Autism spectrum

Autism spectrum, also known as autism spectrum disorder (ASD), is a range of mental disorders of the neurodevelopmental type. It includes autism and Asperger syndrome. Individuals on the autistic spectrum often experience difficulties with social communication and interaction and restricted, repetitive patterns of behavior, interests, or activities. Symptoms are typically recognized between one and two years of age.[2] Long-term problems may include difficulties in performing daily tasks, creating and keeping relationships, and maintaining a job.[9]

Autism spectrum
Other namesAutism spectrum disorder, autistic spectrum disorder (ASD), autism spectrum condition, autistic spectrum condition (ASC)[1]
Repetitively stacking or lining up objects is associated with autism.
SpecialtyPsychiatry
SymptomsProblems with communication, social interaction, restricted interests, repetitive behavior[2]
ComplicationsSocial isolation, employment problems, family stress, bullying[3]
Usual onsetBy the age of 3 years[4]
DurationLifelong[5]
CausesUncertain[5]
Risk factorsAdvanced parental age, exposure to valproate during pregnancy, low birth weight[2]
Diagnostic methodBased on symptoms[5]
Differential diagnosisIntellectual disability, Rett syndrome, ADHD, selective mutism, childhood-onset schizophrenia[2]
TreatmentBehavioral therapy,[6] psychotropic medication[7]
Frequency1% of people[2] (62.2 million 2015)[8]

The cause of autism spectrum is uncertain.[5] Risk factors include having an older parent, a family history of autism, and certain genetic conditions.[5] It is estimated that between 64% and 91% of risk is due to family history.[10] Diagnosis is based on symptoms.[5] The DSM-5 redefined the autism spectrum disorders to encompass the previous diagnoses of autism, Asperger syndrome, pervasive developmental disorder not otherwise specified (PDD-NOS), and childhood disintegrative disorder.[11]

Treatment efforts are generally individualized, and can include behavioural therapy and the teaching of coping skills.[5] Medications may be used to try to help improve symptoms.[5] Evidence to support the use of medications, however, is not very strong.[7]

Autism spectrum is estimated to affect about 1% of people (62.2 million globally) as of 2015.[2][8] In the United States it is estimated to affect more than 2% of children (about 1.5 million) as of 2016.[12] Males are diagnosed four times more often than females.[9][13] The term "spectrum" can refer to the range of symptoms or their severity, leading some to favor a distinction between severely disabled autistics who cannot speak or look after themselves, and higher functioning autistics.

Classification
Further information: Autism § Classification

In the United States, a revision to autism spectrum disorder (ASD) was presented in the Diagnostic and Statistical Manual of Mental Disorders version 5 (DSM-5), released May 2013.[14] The new diagnosis encompasses previous diagnoses of autistic disorder, Asperger syndrome, childhood disintegrative disorder, and PDD-NOS. Compared with the DSM-IV diagnosis of autistic disorder, the DSM-5 diagnosis of ASD no longer includes communication as a separate criterion, and has merged social interaction and communication into one category.[15] Slightly different diagnostic definitions are used in other countries. For example, the ICD-10 is the most commonly-used diagnostic manual in the UK and European Union.[16] Rather than categorizing these diagnoses, the DSM-5 has adopted a dimensional approach to diagnosing disorders that fall underneath the autism spectrum umbrella. Some have proposed that individuals on the autism spectrum may be better represented as a single diagnostic category. Within this category, the DSM-5 has proposed a framework of differentiating each individual by dimensions of severity, as well as associated features (i.e., known genetic disorders, and intellectual disability).

Another change to the DSM includes collapsing social and communication deficits into one domain. Thus, an individual with an ASD diagnosis will be described in terms of severity of social communication symptoms, severity of fixated or restricted behaviors or interests, hyper- or hyposensitivity to sensory stimuli, and associated features. The restricting of onset age has also been loosened from 3 years of age to "early developmental period", with a note that symptoms may manifest later when social demands exceed capabilities.[17]

Autism forms the core of the autism spectrum disorders. Asperger syndrome is closest to autism in signs and likely causes;[18] unlike autism, people with Asperger syndrome usually have no significant delay in language development, according to the older DSM-IV criteria.[19] PDD-NOS is diagnosed when the criteria are not met for a more specific disorder. Some sources also include Rett syndrome and childhood disintegrative disorder, which share several signs with autism but may have unrelated causes; other sources differentiate them from ASD, but group all of the above conditions into the pervasive developmental disorders.[18][20]

Autism, Asperger syndrome, and PDD-NOS are sometimes called the autistic disorders instead of ASD,[21] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism.[22] Although the older term pervasive developmental disorder and the newer term autism spectrum disorder largely or entirely overlap,[20] the earlier was intended to describe a specific set of diagnostic labels, whereas the latter refers to a postulated spectrum disorder linking various conditions.[23] ASD is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.[22]

Signs and symptoms

Autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, and lead to clinically significant functional impairment.[24] There is also a unique form of autism called autistic savantism, where a child can display outstanding skills in music, art, and numbers with no practice.[25] Because of its relevance to different populations, self-injurious behaviors (SIB) are not considered a core characteristic of the ASD population however approximately 50% of those with ASD take part in some type of SIB (head-banging, self-biting) and are more at risk than other groups with developmental disabilities.[26]

Other characteristics of ASD include restricted and repetitive behaviors (RRBs) which include a large range of specific gestures and acts, it can even include certain behavioral traits as defined in the Diagnostic and Statistic Manual for Mental Disorders.[27]

Asperger syndrome was distinguished from autism in the DSM-IV by the lack of delay or deviance in early language development.[28] Additionally, individuals diagnosed with Asperger syndrome did not have significant cognitive delays.[29] PDD-NOS was considered "subthreshold autism" and "atypical autism" because it was often characterized by milder symptoms of autism or symptoms in only one domain (such as social difficulties).[30] The DSM-5 eliminated the four separate diagnoses: Asperger Syndrome, Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS), Childhood Disintegrative Disorder, and Autistic Disorder and combined them under the diagnosis of Autism Spectrum Disorder.[24]

Behavioral characteristics

Autism spectrum disorders include a wide variety of characteristics. Some of these include behavioral characteristics which widely range from slow development of social and learning skills to difficulties creating connections with other people. They may develop these difficulties of creating connections due to anxiety or depression, which people with autism are more likely to experience, and as a result isolate themselves.[31] Other behavioral characteristics include abnormal responses to sensations including sights, sounds, touch, and smell, and problems keeping a consistent speech rhythm. The latter problem influences an individual's social skills, leading to potential problems in how they are understood by communication partners. Behavioral characteristics displayed by those with autism spectrum disorder typically influence development, language, and social competence. Behavioral characteristics of those with autism spectrum disorder can be observed as perceptual disturbances, disturbances of development rate, relating, speech and language, and motility.[32]

Developmental course

Autism spectrum disorders are thought to follow two possible developmental courses, although most parents report that symptom onset occurred within the first year of life.[33][34] One course of development is more gradual in nature, in which parents report concerns in development over the first two years of life and diagnosis is made around 3–4 years of age. Some of the early signs of ASDs in this course include decreased looking at faces, failure to turn when name is called, failure to show interests by showing or pointing, and delayed imaginative play.[35]

A second course of development is characterized by normal or near-normal development in the first 15 months to 3 years before onset of regression or loss of skills. Regression may occur in a variety of domains, including communication, social, cognitive, and self-help skills; however, the most common regression is loss of language.[36][37]

There continues to be a debate over the differential outcomes based on these two developmental courses. Some studies suggest that regression is associated with poorer outcomes and others report no differences between those with early gradual onset and those who experience a regression period.[38] While there is conflicting evidence surrounding language outcomes in ASD, some studies have shown that cognitive and language abilities at age ​2 1⁄2 may help predict language proficiency and production after age 5.[39] Overall, the literature stresses the importance of early intervention in achieving positive longitudinal outcomes.[40]

Social skills

Social skills present the most challenges for individuals with ASD. This leads to problems with friendships, romantic relationships, daily living, and vocational success.[41] Marriages are less common for those with ASD. Many of these challenges are linked to their atypical patterns of behavior and communication. It is common for children and adults with autism to struggle with social interactions because they are unable to relate to their peers.[42] All of these issues stem from cognitive impairments. Difficulty in this thought process is called "theory of the mind" or mind blindness which means that the mind has difficulty with thought process as well as being aware of what is going on around them.[43] Theory of mind is closely related to the pragmatic difficulties children with autism experience.[44]

Communication skills

Communication deficits are generally characterized by impairments regarding joint attention and social reciprocity, challenges with verbal language cues, and poor nonverbal communication skills [45] such as lack of eye contact and meaningful gestures and facial expressions.[46] Language behaviors typically seen in children with autism may include repetitive or rigid language, specific interests in conversation, and atypical language development.[46] ASD is a complex pragmatic language disorder which influences communication skills significantly.[47] Many children with ASD develop language skills at an uneven pace where they easily acquire some aspects of communication, while never fully developing other aspects.[46] In some cases, individuals remain completely nonverbal throughout their lives, although the accompanying levels of literacy and nonverbal communication skills vary.

They may not pick up on body language or social cues such as eye contact and facial expressions if they provide more information than the person can process at that time. Similarly, they have trouble recognizing subtle expressions of emotion and identifying what various emotions mean for the conversation. They struggle with understanding the context and subtext of conversational or printed situations, and have trouble forming resulting conclusions about the content. This also results in a lack of social awareness and atypical language expression.[48]

It is also common for individuals with ASD to communicate strong interest in a specific topic, speaking in lesson-like monologues about their passion instead of enabling reciprocal communication with whomever they are speaking to.[46] What looks like self-involvement or indifference toward others stems from a struggle to recognize or remember that other people have their own personalities, perspectives, and interests.[48] The ability to be focused in on one topic in communication is known as monotropism, and can be compared to "tunnel vision" in the mind for those individuals with ASD.[49] Language expression by those on the autism spectrum is often characterized by repetitive and rigid language. Often children with ASD repeat certain words, numbers, or phrases during an interaction, words unrelated to the topic of conversation. They can also exhibit a condition called echolalia in which they respond to a question by repeating the inquiry instead of answering.[46] However, this repetition can be a form of meaningful communication, a way that individuals with ASD try to express a lack of understanding or knowledge regarding the answer to the question.[50]

Causes
Main article: Causes of autism

While specific causes of autism spectrum disorders have yet to be found, many risk factors identified in the research literature may contribute to their development. These risk factors include genetics, prenatal and perinatal factors, neuroanatomical abnormalities, and environmental factors. It is possible to identify general risk factors, but much more difficult to pinpoint specific factors. Given the current state of knowledge, prediction can only be of a global nature and therefore requires the use of general markers.[51]

Genetic risk factors

As of 2018, understanding of genetic risk factors had shifted from a focus on a few alleles, to an understanding that genetic involvement in ASD is probably diffuse, depending on a large number of variants, some of which are common and have a small effect, and some of which are rare and have a large effect. The most common gene disrupted with large effect rare variants appeared to be CHD8, but less than 0.5% of people with ASD have such a mutation. Some ASD is associated with clearly genetic conditions, like fragile X syndrome; however only around 2% of people with ASD have fragile X.[52]

As of 2018, it appeared that somewhere between 74% and 93% of ASD risk is heritable and that after an older child is diagnosed with ASD, 7–20% of subsequent children are likely to be as well.[52] If parents have a child with ASD they have a 2% to 8% chance of having a second child with ASD. If the child with ASD is an identical twin the other will be affected 36 to 95 percent of the time. If they are fraternal twins the other will only be affected up to 31 percent of the time.[53]

Some of the alterations that contribute to the development of the autistic spectrum: SNVs (single-nucleotide variations), indels (insertions-deletions) and SVs (structural variants). These associations have been identified through whole-genome studies, such as WGS (whole-genome sequencing) and GWAS (genome-wide analysis association studies).

In early onset disorders, such as autism, de novo mutations have been identified as risk factors. One study has identified 64 SNVs and 5 indels de novo on average. By performing an analysis of these variants, comparing cases and controls, considering SNVs and indels in 179 genes associated with autism or close to them, studies observed that the relative risk of missense mutations or variants in promoter regions and UTR (untranslated region), increases versus controls.

The identification of SVs has been very useful too, since structural alterations in the chromosomes are able to rearrange the genome, altering its functionality, depending on the size and the region they affect.

After the analysis, 98,785 SVs were identified, with an average of 5,843 variants per individual: 171 SVs were de novo, more frequent in the germ line. Some of these variants affected genes associated with autism, such as the GRIN2B gene, balanced translocation, or the deletion of exons 8, 9, and 10 of the CHD2 gene.

No significant differences were observed regarding the size of certain rearrangements in cases and controls, though a slight increase in number was observed for cases relative to controls.

All these genetic variants contribute to the development of the autistic spectrum, however, it can not be guaranteed that they are determinants for the development.[54]

Prenatal and perinatal risk factors

Several prenatal and perinatal complications have been reported as possible risk factors for autism. These risk factors include maternal gestational diabetes, maternal and paternal age over 30, bleeding after first trimester, use of prescription medication (e.g. valproate) during pregnancy, and meconium in the amniotic fluid. While research is not conclusive on the relation of these factors to autism, each of these factors has been identified more frequently in children with autism, compared to their siblings who do not have autism, and other typically developing youth.[55] While it is unclear if any single factors during the prenatal phase affect the risk of autism,[56] complications during pregnancy may be a risk.[56]

Low vitamin D levels in early development has been hypothesized as a risk factor for autism.[57]

Disproven vaccine hypothesis
Main article: MMR vaccine and autism

In 1998 Andrew Wakefield led a fraudulent study that suggested that the MMR vaccine may cause autism.[58][59][60][61][62] This conjecture suggested that autism results from brain damage caused either by the MMR vaccine itself, or by thimerosal, a vaccine preservative.[63] No convincing scientific evidence supports these claims, and further evidence continues to refute them, including the observation that the rate of autism continues to climb despite elimination of thimerosal from routine childhood vaccines.[64] A 2014 meta-analysis examined ten major studies on autism and vaccines involving 1.25 million children worldwide; it concluded that neither the MMR vaccine, which has never contained thimerosal,[65] nor the vaccine components thimerosal or mercury, lead to the development of ASDs.[66]

Pathophysiology
Main article: Autism § Mechanism

In general, neuroanatomical studies support the concept that autism may involve a combination of brain enlargement in some areas and reduction in others.[67] These studies suggest that autism may be caused by abnormal neuronal growth and pruning during the early stages of prenatal and postnatal brain development, leaving some areas of the brain with too many neurons and other areas with too few neurons.[68] Some research has reported an overall brain enlargement in autism, while others suggest abnormalities in several areas of the brain, including the frontal lobe, the mirror neuron system, the limbic system, the temporal lobe, and the corpus callosum.[69][70]

In functional neuroimaging studies, when performing theory of mind and facial emotion response tasks, the median person on the autism spectrum exhibits less activation in the primary and secondary somatosensory cortices of the brain than the median member of a properly sampled control population. This finding coincides with reports demonstrating abnormal patterns of cortical thickness and grey matter volume in those regions of autistic persons' brains.[71]

Mirror neuron system
Further information: Mirror neuron § Autism

The mirror neuron system (MNS) consists of a network of brain areas that have been associated with empathy processes in humans.[72] In humans, the MNS has been identified in the inferior frontal gyrus (IFG) and the inferior parietal lobule (IPL) and is thought to be activated during imitation or observation of behaviors.[73] The connection between mirror neuron dysfunction and autism is tentative, and it remains to be seen how mirror neurons may be related to many of the important characteristics of autism.[74][75]

"Social brain" interconnectivity

A number of discrete brain regions and networks among regions that are involved in dealing with other people have been discussed together under the rubric of the "social brain". As of 2012, there was a consensus that autism spectrum is likely related to problems with interconnectivity among these regions and networks, rather than problems with any specific region or network.[76]

Temporal lobe

Functions of the temporal lobe are related to many of the deficits observed in individuals with ASDs, such as receptive language, social cognition, joint attention, action observation, and empathy. The temporal lobe also contains the superior temporal sulcus (STS) and the fusiform face area (FFA), which may mediate facial processing. It has been argued that dysfunction in the STS underlies the social deficits that characterize autism. Compared to typically developing individuals, one fMRI study found that individuals with high-functioning autism had reduced activity in the FFA when viewing pictures of faces.[77]

Mitochondrial dysfunction

It has been suggested that ASD could be linked to mitochondrial disease (MD), a basic cellular abnormality with the potential to cause disturbances in a wide range of body systems.[78] A recent meta-analysis study, as well as other population studies have shown that approximately 5% of children with ASD meet the criteria for classical MD.[79] It is unclear why the MD occurs considering that only 23% of children with both ASD and MD present with mitochondrial DNA (mtDNA) abnormalities.[79]

Serotonin

It has been hypothesized that increased activity of serotonin in the developing brain may facilitate the onset of autism spectrum disorder, with an association found in six out of eight studies between the use of selective serotonin reuptake inhibitors (SSRIs) by the pregnant mother and the development of ASD by the child exposed to SSRI in the antenatal environment. The study could not definitively conclude SSRIs caused the increased risk for ASDs due to the biases found in those studies, and the authors called for more definitive, better conducted studies.[80]

Diagnosis

Evidence-based assessment

ASD can be detected as early as 18 months or even younger in some cases.[81] A reliable diagnosis can usually be made by the age of two years.[82] The diverse expressions of ASD symptoms pose diagnostic challenges to clinicians. Individuals with an ASD may present at various times of development (e.g., toddler, child, or adolescent), and symptom expression may vary over the course of development.[83] Furthermore, clinicians must differentiate among pervasive developmental disorders, and may also consider similar conditions, including intellectual disability not associated with a pervasive developmental disorder, specific language disorders, ADHD, anxiety, and psychotic disorders.[84]

Considering the unique challenges in diagnosing ASD, specific practice parameters for its assessment have been published by the American Academy of Neurology,[85] the American Academy of Child and Adolescent Psychiatry,[83] and a consensus panel with representation from various professional societies.[86] The practice parameters outlined by these societies include an initial screening of children by general practitioners (i.e., "Level 1 screening") and for children who fail the initial screening, a comprehensive diagnostic assessment by experienced clinicians (i.e. "Level 2 evaluation"). Furthermore, it has been suggested that assessments of children with suspected ASD be evaluated within a developmental framework, include multiple informants (e.g., parents and teachers) from diverse contexts (e.g., home and school), and employ a multidisciplinary team of professionals (e.g., clinical psychologists, neuropsychologists, and psychiatrists).[87]

After a child shows initial evidence of ASD tendencies, psychologists administer various psychological assessment tools to assess for ASD.[87] Among these measurements, the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) are considered the "gold standards" for assessing autistic children.[88][89] The ADI-R is a semi-structured parent interview that probes for symptoms of autism by evaluating a child's current behavior and developmental history. The ADOS is a semistructured interactive evaluation of ASD symptoms that is used to measure social and communication abilities by eliciting several opportunities (or "presses") for spontaneous behaviors (e.g., eye contact) in standardized context. Various other questionnaires (e.g., The Childhood Autism Rating Scale, Autism Treatment Evaluation Checklist) and tests of cognitive functioning (e.g., The Peabody Picture Vocabulary Test) are typically included in an ASD assessment battery.

In the UK, there is some diagnostic use of the Diagnostic Interview for Social and Communication Disorders (DISCO)[90] which was developed for use at The Centre for Social and Communication Disorders, by Lorna Wing and Judith Gould, as both a clinical and a research instrument for use with children and adults of any age. The DISCO is designed to elicit a picture of the whole person through the story of their development and behavior. In clinical work, the primary purpose is to facilitate understanding of the pattern over time of the specific skills and impairments that underlie the overt behavior. If no information is available, the clinician has to obtain as much information as possible concerning the details of current skills and pattern of behavior of the person. This type of dimensional approach to clinical description is useful for prescribing treatment.[91]

Comorbidity
Main article: Conditions comorbid to autism spectrum disorders

Autism spectrum disorders tend to be highly comorbid with other disorders. Comorbidity may increase with age and may worsen the course of youth with ASDs and make intervention/treatment more difficult. Distinguishing between ASDs and other diagnoses can be challenging, because the traits of ASDs often overlap with symptoms of other disorders, and the characteristics of ASDs make traditional diagnostic procedures difficult.[92][93]

  • The most common medical condition occurring in individuals with autism spectrum disorders is seizure disorder or epilepsy, which occurs in 11–39% of individuals with ASD.[94]
  • Tuberous sclerosis, an autosomal dominant genetic condition in which non-malignant tumors grow in the brain and on other vital organs, is present in 1–4% of individuals with ASDs.[95]
  • Intellectual disabilities are some of the most common comorbid disorders with ASDs. Recent estimates suggest that 40–69% of individuals with ASD have some degree of an intellectual disability,[38] more likely to be severe for females. A number of genetic syndromes causing intellectual disability may also be comorbid with ASD, including fragile X, Down, Prader-Willi, Angelman, and Williams syndrome.[96]
  • Learning disabilities are also highly comorbid in individuals with an ASD. Approximately 25–75% of individuals with an ASD also have some degree of a learning disability.[97]
  • Various anxiety disorders tend to co-occur with autism spectrum disorders, with overall comorbidity rates of 7–84%.[38] Rates of comorbid depression in individuals with an ASD range from 4–58%.[98] The relationship between ASD and schizophrenia remains a controversial subject under continued investigation, and recent meta-analyses have examined genetic, environmental, infectious, and immune risk factors that may be shared between the two conditions.[99][100][101]
  • Deficits in ASD are often linked to behavior problems, such as difficulties following directions, being cooperative, and doing things on other people's terms.[102] Symptoms similar to those of attention deficit hyperactivity disorder (ADHD) can be part of an ASD diagnosis.[103]
  • Sensory processing disorder is also comorbid with ASD, with comorbidity rates of 42–88%.[104]
  • Starting in adolescence, some people with Asperger syndrome (26% in one sample)[105] fall under the criteria for the similar condition schizoid personality disorder, which is characterised by a lack of interest in social relationships, a tendency towards a solitary or sheltered lifestyle, secretiveness, emotional coldness, detachment and apathy.[105][106][107] Asperger syndrome was traditionally called "schizoid disorder of childhood".

Treatment
Main article: Autism therapies

There is no known cure for autism, although those with Asperger syndrome and those who have autism and require little-to-no support are more likely to experience a lessening of symptoms over time.[108][109][110] Several interventions can help children with Autism.[13] The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes.[111][112] Although evidence-based interventions for autistic children vary in their methods, many adopt a psychoeducational approach to enhancing cognitive, communication, and social skills while minimizing problem behaviors. It has been argued that no single treatment is best and treatment is typically tailored to the child's needs.[113]

Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills. Available approaches include applied behavior analysis, developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.[113] Among these approaches, interventions either treat autistic features comprehensively, or focus treatment on a specific area of deficit.[112] Generally, when educating those with autism, specific tactics may be used to effectively relay information to these individuals. Using as much social interaction as possible is key in targeting the inhibition autistic individuals experience concerning person-to-person contact. Additionally, research has shown that employing semantic groupings, which involves assigning words to typical conceptual categories, can be beneficial in fostering learning.[114]

There has been increasing attention to the development of evidence-based interventions for young children with ASD. Two theoretical frameworks outlined for early childhood intervention include applied behavioral analysis (ABA) and the developmental social-pragmatic model (DSP).[112] Although ABA therapy has a strong evidence base, particularly in regard to early intensive home-based therapy, ABA's effectiveness may be limited by diagnostic severity and IQ of the person affected by ASD.[115] The Journal of Clinical Child and Adolescent Psychology has deemed two early childhood interventions as "well-established": individual comprehensive ABA, and focused teacher-implemented ABA combined with DSP.[112]

Another evidence-based intervention that has demonstrated efficacy is a parent training model, which teaches parents how to implement various ABA and DSP techniques themselves.[112] Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation.

A multitude of unresearched alternative therapies have also been implemented. Many have resulted in harm to autistic people and should not be employed unless proven to be safe.[113]

In October 2015, the American Academy of Pediatrics (AAP) proposed new evidence-based recommendations for early interventions in ASD for children under 3.[116] These recommendations emphasize early involvement with both developmental and behavioral methods, support by and for parents and caregivers, and a focus on both the core and associated symptoms of ASD.[116] Studies on pet therapy have shown positive effects.[117]

Epidemiology
Main article: Epidemiology of autism

The U.S. Center for Disease Control's most recent estimate is that 1 out of every 68 children, or 14.7 per 1,000, are affected by some form of ASD as of 2010.[118] Reviews tend to estimate a prevalence of 6 per 1,000 for autism spectrum disorders as a whole,[119] although prevalence rates vary for each of the developmental disorders in the spectrum. Autism prevalence has been estimated at 1-2 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, childhood disintegrative disorder at 0.02 per 1,000, and PDD-NOS at 3.7 per 1,000.[119] These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder.[38]

While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1,[120] affecting 1 in 70 boys, but only 1 in 315 girls.[121] Girls, however, are more likely to have associated cognitive impairment. Among those with an ASD and intellectual disability, the sex ratio may be closer to 2:1.[122] Prevalence differences may be a result of gender differences in expression of clinical symptoms, with women and girls with autism showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.[123]

History
Further information: Autism § History

Controversies have surrounded various claims regarding the etiology of autism spectrum disorders. In the 1950s, the "refrigerator mother theory" emerged as an explanation for autism. The hypothesis was based on the idea that autistic behaviors stem from the emotional frigidity, lack of warmth, and cold, distant, rejecting demeanor of a child's mother.[124] Naturally, parents of children with an autism spectrum disorder suffered from blame, guilt, and self-doubt, especially as the theory was embraced by the medical establishment and went largely unchallenged into the mid-1960s. The "refrigerator mother" theory has since continued to be refuted in scientific literature, including a 2015 systematic review which showed no association between caregiver interaction and language outcomes in ASD.[125]

Another controversial claim suggests that watching extensive amounts of television may cause autism. This hypothesis was largely based on research suggesting that the increasing rates of autism in the 1970s and 1980s were linked to the growth of cable television at this time.[64]

Society and culture

Caregivers

Families who care for an autistic child face added stress from a number of different causes. Parents may struggle to understand the diagnosis and to find appropriate care options. Parents often take a negative view of the diagnosis, and may struggle emotionally. In the words of one parent whose two children were both diagnosed with autism, "In the moment of diagnosis, it feels like the death of your hopes and dreams."[126] More than half of parents over the age of 50 are still living with their child as about 85% of people with ASD have difficulties living independently.[127]

Autism rights movement

The autism rights movement is a social movement within the context of disability rights that emphasizes the concept of neurodiversity, viewing the autism spectrum as a result of natural variations in the human brain rather than a disorder to be cured.[128] The autism rights movement advocates for including greater acceptance of autistic behaviors; therapies that focus on coping skills rather than imitating the behaviors of those without autism;[129] and the recognition of the autistic community as a minority group.[129][130] Autism rights or neurodiversity advocates believe that the autism spectrum is genetic and should be accepted as a natural expression of the human genome. This perspective is distinct from two other likewise distinct views: the medical perspective, that autism is caused by a genetic defect and should be addressed by targeting the autism gene(s), and fringe theories that autism is caused by environmental factors such as vaccines.[128] A common criticism against autistic activists is that the majority of them are "high-functioning" or have Asperger syndrome and do not represent the views of "low-functioning" autistic people.[130]

Academic performance

The number of students identified and served as eligible for autism services in the United States has increased from 5,413 children in 1991-1992 to 370,011 children in the 2010-2011 academic school year.[131] The United States Department of Health and Human Services reported approximately 1 in 68 children at age 8 are diagnosed with autism spectrum disorder (ASD) although onset is typically between ages 2 and 4.[131]

The increasing number of students with ASD in the schools presents significant challenges to teachers, school psychologists, and other school professionals.[131] These challenges include developing a consistent practice that best support the social and cognitive development of the increasing number of students with ASD.[131] Although there is considerable research addressing assessment, identification, and support services for children with ASD, there is a need for further research focused on these topics within the school context.[131] Further research on appropriate support services for students with ASD will provide school psychologists and other education professionals with specific directions for advocacy and service delivery that aim to enhance school outcomes for students with ASD.[131]

Attempts to identify and use best intervention practices for students with autism also pose a challenge due to overdependence on popular or well-known interventions and curricula.[131] Some evidence suggests that although these interventions work for some students, there remains a lack of specificity for which type of student, under what environmental conditions (one-on-one, specialized instruction or general education) and for which targeted deficits they work best.[131] More research is needed to identify what assessment methods are most effective for identifying the level of educational needs for students with ASD.

A difficulty for academic performance in students with ASD, is the tendency to generalize learning.[49] Learning is different for each student, which is the same for students with ASD. To assist in learning, accommodations are commonly put into place for students with differing abilities. The existing schema of these students works in different ways and can be adjusted to best support the educational development for each student.[132]

The cost of educating a student with ASD in the US is about $8,600 a year.[133]

Employment

About half of people with autism are unemployed, and one third of those with graduate degrees may be unemployed.[134] Among those on the autism spectrum who find work, most are employed in sheltered settings working for wages below the national minimum.[135] While employers state hiring concerns about productivity and supervision, experienced employers of autistics give positive reports of above average memory and detail orientation as well as a high regard for rules and procedure in autistic employees.[134] A majority of the economic burden of autism is caused by lost productivity in the job market.[136] Some studies also find decreased earning among parents who care for autistic children.[137][138] Adding content related to autism in existing diversity training can clarify misconceptions, support employees, and help provide new opportunities for autistics.

References
  1. Baron-Cohen S, Scott FJ, Allison C, Williams J, Bolton P, Matthews FE, Brayne C (June 2009). "Prevalence of autism-spectrum conditions: UK school-based population study". The British Journal of Psychiatry. 194 (6): 500–9. doi:10.1192/bjp.bp.108.059345. PMID 19478287. We favour use of the term 'autism-spectrum condition' rather than 'autism-spectrum disorder' as it is less stigmatising, and it reflects that these individuals have not only disabilities which require a medical diagnosis, but also areas of cognitive strength
  2. American Psychiatric Association (2013). "Autism Spectrum Disorder. 299.00 (F84.0)". Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Arlington, VA: American Psychiatric Publishing. pp. 50–59. doi:10.1176/appi.books.9780890425596. ISBN 978-0-89042-559-6.
  3. "Autism spectrum disorder - Symptoms and causes". Mayo Clinic. Retrieved 13 July 2019.
  4. "F84.0 Childhood autism" (PDF). The ICD-10 Classification of Mental and Behavioural Disorders – Clinical descriptions and diagnostic guidelines. Geneva: World Health Organization. p. 198.
  5. "Autism Spectrum Disorder". NIMH. October 2016. Retrieved 22 January 2018.
  6. Case-Smith J, Arbesman M (2008). "Evidence-based review of interventions for autism used in or of relevance to occupational therapy". The American Journal of Occupational Therapy. 62 (4): 416–29. doi:10.5014/ajot.62.4.416. PMID 18712004.
  7. Accordino RE, Kidd C, Politte LC, Henry CA, McDougle CJ (2016). "Psychopharmacological interventions in autism spectrum disorder". Expert Opinion on Pharmacotherapy. 17 (7): 937–52. doi:10.1517/14656566.2016.1154536. PMID 26891879.
  8. Vos T, Allen C, Arora M, Barber RM, Bhutta ZA, Brown A, et al. (GBD 2015 Disease and Injury Incidence and Prevalence Collaborators) (October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
  9. Comer RJ (2016). Fundamentals of Abnormal Psychology. New York: Worth /Macmillan Learning. p. 457.
  10. Tick B, Bolton P, Happé F, Rutter M, Rijsdijk F (May 2016). "Heritability of autism spectrum disorders: a meta-analysis of twin studies". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 57 (5): 585–95. doi:10.1111/jcpp.12499. PMC 4996332. PMID 26709141.
  11. "Autism spectrum disorder fact sheet" (PDF). DSM5.org. American Psychiatric Publishing. 2013. Archived from the original (PDF) on 6 October 2013. Retrieved 13 October 2013.
  12. "HRSA-led study estimates 1 in 40 U.S. children has diagnosed autism". www.hrsa.gov. 19 November 2018. Retrieved 17 October 2019.
  13. "10 Facts about Autism Spectrum Disorder (ASD)". Early Childhood Development | ACF. Retrieved 6 November 2019.
  14. "Home | APA DSM-5". Dsm5.org. Archived from the original on 19 November 2008. Retrieved 21 February 2012.
  15. Kulage KM, Smaldone AM, Cohn EG (August 2014). "How will DSM-5 affect autism diagnosis? A systematic literature review and meta-analysis". Journal of Autism and Developmental Disorders. 44 (8): 1918–32. doi:10.1007/s10803-014-2065-2. PMID 24531932.
  16. "Profiles and criteria - NAS". www.autism.org.uk.
  17. "DSM-5 Diagnostic Criteria". U.S. Department of Health & Human Services Interagency Autism Coordinating Committee. Retrieved 17 May 2017.
  18. Lord C, Cook EH, Leventhal BL, Amaral DG (November 2000). "Autism spectrum disorders". Neuron. 28 (2): 355–63. doi:10.1016/S0896-6273(00)00115-X. PMID 11144346.
  19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed., text revision (DSM-IV-TR). 2000. ISBN 0890420254. Diagnostic criteria for 299.80 Asperger's Disorder (AD).
  20. National Institute of Mental Health. Autism spectrum disorders (pervasive developmental disorders); 2009 [archived 29 April 2009].
  21. Freitag CM (January 2007). "The genetics of autistic disorders and its clinical relevance: a review of the literature". Molecular Psychiatry. 12 (1): 2–22. doi:10.1038/sj.mp.4001896. PMID 17033636.
  22. Piven J, Palmer P, Jacobi D, Childress D, Arndt S (February 1997). "Broader autism phenotype: evidence from a family history study of multiple-incidence autism families". The American Journal of Psychiatry. 154 (2): 185–90. doi:10.1176/ajp.154.2.185. PMID 9016266.
  23. Klin A (May 2006). "[Autism and Asperger syndrome: an overview]". Revista Brasileira de Psiquiatria. 28 Suppl 1 (suppl 1): S3–11. doi:10.1590/S1516-44462006000500002. PMID 16791390.
  24. American Psychiatric Association, ed. (2013). "Autism Spectrum Disorder, 299.00 (F84.0)". Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Publishing. pp. 50–59.
  25. Weintraub AG. "Autism: Topic Overview". National Institute of Health. U.S. Food and Drug Administration. CDC. 12 May 2013.
  26. Minshawi NF, Hurwitz S, Fodstad JC, Biebl S, Morriss DH, McDougle CJ (April 2014). "The association between self-injurious behaviors and autism spectrum disorders". Psychology Research and Behavior Management. 7: 125–36. doi:10.2147/PRBM.S44635. PMC 3990505. PMID 24748827.
  27. Richler J, Huerta M, Bishop SL, Lord C (1 January 2010). "Developmental trajectories of restricted and repetitive behaviors and interests in children with autism spectrum disorders". Development and Psychopathology. 22 (1): 55–69. doi:10.1017/S0954579409990265. PMC 2893549. PMID 20102647.
  28. Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.). Washington, D.C.: American Psychiatric Association. 2000.
  29. "NINDS Asperger Syndrome Information Page". National Institute of Neurological Disorders and Stroke.
  30. Mesibov GB (1997). "Ask the Editor: What is PDD-NOS and how is it diagnosed?". Journal of Autism and Developmental Disorders. 27 (4).
  31. "Media release: Autism Spectrum Australia". Autism Spectrum Australia. 7 October 2013. ProQuest 1439836954. Missing or empty |url= (help)
  32. Shaughnessy Hinerman P (1983). Teaching Autistic Children to Communicate. Rockville, Maryland: Aspens System Corporation. p. 180. ISBN 978-0-89443-884-4.
  33. Zwaigenbaum L, Bryson S, Lord C, Rogers S, Carter A, Carver L, et al. (May 2009). "Clinical assessment and management of toddlers with suspected autism spectrum disorder: insights from studies of high-risk infants". Pediatrics. 123 (5): 1383–91. doi:10.1542/peds.2008-1606. PMC 2833286. PMID 19403506.
  34. Lord C (November 1995). "Follow-up of two-year-olds referred for possible autism". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 36 (8): 1365–82. doi:10.1111/j.1469-7610.1995.tb01669.x. PMID 8988272.
  35. Zwaigenbaum L (October 2001). "Autistic spectrum disorders in preschool children". Canadian Family Physician. 47 (10): 2037–42. PMC 2018435. PMID 11723598.
  36. Martínez-Pedraza F, Carter AS (July 2009). "Autism spectrum disorders in young children". Child and Adolescent Psychiatric Clinics of North America. 18 (3): 645–63. doi:10.1016/j.chc.2009.02.002. PMC 3166636. PMID 19486843.
  37. Werner E, Dawson G, Munson J, Osterling J (June 2005). "Variation in early developmental course in autism and its relation with behavioral outcome at 3-4 years of age". Journal of Autism and Developmental Disorders. 35 (3): 337–50. doi:10.1007/s10803-005-3301-6. PMID 16119475.
  38. Mash EJ, Barkley RA (2003). Child Psychopathology. New York: The Guilford Press. pp. 409–454.
  39. Ellis Weismer S, Kover ST (December 2015). "Preschool language variation, growth, and predictors in children on the autism spectrum". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 56 (12): 1327–37. doi:10.1111/jcpp.12406. PMC 4565784. PMID 25753577.
  40. Dawson & Osterling (1997). The effectiveness of early intervention. Baltimore: Brookes. pp. 307–326.
  41. Barnhill GP (2007). "Outcomes in adults with Asperger syndrome". Focus on Autism and Other Developmental Disabilities. 22 (2): 116–126. doi:10.1177/10883576070220020301.
  42. Davis MA, Spriggs A, Rodgers A, Campbell J (June 2018). "The Effects of a Peer-Delivered Social Skills Intervention for Adults with Comorbid Down Syndrome and Autism Spectrum Disorder". Journal of Autism and Developmental Disorders. 48 (6): 1869–1885. doi:10.1007/s10803-017-3437-1. PMID 29274009.
  43. O'Brien T (2013). The Early Identification of Autism Spectrum Disorders : A Visual Guide. London: Jessica Kingsley Publishers.
  44. Bottema-Beutel K, Lloyd B, Watson L, Yoder P (May 2018). "Bidirectional influences of caregiver utterances and supported joint engagement in children with and without autism spectrum disorder". Autism Research. 11 (5): 755–765. doi:10.1002/aur.1928. PMC 5991996. PMID 29356414.
  45. "Autism: Overview". American Speech-Language-Hearing Association. Retrieved 17 December 2017.
  46. "Autism Spectrum Disorder: Communication Problems in Children". NIDCD. 18 August 2015. Retrieved 17 December 2017.
  47. Kasper G, Ross SJ (2013), Assessing Second Language Pragmatics, Palgrave Macmillan, doi:10.1057/9781137003522.0007, ISBN 9781137003522
  48. Vicker B. "Social communication and language characteristics associated with high-functioning, verbal children and adults with autism spectrum disorder". Indiana Resource Center for Autism. Retrieved 17 December 2017.
  49. Lawson W (2001). Understanding and Working With the Spectrum of Autism An Insider's View. Philadelphia, PA: Jessica Kingsley Publishers London and Philadelphia. p. 33. ISBN 978-1853029714.
  50. "Communicating".
  51. Tager-Flusberg H (2010). "The origins of social impairments in autism spectrum disorder: studies of infants at risk". Neural Networks. 23 (8–9): 1072–6. doi:10.1016/j.neunet.2010.07.008. PMC 2956843. PMID 20800990.
  52. Lord C, Elsabbagh M, Baird G, Veenstra-Vanderweele J (August 2018). "Autism spectrum disorder". Lancet. 392 (10146): 508–520. doi:10.1016/S0140-6736(18)31129-2. PMID 30078460.
  53. CDC (26 February 2015). "Signs & Symptoms - Autism Spectrum Disorder (ASD) - NCBDDD - CDC". Centers for Disease Control and Prevention.
  54. Werling DM, Brand H, An JY, Stone MR, Zhu L, Glessner JT, et al. (May 2018). "An analytical framework for whole-genome sequence association studies and its implications for autism spectrum disorder". Nature Genetics. 50 (5): 727–736. doi:10.1038/s41588-018-0107-y. PMC 5961723. PMID 29700473.
  55. Gardener H, Spiegelman D, Buka SL (August 2011). "Perinatal and neonatal risk factors for autism: a comprehensive meta-analysis". Pediatrics. 128 (2): 344–55. doi:10.1542/peds.2010-1036. PMC 3387855. PMID 21746727.
  56. Gardener H, Spiegelman D, Buka SL (July 2009). "Prenatal risk factors for autism: comprehensive meta-analysis". The British Journal of Psychiatry. 195 (1): 7–14. doi:10.1192/bjp.bp.108.051672. PMC 3712619. PMID 19567888.
  57. Mazahery H, Camargo CA, Conlon C, Beck KL, Kruger MC, von Hurst PR (April 2016). "Vitamin D and Autism Spectrum Disorder: A Literature Review". Nutrients. 8 (4): 236. doi:10.3390/nu8040236. PMC 4848704. PMID 27110819.
  58. Deer B (8 February 2009). "MMR doctor Andrew Wakefield fixed data on autism". The Sunday Times.
  59. Boseley S (2 February 2010). "Lancet retracts 'utterly false' MMR paper". The Guardian – via www.theguardian.com.
  60. Medicine, Institute of; Practice, Board on Population Health Public Health; Vaccines, Committee to Review Adverse Effects of; Ford, A.; Rusch, E.; Clayton, E. W. (2012). Read "Adverse Effects of Vaccines: Evidence and Causality" at NAP.edu. doi:10.17226/13164. ISBN 978-0-309-21435-3. PMID 24624471.
  61. Flaherty DK (October 2011). "The vaccine-autism connection: a public health crisis caused by unethical medical practices and fraudulent science". The Annals of Pharmacotherapy. 45 (10): 1302–4. doi:10.1345/aph.1Q318. PMID 21917556.
  62. Godlee F, Smith J, Marcovitch H (January 2011). "Wakefield's article linking MMR vaccine and autism was fraudulent". BMJ. 342: c7452. doi:10.1136/bmj.c7452. PMID 21209060.
  63. Tan M, Parkin JE (November 2000). "Route of decomposition of thiomersal (thimerosal)". International Journal of Pharmaceutics. 208 (1–2): 23–34. doi:10.1016/S0378-5173(00)00514-7. PMID 11064208.
  64. Waterhouse L (December 2008). "Autism overflows: increasing prevalence and proliferating theories". Neuropsychology Review. 18 (4): 273–86. doi:10.1007/s11065-008-9074-x. PMID 19015994.
  65. "Frequently Asked Questions about Thimerosal". www.cdc.gov. Centers for Disease Control and Prevention. Retrieved 21 February 2017.
  66. Taylor LE, Swerdfeger AL, Eslick GD (June 2014). "Vaccines are not associated with autism: an evidence-based meta-analysis of case-control and cohort studies". Vaccine. 32 (29): 3623–9. doi:10.1016/j.vaccine.2014.04.085. PMID 24814559. Lay summary – news.com.au.
  67. Koenig K, Tsatsanis KD, Volkmar FR (2001). "Neurobiology and Genetics of Autism : A Developmental Perspective". In Burack JA, Charman T, Yirmiya N, Zelazo PR (eds.). The development of autism: perspectives from theory and research. Mahwah, N.J.: L. Erlbaum. pp. 73–92. ISBN 9780805832457. OCLC 806185029.
  68. Minshew NJ (April 1996). "Brief report: brain mechanisms in autism: functional and structural abnormalities". Journal of Autism and Developmental Disorders. 26 (2): 205–9. doi:10.1007/BF02172013. PMID 8744486.
  69. Stanfield AC, McIntosh AM, Spencer MD, Philip R, Gaur S, Lawrie SM (June 2008). "Towards a neuroanatomy of autism: a systematic review and meta-analysis of structural magnetic resonance imaging studies". European Psychiatry. 23 (4): 289–99. doi:10.1016/j.eurpsy.2007.05.006. PMID 17765485.
  70. Lefebvre A, Beggiato A, Bourgeron T, Toro R (July 2015). "Neuroanatomical Diversity of Corpus Callosum and Brain Volume in Autism: Meta-analysis, Analysis of the Autism Brain Imaging Data Exchange Project, and Simulation". Biological Psychiatry. 78 (2): 126–34. doi:10.1016/j.biopsych.2015.02.010. PMID 25850620.
  71. Sugranyes G, Kyriakopoulos M, Corrigall R, Taylor E, Frangou S (2011). "Autism spectrum disorders and schizophrenia: meta-analysis of the neural correlates of social cognition". PLOS ONE. 6 (10): e25322. Bibcode:2011PLoSO...625322S. doi:10.1371/journal.pone.0025322. PMC 3187762. PMID 21998649.
  72. Fadiga L, Craighero L, Olivier E (April 2005). "Human motor cortex excitability during the perception of others' action". Current Opinion in Neurobiology. 15 (2): 213–8. doi:10.1016/j.conb.2005.03.013. PMID 15831405.
  73. Shamay-Tsoory SG (February 2011). "The neural bases for empathy". The Neuroscientist. 17 (1): 18–24. doi:10.1177/1073858410379268. PMID 21071616.
  74. Dinstein I, Thomas C, Behrmann M, Heeger DJ (January 2008). "A mirror up to nature". Current Biology. 18 (1): R13–8. doi:10.1016/j.cub.2007.11.004. PMC 2517574. PMID 18177704.
  75. Kalat J (2009). Biological Psychology (Tenth ed.). pp. 237–8. ISBN 978-0-495-60300-9.
  76. Kennedy DP, Adolphs R (November 2012). "The social brain in psychiatric and neurological disorders". Trends in Cognitive Sciences. 16 (11): 559–72. doi:10.1016/j.tics.2012.09.006. PMC 3606817. PMID 23047070.
  77. Schultz RT (2005). "Developmental deficits in social perception in autism: the role of the amygdala and fusiform face area". International Journal of Developmental Neuroscience. 23 (2–3): 125–41. doi:10.1016/j.ijdevneu.2004.12.012. PMID 15749240.
  78. Haas RH, Parikh S, Falk MJ, Saneto RP, Wolf NI, Darin N, Cohen BH (December 2007). "Mitochondrial disease: a practical approach for primary care physicians". Pediatrics. 120 (6): 1326–33. doi:10.1542/peds.2007-0391. PMID 18055683.
  79. Rossignol DA, Frye RE (March 2012). "Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis". Molecular Psychiatry. 17 (3): 290–314. doi:10.1038/mp.2010.136. PMC 3285768. PMID 21263444.
  80. Gentile S (August 2015). "Prenatal antidepressant exposure and the risk of autism spectrum disorders in children. Are we looking at the fall of Gods?". Journal of Affective Disorders. 182: 132–7. doi:10.1016/j.jad.2015.04.048. PMID 25985383.
  81. "Autism Spectrum Disorder (ASD): Screening and Diagnosis". Centers for Disease Control and Prevention. 26 February 2015.
  82. Lord C, Risi S, DiLavore PS, Shulman C, Thurm A, Pickles A (June 2006). "Autism from 2 to 9 years of age". Archives of General Psychiatry. 63 (6): 694–701. doi:10.1001/archpsyc.63.6.694. PMID 16754843.
  83. Volkmar F, Cook EH, Pomeroy J, Realmuto G, Tanguay P (December 1999). "Practice parameters for the assessment and treatment of children, adolescents, and adults with autism and other pervasive developmental disorders. American Academy of Child and Adolescent Psychiatry Working Group on Quality Issues". Journal of the American Academy of Child and Adolescent Psychiatry. 38 (12 Suppl): 32S–54S. doi:10.1016/s0890-8567(99)80003-3. PMID 10624084.
  84. Constantino JN, Charman T (March 2016). "Diagnosis of autism spectrum disorder: reconciling the syndrome, its diverse origins, and variation in expression" (PDF). The Lancet. Neurology. 15 (3): 279–91. doi:10.1016/s1474-4422(15)00151-9. PMID 26497771.
  85. Filipek PA, Accardo PJ, Ashwal S, Baranek GT, Cook EH, Dawson G, et al. (August 2000). "Practice parameter: screening and diagnosis of autism: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Child Neurology Society". Neurology. 55 (4): 468–79. doi:10.1212/wnl.55.4.468. PMID 10953176.
  86. Filipek PA, Accardo PJ, Baranek GT, Cook EH, Dawson G, Gordon B, et al. (December 1999). "The screening and diagnosis of autistic spectrum disorders". Journal of Autism and Developmental Disorders. 29 (6): 439–84. doi:10.1023/A:1021943802493. PMID 10638459.
  87. Ozonoff S, Goodlin-Jones BL, Solomon M (September 2005). "Evidence-based assessment of autism spectrum disorders in children and adolescents" (PDF). Journal of Clinical Child and Adolescent Psychology. 34 (3): 523–40. doi:10.1207/s15374424jccp3403_8. PMID 16083393.
  88. Corsello C, Hus V, Pickles A, Risi S, Cook EH, Leventhal BL, Lord C (September 2007). "Between a ROC and a hard place: decision making and making decisions about using the SCQ". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 48 (9): 932–40. doi:10.1111/j.1469-7610.2007.01762.x. hdl:2027.42/74877. PMID 17714378.
  89. Huerta M, Lord C (February 2012). "Diagnostic evaluation of autism spectrum disorders". Pediatric Clinics of North America. 59 (1): 103–11, xi. doi:10.1016/j.pcl.2011.10.018. PMC 3269006. PMID 22284796.
  90. Wing L, Leekam SR, Libby SJ, Gould J, Larcombe M (2002). "The Diagnostic Interview for Social and Communication Disorders: background, inter-rater reliability and clinical use". Journal of Child Psychology and Psychiatry. 43 (3): 307–325. doi:10.1111/1469-7610.00023. PMID 11944874.
  91. "Why use the DISCO? - NAS". www.autism.org.uk.
  92. Helverschou SB, Bakken TL, Martinsen H (2011). Matson JL, Sturmey P (eds.). Psychiatric Disorders in People with Autism Spectrum Disorders: Phenomenology and Recognition. International handbook of autism and pervasive developmental disorders. New York: Springer. pp. 53–74. ISBN 9781441980649. OCLC 746203105.
  93. Underwood L, McCarthy J, Tsakanikos E (September 2010). "Mental health of adults with autism spectrum disorders and intellectual disability". Current Opinion in Psychiatry. 23 (5): 421–6. doi:10.1097/YCO.0b013e32833cfc18. PMID 20613532.
  94. Ballaban-Gil K, Tuchman R (2000). "Epilepsy and epileptiform EEG: association with autism and language disorders". Mental Retardation and Developmental Disabilities Research Reviews. 6 (4): 300–8. doi:10.1002/1098-2779(2000)6:4<300::AID-MRDD9>3.0.CO;2-R. PMID 11107195.
  95. Wiznitzer M (September 2004). "Autism and tuberous sclerosis". Journal of Child Neurology. 19 (9): 675–9. doi:10.1177/08830738040190090701. PMID 15563013.
  96. Zafeiriou DI, Ververi A, Vargiami E (June 2007). "Childhood autism and associated comorbidities". Brain & Development. 29 (5): 257–72. doi:10.1016/j.braindev.2006.09.003. PMID 17084999.
  97. O'Brien G, Pearson J (June 2004). "Autism and learning disability". Autism. 8 (2): 125–40. doi:10.1177/1362361304042718. PMID 15165430.
  98. Lainhart J (1999). "Psychiatric problems in individuals with autism, their parents and siblings". International Review of Psychiatry. 11 (4): 278–298. doi:10.1080/09540269974177.
  99. Chisholm K, Lin A, Abu-Akel A, Wood SJ (August 2015). "The association between autism and schizophrenia spectrum disorders: A review of eight alternate models of co-occurrence" (PDF). Neuroscience and Biobehavioral Reviews. 55: 173–83. doi:10.1016/j.neubiorev.2015.04.012. PMID 25956249.
  100. Hamlyn J, Duhig M, McGrath J, Scott J (May 2013). "Modifiable risk factors for schizophrenia and autism--shared risk factors impacting on brain development". Neurobiology of Disease. 53: 3–9. doi:10.1016/j.nbd.2012.10.023. PMID 23123588.
  101. Crespi BJ, Thiselton DL (October 2011). "Comparative immunogenetics of autism and schizophrenia". Genes, Brain, and Behavior. 10 (7): 689–701. doi:10.1111/j.1601-183X.2011.00710.x. PMID 21649858.
  102. Tsakanikos E, Costello H, Holt G, Sturmey P, Bouras N (July 2007). "Behaviour management problems as predictors of psychotropic medication and use of psychiatric services in adults with autism" (PDF). Journal of Autism and Developmental Disorders. 37 (6): 1080–5. doi:10.1007/s10803-006-0248-1. PMID 17053989.
  103. Rommelse NN, Franke B, Geurts HM, Hartman CA, Buitelaar JK (March 2010). "Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder". European Child & Adolescent Psychiatry. 19 (3): 281–95. doi:10.1007/s00787-010-0092-x. PMC 2839489. PMID 20148275.
  104. Baranek GT (October 2002). "Efficacy of sensory and motor interventions for children with autism". Journal of Autism and Developmental Disorders. 32 (5): 397–422. doi:10.1023/A:1020541906063. PMID 12463517.
  105. Lugnegård, Tove; Hallerbäck, Maria Unenge; Gillberg, Christopher (May 2012). "Personality disorders and autism spectrum disorders: what are the connections?". Comprehensive Psychiatry. 53 (4): 333–340. doi:10.1016/j.comppsych.2011.05.014. ISSN 1532-8384. PMID 21821235.
  106. Tantam, D. (December 1988). "Lifelong eccentricity and social isolation. II: Asperger's syndrome or schizoid personality disorder?". The British Journal of Psychiatry: The Journal of Mental Science. 153: 783–791. doi:10.1192/bjp.153.6.783. ISSN 0007-1250. PMID 3256377.
  107. Sharon C. Ekleberry (2008). "Cluster A - Schizoid Personality Disorder and Substance Use Disorders". Integrated Treatment for Co-Occurring Disorders: Personality Disorders and Addiction. Routledge. pp. 31–32. ISBN 978-0789036933.
  108. McPartland J, Klin A (October 2006). "Asperger's syndrome". Adolescent Medicine Clinics. 17 (3): 771–88, abstract xiii. doi:10.1016/j.admecli.2006.06.010 (inactive 3 December 2019). PMID 17030291.
  109. Woodbury-Smith MR, Volkmar FR (January 2009). "Asperger syndrome". European Child & Adolescent Psychiatry (Submitted manuscript). 18 (1): 2–11. doi:10.1007/s00787-008-0701-0. PMID 18563474.
  110. Coplan J, Jawad AF (July 2005). "Modeling clinical outcome of children with autistic spectrum disorders". Pediatrics. 116 (1): 117–22. doi:10.1542/peds.2004-1118. PMID 15995041. Lay summary – press release (5 July 2005).
  111. Eldevik S, Hastings RP, Hughes JC, Jahr E, Eikeseth S, Cross S (May 2009). "Meta-analysis of Early Intensive Behavioral Intervention for children with autism". Journal of Clinical Child and Adolescent Psychology. 38 (3): 439–50. CiteSeerX 10.1.1.607.9620. doi:10.1080/15374410902851739. PMID 19437303.
  112. Smith T, Iadarola S (2015). "Evidence Base Update for Autism Spectrum Disorder". Journal of Clinical Child and Adolescent Psychology. 44 (6): 897–922. doi:10.1080/15374416.2015.1077448. PMID 26430947.
  113. Myers SM, Johnson CP (November 2007). "Management of children with autism spectrum disorders". Pediatrics. 120 (5): 1162–82. doi:10.1542/peds.2007-2362. PMID 17967921. Lay summary – AAP (29 October 2007).
  114. Sigman, Marian, and Lisa Capps. Children with Autism: A Developmental Perspective. Cambridge: Harvard UP, 2002: 178–179. Print.
  115. Rogers SJ, Vismara LA (January 2008). "Evidence-based comprehensive treatments for early autism". Journal of Clinical Child and Adolescent Psychology. 37 (1): 8–38. doi:10.1080/15374410701817808. PMC 2943764. PMID 18444052.
  116. Zwaigenbaum L, Bauman ML, Choueiri R, Kasari C, Carter A, Granpeesheh D, Mailloux Z, Smith Roley S, Wagner S, Fein D, Pierce K, Buie T, Davis PA, Newschaffer C, Robins D, Wetherby A, Stone WL, Yirmiya N, Estes A, Hansen RL, McPartland JC, Natowicz MR (October 2015). "Early Intervention for Children With Autism Spectrum Disorder Under 3 Years of Age: Recommendations for Practice and Research". Pediatrics. 136 Suppl 1 (Supplement 1): S60–81. doi:10.1542/peds.2014-3667E. PMID 26430170.
  117. Siewertsen, Caitlin M.; French, Emma D.; Teramoto, Masaru (2015). "Autism spectrum disorder and pet therapy". Advances in Mind-Body Medicine. 29 (2): 22–25. ISSN 1532-1843. PMID 25831431.
  118. "Autism Spectrum Disorder (ASD) - NCBDDD - CDC". cdc.gov. 4 May 2018.
  119. Newschaffer CJ, Croen LA, Daniels J, Giarelli E, Grether JK, Levy SE, Mandell DS, Miller LA, Pinto-Martin J, Reaven J, Reynolds AM, Rice CE, Schendel D, Windham GC (2007). "The epidemiology of autism spectrum disorders". Annual Review of Public Health. 28: 235–58. doi:10.1146/annurev.publhealth.28.021406.144007. PMID 17367287.
  120. Fombonne E (June 2009). "Epidemiology of pervasive developmental disorders". Pediatric Research. 65 (6): 591–8. doi:10.1203/PDR.0b013e31819e7203. PMID 19218885.
  121. (ADDM) Autism and Developmental Disabilities Monitoring Network Surveillance Year 2006 Principal Investigators (2009). "Prevalence of autism spectrum disorders-Autism and Developmental Disabilities Monitoring Network". MMWR Surveillance Summaries. 58: 1–20.
  122. Volkmar FR, Lord C, Bailey A, Schultz RT, Klin A (January 2004). "Autism and pervasive developmental disorders". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 45 (1): 135–70. doi:10.1046/j.0021-9630.2003.00317.x. PMID 14959806.
  123. Tsakanikos E, Underwood L, Kravariti E, Bouras N, McCarthy J (2011). "Gender differences in co-morbid psychopathology and clinical management in adults with autism spectrum disorders". Research in Autism Spectrum Disorders. 5 (2): 803–808. doi:10.1016/j.rasd.2010.09.009. ISSN 1750-9467.
  124. Kanner L (July 1949). "Problems of nosology and psychodynamics of early infantile autism". The American Journal of Orthopsychiatry. 19 (3): 416–26. doi:10.1111/j.1939-0025.1949.tb05441.x. PMID 18146742.
  125. Tager-Flusberg H (February 2016). "Risk Factors Associated With Language in Autism Spectrum Disorder: Clues to Underlying Mechanisms". Journal of Speech, Language, and Hearing Research. 59 (1): 143–54. doi:10.1044/2015_jslhr-l-15-0146. PMC 4867927. PMID 26502110.
  126. Levinovitz A. "An Alternative-Medicine Believer's Journey Back to Science". WIRED. Retrieved 13 February 2017. The entire diagnosis and explanation took no more than 45 minutes. 'In the moment of diagnosis, it feels like the death of your hopes and dreams,' Louise [Laidler] says. There's a quiet grief in her voice, even though two decades have passed. 'In a way, it's even harder than a death, because you can't mourn and go on,' she says. 'You have to figure out how to care for your new child.'
  127. Karst JS, Van Hecke AV (September 2012). "Parent and family impact of autism spectrum disorders: a review and proposed model for intervention evaluation". Clinical Child and Family Psychology Review. 15 (3): 247–77. doi:10.1007/s10567-012-0119-6. PMID 22869324.
  128. Solomon, Andrew (25 May 2008). "The autism rights movement". New York. Archived from the original on 27 May 2008. Retrieved 27 May 2008.
  129. Ratner, Paul (10 July 2016). "Should Autism Be Cured or Is "Curing" Offensive?". Big Think. Retrieved 16 June 2019.
  130. Jaarsma, Pier; Welin, Stellan (2012). "Autism as a natural human variation: reflections on the claims of the neurodiversity movement". Health Care Analysis. 20 (1): 20–30. doi:10.1007/s10728-011-0169-9. ISSN 1573-3394. PMID 21311979.
  131. Stichter JP, Riley-Tillman TC, Jimerson SR (December 2016). "Assessing, understanding, and supporting students with autism at school: Contemporary science, practice, and policy". School Psychology Quarterly. 31 (4): 443–449. doi:10.1037/spq0000184. PMID 27929316.
  132. "Jean Piaget's Theory of Cognitive Development | Simply Psychology". www.simplypsychology.org. Retrieved 19 February 2019.
  133. "Facts and Statistics". Autism Society. Retrieved 6 November 2019.
  134. Ohl A, Grice Sheff M, Small S, Nguyen J, Paskor K, Zanjirian A (2017). "Predictors of employment status among adults with Autism Spectrum Disorder". Work. 56 (2): 345–355. doi:10.3233/WOR-172492. PMID 28211841.
  135. DePillis L (12 February 2016). "Disabled people are allowed to work for pennies per hour – but maybe not for much longer". Washington Post. Retrieved 31 December 2018.
  136. Ganz ML (2007). "The lifetime distribution of the incremental societal costs of autism". Arch Pediatr Adolesc Med. 161 (4): 343–49. doi:10.1001/archpedi.161.4.343. PMID 17404130. Lay summary – Harvard School of Public Health (25 April 2006).
  137. Montes G, Halterman JS (2008). "Association of childhood autism spectrum disorders and loss of family income". Pediatrics. 121 (4): e821–26. doi:10.1542/peds.2007-1594. PMID 18381511. Archived from the original on 4 March 2010.
  138. Montes G, Halterman JS (2008). "Child care problems and employment among families with preschool-aged children with autism in the United States". Pediatrics. 122 (1): e202–08. doi:10.1542/peds.2007-3037. PMID 18595965. Archived from the original on 6 December 2009.
Classification
External resources
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.