essays on autism spectrum

Autism Spectrum Disorder (ASD) Essay

Introduction, biological and genetic aspects of autism spectrum disorders, asd etiology, prevalence of asd, diagnosis of asd, treatment of asd.

Autism is a serious disorder that has the potential to disrupt the success of people living with it. This report shall set out to explore various aspects regarding this disorder. To this end, an overview of the symptoms, causes, diagnosis and treatment shall be offered. This shall aim at expanding our understanding regarding this disorder so as to enable us to be better prepared to handle it whenever the need arises.

Autism has been noted to be among the most prevalent childhood psychiatric disorder. Kuder (2003) denotes that in the USA, an estimated 2.1% of the population aged between 8 and 17 is affected by autism in its various forms.

Autism is manifested by varied behavior but it is chiefly characterized by inability to communicate, lingual deficits, lack of a sustained attention, low level of activity, temper tantrums, sleep disturbance, aggression inadequate motor control and other non-compliant behavior. These behaviors are detrimental to the social and educational endeavors of the people involved.

Autism spectrum is a medical term that is used to describe children and adults who experience difficulties in motor coordination, socializing, communicating (verbal and non-verbal) and language acquisition (Tager-Flusberg, Paul and Lord, 2005). The authors describe autism as a neurological disorder that stems from the brain’s inability to carryout some functions normally.

The causes of Autism as well as the reasons why it affects lingual and communication skills are not entirely known though there is a close linkage between Autism and genetics.

Studies indicate that Autism Spectrum Disorder (ASD) is inherited between family members. A study conducted by the American Psychiatric Association (2000) indicated that there is a 3-6% chance of getting autism amongst siblings.

However, Korvatska et al (2002) state that the difficulty experienced by scientists in pinpointing the genetic aspects of autism emanates from the lack of extended family histories. In most cases, autistic individual become more detached socially that they rarely marry or have children. As such, finding a family that has detailed genetic information regarding autism is difficult.

On a brighter note, twins have been used to explore the genetics behind autism (Beaudet, 2007). One study indicated an 82% likelihood of an autistic identical twin having the same disorder. This is in contrast to the 10% likelihood indicated by results from fraternal twins. More sophisticated studies have in the recent past concluded that 90% of autism related behavioral phenotypes are as a result of inherited genes (Happé & Ronald, 2008). This shows that there is a strong relationship between autism and genes.

Biologically, the root cause of autism has been difficult due to relative inability to access and study the brain systematically. However, technological innovations and advancements such as MRIs, CT scans and SPECT have made it possible to study the structure and functionality of the brain.

As a result, specialists have been able to deduce that majority of the brain’s structures play a pivotal role in the development of ASD. According to NIMH (2009, p. 1) they include but are not limited to “the cerebellum, cerebral cortex, limbic system, corpus callosum, basal ganglia, and brain stem”.

Similarly, other studies indicate that various neurotransmitters such as serotonin and epinephrine have a strong link to autism. The diagram below shows the biological basis of Autism Spectrum Disorder. It shows various structures of the brain and explains the functions that each play. Various symptoms of ASD are as a result of the structures’ inability to carry out their normal function.

A diagram showing brain structures linked to ASD

As mentioned earlier, the causes of ASD are not well known. However, researches conducted in this regard indicate that genetic, nutritional and environmental factors play a pivotal role in the development of the disorders. Results from numerous studies indicate that genetic factors predominate.

Others indicate that certain foods, infectious diseases, plastic and metallic extracts could cause autism. Similarly, smoking, alcohol, illicit drugs and some (mercury-based) childhood vaccines have also been attributed to causing autism. However, none of these causes are conclusive and more research needs to be conducted. This is to mean that the theory of causation regarding autism is not complete as yet.

The most recent survey conducted by center of disease control (CDC) indicated that autism rates have increased significantly over the past three decades. In most cases, studies indicate that autism is most prevalent among children. According to Rutter (2005), boys are four times more likely to be autistic than their female counterparts.

In addition, the author states that the symptoms of autism exhibit themselves from childbirth until three years of age. Parents are the most likely to discover these symptoms. As a result, they should ensure that they have their children checked at the onset of various abnormal behaviors.

Rutter (2005) asserts that the prevalence of autism disorder has been facilitated by ignorance and assumptions made by caretakers. In some cases, parents assume that their children are ‘slow and that they will develop as they grow up. However, this approach has proven to be costly since autism can best be handled as soon as it is detected.

Delaying makes it difficult to come up with remedies and coping mechanisms for both parents and the individuals having autism disorders. The main symptoms of this disorder include communication (verbal and non-verbal) difficulties, inability to develop and maintain relations with other people, abnormal lingual patterns and repetitive behaviors. Whenever any of these symptoms are discovered, it is highly recommended that medical or psychiatric assistance be sought.

An early diagnosis of ASD is important since it enables the people involved to come up with effective interventions before its too late. Recent studies show that intensive interventions administered in a control environment for a minimum of two years during preschool leads to behavioral and social improvements among children with ASD.

Clinicians base their diagnosis depending on the behavioral traits exhibited by a child. For a diagnosis to be made, NIMH (2009) asserts that at least one of the symptoms associated with ASD must be present. This means that a patient must have abnormal patterns of communication, socialization and restrictive behaviors.

In most cases, the diagnosis is made through a two-stage process. The first stage is “a developmental screening normally conducted during the routine childhood check-ups, while the second one involves a more comprehensive behavioral analysis by a team of experts (NIMH, 2009, p. 1).” Below are the stages that are followed to diagnose ASD.

The American Psychiatric Association (2000) recommends that every parent should ensure that a developmental screening test is carried out for his/her child during the “well child” check-up. The author contends that screening plays a pivotal role in the early identification of ASD symptoms.

Due to its importance, there are various screening instruments that have been developed to facilitate the diagnosis process. They include but are not limited to Checklist of Autism in Toddlers (CHAT) and its modified version; M-CHAT. Similarly, the Screening Tool for Autism in Two-Year-Olds (STAT) as well as the Social Communication Questionnaire (SCQ) have proven to be effective in diagnosing ASD in children aged between two years old and above four years old respectively.

According to Tadevosyan-Leyfer et al (2003), questionnaires given to parents provide important information during the diagnosis process. As such, some instruments rely on such responses while others depend on these responses as well as observations made by the caregiver. However, these screening instruments are not as effective as they should be when it comes to identifying mild ASD or Asperger syndrome. As a result, other screening instruments such as the Autism Spectrum Screening Questionnaire (ASSQ) and the Childhood Asperger Syndrome Test (CAST) among others have been developed so as to diagnose these forms of ASD (NIMH, 2009).

Comprehensive Diagnostic Evaluation

This is the second stage of diagnosis and it relies on the skills of a team of different experts such as psychologists, psychiatrists, neurologists, and therapists among others. This evaluation entails a comprehensive analysis of neural, genetic, cognitive and language testing in order to conclude whether a patient is suffering from autism or other behavioral disorders.

Some of the instruments used at this stage include: Autism Diagnosis Interview-Revised (ADI-R), which is a structured interview designed to test a child’s “communication, social interaction, restrictive behaviors and age-of-onset symptoms, and the Autism Diagnosis Observation Scheduling (ADOS-G), which is designed to identify abnormal, missing or delayed communication and social behaviors (NIMH, 2009, p. 1).”

The teams of experts that conduct this diagnosis determine the strengths and weaknesses of the child and recommend various treatment options that should be undertaken.

According to Freitag (2007) there is no one-shoe-fits-all approach to treating ASD. However, specialists in this area seem to agree on the fact that early interventions are of great importance. Arguably, the best treatment is one that considers the interests of the patient, allows the patient to learn in accordance to his/her ability and causes no harm to the overall well being of the patient. With this in mind, there are specialized programs and treatments that have proven to be effective against ASD symptoms.

For starters, Applied Behavioral Analysis (ABA) is among the most used intervention in treating ASD (SAMHSA, 2011). Similarly, there are dietary and medical interventions that help suppress unwanted behaviors among autistic children (NIMH, 2009). In regard to learning, there are specialized educational programs that seek to enhance the socio-communicative, cognitive and language skills of autistic students.

It can be articulated from this report that Autism is a problem that needs to be focused on. With proper understanding as to what the condition entails, parents and practitioners are better armed to assist patients overcome the weaknesses brought about by the condition and therefore achieve successful lives.

From this study, it can be authoritatively stated that early diagnosis and treatment of Autism spectrum is necessary to increase the chances of success in learning for the child suffering from this disease. Whereas Autism is not curable, it can be managed so as to ensure that it is not disruptive to the life of the individual during his/her future endeavors.

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders: DSM-IV-TR (fourth edition, text revision). Washington DC: American Psychiatric Association.

Beaudet, A. L. (2007). Autism: highly heritable but not inherited. Nat Med, 13(5): 534–6.

Freitag, C. M. (2007). The genetics of autistic disorders and its clinical relevance: a review of the literature. Mol Psychiatry. 12(1): 2–22.

Happé, F., & Ronald, A. (2008). The ‘fractionable autism triad’: a review of evidence from behavioral, genetic, cognitive and neural research. Neuropsychol Rev, 18(4): 287–304.

Korvatska, E et al. (2002). Genetic and immunologic considerations in autism. Neurobiology of Disease , 9: 107-125.

Kuder, S. (2003). Teaching Students with Language and Communication Disabilities. USA: Allyn and Bacon.

NIMH. (2009) Autism Spectrum Disorders (Pervasive Developmental Disorders) . Web.

Rutter, M. (2005). Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatr. 94(1): 2–15.

SAMHSA. (2011). Autism Spectrum Disorders . Web.

Tadevosyan-Leyfer, O et al. (2003). A principal components analysis of the autism diagnostic interview-revised. Journal of the American Academy of Child and Adolescent Psychiatry, 42(7): 864-872.

Tager-Flusberg, H., & Lord, C. (2005). Language and Communication in Autism. Web.

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Autism - List of Essay Samples And Topic Ideas

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How To Write an Essay About Autism

Understanding autism.

Before writing an essay about autism, it's essential to understand what autism is and the spectrum of conditions it encompasses. Autism, or Autism Spectrum Disorder (ASD), is a complex developmental disorder that affects communication and behavior. It is characterized by challenges with social skills, repetitive behaviors, speech, and nonverbal communication. Start your essay by explaining the nature of autism, its symptoms, and the spectrum concept, which acknowledges a range of strengths and challenges experienced by individuals with autism. It's also important to discuss the causes and diagnosis of autism, as well as the common misconceptions and stereotypes surrounding it. This foundational knowledge will set the stage for a more in-depth exploration of the topic.

Developing a Focused Thesis Statement

A strong essay on autism should be centered around a clear, focused thesis statement. This statement should present a specific angle or argument about autism. For example, you might discuss the importance of early intervention and therapy, the representation of autism in media, or the challenges faced by individuals with autism in education and employment. Your thesis will guide the direction of your essay and ensure that your analysis is structured and coherent.

Gathering and Analyzing Data

To support your thesis, gather relevant data and research from credible sources. This might include scientific studies, statistics, reports from autism advocacy organizations, and personal narratives. Analyze this data critically, considering different perspectives and the quality of the evidence. Including a range of viewpoints will strengthen your argument and demonstrate a comprehensive understanding of the topic.

Discussing Implications and Interventions

A significant portion of your essay should be dedicated to discussing the broader implications of autism and potential interventions. This can include the impact of autism on individuals and families, educational strategies, therapeutic approaches, and social support systems. Evaluate the effectiveness of these interventions, drawing on case studies or research findings. Discussing both the successes and challenges in managing and understanding autism will provide a balanced view and demonstrate a comprehensive understanding of the topic.

Concluding the Essay

Conclude your essay by summarizing the key points of your discussion and restating your thesis in light of the evidence and examples provided. Your conclusion should tie together your analysis and emphasize the significance of understanding and supporting individuals with autism. You might also want to highlight areas where further research or development is needed or the potential for societal changes to improve the lives of those with autism.

Final Review and Editing

After completing your essay, it's important to review and edit your work. Ensure that your arguments are clearly articulated and supported by evidence. Check for grammatical accuracy and ensure that your essay flows logically from one point to the next. Consider seeking feedback from peers or experts in the field to refine your essay further. A well-crafted essay on autism will not only inform but also engage readers in considering the complexities of this condition and the collective efforts required to support those affected by it.

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A Short Review on the Current Understanding of Autism Spectrum Disorders

Hye ran park.

1 Department of Neurosurgery, Seoul National University Hospital, Seoul 03080, Korea.

Jae Meen Lee

Hyo eun moon, dong soo lee.

2 Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul 03080, Korea.

Bung-Nyun Kim

3 Division of Child and Adolescent Psychiatry, Department of Psychiatry, Seoul National University College of Medicine, Seoul 03080, Korea.

Jinhyun Kim

4 Center for Functional Connectomics, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.

Dong Gyu Kim

Sun ha paek.

Autism spectrum disorder (ASD) is a set of neurodevelopmental disorders characterized by a deficit in social behaviors and nonverbal interactions such as reduced eye contact, facial expression, and body gestures in the first 3 years of life. It is not a single disorder, and it is broadly considered to be a multi-factorial disorder resulting from genetic and non-genetic risk factors and their interaction. Genetic studies of ASD have identified mutations that interfere with typical neurodevelopment in utero through childhood. These complexes of genes have been involved in synaptogenesis and axon motility. Recent developments in neuroimaging studies have provided many important insights into the pathological changes that occur in the brain of patients with ASD in vivo. Especially, the role of amygdala, a major component of the limbic system and the affective loop of the cortico-striatothalamo-cortical circuit, in cognition and ASD has been proved in numerous neuropathological and neuroimaging studies. Besides the amygdala, the nucleus accumbens is also considered as the key structure which is related with the social reward response in ASD. Although educational and behavioral treatments have been the mainstay of the management of ASD, pharmacological and interventional treatments have also shown some benefit in subjects with ASD. Also, there have been reports about few patients who experienced improvement after deep brain stimulation, one of the interventional treatments. The key architecture of ASD development which could be a target for treatment is still an uncharted territory. Further work is needed to broaden the horizons on the understanding of ASD.

INTRODUCTION

Autism spectrum disorder (ASD) is a set of neurodevelopmental disorders characterized by a lack of social interaction, verbal and nonverbal communication in the first 3 years of life. The distinctive social behaviors include an avoidance of eye contact, problems with emotional control or understanding the emotions of others, and a markedly restricted range of activities and interests [ 1 ]. The current prevalence of ASD in the latest large-scale surveys is about 1%~2% [ 2 , 3 ]. The prevalence of ASD has increased in the past two decades [ 4 ]. Although the increase in prevalence is partially the result of changes in DSM diagnostic criteria and younger age of diagnosis, an increase in risk factors cannot be ruled out [ 5 , 6 ]. Studies have shown a male predominance; ASD affects 2~3 times more males than females [ 2 , 3 , 7 ]. This diagnostic bias towards males might result from under-recognition of females with ASD [ 8 ]. Also, some researchers have suggested the possibility that the female-specific protective effects against ASD might exist [ 9 ].

A Swiss psychiatrist, Paul Eugen Bleuler used the term "autism" to define the symptoms of schizophrenia for the first time in 1912 [ 10 ]. He derived it from the Greek word αὐτὀς (autos), which means self. Hans Asperger adopted Bleuler's terminology "autistic" in its modern sense to describe child psychology in 1938. Afterwards, he reported about four boys who did not mix with their peer group and did not understand the meaning of the terms 'respect' and 'polite', and regard for the authority of an adult. The boys also showed specific unnatural stereotypic movement and habits. Asperger describe this pattern of behaviors as "autistic psychopathy", which is now called as Asperger's Syndrome [ 11 ]. The person who first used autism in its modern sense is Leo Kanner. In 1943, he reported about 8 boys and 3 girls who had "an innate inability to form the usual, biologically provided affective contact with people", and introduced the label early infantile autism [ 12 ]. Hans Asperger and Leo Kanner have been considered as those who designed the basis of the modern study of autism.

Most recently, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) adopted the term ASD with a dyadic definition of core symptoms: early-onset of difficulties in social interaction and communication, and repetitive, restricted behaviors, interests, or activities [ 13 ]. Atypical language development, which had been included into the triad of ASD, is now regarded as a co-occurring condition.

As stated earlier, the development of the brain in individuals with ASD is complex and is mediated by many genetic and environmental factors, and their interactions. Genetic studies of ASD have identified mutations that interfere with typical neurodevelopment in utero through childhood. These complexes of genes have been involved in synaptogenesis and axon motility. Also, the resultant microstructural, macrostructural, and functional abnormalities that emerge during brain development create a pattern of dysfunctional neural networks involved in socioemotional processing. Microstructurally, an altered ratio of short- to long-diameter axons and disorganization of cortical layers are observed. Macrostructurally, MRI studies assessing brain volume in individuals with ASD have consistently shown cortical and subcortical gray matter overgrowth in early brain development. Functionally, resting-state fMRI studies show a narrative of widespread global underconnectivity in socioemotional networks, and task-based fMRI studies show decreased activation of networks involved in socioemotional processing. Moreover, electrophysiological studies demonstrate alterations in both resting-state and stimulus-induced oscillatory activities in patients with ASD [ 14 ].

The well-conserved sets of genes and genetic pathways were implicated in ASD, many of which contribute toward the formation, stabilization, and maintenance of functional synapses. Therefore, these genetic aspects coupled with an in-depth phenotypic analysis of the cellular and behavioral characteristics are essential to unraveling the pathogenesis of ASD. The number of genes already discovered in ASD holds the promise to translate the knowledge into designing new therapeutic interventions. Also, the fundamental research using animal models is providing key insights into the various facets of human ASD. However, a better understanding of the genetic, molecular, and circuit level aberrations in ASD is still needed [ 15 ].

Neuroimaging studies have provided many important insights into the pathological changes that occur in the brain of patients with ASD in vivo. Importantly, ASD is accompanied by an atypical path of brain maturation, which gives rise to differences in neuroanatomy, functioning, and connectivity. Although considerable progress has been made in the development of animal models and cellular assays, neuroimaging approaches allow us to directly examine the brain in vivo, and to probably facilitate the development of a more personalized approach to the treatment of ASD [ 16 ].

ASD is not a single disorder. It is now broadly considered to be a multi-factorial disorder resulting from genetic and non-genetic risk factors and their interaction.

Genetic causes including gene defects and chromosomal anomalies have been found in 10%~20% of individuals with ASD [ 17 , 18 ]. Siblings born in families with an ASD subject have a 50 times greater risk of ASD, with a recurrence rate of 5%~8% [ 19 ]. The concordance rate reaches up to 82%~92% in monozygotic twins, compared with 1%~10% in dizygotic twins. Genetic studies suggested that single gene mutations alter developmental pathways of neuronal and axonal structures involved in synaptogenesis [ 20 , 21 , 22 ]. In the cases of related with fragile X syndrome and tuberous sclerosis, hyperexcitability of neocortical circuits caused by alterations in the neocortical excitatory/inhibitory balance and abnormal neural synchronization is thought to be the most probable mechanisms [ 23 , 24 ]. Genome-wide linkage studies suggested linkages on chromosomes 2q, 7q, 15q, and 16p as the location of susceptibility genes, although it has not been fully elucidated [ 25 , 26 ]. These chromosomal abnormalities have been implicated in the disruption of neural connections, brain growth, and synaptic/dendritic morphology [ 27 , 28 , 29 ]. Metabolic errors including phenylketonuria, creatine deficiency syndromes, adenylosuccinate lyase deficiency, and metabolic purine disorders are also account for less than 5% of individuals with ASD [ 30 ]. Recently, the correlation between cerebellar developmental patterning gene ENGRAILED 2 and autism was reported [ 31 ]. It is the first genetic allele that contributes to ASD susceptibility in as many as 40% of ASD cases. Other genes such as UBE3A locus, GABA system genes, and serotonin transporter genes have also been considered as the genetic factors for ASD [ 18 ].

Diverse environmental causative elements including pre-natal, peri-natal, and post-natal factors also contribute to ASD [ 32 ]. Prenatal factors related with ASD include exposure to teratogens such as thalidomide, certain viral infections (congenital rubella syndrome), and maternal anticonvulsants such as valproic acid [ 33 , 34 ]. Low birth weight, abnormally short gestation length, and birth asphyxia are the peri-natal factors [ 34 ]. Reported post-natal factors associated with ASD include autoimmune disease, viral infection, hypoxia, mercury toxicity, and others [ 33 , 35 , 36 ]. Table 1 summarizes the known and putative ASD-related genes and environmental factors contributing to the ASD.

In recent years, some researchers suggest that ASD is the result of complex interactions between genetic and environmental risk factors [ 37 ]. Understanding the interaction between genetic and environmental factors in the pathogenesis of ASD will lead to optimal treatment strategy.

Clinical features and Diagnosis

ASD is typically noticed in the first 3 years of life, with deficits in social behaviors and nonverbal interactions such as reduced eye contact, facial expression, and body gestures [ 1 ]. Children also manifest with non-specific symptoms such as unusual sensory perception skills and experiences, motor clumsiness, and insomnia. Associated phenomena include mental retardation, emotional indifference, hyperactivity, aggression, self-injury, and repetitive behaviors such as body rocking or hand flapping. Repetitive, stereotyped behaviors are often accompanied by cognitive impairment, seizures or epilepsy, gastrointestinal complaints, disturbedd sleep, and other problems. Differential diagnosis includes childhood schizophrenia, learning disability, and deafness [ 38 , 39 ].

ASD is diagnosed clinically based on the presence of core symptoms. However, caution is required when diagnosing ASD because of non-specific manifestations in different age groups and individual abilities in intelligence and verbal domains. The earliest nonspecific signs recognized in infancy or toddlers include irritability, passivity, and difficulties with sleeping and eating, followed by delays in language and social engagement. In the first year of age, infants later diagnosed with ASD cannot be easily distinguished from control infants. However, some authors report that about 50% of infants show behavioral abnormalities including extremes of temperament, poor eye contact, and lack of response to parental voices or interaction. At 12 months of age, individuals with ASD show atypical behaviors, across the domains of visual attention, imitation, social responses, motor control, and reactivity [ 40 ]. There is also report about atypical language trajectories, with mild delays at 12 months progressing to more severe delays by 24 months [ 40 ]. By 3 years of age, the typical core symptoms such as lack of social communication and restricted/repetitive behaviors and interests are manifested. ASD can be easily differentiated from other psychosocial disorders in late preschool and early school years.

Amygdala and ASD

The frontal and temporal lobes are the markedly affected brain areas in the individuals with ASD. In particular, the role of amygdala in cognition and ASD has been proved in numerous neuropathological and neuroimaging studies. The amygdala located the medial temporal lobe anterior to the hippocampal formation has been thought to have a strong association with social and aggressive behaviors in patients with ASD [ 41 , 42 ]. The amygdala is a major component of the limbic system and affective loop of the cortico-striato-thalamo-cortical circuit [ 43 ].

The amygdala has 2 specific functions including eye gaze and face processing [ 44 ]. The lesion of the amygdala results in fear-processing, modulation of memory with emotional content, and eye gaze when looking at human face [ 45 , 46 , 47 ]. The findings in individuals with amygdala lesion are similar to the phenomena in ASD. The amygdala receives highly processed somatosensory, visual, auditory, and all types of visceral inputs. It sends efferents through two major pathways, the stria terminalis and the ventral amygdalofugal pathway.

The amygdala comprises a collection of 13 nuclei. Based on histochemical analyses, these 13 nuclei are divided into three primary subgroups: the basolateral (BL), centromedial (CM), and superficial groups [ 42 ]. The BL group attributes amygdala to have a role as a node connecting sensory stimuli to higher social cognition level. It links the CM and superficial groups, and it has reciprocal connection with the orbitofrontal cortex, anterior cingulate cortex (ACC), and the medial prefrontal cortex (mPFC) [ 48 ]. The BL group contains neurons responsive to faces and actions of others, which is not found in the other two groups of amygdala [ 49 , 50 ]. The CM group consists of the central, medial, cortical nuclei, and the periamygdaloid complex. It innervates many of the visceral and autonomic effector regions of the brain stem, and provides a major output to the hypothalamus, thalamus, ventral tegmental area, and reticular formation [ 51 ]. The superficial group includes the nucleus of the lateral olfactory tract [ 42 ].

Neurochemistrial studies revealed high density of benzodiazepine/GABAa receptors and a substantial set of opiate receptors in the amygdala. It also includes serotonergic, dopaminergic, cholinergic, and noradrenergic cell bodies and pathways [ 52 ]. Since some patients with temporal epilepsy and aggressive behavior experienced improvement in aggressiveness after bilateral stereotactic ablation of basal and corticomedial amygdaloid nuclei, the role of amygdala in emotional processing, especially rage processing has been investigated [ 53 , 54 , 55 , 56 ]. Some evidences for the amygdala deficit in patients with ASD have been suggested. Post-mortem studies found the pathology in the amygdala of individuals with ASD compared to age- and sex-matched controls [ 57 , 58 , 59 ]. Small neuronal size and increased cell density in the cortical, medial, and central nuclei of the amygdala were detected in ASD patients.

Several studies proposed the use of an animal model to confirm the evidence for the association between amygdala and ASD [ 60 , 61 ]. Despite the limitation which stems from the need to prove higher order cognitive disorder, the studies suggested that disease-associated alterations in the temporal lobes during experimental manipulations of the amygdala in animals have produced some symptoms of ASD [ 62 ]. Especially, the Kluver-Bucy syndrome, which is caused by bilateral damage to the anterior temporal lobes in monkeys, has characteristic manifestations similar to ASD [ 63 , 64 ]. Monkeys with the Kluver-Bucy syndrome shows absence of social chattering, lack of facial expression, absence of emotional reactions, repetitive abnormal movement patterns, and increased aggression. Sajdyk et al. performed experiments on rats and discovered that physiological activation of the BL nucleus of the amygdala by blocking tonic GABAergic inhibition or enhancing glutamate or the stress-associated peptide corticotropin-releasing factor (CRF)-mediated excitation caused reduction in social behaviors [ 65 ]. On the contrary, lesioning of the amygdala or blocking amygdala excitability with glutamate antagonist increased dyadic social interactions [ 60 ]. Besides animals, humans who underwent lesioning of the amygdala showed impairments in social judgment. This phenomenon is called acquired ASD [ 66 , 67 , 68 ]. The pattern of social deficits was similar in idiopathic and acquired ASD [ 69 ]. Felix-Ortiz and Tye sought to understand the role of projections from the BL amygdala to the ventral hippocampus in relation to behavior. Their study using mice showed that the BLS-ventral hippocampus pathway involved in anxiety plays a role in the mediation of social behavior as well [ 70 ].

The individuals with temporal lobe tumors involving the amygdala and hippocampus provide another evidence of the correlation between the amygdala and ASD. Some authors reported that patients experienced autistic symptoms after temporal lobe was damaged by a tumor [ 71 , 72 ]. Also, individuals with tuberous sclerosis experienced similar symptoms including facial expression due to a temporal lobe hamartoma [ 73 ].

Although other researchers failed to find structural abnormalities in the mesial temporal lobe of autistic subjects by performing magnetic resonance imaging (MRI) studies [ 74 , 75 , 76 ], recent development in neuroimaging has facilitated the investigation of amygdala pathology in ASD. Studies using structural MRI estimated volumes of the amygdala and related structures in individuals with ASD and age-, gender, and verbal IQ-matched healthy controls [ 77 ]. Increase in bilateral amygdala volume and reduction in hippocampal and parahippocampal gyrus volumes were noted in individuals with ASD. Also, the lateral ventricles and intracranial volumes were significantly increased in the autistic subjects; however, overall temporal lobe volumes were similar between the ASD and control groups.

There was a significant difference in the whole brain voxel-based scans of individuals with ASD and control groups [ 78 ]. Individuals with ASD showed decreased gray matter volume in the right paracingulate sulcus, the left occipito-temporal cortex, and the left inferior frontal sulcus. On the contrary, the gray matter volume in the bilateral cerebellum was increased. Otherwise, they showed increased volume in the left amygdala/periamygdaloid cortex, the right inferior temporal gyrus, and the middle temporal gyrus.

Recently, the development of functional neuroimaging also provided some evidence for the correlation between amygdala deficit and ASD. A study using Technetium-99m (Tc-99m) single-photon emission computed tomography (SPECT) found that regional cerebral blood flow (rCBF) was decreased in the bilateral insula, superior temporal gyri, and left prefrontal cortices in individuals with ASD compared to age- and gender-matched controls with mental retardation [ 79 ]. Also, the authors found that rCBF in both the right hippocampus and amygdala was correlated with a behavioral rating subscale.

On proton magnetic resonance spectroscopy (MRS) in the right hippocampal-amygdala region and the left cerebellar hemisphere, autistic subjects showed decreased level of N-acetyl aspartate (NAA) in both areas [ 80 ]. There was no difference in the level of the other metabolites, such as creatine and choline. This study implies that a decreased level of NAA might be associated with neuronal hypofunction or immature neurons.

These findings support the claim that amygdala might be a key structure in the development of ASD and a target for the management of the disease.

Prefrontal cortex and ASD

Frontal lobe has been considered as playing an important role in higher-level control and a key structure associated with autism. Individuals with frontal lobe deficit demonstrate higher-order cognitive, language, social, and emotion dysfunction, which is deficient in autism [ 81 ]. Recently, neuroimaging and neuropsychological studies have attempted to delineate distinct regions of prefrontal cortex supporting different aspects of executive function. Some authors have reported that the excessive rates of brain growth in infants with ASD, which is mainly contributed by the increase of frontal cortex volume [ 82 , 83 ]. Especially, the PFC including Brodmann areas 8, 9, 10, 11, 44, 45, 46, and 47 has been noted for the structure related with ASD [ 84 ]. The PFC is cytoarchitectonically defined as the presence of a cortical granular layer IV [ 85 ], and anatomically refers to the regions of the cerebral cortex that are anterior to premotor cortex and the supplementary motor area [ 86 ]. The PFC has extensive connections with other cortical, subcortical and brain stem sites [ 87 ]. It receives inputs from the brainstem arousal systems, and its function is particularly dependent on its neurochemical environment [ 88 ].

The PFC is broadly divided into the medial PFC (mPFC) and the lateral PFC (lPFC). The mPFC is further divided into four distinct regions: medial precentral cortex, anterior cingulate cortex, prelimbic and infralimbic prefrontal cortex [ 89 ]. While the lPFC is thought to support cognitive control process [ 90 ], the mPFC has reciprocal connections with brain regions involved in emotional processing (amygdala), memory (hippocampus) and higher-order sensory regions (within temporal cortex) [ 91 ]. This involvement of mPFC in social cognition and interaction implies that mPFC might be a key region in understanding self and others [ 92 ].

The mPFC involves in fear learning and extinction by reciprocal synaptic connections with the basolateral amygdala [ 93 , 94 ]. It is believed that the mPFC regulates and controls amygdala output and the accompanying behavioral phenomena [ 95 , 96 ]. Previous authors investigated how memory processing is regulated by interactions between BLA and mPFC by means of functional disconnection [ 97 , 98 ]. Disturbed communication within amygdala-mPFC circuitry caused deficits in memory processing. These informations provide support for a role of the mPFC in the development of ASD.

Nucleus Accumbens and ASD

Besides amygdala, nucleus accumbens (NAc) is also considered as the key structure which is related with the social reward response in ASD. NAc borders ventrally on the anterior limb of the internal capsule, and the lateral subventricular fundus of the NAc is permeated in rostral sections by internal capsule fiber bundles. The rationale for NAc to be considered as the potential target of DBS for ASD is its predominant role in modulating the processing of reward and pleasure [ 99 ]. Anticipation of rewarding stimuli recruits the NAc as well as other limbic structures, and the experience of pleasure activates the NAc as well as the caudate, putamen, amygdala, and VMPFC [ 100 , 101 , 102 ]. It is well known that dysfunction of NAc regarding rewarding stimuli in subjects with depression. Bewernick et al. demonstrated antidepressant effects of NAc-DBS in 5 of the 10 patients suffering from severe treatment-resistant depression [ 103 ].

Two groups reported about the neural basis of social reward processing in ASD. Schmitz et al. examined responses to a task that involved monetary reward. They investigated the neural substrates of reward feedback in the context of a sustained attention task, and found increased activation in the left anterior cingulate gyrus and left mid-frontal gyrus on rewarded trials in ASD [ 104 ]. Scott-Van Zeeland et al. investigated the neural correlates of rewarded implicit learning in children with ASD using both social and monetary rewards. They found diminished ventral striatal response during social, but not monetary, rewarded learning [ 105 ]. According to them, activity within the ventral striatum predicted social reciprocity within the control group, but not within the ASD group.

Anticipation of pleasurable stimuli recruits the NAc, whereas the experience of pleasure activates VMPFC [ 106 ]. NAc is activated by incentive motivation to reach salient goals [ 106 ]. Increased activation in the left anterior cingulate gyrus and left mid-frontal gyrus was noted during both the anticipatory and consummatory phase of the reward response [ 104 , 107 , 108 ]. However, the activity within the ventral striatum was decreased in autistic subjects, which caused impairment in social reciprocity [ 105 ].

These findings indicate that reward network function in ASD is contingent on both the temporal phase of the response and the type of reward processed, suggesting that it is critical to assess the temporal chronometry of responses in a study of reward processing in ASD. NAc might be one of the candidates as a target of DBS which is introduced as below.

Various educational and behavioral treatments have been the mainstay of the management of ASD. Most experts agree that the treatment for ASD should be individualized. Treatment of disabling symptoms such as aggression, agitation, hyperactivity, inattention, irritability, repetitive and self-injurious behavior may allow educational and behavioral interventions to proceed more effectively [ 109 ].

Increasing interest is being shown in the role of various pharmacological treatments. Medical management includes typical antipsychotics, atypical antipsychotics, antidepressants, selective serotonin reuptake inhibitors, α2-adrenergic agonists, β-adrenergic antagonist, mood stabilizers, and anticonvulsants [ 110 , 111 ]. So far, there has been no agent which has been proved effective in social communication [ 112 ]. A major factor in the choice of pharmacologic treatment is awareness of specific individual physical, behavioral or psychiatric conditions comorbid with ASD, such as obsessive-compulsive disorder, schizophrenia, mood disorder, and intellectual disability [ 113 ]. Antidepressants were the most commonly used agents followed by stimulants and antipsychotics. The high prevalence of comorbidities is reflected in the rates of psychotropic medication use in people with ASD. Antipsychotics were effective in treating the repetitive behaviors in children with ASD; however, there was not sufficient evidence on the efficacy and safety in adolescents and adults [ 114 ]. There are also alternative options including opiate antagonist, immunotherapy, hormonal agents, megavitamins and other dietary supplements [ 109 , 113 ].

However, the autistic symptoms remain refractory to medication therapy in some patients [ 115 ]. These individuals have severely progressed disease and multiple comorbidities causing decreased quality of life [ 44 , 110 ]. Interventional therapy such as deep brain stimulation (DBS) may be an alternative therapeutic option for these patients.

Two kinds of interventions have been used for treating ASD; focused intervention practices and comprehensive treatments [ 116 ]. The focused intervention practices include prompting, reinforcement, discrete trial teaching, social stories, or peer-mediated interventions. These are designed to produce specific behavioral or developmental outcomes for individual children with ASD, and used for a limited time period with the intent of demonstrating a change in the targeted behaviors. The comprehensive treatment models are a set of practices performed over an extended period of time and are intense in their application, and usually have multiple components [ 116 ].

Since it was approved by the FDA in 1997, DBS has been used to send electrical impulses to specific parts of the brain [ 117 , 118 ]. In recent years, the spectrum for which therapeutic benefit is provided by DBS has widely been expanded from movement disorders such as Parkinson's disease, essential tremor, and dystonia to psychiatric disorders. Some authors have demonstrated the efficacy of DBS for psychiatric disorders including refractory obsessive-compulsive disorder, depression, Tourette syndrome, and others for the past few years [ 119 , 120 , 121 ].

To the best of our knowledge, there have been 2 published articles of 3 patients who underwent DBS for ASD accompanied by life-threatening self-injurious behaviors not alleviated by antipsychotic medication [ 122 , 123 ]. The targets were anterior limb of the internal capsule and globus pallidus internus, only globus pallidus, and BL nucleus of the amygdala, respectively. All patients obtained some benefit from DBS. Although the first patient showed gradual re-deterioration after temporary improvement, the patient who underwent DBS of the BL nucleus experienced substantial improvement in self-injurious behavior and social communication. These experiences suggested the possibility of DBS for the treatment of ASD. For patients who did not obtain benefit from other treatments, DBS may be a viable therapeutic option. Understanding the structures which contribute to the occurrence of ASD might open a new horizon for management of ASD, particularly DBS. Accompanying development of neuroimaging technique enables more accurate targeting and heightens the efficacy of DBS. However, the optimal DBS target and stimulation parameters are still unknown, and prospective controlled trials of DBS for various possible targets are required to determine optimal target and stimulation parameters for the safety and efficacy of DBS.

ASD should be considered as a complex disorder. It has many etiologies involving genetic and environmental factors, and further evidence for the role of amygdala and NA in the pathophysiology of ASD has been obtained from numerous studies. However, the key architecture of ASD development which could be a target for treatment is still an uncharted territory. Further work is needed to broaden the horizons on the understanding of ASD.

Acknowledgements

This study was partly supported by the Korea Institute of Planning & Evaluation for Technology in Food, Agriculture, Forestry, and Fisheries, Republic of Korea (311011-05-3-SB020), by the Korea Healthcare Technology R&D Project (HI11C21100200) funded by Ministry of Health & Welfare, Republic of Korea, by the Technology Innovation Program (10050154, Business Model Development for Personalized Medicine Based on Integrated Genome and Clinical Information) funded by the Ministry of Trade, Industry & Energy (MI, Korea), and by the Bio & Medical Technology Development Program of the NRF funded by the Korean government, MSIP (2015M3C7A1028926).

Jackie Schuld Art Therapy Blog

• Feb 17, 2023

The Great List of Autistic Essays

I’m a late-identified autistic who loves writing about autism. How much do I love it? I’ve written over 150 essays on it in the past six months alone.

How do I think of so many autistic topics to write about? I’m an art therapist who specializes in late-identified autistic adults. That means I not only have my personal experience to draw from, but also the hundreds of hours spent listening to my clients.

I share most of my essays here on Medium, which means it has now become quite the library. In an effort to make my essays more accessible to those wanting clear, relatable information about late-identified autism in adults, I’ve sorted my essays into topics below. While I wish I could provide a link to each of them for you… I’ve got to prioritize my time and energy. So if a specific essay interests you, just pop it into the search and it’ll come up

Autism in a Neurotypical World

What Would a World Designed by Autistic People Be Like

The Harm in "They're a Little Autistic"

Autism Does Not Directly Cause Socializing Problems

Please Trust My Lived Autistic Experience

Can Someone Please Create a Neurodivergent Intentional Living Community

What if I Accept that Most Neurotypicals Won't Like Me

How Neuro-Bias Shows Up in Professional Testing

Your Autistic Experience Sounds Just LIke my Neurotypical One

Neurotypical Words that Don't Work for Autistics: Overachiever

But Neurotypicals Experience That, Too!

Neurotypical Norms That Don’t Work for Autistics: Hustle Goals

The Fear of Being a Hypocritical Autistic

Neurodiversity: Us vs Them?

How to Meet an Autistic Adult Exactly Where They're At

Autism Characteristics

The Autistic Mind Loves to Take Detours

4 Reasons Why Autism Symptoms Lists are Confusing

My Autistic Brain: Sunshine and Detours

The Joys of Being Autistic: Part 1

Stop Saying Autistic People Can't Empathize

Redefining Fun for Autistic Adults

9 Reasons Why Autism Looks So Similar to CPTSD

We Need More Depictions of the Interior Experience of Autism

Clarity is What my Autistic Mind Craves

How Trauma and Autism Can be a Confusing Mix to Decipher

Why am I like This? Understanding the Autistic Brain

My Autistic Mind Does What it Wants

The Dissociated Autistic Performance State

The Joys of Being Autistic: Increased Creativity and Innovation

My Autistic Memory Is Not the Same as Others

The Firehouse Dilemma: Autism and Infodumping

The Variability of the Autistic Sensory System

5 Reasons Autistics are Especially Hard on Themselves

The Shame That Often Accompanies Autism

Knowing You’re Different as an Autistic Adult

3 Reasons Autism is Worse After You Learn You're Autistic

Disability and Internalized Ableism

I Had to Dismantle My Fear of Autistic People

Is Autism a Disability?

I’m Ok With Saying I have a Disability, Right?

Dog Training

The Difficulties of Adjusting to a New Dog When You're Autistic

Tips for Adjusting to a New Dog When You're Autistic

5 Tips to Integrate a Dog into Your Autistic Life

Defining and Explaining Autism

What I Wish Others Knew About Autism

Let’s Drop the “Disorder” From Autism Spectrum Disorder

How Low and High Autism Labels are Misleading

We Need All the Autism Theories and Models

Autism Can Be a Murky Thing To Understand

How I Explain Autism to Someone Unfamiliar With It

What is Late Identified Autism

Autistic Statistics are Not Accurate for Late-Identified Autistics

I'm Here for the Autistic Awakening

How It Helps to Know You’re Autistic

Why It Matters to Know You're Neurodivergent

What is Neurodiversity and Why Does it Matter

How Neurodivergent Acceptance Can Improve Our Lived Experiences

How Unidentified Autistics are Taught to Socially Camouflage and Mask

Is There a World Where I can Be Unmasked?

The False Dichotomy of Masked and Unmasked Autism

6 Reasons Why UnMasking Is Harder Than it Sounds

What if You have to Mask Everywhere?

My Personal Experience as an Autistic

Hating Cooking as an Autistic Adult

I Make Giant Lists About Autism for Fun

The Challenges of Writing Publically About Autism

The Risk of Sharing my Autistic Passions with Others

I'm Reclaiming Weird for My Autistic Self

I Expand and Then I Contract

I Stopped Seeing Myself As Broken When I learned I was Autistic

Respecting my Limits as an Autistic Business Owner

I Need to Lessen the Pressure on my Autistic Self

My Autistic Brain Doesn’t Want to Watch TV Right Now

Embracing Who I am as an Autistic Adult

I Used to be a Very Judgemental When I Didn’t Know I was Autistic

A Letter from An Autistic Adult to Trust

Don’t Get So Upset: A Line that Doesn’t Work for This Autist

Why This Autistic Writer Didn't Respond to Your Comment

Relationships

Is Dating Worth it as an Autistic Adult?

Is it Possible to be Happily Partnered as an Autistic Adult?

Not Liking People as an Autistic Adult

Self-Identification

So You Think You Might Be Autistic

Dearly Newly Identified Autistic Person

Am I Actually Autistic?

Dearest Smart, Weird, and Caring Autistic

I Am Deeply Unsure About Autism

How to Self Identify Autism as an Adult

When the Past Makes Sense after a Late-Identification of Autism

Where to Start When You First Learn You’re Autistic

6 Strategies to Harness the Hyperfocus Power of an Autistic Mind

Leave the Gremlin In the Cave: Self-Isolation as a Necessary Autistic Tool

No Plans Days as an Autistic Tool

Making Accommodations for Myself as an Autistic Adult

How Many Accommodations Can We Ask for as Autistic Adults?

Using Art to Help Your Autistic Mind

Dissociation as an Autistic Tool

The Power of the Home Environment for Autistics

Is It Ok to Honor My Autistic Needs?

Recognizing When It's Not Time to Make Decisions as an Autistic

Therapy for Autistics

Dearest Autistic Client of Mine

8 Ways Therapy Can Help With Late Identified Autism

Gaslighting the Autistic Experience

Dearest Therapist Who Knows Barely Anything About Autism

I'm an Autistic Therapist: Sometimes It's Easier Than Everyday Life

Does Your Therapist Know Enough About Autism to Help You?

Questions to Ask a Potential Therapist When You're Autistic

How I Work with Newly Identified Autistic People

What to Ask When You're Seeking Therapy for Late-Identified Autism

12 Ways Therapy Can Enhance Life for Late Identified Autistic Adults

Therapy is Not for Fixing Autism

The Harm I Caused When I Didn't Know about Autism

A Newly Identified Autistic Therapist Working with Newly Identified Autistics

Common Therapy Advice That is Counterproductive for Autistics

A Therapist Told Me Treating Autism is Like Treating Depression

Who Can Diagnose Autism in Adults?

Autistic Adults Deserve Better from the Mental Health Field

Undiagnosed Autism

The Correlation Between Intelligence and Undiagnosed Autism

10 Consequences of a Life with Unidentified Autism

The Gap Between “Diagnosable Autism” and a Lifetime of Unidentified Autism

Autism Diagnosis Criteria are Limiting for Men Too

No Autistic Should Receive a Diagnosis Letter Like Mine

Identifying Autism in Undiagnosed Women Abstract

How I Identify Autism in Undiagnosed Women

Autistic Stereotypes Block People From Knowing They're Autistic

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About Autism Spectrum Disorder

• Autism spectrum disorder (ASD) is a developmental disability caused by differences in the brain.
• Some people with ASD have a known difference, such as a genetic condition. Other causes are not yet known.
• Scientists believe there are multiple causes of ASD that act together to change the most common ways people develop. We still have much to learn about these causes and how they impact people with ASD.
• Early intervention services can greatly improve the development of a child with ASD.

People with ASD may behave, communicate, interact, and learn in ways that are different from most other people. There is often nothing about how they look that sets them apart from other people. The abilities of people with ASD can vary significantly. For example, some people with ASD may have advanced conversation skills whereas others may be nonverbal. Some people with ASD need a lot of help in their daily lives; others can work and live with little to no support.

ASD begins before the age of 3 years and can last throughout a person's life, although symptoms may improve over time. Some children show ASD symptoms within the first 12 months of life. In others, symptoms may not show up until 24 months of age or later. Some children with ASD gain new skills and meet developmental milestones until around 18 to 24 months of age, and then they stop gaining new skills or lose the skills they once had.

As children with ASD become adolescents and young adults, they may have difficulties developing and maintaining friendships, communicating with peers and adults, or understanding what behaviors are expected in school or on the job. They may come to the attention of healthcare providers because they also have conditions such as anxiety, depression, or attention-deficit/hyperactivity disorder (ADHD), which occur more often in people with ASD than in people without ASD.

Signs and symptoms

People with ASD often have problems with social communication and interaction, and restricted or repetitive behaviors or interests. People with ASD may also have different ways of learning, moving, or paying attention. These characteristics can make life very challenging . It is important to note that some people without ASD might also have some of these symptoms.

As a parent, you already have what it takes to help your young child learn and grow. CDC has developed materials to help you track your child's developmental milestones and share that progress, or any concerns, with your child's doctor at every check-up.

Track your child's development‎‎

Risk factors.

There is not just one cause of ASD. Many different factors have been identified that may make a child more likely to have ASD, including environmental, biologic, and genetic factors.

Although we know little about specific causes, the available evidence suggests that the following may put children at greater risk for developing ASD:

• Having a sibling with ASD
• Having certain genetic or chromosomal conditions, such as fragile X syndrome or tuberous sclerosis
• Experiencing complications at birth
• Being born to older parents

CDC is currently working on one of the largest US studies to date on ASD. This study, called the Study to Explore Early Development (SEED), was designed to look at the risk factors and behaviors related to ASD. CDC is now conducting a follow-up study of older children who were enrolled in SEED to determine the health, functioning, and needs of people with ASD and other developmental disabilities as they mature.

Screening and diagnosis

Diagnosing ASD can be difficult since there is no medical test, like a blood test, to diagnose the disorder. Doctors look at the child's behavior and development to make a diagnosis.

ASD can sometimes be detected at 18 months of age or younger. By age 2 years, a diagnosis by an experienced professional can be considered reliable. 1 However, many children do not receive a final diagnosis until they are much older. Some people are not diagnosed until they are adolescents or adults. This delay means that people with ASD might not get the early help they need.

Current treatments for ASD seek to reduce symptoms that interfere with daily functioning and quality of life. ASD affects each person differently, meaning that people with ASD have unique strengths and challenges and different treatment needs. 2 Treatment plans usually involve multiple professionals and are catered to the individual.

What CDC is doing

Promoting early identification of asd.

We naturally think of a child's growth as height and weight, but from birth to 5 years, a child should reach milestones in how they play, learn, speak, act, and move. A delay in any of these areas could be a sign of ASD or other developmental disability.

Through the Learn the Signs. Act Early. program, CDC and its partners aim to improve early identification of children with ASD and other developmental disabilities by promoting developmental monitoring , so children and families can get the services and support they need.

Did you know?‎

Understanding risk factors and causes of asd.

Understanding the risk factors that make a person more likely to develop ASD will help us learn more about the causes. CDC is currently funding and working on one of the largest US studies to date, called Study to Explore Early Development (SEED) .

SEED will help identify factors that may put children at risk for ASD and other developmental disabilities. SEED is a multi-year study being conducted at six sites and a data coordinating center, called the Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) network.

Determining how many people have ASD

There continue to be many children living with ASD who need services and support, both now and as they grow into adolescence and adulthood.

By studying the number of people identified with ASD over time, we can find out if the number is rising, dropping, or staying the same. We can also compare the number of children with ASD in different areas of the country and different groups of people. This information can help us look for causes of ASD.

CDC's Autism and Developmental Disabilities Monitoring (ADDM) Network has been estimating the number of 8-year-old children with ASD in the United States since 2000. ASD occurs in all racial, ethnic, and socioeconomic groups. It is more than 4 times more common among boys than among girls.

If you’re concerned

Research shows that early intervention services can greatly improve a child's development. 3 4 In order to make sure your child reaches their full potential, it is very important to receive services as soon as possible. Contact your child's doctor if you think your child might have ASD or if you have any other concerns about the way your child plays, learns, speaks, or acts.

Referral to a specialist

If you are still concerned, ask the doctor for a referral to a specialist who can do a more in-depth evaluation of your child. Specialists who can do a more in-depth evaluation and make a diagnosis include

• Developmental pediatricians (doctors who have special training in child development and children with special needs)
• Child neurologists (doctors who work on the brain, spine, and nerves)
• Child psychologists or psychiatrists (doctors who know about the human mind)

Free evaluations

At the same time, call your state's public early childhood system to request a free evaluation , sometimes called a Child Find evaluation, to find out if your child qualifies for intervention services. You do not need to wait for a doctor's referral or a medical diagnosis to make this call. Where to call for a free evaluation from the state depends on your child's age.

If your child is not yet 3 years old

• Contact your local early intervention system.
• You can find the right contact information for your state by calling the Early Childhood Technical Assistance Center (ECTA) at 919-962-2001.
• Or visit the ECTA website.

If your child is 3 years old or older

• If your child is 3 years old or older, contact your local public school system.
• Even if your child is not yet old enough for kindergarten or enrolled in a public school, call your local elementary school or board of education and ask to speak with someone who can help you have your child evaluated.
• If you're not sure who to contact, call the ECTA at 919-962-2001.
• Lord C, Risi S, DiLavore PS, Shulman C, Thurm A, Pickles A. Autism from 2 to 9 years of age . Arch Gen Psychiatry . 2006;63(6):694-701.
• Hyman SL, Levy SE, Myers SM; COUNCIL ON CHILDREN WITH DISABILITIES, SECTION ON DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS. Identification, Evaluation, and Management of Children With Autism Spectrum Disorder. Pediatrics . 2020;145(1):e20193447.
• Handleman, Jan S., and Sandra L. Harris, eds. Preschool education programs for children with autism . Austin, TX: Pro-Ed, 2001.
• National Research Council. Educating Children with Autism . National Academies Press, 2001.

Autism Spectrum Disorder (ASD)

Autism spectrum disorder (ASD) is a developmental disability that can cause significant social, communication and behavioral challenges. CDC is committed to continuing to provide essential data on ASD and develop resources that help identify children with ASD as early as possible.

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General Information

Autism spectrum disorder, the name adopted in 2013, is a developmental disorder characterized by persistent problems in social communication and interaction, along with restricted and repetitive patterns of behavior, interests or activities. 1  It replaces the older terms of autistic disorder, Asperger's syndrome and other conditions envisioned on "the great continuum" of autism. 2  Still, the defining features of the condition commonly referred to as "autism" remain essentially the same.

But what does autism  look  like? As you observe a person's behavior, what might make you suspect he or she could have autism? To explore this question, we return to the very first written account of autism.

First Accounts of Autism: Defining Characteristics

It is likely that autism has existed through the ages, but the first ever clinical account of the disorder was published by Dr. Leo Kanner in 1943. 3  Dr. Kanner, who developed the first child psychiatric service at a U.S. hospital, described a group of 11 children – eight boys and three girls – who had "autistic disturbances of affective contact." 4

Dr. Kanner based his report on direct observation, and much of what he set down has stood the test of time. He vividly depicted the essential features of autism, all of which are echoed in current-day diagnostic manuals. It is interesting to note that, just as in Kanner's study, the rate of autism in males continues to be much higher than the rate in females.

Hans Asperger, an Austrian pediatrician, was working at nearly the same time as Kanner with a similar group of children on the other side of the Atlantic. A milder form of autism, Asperger syndrome, was named after him.

About Autism

As the word "spectrum" suggests, people with autism spectrum disorder (ASD) may have challenges that run the gamut from mild to severe, with different levels of ability and disability. Someone may have no functional speech, or may have a rich vocabulary. He or she may be intellectually disabled or have an average or above average IQ. He may be socially withdrawn or may be socially active, although in an oblivious, eccentric way. He may be fixated on lining up toys in a certain order, or have an encyclopedic knowledge of animals or another favorite topic.

To learn about the symptoms of autism spectrum disorder, please see our  About Autism  section.

Newly Diagnosed?

Parents of children who have just been diagnosed with ASD often feel both devastated and panicked. In our  Newly Diagnosed  section, we address some of the issues most on the minds of parents in this situation.

Exploring Autism Treatments

When a child is diagnosed with an autism spectrum disorder, families face the next challenge: choosing the right treatments and therapies for their child. What are these treatments and therapies? How much do we know about them? How can a family best evaluate whether a treatment is working for their child?

In our  Autism Treatments  section, we explore current autism treatments, the evidence behind them, and what we are learning from the experience of individuals and families who have tried them.

Challenging Behaviors

Children with autism spectrum disorder may exhibit many behaviors their family, teachers and others find challenging. At the same time, those children often find the world at large a challenge, and the behavior of other people may be confusing to  them .

What are the behaviors that distinguish a child with an ASD from his or her typically-developing peers? Although these will vary according to the severity of a person's autism and their age, there are core issues that affect most people with autism spectrum disorder. See our  Challenging Behaviors  section to explore those topics.

Adults With Autism

Many of the children diagnosed when autism rates began rising in the 1990s are, or soon will be, adults. Visit our  Adults with Autism  section for articles on topics of interest to teenagers and adults, such as the transition to adult services, getting a driver's license, employment, housing and romantic relationships.

So Much Still to Learn: A Quest For Answers

Since the 1940s, when Doctors Kanner and Asperger were putting their remarkable insights regarding socially different children on paper, we have learned a great deal. As you peruse this website and other sources of information on autism, you will see how much has been discovered about autism spectrum disorder from research in a wide variety of fields, including genetics, neuroscience, and cognitive psychology.

What will also become evident is how many questions remain unanswered. We still don't know exactly what causes autism; we haven't yet been able to identify specific subtypes of autism; and we still have very few proven treatments for autism.

The answers to our urgent questions will only come through research. The Interactive Autism Network was created to facilitate just that.

We hope individuals with ASD and their families will use this site to become informed consumers of autism research, and to become part of research studies themselves. Care providers, educators, researchers,

We salute each and every one of you who is committed to finding answers: individuals with autism and their families, researchers and educators, doctors and therapists, advocates and policy makers. We are here for you, and hope you will contact us with your questions, ideas, and concerns.

• American Psychiatric Association. (2013).  Diagnostic and statistical manual of mental disorders  (5th ed.). Arlington, VA: American Psychiatric Publishing.
• Grandin, T. (2006).  Thinking in pictures: My life with autism  (Exp. ed.). New York: Vintage Books. (Pg. 47.)
• Volkmar, F., & Klin, A. (2005). Issues in the classification of autism and related conditions. In F. Volkmar et al. (Eds.),  Handbook of Autism and Pervasive Developmental Disorders  (pp.5-41). Hoboken, NJ: John Wiley & Sons.
• Kanner, L. (1943).  Autistic disturbances of affective contact. Nervous Child, 2 , 217-250.

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• Autism spectrum disorder

Autism spectrum disorder is a condition related to brain development that impacts how a person perceives and socializes with others, causing problems in social interaction and communication. The disorder also includes limited and repetitive patterns of behavior. The term "spectrum" in autism spectrum disorder refers to the wide range of symptoms and severity.

Autism spectrum disorder includes conditions that were previously considered separate — autism, Asperger's syndrome, childhood disintegrative disorder and an unspecified form of pervasive developmental disorder. Some people still use the term "Asperger's syndrome," which is generally thought to be at the mild end of autism spectrum disorder.

Autism spectrum disorder begins in early childhood and eventually causes problems functioning in society — socially, in school and at work, for example. Often children show symptoms of autism within the first year. A small number of children appear to develop normally in the first year, and then go through a period of regression between 18 and 24 months of age when they develop autism symptoms.

While there is no cure for autism spectrum disorder, intensive, early treatment can make a big difference in the lives of many children.

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Some children show signs of autism spectrum disorder in early infancy, such as reduced eye contact, lack of response to their name or indifference to caregivers. Other children may develop normally for the first few months or years of life, but then suddenly become withdrawn or aggressive or lose language skills they've already acquired. Signs usually are seen by age 2 years.

Each child with autism spectrum disorder is likely to have a unique pattern of behavior and level of severity — from low functioning to high functioning.

Some children with autism spectrum disorder have difficulty learning, and some have signs of lower than normal intelligence. Other children with the disorder have normal to high intelligence — they learn quickly, yet have trouble communicating and applying what they know in everyday life and adjusting to social situations.

Because of the unique mixture of symptoms in each child, severity can sometimes be difficult to determine. It's generally based on the level of impairments and how they impact the ability to function.

Below are some common signs shown by people who have autism spectrum disorder.

Social communication and interaction

A child or adult with autism spectrum disorder may have problems with social interaction and communication skills, including any of these signs:

• Fails to respond to his or her name or appears not to hear you at times
• Resists cuddling and holding, and seems to prefer playing alone, retreating into his or her own world
• Has poor eye contact and lacks facial expression
• Doesn't speak or has delayed speech, or loses previous ability to say words or sentences
• Can't start a conversation or keep one going, or only starts one to make requests or label items
• Speaks with an abnormal tone or rhythm and may use a singsong voice or robot-like speech
• Repeats words or phrases verbatim, but doesn't understand how to use them
• Doesn't appear to understand simple questions or directions
• Doesn't express emotions or feelings and appears unaware of others' feelings
• Doesn't point at or bring objects to share interest
• Inappropriately approaches a social interaction by being passive, aggressive or disruptive
• Has difficulty recognizing nonverbal cues, such as interpreting other people's facial expressions, body postures or tone of voice

Patterns of behavior

A child or adult with autism spectrum disorder may have limited, repetitive patterns of behavior, interests or activities, including any of these signs:

• Performs repetitive movements, such as rocking, spinning or hand flapping
• Performs activities that could cause self-harm, such as biting or head-banging
• Develops specific routines or rituals and becomes disturbed at the slightest change
• Has problems with coordination or has odd movement patterns, such as clumsiness or walking on toes, and has odd, stiff or exaggerated body language
• Is fascinated by details of an object, such as the spinning wheels of a toy car, but doesn't understand the overall purpose or function of the object
• Is unusually sensitive to light, sound or touch, yet may be indifferent to pain or temperature
• Doesn't engage in imitative or make-believe play
• Fixates on an object or activity with abnormal intensity or focus
• Has specific food preferences, such as eating only a few foods, or refusing foods with a certain texture

As they mature, some children with autism spectrum disorder become more engaged with others and show fewer disturbances in behavior. Some, usually those with the least severe problems, eventually may lead normal or near-normal lives. Others, however, continue to have difficulty with language or social skills, and the teen years can bring worse behavioral and emotional problems.

When to see a doctor

Babies develop at their own pace, and many don't follow exact timelines found in some parenting books. But children with autism spectrum disorder usually show some signs of delayed development before age 2 years.

If you're concerned about your child's development or you suspect that your child may have autism spectrum disorder, discuss your concerns with your doctor. The symptoms associated with the disorder can also be linked with other developmental disorders.

Signs of autism spectrum disorder often appear early in development when there are obvious delays in language skills and social interactions. Your doctor may recommend developmental tests to identify if your child has delays in cognitive, language and social skills, if your child:

• Doesn't respond with a smile or happy expression by 6 months
• Doesn't mimic sounds or facial expressions by 9 months
• Doesn't babble or coo by 12 months
• Doesn't gesture — such as point or wave — by 14 months
• Doesn't say single words by 16 months
• Doesn't play "make-believe" or pretend by 18 months
• Doesn't say two-word phrases by 24 months
• Loses language skills or social skills at any age

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Autism spectrum disorder has no single known cause. Given the complexity of the disorder, and the fact that symptoms and severity vary, there are probably many causes. Both genetics and environment may play a role.

• Genetics. Several different genes appear to be involved in autism spectrum disorder. For some children, autism spectrum disorder can be associated with a genetic disorder, such as Rett syndrome or fragile X syndrome. For other children, genetic changes (mutations) may increase the risk of autism spectrum disorder. Still other genes may affect brain development or the way that brain cells communicate, or they may determine the severity of symptoms. Some genetic mutations seem to be inherited, while others occur spontaneously.
• Environmental factors. Researchers are currently exploring whether factors such as viral infections, medications or complications during pregnancy, or air pollutants play a role in triggering autism spectrum disorder.

No link between vaccines and autism spectrum disorder

One of the greatest controversies in autism spectrum disorder centers on whether a link exists between the disorder and childhood vaccines. Despite extensive research, no reliable study has shown a link between autism spectrum disorder and any vaccines. In fact, the original study that ignited the debate years ago has been retracted due to poor design and questionable research methods.

Avoiding childhood vaccinations can place your child and others in danger of catching and spreading serious diseases, including whooping cough (pertussis), measles or mumps.

Risk factors

The number of children diagnosed with autism spectrum disorder is rising. It's not clear whether this is due to better detection and reporting or a real increase in the number of cases, or both.

Autism spectrum disorder affects children of all races and nationalities, but certain factors increase a child's risk. These may include:

• Your child's sex. Boys are about four times more likely to develop autism spectrum disorder than girls are.
• Family history. Families who have one child with autism spectrum disorder have an increased risk of having another child with the disorder. It's also not uncommon for parents or relatives of a child with autism spectrum disorder to have minor problems with social or communication skills themselves or to engage in certain behaviors typical of the disorder.
• Other disorders. Children with certain medical conditions have a higher than normal risk of autism spectrum disorder or autism-like symptoms. Examples include fragile X syndrome, an inherited disorder that causes intellectual problems; tuberous sclerosis, a condition in which benign tumors develop in the brain; and Rett syndrome, a genetic condition occurring almost exclusively in girls, which causes slowing of head growth, intellectual disability and loss of purposeful hand use.
• Extremely preterm babies. Babies born before 26 weeks of gestation may have a greater risk of autism spectrum disorder.
• Parents' ages. There may be a connection between children born to older parents and autism spectrum disorder, but more research is necessary to establish this link.

Complications

Problems with social interactions, communication and behavior can lead to:

• Problems in school and with successful learning
• Employment problems
• Inability to live independently
• Social isolation
• Stress within the family
• Victimization and being bullied

More Information

• Autism spectrum disorder and digestive symptoms

There's no way to prevent autism spectrum disorder, but there are treatment options. Early diagnosis and intervention is most helpful and can improve behavior, skills and language development. However, intervention is helpful at any age. Though children usually don't outgrow autism spectrum disorder symptoms, they may learn to function well.

• Autism spectrum disorder (ASD). Centers for Disease Control and Prevention. https://www.cdc.gov/ncbddd/autism/facts.html. Accessed April 4, 2017.
• Uno Y, et al. Early exposure to the combined measles-mumps-rubella vaccine and thimerosal-containing vaccines and risk of autism spectrum disorder. Vaccine. 2015;33:2511.
• Taylor LE, et al. Vaccines are not associated with autism: An evidence-based meta-analysis of case-control and cohort studies. Vaccine. 2014;32:3623.
• Weissman L, et al. Autism spectrum disorder in children and adolescents: Overview of management. https://www.uptodate.com/home. Accessed April 4, 2017.
• Autism spectrum disorder. In: Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th ed. Arlington, Va.: American Psychiatric Association; 2013. http://dsm.psychiatryonline.org. Accessed April 4, 2017.
• Weissman L, et al. Autism spectrum disorder in children and adolescents: Complementary and alternative therapies. https://www.uptodate.com/home. Accessed April 4, 2017.
• Augustyn M. Autism spectrum disorder: Terminology, epidemiology, and pathogenesis. https://www.uptodate.com/home. Accessed April 4, 2017.
• Bridgemohan C. Autism spectrum disorder: Surveillance and screening in primary care. https://www.uptodate.com/home. Accessed April 4, 2017.
• Levy SE, et al. Complementary and alternative medicine treatments for children with autism spectrum disorder. Child and Adolescent Psychiatric Clinics of North America. 2015;24:117.
• Brondino N, et al. Complementary and alternative therapies for autism spectrum disorder. Evidence-Based Complementary and Alternative Medicine. http://dx.doi.org/10.1155/2015/258589. Accessed April 4, 2017.
• Volkmar F, et al. Practice parameter for the assessment and treatment of children and adolescents with autism spectrum disorder. Journal of the American Academy of Child and Adolescent Psychiatry. 2014;53:237.
• Autism spectrum disorder (ASD). Eunice Kennedy Shriver National Institute of Child Health and Human Development. https://www.nichd.nih.gov/health/topics/autism/Pages/default.aspx. Accessed April 4, 2017.
• American Academy of Pediatrics policy statement: Sensory integration therapies for children with developmental and behavioral disorders. Pediatrics. 2012;129:1186.
• James S, et al. Chelation for autism spectrum disorder (ASD). Cochrane Database of Systematic Reviews. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD010766.pub2/abstract;jsessionid=9467860F2028507DFC5B69615F622F78.f04t02. Accessed April 4, 2017.
• Van Schalkwyk GI, et al. Autism spectrum disorders: Challenges and opportunities for transition to adulthood. Child and Adolescent Psychiatric Clinics of North America. 2017;26:329.
• Autism. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed April 4, 2017.
• Autism: Beware of potentially dangerous therapies and products. U.S. Food and Drug Administration. https://www.fda.gov/ForConsumers/ConsumerUpdates/ucm394757.htm?source=govdelivery&utm_medium=email&utm_source=govdelivery. Accessed May 19, 2017.
• Drutz JE. Autism spectrum disorder and chronic disease: No evidence for vaccines or thimerosal as a contributing factor. https://www.uptodate.com/home. Accessed May 19, 2017.
• Weissman L, et al. Autism spectrum disorder in children and adolescents: Behavioral and educational interventions. https://www.uptodate.com/home. Accessed May 19, 2017.
• Huebner AR (expert opinion). Mayo Clinic, Rochester, Minn. June 7, 2017.

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Home — Essay Samples — Nursing & Health — Neurology & Nervous System Diseases — Autism

Essays About Autism

What makes a good autism essay topics.

When it comes to writing an essay on autism, it's important to choose a topic that is not only interesting but also relevant and impactful. The topic you choose can make or break your essay, so it's crucial to select one that is both engaging and thought-provoking. Here are some recommendations on how to brainstorm and choose an essay topic, what to consider, and What Makes a Good essay topic.

When brainstorming for autism essay topics, it's important to consider the audience and the purpose of the essay. Think about what you want to achieve with your essay and who will be reading it. Consider the impact you want to make and the message you want to convey. It's also important to choose a topic that is manageable and can be effectively explored within the constraints of the essay.

A good autism essay topic should be relevant and timely. Consider current issues and debates surrounding autism and choose a topic that is both current and significant. It's also important to choose a topic that is unique and original. Avoid cliché topics and instead focus on something that has not been extensively explored or discussed. A good essay topic should also be specific and focused. Avoid broad and generic topics and instead narrow down your focus to a specific aspect or issue related to autism.

Best Autism Essay Topics

• The impact of early intervention on children with autism
• The role of sensory processing in autism
• The link between autism and genetics
• The portrayal of autism in popular media
• The challenges of parenting a child with autism
• The benefits of music therapy for individuals with autism
• The use of technology in autism interventions
• The importance of inclusive education for children with autism
• The impact of autism on the family dynamics
• The experiences of adults with autism in the workplace
• The connection between autism and co-occurring conditions
• The role of speech therapy in treating autism
• The challenges of accessing autism services in rural communities
• The intersection of race and autism diagnosis
• The potential of animal-assisted therapy for individuals with autism
• The link between autism and mental health
• The experiences of girls and women with autism
• The impact of autism on social relationships
• The role of advocacy in the autism community
• The potential of alternative therapies for individuals with autism

Autism essay topics Prompts

• Imagine a world where autism acceptance is the norm. How would society be different?
• Write a letter to a parent of a newly diagnosed child with autism, offering support and guidance.
• Create a fictional story that explores the experiences of a teenager with autism navigating high school.
• Imagine a future where a cure for autism is discovered. What are the potential implications and consequences?
• Write a reflective essay on your own experiences with autism, whether as an individual on the spectrum or as a caregiver or advocate.

Choosing a topic for an autism essay can be a daunting task, but with careful consideration and creativity, you can choose a topic that is not only engaging but also impactful. Whether you're exploring the latest research on autism interventions or delving into the personal experiences of individuals with autism, there are endless possibilities for compelling and thought-provoking essay topics. So, take your time, brainstorm, and choose a topic that will captivate your audience and leave a lasting impression.

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Sensation and Perception: Autism

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Autism spectrum disorder is a condition related to brain development that impacts how a person perceives and socializes with others, causing problems in social interaction and communication.

Trouble with social interaction, verbal and nonverbal communication, and presence of restricted interests and repetitive behavior.

Autism spectrum disorder has no single known cause. Given the complexity of the disorder, and the fact that symptoms and severity vary, there are probably many causes. Both genetics and environment may play a role.

Autism is about 4 times more likely in boys than girls. Autism affects children of all racial, ethnic, and socioeconomic groups. Autism can be reliably diagnosed by age 2, but children may be diagnosed at earlier ages. ASD affects about 1 in 68 children Visit disclaimer page in the United States.

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Educating Children with Autism (2001)

Chapter: 16 conclusions and recommendations.

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16 Conclusions and Recommendations This chapter summarizes the committee’s conclusions about the state of the science in early intervention for children with autistic spectrum disorders and its recommendations for future intervention strategies, pro- grams, policy, and research. The chapter is organized around seven key areas pertaining to educational interventions for young children with autistic spectrum disorders: how the disorders are diagnosed and as- sessed and how prevalent they are; the effect on and role of families; appropriate goals for educational services; characteristics of effective in- terventions and educational programs; public policy approaches to en- suring access to appropriate education; the preparation of educational personnel; and needs for future research. DIAGNOSIS, ASSESSMENT, AND PREVALENCE Conclusions Autism is a developmental disorder of neurobiologic origin that is defined on the basis of behavioral and developmental features. Autism is best characterized as a spectrum of disorders that vary in severity of symptoms, age of onset, and association with other disorders (e.g., mental retardation, specific language delay, epilepsy). The manifestations of au- tism vary considerably across children and within an individual child over time. There is no single behavior that is always typical of autism and no behavior that would automatically exclude an individual child from a 211 

212 EDUCATING CHILDREN WITH AUTISM diagnosis of autism, even though there are strong and consistent com- monalities, especially relative to social deficits. The large constellation of behaviors that define autistic spectrum dis- orders—generally representing deficits in social interaction, verbal and nonverbal communication, and restricted patterns of interest or behav- iors—are clearly and reliably identifiable in very young children to expe- rienced clinicians and educators. However, distinctions among classical autism and atypical autism, pervasive developmental disorder-not other- wise specified (PDD-NOS), and Asperger’s disorder can be arbitrary and are often associated with the presence or severity of handicaps, such as mental retardation and severe language impairment. Identifying narrow categories within autism is necessary for some research purposes; however, the clinical or educational benefit to subclas- sifying autistic spectrum disorders purely by diagnosis is debated. In contrast, individual differences in language development, verbal and non- verbal communication, sensory or motor skills, adaptive behavior, and cognitive abilities have significant effects on behavioral presentation and outcome, and, consequently, have specific implications for educational goals and strategies. Thus, the most important considerations in pro- gramming have to do with the strengths and weaknesses of the indi- vidual child, the age at diagnosis, and early intervention. With adequate time and training, the diagnosis of autistic spectrum disorders can be made reliably in 2-year-olds by professionals experi- enced in the diagnostic assessment of young children with autistic spec- trum disorders. Many families report becoming concerned about their children’s behavior and expressing this concern, usually to health profes- sionals, even before this time. Research is under way to develop reliable methods of identification for even younger ages. Children with autistic spectrum disorders, like children with vision or hearing problems, re- quire early identification and diagnosis to equip them with the skills (e.g., imitation, communication) to benefit from educational services, with some evidence that earlier initiation of specific services for autistic spectrum disorders is associated with greater response to treatment. Thus, well meaning attempts not to label children with formal diagnoses can deprive children of specialized services. There are clear reasons for early identifi- cation of children, even as young as two years of age, within the autism spectrum. Epidemiological studies and service-based reports indicate that the prevalence of autistic spectrum disorders has increased in the last 10 years, in part due to better identification and broader categorization by educators, physicians, and other professionals. There is little doubt that more children are being identified as requiring specific educational inter- ventions for autistic spectrum disorders. This has implications for the provision of services at many levels. Analysis of data from the Office of 

CONCLUSIONS AND RECOMMENDATIONS 213 Special Education Programs, gathered for school-age children since the autism category was recognized in 1991, would support investigation of whether the dramatic increases in the numbers of children served with autistic spectrum disorders are offset by commensurate decreases in other categories in which children with autistic spectrum disorders might have previously been misclassified or whether these dramatic increases have come about for other reasons. Although children with autistic spectrum disorders share some char- acteristics with children who have other developmental disorders and may benefit from many of the same educational techniques, they offer unique challenges to families, teachers, and others who work with them. Their deficits in nonverbal and verbal communication require intense effort and skill even in the teaching of basic information. The unique difficulties in social interaction (e.g., in joint attention) may require more individual guidance than for other children in order to attract and sustain their children’s attention. Moreover, ordinary social exchanges between peers do not usually occur without deliberate planning and ongoing struc- turing by the adults in the child’s environment. The absence of typical friendships and peer relationships affects children’s motivation systems and the meaning of experiences. Appropriate social interactions may be some of the most difficult and important lessons a child with autistic spectrum disorders will learn. In addition, the frequency of behavior problems, such as tantrums and self-stimulatory and aggressive behavior, is high. The need for sys- tematic selection of rewards for many children with autistic spectrum disorders, whose motivation or interests can be limited, requires creativ- ity and continued effort from teachers and parents to maximize the child’s potential. Although general principles of learning and behavior analysis apply to autistic spectrum disorders, familiarity with the specific nature of the disorder should contribute to analysis of the contexts (e.g., commu- nicative and social) of behaviors for individual children and result in more effective programming. For example, conducting a functional as- sessment that considers contexts, and then replacing problem behaviors with more appropriate ways to communicate can be an effective method for reducing problem behaviors. Recommendations 1-1 Because of their shared continuities and their unique social diffi- culties, children with any autistic spectrum disorder (autistic disorder, Asperger’s disorder, atypical autism, PDD-NOS, child- hood disintegrative disorder), regardless of level of severity or function, should be eligible for special educational services within the category of autistic spectrum disorders, as opposed to other 

214 EDUCATING CHILDREN WITH AUTISM terminology used by school systems, such as other health im- paired, social emotionally maladjusted, significantly developmen- tally delayed, or neurologically impaired. 1-2 Identification of autistic spectrum disorders should include a for- mal multidisciplinary evaluation of social behavior, language and nonverbal communication, adaptive behavior, motor skills, atypi- cal behaviors, and cognitive status by a team of professionals experienced with autistic spectrum disorders. An essential part of this evaluation is the systematic gathering of information from parents on their observations and concerns. If the school system cannot carry out such an assessment, the local education author- ity should fund the assessment through external sources. Early diagnosis should be emphasized. Because of variability in early development, younger children with autistic spectrum disorders should receive a follow-up diagnostic and educational assess- ment within one to two years of initial evaluation. 1-3 Professional organizations, with the support of the National Insti- tutes of Health (NIH) and the Department of Education’s Office of Special Education Programs (OSEP), should disseminate infor- mation concerning the nature and range of autistic spectrum dis- orders in young children to all professionals who have contact with children, particularly those who work with infants, toddlers, and preschool children. This information should include the vari- able presentations and patterns of behavior seen in autistic spec- trum disorders from toddlers to school age children. Members of “child find” teams within the early intervention systems, as well as primary care providers, should be trained in identifying the “red flags of autistic spectrum disorders” and the importance and means of early referral for comprehensive diagnostic evaluation. Advocacy groups and relevant federal agencies, as well as profes- sional organizations, should use effective media resources, in- cluding the Internet, to provide information concerning the range of behaviors in autistic spectrum disorders. ROLE OF FAMILIES Conclusions Having a child with an autistic spectrum disorder is a challenge for any family. Involvement of families in the education of young children with autistic spectrum disorders can occur at multiple levels, including advocacy, parents as participating partners in and agents of education or 

CONCLUSIONS AND RECOMMENDATIONS 215 behavior change, and family-centered consideration of the needs and strengths of the family as a unit. Nearly all empirically supported treat- ments reviewed by the committee included a parent component, and most research programs used a parent-training approach. More informa- tion is needed about the benefits of a family-centered orientation or com- bined family-centered and formalized parent training in helping parents. It is well established that parents can learn and successfully apply skills to changing the behavior of their children with autistic spectrum disorders, though little is known about the effects of cultural differences, such as race, ethnicity, and social class, nor about the interactions among family factors, child characteristics, and features of educational interven- tion. For most families, having a child with an autistic spectrum disorder creates added stress. Parents’ use of effective teaching methods can have a significant effect on that stress, as can support from within the family and the community. Parents need access to balanced information about autistic spectrum disorders and the range of appropriate services and technologies in order to carry out their responsibilities. They also need timely information about assessments, educational plans, and the avail- able resources for their children. This information needs to be conveyed to them in a meaningful way that gives them time to prepare to fulfill their roles and responsibilities. In the last ten years the widespread availability of the Internet and media attention to autistic spectrum disorders have increased parents’ knowledge but often conveyed perspectives that were not balanced nor well-supported scientifically. Of crucial importance is the question of how to make information available to parents and to ensure their active role in advocacy for their children’s education. Recommendations 2-1 Parents’ concerns and perspectives should actively help to shape educational planning. Specifically: a. In order for a family to be effective members of the Indi- vidualized Education Plan (IEP) team that plans a child’s educa- tion, the local school system should provide to the parents, at the beginning of the assessment process, written information con- cerning the nature of autistic spectrum disorders and eligibility categories, the range of alternatives within best practices in early education of autistic spectrum disorders, sources of funding and support (e.g., a support guide and bibliography), and their child’s rights. b. Prior to the IEP meeting, the local school system should provide to each family the written results of their child’s assess- 

216 EDUCATING CHILDREN WITH AUTISM ment, and a contact person to explain the findings if they wish, and should indicate that they will have the opportunity to present their concerns. Early during the IEP meeting, parents should be given an opportunity to voice their questions, concerns, and per- spectives about their child’s development and educational pro- gramming. 2-2 As part of local educational programs and intervention programs for children from birth to age 3, families of children with autistic spectrum disorders should be provided the opportunity to learn techniques for teaching their child new skills and reducing prob- lem behaviors. These opportunities should include not only di- dactic sessions, but also ongoing consultation in which individu- alized problem-solving, including in-home observations or training, occur for a family, as needed, to support improvements at home as well as at school. 2-3 Families that are experiencing stress in raising their children with an autistic spectrum disorder should be provided with mental health support services. Under Part C of the Individuals with Disabilities Education Act (IDEA), which addresses family sup- port and service coordination, including private service provid- ers, services should be extended to include families of children at least up to age 8 years. GOALS FOR EDUCATIONAL SERVICES Conclusions At the root of questions about the most appropriate educational inter- ventions lie differences in assumptions about what is possible and what is important to give students with autistic spectrum disorders through edu- cation. The appropriate goals for educational services are the same as those for other children: personal independence and social responsibility. These goals imply continuous progress in social and cognitive abilities, verbal and nonverbal communication skills, adaptive skills, amelioration of behavioral difficulties, and generalization of abilities across multiple environments. In some cases, reports have suggested that particular treat- ments can foster permanent “recovery”. However, as with other develop- mental disabilities, the core deficits of autistic spectrum disorders have generally been found to persist, to some degree, in most individuals. Research concerning outcomes can be characterized by whether the goal of intervention is broadly defined (e.g., “recovery” or “best out- 

CONCLUSIONS AND RECOMMENDATIONS 217 come”) or more specifically defined (e.g., increasing vocabulary or peer- directed social behavior); whether the design involves reporting results in terms of group or individual changes; and whether the goals are short term (i.e., to be achieved in a few weeks or months) or longer term (i.e., over years). A large body of single-subject research has demonstrated substantial progress in individual responses to specific intervention tech- niques in relatively short periods of times (e.g., several months) in many specific areas, including gains in social skills, language acquisition, non- verbal communication, and reductions in challenging behaviors. Studies over longer periods of time have documented joint attention, symbolic play, early language skills, and imitation as core deficits and hallmarks of the disorder that are predictive of longer term outcome in the domains of language, adaptive behaviors, and academic skills. Many treatment studies report postintervention placement as an out- come measure. While successful participation in regular classrooms is an important goal for some children with autistic spectrum disorders, the usefulness of placement in regular education classes as an outcome mea- sure is limited, because placement may be related to many variables other than the characteristics of the child (e.g., prevailing trends in inclusion, availability of other services). The most commonly reported outcome measure in group treatment studies of children with autistic spectrum disorders has been changes in IQ scores, which also have many limita- tions. Studies have reported substantial changes in large numbers of chil- dren in intervention studies and longitudinal studies in which children received a variety of interventions. Even in the treatment studies that have shown the strongest gains, children’s outcomes are variable, with some children making substantial progress and others showing very slow gains. The needs and strengths of young children with autistic spectrum disorders are very heterogeneous. Although there is evidence that many interventions lead to improvements and that some children shift in spe- cific diagnosis along the autism spectrum during the preschool years, there does not appear to be a simple relationship between any particular intervention and “recovery” from autistic spectrum disorders. Thus, while substantial evidence exists that treatments can reach short-term specific goals in many areas, gaps remain in addressing larger questions of the relationships between particular techniques, child characteristics, and outcomes. Recommendations The IEP and Individual Family Service Plan (IFSP) should be the vehicles for planning and implementing educational objectives. 

218 EDUCATING CHILDREN WITH AUTISM 3-1 Appropriate educational objectives for children with autistic spec- trum disorders should be observable, measurable behaviors and skills. These objectives should be able to be accomplished within 1 year and expected to affect a child’s participation in education, the community, and family life. They should include the devel- opment of: a. Social skills to enhance participation in family, school, and community activities (e.g., imitation, social initiations and re- sponse to adults and peers, parallel and interactive play with peers and siblings); b. Expressive verbal language, receptive language, and non- verbal communication skills; c. A functional symbolic communication system; d. Increased engagement and flexibility in developmentally appropriate tasks and play, including the ability to attend to the environment and respond to an appropriate motivational system; e. Fine and gross motor skills used for age appropriate func- tional activities, as needed; f. Cognitive skills, including symbolic play and basic con- cepts, as well as academic skills; g. Replacement of problem behaviors with more conven- tional and appropriate behaviors; and h. Independent organizational skills and other behaviors that underlie success in regular education classrooms (e.g., complet- ing a task independently, following instructions in a group, ask- ing for help). 3-2 Ongoing measurement of educational objectives must be docu- mented in order to determine whether a child is benefiting from a particular intervention. Every child’s response to the educational program should be assessed after a short period of time. Progress should be monitored frequently and objectives adjusted accord- ingly. CHARACTERISTICS OF EFFECTIVE INTERVENTIONS Conclusions In general, there is consistent agreement across comprehensive inter- vention programs about a number of features, though practical and, some- times, ethical considerations have made well-controlled studies with ran- dom assignment very difficult to conduct without direct evaluation. Characteristics of the most appropriate intervention for a given child must 

CONCLUSIONS AND RECOMMENDATIONS 219 be tied to that child’s and family’s needs. However, without direct evalu- ation, it is difficult to know which features are of greatest importance in a program. Across primarily preschool programs, there is a very strong consensus that the following features are critical: • entry into intervention programs as soon as an autism spectrum diagnosis is seriously considered; • active engagement in intensive instructional programming for a minimum of the equivalent of a full school day, 5 days (at least 25 hours) a week, with full year programming varied according to the child’s choronological age and developmental level; • repeated, planned teaching opportunities generally organized around relatively brief periods of time for the youngest children (e.g., 15- 20 minute intervals), including sufficient amounts of adult attention in one-to-one and very small group instruction to meet individualized goals; • inclusion of a family component, including parent training; • low student/teacher ratios (no more than two young children with autistic spectrum disorders per adult in the classroom); and • mechanisms for ongoing program evaluation and assessments of individual children’s progress, with results translated into adjustments in programming. Curricula across different programs differ in a number of ways. They include the ways in which goals are prioritized, affecting the relative time spent on verbal and nonverbal communication, social activities, behav- ioral, academic, motor, and other domains. Strategies from various pro- grams represent a range of techniques, including discrete trials, incidental teaching, structured teaching, “floor time”, and individualized modifica- tions of the environment, including schedules. Some programs adopt a unilateral use of one set of procedures, and others use a combination of approaches. Programs also differ in the relative amount of time spent in homes, centers, or schools, when children are considered ready for inclu- sion into regular classrooms, how the role of peers as intervention agents is supported, and in the use of distraction-free or natural environments. Programs also differ in the credentials that are required of direct support and supervisory staff and the formal and informal roles of collateral staff, such as speech language pathologists and occupational therapists. Overall, many of the programs are more similar than different in terms of levels of organization, staffing, ongoing monitoring, and the use of certain techniques, such as discrete trials, incidental learning, and struc- tured teaching. However, there are real differences in philosophy and practice that provide a range of alternatives for parents and school sys- tems considering various approaches. The key to any child’s educational program lies in the objectives specified in the IEP and the ways they are 

220 EDUCATING CHILDREN WITH AUTISM addressed. Much more important than the name of the program attended is how the environment and educational strategies allow implementation of the goals for a child and family. Thus, effective services will and should vary considerably across individual children, depending on a child’s age, cognitive and language levels, behavioral needs, and family priorities. Recommendations The committee’s recommendations for effective treatment are made on the basis of empirical findings, information from selected representa- tive programs, and findings in the general education and developmental literature. In particular, it is well established that children with autism spend much less time in focused and socially directed activity when in unstructured situations than do other children. Therefore, it becomes crucial to specify time engaged in social and focused activity as part of a program for children with autistic spectrum disorders. 4-1 Based on a set of individualized, specialized objectives and plans that are systematically implemented, educational services should begin as soon as a child is suspected of having an autistic spec- trum disorder. Taking into account the needs and strengths of an individual child and family, the child’s schedule and educational environment, in and out of the classroom, should be adapted as needed in order to implement the IEP. Educational services should include a minimum of 25 hours a week, 12 months a year, in which the child is engaged in systematically planned, develop- mentally appropriate educational activity aimed toward identi- fied objectives. Where this activity takes place and the content of the activity should be determined on an individual basis, de- pending on characteristics of both the child and the family. 4-2 A child must receive sufficient individualized attention on a daily basis so that individual objectives can be effectively implemented; individualized attention should include individual therapies, de- velopmentally appropriate small group instruction, and direct one-to-one contact with teaching staff. 4-3 Assessment of a child’s progress in meeting objectives should be used on an ongoing basis to further refine the IEP. Lack of objec- tively documentable progress over a 3 month period should be taken to indicate a need to increase intensity by lowering stu- 

CONCLUSIONS AND RECOMMENDATIONS 221 dent/teacher ratios, increasing programming time, reformulat- ing curricula, or providing additional training and consultation. 4-4 To the extent that it leads to the specified educational goals (e.g., peer interaction skills, independent participation in regular edu- cation), children should receive specialized instruction in settings in which ongoing interactions occur with typically developing children. 4-5 Six kinds of interventions should have priority: a. Functional, spontaneous communication should be the pri- mary focus of early education. For very young children, pro- gramming should be based on the assumption that most children can learn to speak. Effective teaching techniques for both verbal language and alternative modes of functional communication, drawn from the empirical and theoretical literature, should be vigorously applied across settings. b. Social instruction should be delivered throughout the day in various settings, using specific activities and interventions planned to meet age-appropriate, individualized social goals (e.g., with very young children, response to maternal imitation; with preschool children, cooperative activities with peers). c. The teaching of play skills should focus on play with peers, with additional instruction in appropriate use of toys and other materials. d. Other instruction aimed at goals for cognitive develop- ment should also be carried out in the context in which the skills are expected to be used, with generalization and maintenance in natural contexts as important as the acquisition of new skills. Because new skills have to be learned before they can be general- ized, the documentation of rates of acquisition is an important first step. Methods of introduction of new skills may differ from teaching strategies to support generalization and maintenance. e. Intervention strategies that address problem behaviors should incorporate information about the contexts in which the behaviors occur; positive, proactive approaches; and the range of techniques that have empirical support (e.g., functional assess- ment, functional communication training, reinforcement of alter- native behaviors). f. Functional academic skills should be taught when appro- priate to the skills and needs of a child. 

222 EDUCATING CHILDREN WITH AUTISM PUBLIC POLICIES Conclusions The Individuals with Disabilities Education Act (IDEA) contains the necessary provisions for ensuring rights to appropriate education for chil- dren with autistic spectrum disorders. However, the implementation and specification of these services are variable. Early intervention for young children with autistic spectrum disorders is expensive, and most local schools need financial help from the state and federal programs to pro- vide appropriate services. The large number of court cases is a symptom of the tension between families and school systems. Case law has yielded an inconsistent pattern of findings that vary according to the characteristics of the individual cases. The number of challenges to decision-making for programming within school systems reflects parents’ concerns about the adequacy of knowledge and the expertise of school systems in determining their children’s education and implementing appropriate techniques. The treatment of autistic spectrum disorders often involves many disciplines and agencies. This confuses lines of financial and intellectual responsibility and complicates assessment and educational planning. When communication between families and school systems goes awry, it can directly affect children’s programming and the energy and financial resources that are put into education rather than litigation. Support sys- tems are not generally adequate in undergirding local service delivery programs and maximizing the usefulness of different disciplines and agencies, and transitions between service delivery agencies are often prob- lematic. A number of states have successful models for providing services to children with autism, and mechanisms are becoming increasingly effi- cient and flexible in some states. In most cases, existing agencies at state and federal levels can develop appropriate programs without restructur- ing—with the possible addition of special task forces or committees de- signed to deal with issues particular to children with autistic spectrum disorders. Recommendations The committee recommends that a variety of steps be taken to ensure that policies are effectively carried out at the state and local levels. 5-1 At the federal level, the National Institutes of Health’s Autism Coordinating Committee and the Federal Interagency Coordinat- ing Council should jointly appoint a clinical research oversight 

CONCLUSIONS AND RECOMMENDATIONS 223 task force of professionals knowledgeable in the field of autistic spectrum disorders, to review and periodically report on basic and applied research programs to the parent agencies and to track program implementation through the State Interagency Coordi- nating Councils or relevant state agencies. Administrative sup- port for these efforts should be provided by the appropriate de- partment of the Secretary’s office. 5-2 States should have regional resource and training centers with expertise in autistic spectrum disorders to provide training and technical support to local schools. States should also have a mechanism to evaluate the adequacy of current support systems to local schools and recommend ways for improvement. One such mechanism could be an autistic spectrum disorders support systems task force that would examine the relevant provisions for personnel preparation, technical assistance, and demonstration of exemplary programs and would make recommendations as to what would be needed to bring a state’s support systems into alignment with quality education for children with autistic spec- trum disorders. States should monitor coordination among and transitions between service delivery systems and should develop ways to facilitate these processes. 5-3 Families should have access to consultation and legal knowledge such as provided by an ombudsman who is independent of the school system and who could be a standard part of Individual- ized Educational Plan planning and meetings. The ombudsman should be knowledgeable about autistic spectrum disorders and about relevant law and court decisions. The ombudsman’s role should include attending IEP meetings, interpreting the school system’s communications about a child to parents, and propos- ing, at the parents’ request, alternatives to those presented by the school system. Professional and advocacy groups should work together to provide this service, with the Governor’s Council for Developmental Disabilities or the Autistic Spectrum Disorders Support Systems Task Force responsible for ensuring funding for training and support of this service. 5-4 State and federal agencies should consider ways to work with and support professional and advocacy groups to provide up-to- date, practical, scientifically valid information to parents and practitioners. 

224 EDUCATING CHILDREN WITH AUTISM 5-5 States should have clearly defined minimum standards for per- sonnel in educational settings for children with autistic spectrum disorders. For example, at a minimum, teachers should have some special preparation (e.g., preservice course work, equiva- lent inservice training, workshops, and supervised practice in re- search-based practices in autistic spectrum disorders) and should have well-trained, experienced support personnel available to provide ongoing training and additional consultation. 5-6 States should develop a systematic strategy to fund the interven- tions that are necessary for children with autistic spectrum disor- ders in local schools, so that this cost is not borne primarily by the parents or local school systems. State education departments should develop interagency collaborations to pool support for local systems. A state fund for intensive intervention, or more systematic use of Medicaid waivers or other patterns of funding currently in place in some states, should be considered. Families should not be expected to fund or provide the majority of educa- tional programming for their children. 5-7 An updated, accurate summary of case law, consultation services, and mediation mechanisms in autistic spectrum disorders should be made accessible by the Office of Special Education Programs so that schools and parents can understand the options available to them when conflicts arise. 5-8 Since levels of information about autistic spectrum disorders vary greatly within the groups and agencies that make funding and policy decisions about autistic spectrum disorders, including state task forces in education and review panels in federal agencies, it is crucial that persons knowledgeable in the range of needs and interventions associated with autistic spectrum disorders be in- cluded in those decision-making activities. PERSONNEL PREPARATION Conclusions The nature of autistic spectrum disorders and other disabilities that frequently accompany them has significant implications for approaches to education and intervention at school, in the home, and in the commu- nity. Approaches that emphasize the use of specific “packages” of mate- rials and methods associated with comprehensive intervention programs 

CONCLUSIONS AND RECOMMENDATIONS 225 may understate the multiple immediate and long-term needs of children for behavior support and for instruction across areas. Teachers are faced with a huge task. They must be familiar with theory and research concerning best practices for children with autistic spectrum disorders, including methods of applied behavior analysis, naturalistic learning, assistive technology, socialization, communication, inclusion, adaptation of the environment, language interventions, assess- ment, and the effective use of data collection systems. Specific problems in generalization and maintenance of behaviors also affect the need for training in methods of teaching children with autistic spectrum disorders. The wide range of IQ scores and verbal skills associated with autistic spectrum disorders, from profound mental retardation and severe lan- guage impairments to superior intelligence, intensify the need for person- nel training. To enable teachers to adequately work with parents and with other professionals to set appropriate goals, teachers need familiar- ity with the course of autistic spectrum disorders and the range of pos- sible outcomes. Teachers learn according to the same principles as their students. Multiple exposures, opportunities to practice, and active involvement in learning are all important aspects of learning for teachers, as well as stu- dents. Many states and community organizations have invested substan- tial funds in teacher preparation through workshops and large-audience lectures by well-known speakers. While such presentations can stimulate enthusiasm, they do not substitute for ongoing consultation and hands- on opportunities to observe and practice skills working with children with autistic spectrum disorders. Personnel preparation remains one of the weakest elements of effec- tive programming for children with autistic spectrum disorders and their families. Ways of building on the knowledge of teachers as they acquire experience with children with autistic spectrum disorders, and ways of keeping skilled personnel within the field, are critical. This is particularly true given recent trends for dependence on relatively inexperienced assis- tants for in-home programs. Providing knowledge about autistic spec- trum disorders to special education and regular education administra- tors, as well as to specialized providers with major roles in early intervention (e.g., speech language pathologists) will be critical in effect- ing change that is proactive. Findings concerning change in educational and other opportunities suggest that administrative attitudes and sup- port are critical in improving schools. Recommendations The committee recommends that relevant state and federal agencies institute an agenda for upgrading personnel preparation for those who 

226 EDUCATING CHILDREN WITH AUTISM work with, and are responsible for, children with autistic spectrum disor- ders and their families. These efforts should be part of a larger effort to coordinate and collaborate with the already established infrastructure of special education, regional resource centers, technical assistance pro- grams, personnel preparation, communication sharing, and other relevant aspects of the existing infrastructure. Professionals aware of the special nature of these children are already carrying out many of these recom- mendations in a limited fashion. The committee urges agencies to pro- vide the personnel preparation resources needed for intensified efforts to build a viable support structure for educating children with autistic spec- trum disorders. 6-1 The Office of Special Education Programs should establish a 5- year plan to provide priority funds for preservice and inservice preparation for teachers, paraprofessionals, and other personnel providing services for children with autistic spectrum disorders, including children under age 3 years. 6-2 The need for a team approach involving many professions should be addressed by personnel preparation and practicum work within multidisciplined organizations and teams. 6-3 A special emphasis should be placed on training of trainers. There is a short supply of expertise and experience in the field of educa- tion for children with autistic spectrum disorders, and special attention should be paid to rapidly increase the capabilities of the trainers, who may have experience in special education or related fields, but not in the special skills and practices for children with autistic spectrum disorders. 6-4 The existing support systems that provide short-term training (e.g., technical assistance systems, resource centers, etc.) should include people with special expertise in autistic spectrum disor- ders on their staff. 6-5 The content of the curriculum for children with autistic spectrum disorders should be based on sound research. A continuing pro- gram should be established from such agencies as the National Institute of Mental Health and the National Institute of Child Health and Human Development to translate their research into usable information for practitioners. Work on family research is particularly relevant. 

CONCLUSIONS AND RECOMMENDATIONS 227 NEEDED RESEARCH Conclusions There are several distinct and substantial bodies of research relevant to young children with autistic spectrum disorders. One body identifies neurological, behavioral, and developmental characteristics. Another body of research addresses diagnostic practices and related issues of prevalence. Another has examined the effects of comprehensive early treatment programs on the immediate and long-term outcomes of chil- dren and their families. These treatment studies tended to use some form of group experimental design. An additional body of research has ad- dressed individual instructional or intervention approaches, with many studies in this literature using single-subject experimental methodology. Altogether, a large research base exists, but with relatively little integra- tion across bodies of literature. Highly knowledgeable researchers in one area of autistic spectrum disorders may have minimal information from other perspectives, even about studies with direct bearing on their find- ings. Most researchers have not used randomized group comparison de- signs because of the practical and ethical difficulties in randomly assign- ing children and families to treatment groups. In addition, there have been significant controversies over the type of control or contrast group to use and the conditions necessary for demonstrating effectiveness. Al- though a number of comprehensive programs have provided data on their effectiveness, and, in some cases, claims have been made that certain treatments are superior to others, there have been virtually no compari- sons of different comprehensive interventions of equal intensity. Across several of the bodies of literature, the children and families who have participated in studies are often inadequately described. Stan- dardized diagnoses, descriptions of ethnicity, the social class, and associ- ated features of the children (such as mental retardation and language level) are often not specified. Fidelity of treatment implementation has not been consistently assessed. Generalization, particularly across set- tings, and maintenance of treatment effects are not always measured. Though there is little evidence concerning the effectiveness of discipline- specific therapies, there is substantial research supporting the effective- ness of many specific therapeutic techniques. Recommendations 7-1 Funding agencies and professional journals should require minimium standards in design and description of intervention projects. All intervention studies should provide the following information: 

228 EDUCATING CHILDREN WITH AUTISM a. Adequate information concerning the children and fami- lies who participated, and who chose not to participate or with- drew from participation, including chronological age, develop- mental assessment data (including verbal and nonverbal IQ levels), standardized diagnoses, gender, race, family characteris- tics, socioeconomic status, and relevant health or other biological impairments; b. description of the intervention in sufficient detail so that an external group could replicate it; detailed documentation is crucial especially if no treatment manual is available; c. fidelity of treatment and degree of implementation; d. specific objective measures of expected outcomes, assessed at regular intervals; and e. measures of outcome that are independent of the interven- tion, in terms of both the evaluators and the measures, and in- clude broad immediate and long-term effects on children and families, particularly generalization and maintenance effects. 7-2 Funders and performers of research should recognize that valu- able information can be provided by a variety of approaches to research in intervention, including group experimental and single-subject designs. 7-3 In order to help educators and consumers make informed deci- sions about appropriate methods of intervention for particular children, federal agencies involved in autistic spectrum disorders initiatives (including the Office of Special Education Programs, the Office of Educational Research and Improvement, the Na- tional Institute of Child Health and Human Development, the National Institute of Mental Health, the National Institute of Neu- rological Disorders and Stroke, and the National Institute on Deaf- ness and Other Communication Disorders) and nonprofit agen- cies with similar national missions (such as Autism Society of America Foundation, Cure Autism Now, and National Alliance for Autism Research) should form a research task force and spe- cifically allocate federal responsibilites for recruiting and funding a comprehensive program of research related to intervention and treatment. This program should include: a. development of more specific, precise measures of impor- tant areas of outcome, such as social functioning, peer relation- ships, spontaneous communication and language, and the acqui- sition of competence in natural contexts (e.g., classroom, home); 

CONCLUSIONS AND RECOMMENDATIONS 229 b. definition of appropriate educational skills and sequences in social and cognitive development, informed by normal devel- opmental literature; c. measurement of the effects of the interactions between fam- ily variables (e.g., family structure, family supports, socioeco- nomic status), child factors (such as degree of language impair- ment), and responses to educational interventions (including family-centered, parent training, and other approaches) on out- comes. d. longitudinal treatment studies, where feasible, built on a clinical model with randomly assigned samples of sufficient size to assess the effectiveness of differing modes of treatment. 7-4 Treatment studies should recognize the common components of many comprehensive programs (e.g., standardized curriculum, family training, presence of typically developing peers) and should target and measure, longitudinally when feasible, “active ingredients” and mediating variables that influence the effects of intervention (e.g., communication and interaction opportunities for engagement, levels of interaction and initiation, specific teach- ing techniques, proportion of time in close proximity of peers). The concomitant development of innovative treatments building on these “active ingredients” should be supported. 7-5 In response to amendments in IDEA to make education more outcome oriented, a federal initiative should solicit and fund stud- ies in the following areas, not easily supported under the current review system: a. the development of instruments for measurement of diag- nosis and critical aspects of development, particularly tools for early screening of autistic spectrum disorders and for measure- ment of response to interventions; b. the development and application of sophisticated statisti- cal methods of analysis of change and growth, particularly multi- variate designs and those applicable to small samples; and c. the development and dissemination of novel research de- signs that combine individual and group approaches in ways that minimize biases and maximize the power of small samples. 7-6 Competitively funded initiatives in early education in autistic spectrum disorders should require plans and contain sufficient funding for short- and long-term assessment of child outcomes and measures of program efficacy. 

Autism is a word most of us are familiar with. But do we really know what it means?

Children with autism are challenged by the most essential human behaviors. They have difficulty interacting with other people—often failing to see people as people rather than simply objects in their environment. They cannot easily communicate ideas and feelings, have great trouble imagining what others think or feel, and in some cases spend their lives speechless. They frequently find it hard to make friends or even bond with family members. Their behavior can seem bizarre.

Education is the primary form of treatment for this mysterious condition. This means that we place important responsibilities on schools, teachers and children's parents, as well as the other professionals who work with children with autism. With the passage of the Individuals with Disabilities Education Act of 1975, we accepted responsibility for educating children who face special challenges like autism. While we have since amassed a substantial body of research, researchers have not adequately communicated with one another, and their findings have not been integrated into a proven curriculum.

Educating Children with Autism outlines an interdisciplinary approach to education for children with autism. The committee explores what makes education effective for the child with autism and identifies specific characteristics of programs that work. Recommendations are offered for choosing educational content and strategies, introducing interaction with other children, and other key areas.

This book examines some fundamental issues, including:

• How children's specific diagnoses should affect educational assessment and planning
• How we can support the families of children with autism
• Features of effective instructional and comprehensive programs and strategies
• How we can better prepare teachers, school staffs, professionals, and parents to educate children with autism
• What policies at the federal, state, and local levels will best ensure appropriate education, examining strategies and resources needed to address the rights of children with autism to appropriate education.

Children with autism present educators with one of their most difficult challenges. Through a comprehensive examination of the scientific knowledge underlying educational practices, programs, and strategies, Educating Children with Autism presents valuable information for parents, administrators, advocates, researchers, and policy makers.

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My son is profoundly autistic. Please don’t say he’s merely ‘neurodiverse.’

Advocates are fighting to eliminate terminology that accurately describes my son and thousands of people like him — who can’t speak up for themselves..

I t was pure coincidence that I happened upon the bloody site. Hoping to surprise my son, I drove to his favorite walking trail, along a lakefront, where I caught sight of police officers in a tense confrontation. Three officers stood side by side in an impenetrable wall while instructing someone splayed out and writhing on the ground. I hope Zack doesn’t get distracted by this scene , I thought.

As I neared the trail, I saw Zack’s aide, slouched inside her car, fully absorbed in texting. She was supposed to remain beside him at all times, but he was not with her. I called out to her, “Where’s Zack?” as my throat tightened with the realization he was nowhere in sight. I began sprinting toward the police officers — only to discover with mounting horror that Zack was the scene they were dealing with.

He was ravaging his forearms with deep, mutilating bites, thrashing angrily on the ground, and then rising to charge at the officers, who patiently but sternly reminded him to “stay seated” and repeated “Don’t panic, you’re not in trouble.” Breaking into the scene, I began a frantic avalanche of contrition. “I’m so sorry, I don’t know what triggered this —” But I was abruptly cut off by an officer who stated calmly, “Yes, we understand who he is and that he’s petrified.”

Somewhere during his sojourn along the lake, Zack, who was 20 years old at the time, had abruptly sat down too close to a woman seated on a bench, who gingerly told him to put on a COVID mask — and Zack bit her on the shoulder for what he perceived as a reprimand. The woman immediately summoned the police, not in anger but in compassion, realizing this young man was seriously disabled and apparently unattended.

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“He’s not in trouble, the woman’s not pressing charges,” the officer assured me. “We’ve been trying to get him to recount a phone number of someone we could contact —” He halted, spying a robust purple bruise on my calf and deep bite marks encrusted with dried blood along my arms. His tone turned solemn. “I can only imagine what you’ve been through. I do understand.”

I stood in stunned silence. I was not prepared for them to be prepared. It had been 45 minutes since they first gathered around Zack with no identifying information, 45 minutes during which his very safety hinged not only on the instincts of a benevolent stranger whom he assaulted but on a shared understanding by all involved of his clinical identity — that Zack is profoundly autistic.

What’s remarkable about Zack’s behavior is how unremarkable it is. Autism has been on an inexplicable rise with no signs of a plateau. The Centers for Disease Control and Prevention estimates that 1 in every 36 children born today has autism, and 1 in every 4 of those will have “profound autism,” a clinical distinction for those with much higher needs than the more verbally and intellectually able people who also have an autism diagnosis. Individuals like Zack with profound autism have minimal or no expressive language and require round-the-clock care to assist with daily living activities and safeguard them from extreme behaviors such as self-injury, the destruction of property, and “elopement” — the term for running or wandering away from caregivers or secure locations.

But while parents like me struggle to manage our children’s dangerous impulses, a powerful cultural movement has taken hold that forbids open discussion of profound autism and its manifestations. Advocates for “neurodiversity” are seeking to eliminate the term “profound autism” — on the grounds, they say, that it makes it seem as if autism is always an affliction. And now they are bullying doctors, researchers, lawmakers, and the rest of society into ignoring truths about Zack’s disorder that define his life.

Sanitizing Zack’s diagnosis and intense needs is dangerous. That day out on the lakefront trail, my son’s safety turned on the officers’ ability to decode from his conspicuous behaviors that he has profound autism in particular. They told me they realized that Zack’s refusal to identify himself to them despite repeated requests stemmed from an inability to articulate salient information in a moment of acute stress. They employed a measured response to his rage by speaking in succinct, assertive phrases, repeating reassurances, and maintaining a physical distance. If they hadn’t had such precise training , which depends on recognizing precise clinical criteria rather than employing general descriptors such as “neurodiverse,” the scenario could have gone very differently — with his arrest, forcible restraint, and even suffocation and death.

The intimidation campaign

I embrace many of neurodiversity’s fundamental tenets, especially the idea that people with intellectual disabilities should be broadly accepted and included in society.

I’ve staked my career on this principle — I used to work in the US Department of Justice as a disability rights attorney. I witnessed firsthand the exclusion of people with physical and cognitive disabilities from the rituals of daily life most other people take for granted. And I believe parents and professionals must aspire to discern a child’s authentic needs rather than superimpose our own preferences on them or force them into compliant molds of “normal.” Our children do not need to be “typical” to thrive in a society designed for its vast majority, nor is that an attainable goal.

But the concept of neurodiversity is going into dangerous territory if diagnostic distinctions across the spectrum are now considered archaic and bigoted.

In 2021, the medical journal The Lancet published a report from a commission of worldwide medical experts who recognized the need for “profound autism” as a discrete diagnostic category. The backlash was swift and mighty.

Autistic self-advocates launched a virulent campaign to quash the term, arguing that it had arisen, in the words of self-advocate Julia Bascom , “because some parents . . . see their kids as needing different kinds of support and different levels of restriction. But they are wrong on all counts.” The Global Autistic Task Force on Autism Research, an advocacy group, responded to The Lancet commission by saying : “For more than 30 years, autistic people have resisted functioning labels as misleading and offensive.”

As neurodiversity advocates denounce any framing of autism as a disability that requires medical intervention, they demand more support systems for people with autism, such as independent living “that honors authentic forms of human diversity.” Groups like the Autistic Self-Advocacy Network, people who identify on social media as #ActuallyAutistic, and parent activists insist that there is no such thing as a “normal” brain, only relative differences that render all humans “differently abled.”

To them, frank discussions about profound autism give a distorted image of people like Zack as unpredictable, cognitively limited, and presenting more behavioral challenges than the general population. Except the image is not distorted. While it’s painful to accept, these descriptors are accurate. Over the course of a single day, Zack, who is now 23, might furiously pummel his head in rage, slam his body into a wall, and bite me hard enough to draw blood.

The neurodiversity advocates — whose members are distinguished precisely by their ability to advocate for themselves, as Zack cannot — are not illuminating the complexity of autism; they are castigating into submission anyone who dares to deviate from their accepted language.

Intolerance for the term “profound autism” is leaching into medical journals and doctors’ practices. Doctors who’ve devoted their careers to treating children who compulsively ravage their flesh and slam their skulls into the ground are now verbally castrated on social media and “canceled” from lectures so regularly that preserving their livelihood requires stifling crucial medical data . It’s become common for autism self-advocates to “shout down” researchers imparting medical data at conferences or to call the researchers out on social media for online hazing and threats by neurodiverse mobs.

Today, both experienced and newer autism researchers contemplate leaving the field because, as one University of California scientist, David Amaral , observed, “People are getting reluctant to give public presentations or to be too vocal about what they’re finding,” despite the fact that “science is supposed to be about communication.” Top research institutions like the National Institutes of Health (NIH), tasked with conducting clinical trials to illuminate the disorder, face vitriolic accusations of being “ableist” and uncomprehending of the very people they are trying to help.

After the The Lancet’s commission recognized “profound autism” in 2021, the journal published an article by a doctor who wrote: “Generally, physicians think that disability is medical, and that if a patient’s condition interferes with their daily life, they are disabled. This traditional, medical model of disability does not address societal factors that influence disability, nor does it recognize disability as a cultural identity. Viewing disability as an issue stemming from an impaired body can encourage physicians to view disabled patients’ quality of life negatively . . . and to offer treatments aiming to fix the patient.”

This is absurd. I know of no person with profound autism who proudly identifies self-mutilating or violent impulses as core to their “cultural” identity. There is nothing bigoted about striving to ameliorate dangerous behaviors.

More critically, it is not the role of medical researchers to kowtow to trending cultural demands at the expense of addressing medically life-threatening conditions. Erasing diagnostic distinctions will make it impossible to perform research into the behaviors that are associated with profound autism — research that could lead to drugs that could benefit people across the entire autism spectrum. Although about 27 percent of all people with autism have profound autism, the condition is already underrepresented in clinical trials, which typically exclude those with an IQ lower than 70.

Two years ago, my son was abruptly ensnared in a cycle of self-injury, physical assaults, and chronic insomnia that within days catapulted him into a dangerously manic state — during which he risked seizures and seriously injuring anyone in proximity to him. Introducing anti-psychotic medicine delivered the jolt of serotonin to Zack’s brain that allowed him to reclaim his stability. Might other medicines become available that would work better? A movement that vilifies any medical mention of “risk,” “limitations,” or extreme behaviors has the power to thwart the development of such urgently needed drugs.

I hope Congress hears parents like me

The Autism CARES Act, which allocates NIH-funded research and services, sunsets on Sept. 30. Fierce debates are already underway about what Congress should do when it reauthorizes this funding. On one side stand autistic self-advocates who rally against any research not explicitly approved by them. On the other are parents who are desperate for clinical advancements but are so engulfed in the daily ordeal of managing their profoundly autistic children’s aggression and property destruction that they are largely incapable of organizing. The few dedicated parents calling for NIH to set aside funding to specifically address “profound autism” are vastly outnumbered by neurodiverse advocates who seek to block the act from passing if such “stigmatizing” language is included.

The loudest voices seek to abolish all spending on autism medical research and replace it with select services, such as workforce initiatives, that assist only those with milder autism. It’s here that the idea of neurodiversity poses the greatest threat — a movement that celebrates autism in all its forms, and depicts even the most severe afflictions as “merely a difference,” vehemently opposes any investigation into autism’s causes as ableist.

The truth is that we still don’t know what explains the steep rise in autism — perhaps it’s the product of widespread environmental contaminants altering our children’s brains — and this increase needs urgent attention. As these children age, state programs already strained by the deluge of adults needing lifelong services threaten to collapse entirely. Capitulating to self-advocates’ demands amid a global proliferation of one of the gravest disorders of our time is not only morally incoherent but medical malpractice.

In the natural course of events, every profoundly autistic child will eventually be orphaned by the most qualified and dedicated caretakers he’s ever known — his parents. Absent meticulous advance planning and abundant resources, that child will be automatically transitioned by the state to placement in a residential living arrangement. For that child to be placed appropriately depends entirely upon having accurate clinical information about the intensity of his needs, taking into account the possibility of physical aggression, self-injury, elopement, property destruction, seizures, and other overlapping medical needs. I’m confident that if a person facing homelessness and a precariously uncertain future were asked whether he values a safe residential arrangement over semantics that obscure his diagnosis, he would choose the former.

For the record, any language that contorts or constricts the full scope of Zack’s identity is something I find deeply offensive. Zack has struggled with innumerable obstacles and heartbreak in navigating a world that does not come naturally to him, and his competence is strengthening to this day. Blurring his identity under the indistinct banner of “neurodiverse” erases Zack’s lived history — all that he has endured and overcome to get here.

Whitney Ellenby is a former disability rights attorney in the US Department of Justice and the author of the 2018 book “Autism Uncensored: Pulling Back the Curtain.” She is also the founder of Autism Ambassadors, which runs recreational events for over 800 families affected by autism in the Washington, D.C., area.

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Association between exposure to antibiotics during pregnancy or early infancy and risk of autism spectrum disorder, intellectual disorder, language disorder, and epilepsy in children: population based cohort study

• Related content
• Peer review
• Ahhyung Choi , postdoctoral research fellow 1 2 ,
• Hyesung Lee , research professor 1 3 ,
• Han Eol Jeong , postdoctoral research fellow 1 3 ,
• Seo-Young Lee , professor 4 5 ,
• Jun Soo Kwon , professor 6 7 8 ,
• Jung Yeol Han , professor 9 ,
• Young June Choe , associate professor 10 ,
• Ju-Young Shin , associate professor 1 3 11
• 1 School of Pharmacy, Sungkyunkwan University, Suwon, South Korea
• 2 Harvard-MIT Center for Regulatory Science, Harvard Medical School, Boston, MA, USA
• 3 Department of Biohealth Regulatory Science, Sungkyunkwan University, Suwon, South Korea
• 4 Department of Neurology, College of Medicine, Kangwon National University, Chuncheon, South Korea
• 5 Interdisciplinary Graduate Program in Medical Bigdata Convergence, Kangwon National University, Chuncheon, South Korea
• 6 Department of Psychiatry, Seoul National University College of Medicine, Seoul, South Korea
• 7 Department of Brain and Cognitive Sciences, Seoul National University College of Natural Sciences, Seoul, South Korea
• 8 Institute of Human Behavioral Medicine, Seoul National University Medical Research Center, Seoul, South Korea
• 9 Korean Mothersafe Counselling Center, Department of Obstetrics and Gynecology, Inje University Ilsan Paik Hospital, Goyang, South Korea
• 10 Department of Pediatrics, Korea University Anam Hospital, Korea University College of Medicine, Seoul, South Korea
• 11 Department of Clinical Research Design & Evaluation, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, South Korea
• Correspondence to: J-Y Shin shin.jy{at}skku.edu
• Accepted 11 April 2024

Objective To evaluate the association between antibiotic use during pregnancy or early infancy and the risk of neurodevelopmental disorders in children.

Design Nationwide population based cohort study and sibling analysis.

Setting Korea’s National Health Insurance Service mother-child linked database, 2008-21.

Participants All children live born between 2009 and 2020, followed up until 2021 to compare those with and without antibiotic exposure during pregnancy or early infancy (first six months of life).

Main outcomes measures Autism spectrum disorder, intellectual disorder, language disorder, and epilepsy in children. After 1:1 propensity score matching based on many potential confounders, hazard ratios with 95% confidence interval were estimated using Cox proportional hazard models. A sibling analysis additionally accounted for unmeasured familial factors.

Results After propensity score matching, 1 961 744 children were identified for the pregnancy analysis and 1 609 774 children were identified for the early infancy analysis. Although antibiotic exposure during pregnancy was associated with increased risks of all four neurodevelopmental disorders in the overall cohort, these estimates were attenuated towards the null in the sibling analyses (hazard ratio for autism spectrum disorder 1.06, 95% confidence interval 1.01 to 1.12; intellectual disorder 1.00, 0.93 to 1.07; language disorder 1.05, 1.02 to 1.09; and epilepsy 1.03, 0.98 to 1.08). Likewise, no association was observed between antibiotic exposure during early infancy and autism spectrum disorder (hazard ratio 1.00, 0.96 to 1.03), intellectual disorder (1.07, 0.98 to 1.15), and language disorder (1.04, 1.00 to 1.08) in the sibling analyses; however, a small increased risk of epilepsy was observed (1.13, 1.09 to 1.18). The results generally remained consistent across several subgroup and sensitivity analyses, except for slightly elevated risks observed among children who used antibiotics during very early life and those who used antibiotics for more than 15 days.

Conclusions In this large cohort study, antibiotic exposure during pregnancy or early infancy was not associated with an increased risk of autism spectrum disorder, intellectual disorder, or language disorder in children. However, elevated risks were observed in several subgroups such as children using antibiotics during very early life and those with long term antibiotic use, which warrants attention and further investigation. Moreover, antibiotic use during infancy was modestly associated with epilepsy, even after control for indications and familial factors. When prescribing antibiotics to pregnant women and infants, clinicians should carefully balance the benefits of use against potential risks.

Introduction

Neurodevelopmental disorders are emerging as a critical public health problem among children, given the long lasting effect of these disorders on individuals’ lives and society. 1 2 The global prevalence of neurodevelopmental disorders, including autism spectrum disorders, has been steadily increasing. 3 4 5 Although the causes of neurodevelopmental disorders are not yet fully understood, several potential risk factors include advanced maternal age, preterm birth, and environmental factors. 1 6 In recent years, a growing body of evidence is also highlighting that alterations in the microbiome may play a significant role in the development of neurodevelopmental disorders. 6 7

Antibiotics, which are known to disturb the composition of the microbiome, are commonly used during pregnancy and infancy to treat infections. 8 9 10 Given that fetal and early life is the critical period for the extensive development of the gut microbiome, concern is growing about antibiotic use during these periods. 11 Few epidemiological studies have investigated an association between prenatal or infant antibiotic use and neurodevelopmental disorders such as autism spectrum disorder and epilepsy. 12 13 14 15 However, the evidence remains limited and inconclusive, possibly owing to insufficient control for confounding in some studies. Because infection, in both severe and less severe forms, has been linked with neurodevelopmental consequences, confounding by indication is of particular concern in investigating the role of antibiotics in neurodevelopmental disorders. 16 17 18 In addition, familial confounding presents another potential source of bias, as the pathophysiology of neurodevelopmental disorders involves both genetic and environmental factors. Therefore, comprehensive investigation on this topic based on real world data is warranted, while controlling for these potential confounding, as pregnant women and infants are generally excluded from randomised trials.

In this study, we aimed to evaluate whether exposure to antibiotics during pregnancy or early infancy is associated with subsequent development of autism spectrum disorder, intellectual disorder, language disorder, and epilepsy in children by using a large nationwide database in South Korea. Although intellectual disorder and language disorder are recognised as another common type of neurodevelopmental disorder, no study to date has thoroughly evaluated whether these disorders are associated with antibiotic use. To account for confounding by indication and unmeasured familial factors, we implemented two designs: a propensity score matched cohort study and a sibling analysis.

Data source and study design

We conducted a nationwide retrospective cohort study using the National Health Insurance Service (NHIS) mother-child linked database from 2008 to 2021. 19 The NHIS database contains claims data of the entire population (>50 million) in South Korea, and construction of the mother-child linkage has been described previously. 20 21 This database comprises comprehensive information on socioeconomics, healthcare utilisation (for example, diagnosis, drug prescription, and medical procedures) from both inpatient and outpatient settings, health examination records for mothers and infants, and vital statistics data. We estimated the start of pregnancy on the basis of a previously validated algorithm developed using administrative data. 22 This study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline. 23

Study cohorts

We constructed two separate cohorts among all children born between 1 April 2009 and 31 December 2020 ( fig 1 ). The first cohort (hereafter referred to as the pregnancy cohort), for analysing antibiotic exposure during pregnancy, consisted of all children after exclusion of children with chromosomal abnormalities and those whose mothers took antibiotics one month before the start of pregnancy but not during pregnancy to avoid classifying those who actually took their antibiotics or had available antibiotics after the start of pregnancy in the unexposed group. The second cohort (hereafter referred to as the infant cohort), for analysing antibiotic exposure during early infancy, comprised all children after exclusion of those who died during the first six months of life, children with chromosomal abnormalities, and those who received a diagnosis of one of the study outcomes during the first six months of life.

Flowchart of study cohort identification. NHIS=National Health Insurance Service

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Antibiotic exposure

We defined exposure as the presence of one or more prescriptions for a systemic antibiotic (Anatomical Therapeutic Chemical classification system code J01). For the pregnancy cohort, we defined the exposed group as children whose mothers had at least one prescription for antibiotics at any time during pregnancy and the unexposed group as children whose mothers had no history of prescriptions for antibiotics from 30 days before pregnancy to the end of the pregnancy. For the infant cohort, we defined the exposed group as children who had at least one prescription for antibiotics during the first six months of life and the unexposed group as children with no history of prescriptions for antibiotics during this period.

Study outcomes were autism spectrum disorder (ICD-10 (international classification of diseases, 10th revision) code F84), intellectual disorder (F70-F73), language disorder (F80), and epilepsy (G40, G41, F803, R56, and prescription for antiepileptic medication) (supplementary table A). Autism spectrum disorder, intellectual disorder, and language disorder are typically diagnosed by psychiatrists or paediatricians in South Korea on the basis of clinical evaluation and standardised tests and recorded with ICD-10 codes. A previous study found a high positive predictive value of diagnostic codes in Korea’s claims data, 24 and our definition of epilepsy has been validated with high positive predictive values especially among children (1-4 years old: 84.7%; 5-9 years old: 92.9%). 25 We followed up all children from birth (pregnancy cohort) or six months after birth (infant cohort) until the occurrence of an outcome, death, or the end of the study period (31 December 2021), whichever came first.

For the analyses of both pregnancy and infant cohorts, we considered a broad range of potential confounders including demographics (for example, maternal age, insurance type, and income level at delivery), indications for antibiotic use (for example, respiratory infection, urinary infection), infection related healthcare utilisation as a proxy for severity of infection (for example, number of hospital visits for infection diagnoses, number of distinct infection diagnoses), maternal conditions (for example, attention deficit/hyperactivity disorder, autoimmune diseases, diabetes mellitus), medication use (for example, paracetamol, antidepressants, antipsychotics), obstetric conditions (for example, nulliparity, multiple gestations), measures of healthcare utilisation (for example, obstetric comorbidity index), 26 27 smoking status, and body mass index. For the analyses of the infant cohort, we additionally considered maternal use of antibiotics, sex of child, preterm birth, caesarean section, birth weight, and type of feeding. We considered maternal antibiotic use during pregnancy as a covariate in the infant cohort as it may influence the infant’s exposure and the study outcomes, whereas we did not consider maternal antibiotic use during early infancy as a covariate in the pregnancy cohort as the infant’s exposure occurs after the prenatal exposure. Details of the covariates and their assessment windows are presented in supplementary table A.

Statistical analyses

To control for potential confounding, we did one-to-one propensity score matching using the greedy nearest neighbour matching algorithm without replacement. 28 We estimated the propensity score, or the probability of antibiotic exposure in our study, by using a logistic regression model based on all pre-defined covariates except for smoking status and body mass index given their high proportion of missing data. We evaluated the distribution of covariates between exposed and unexposed groups by using the standardised mean difference, considering a value less than 0.1 on the absolute scale to indicate well balanced groups. In the propensity score matched cohort, we calculated the incidence of outcomes per 1000 person years and absolute rate differences with 95% confidence intervals on the basis of Poisson regression. We also estimated hazard ratios with 95% confidence intervals by using Cox proportional hazard regression models, while applying robust standard errors to account for data clustering. In each outcome model, we additionally adjusted for covariates that were unbalanced after propensity score matching. We considered a P value of <0.05 to be statistically significant. We used SAS Enterprise Guide, version 7.1, for data management and analysis.

Sibling analyses

Given the concerns about unmeasured confounding from familial factors, we additionally did sibling controlled analyses by restricting the population to children who had at least one sibling during the study period. Sibling analyses, by design, can control for time invariant shared factors at the family level. Using a stratified Cox proportional hazard regression model, we calculated hazard ratios with 95% confidence intervals for each outcome that were adjusted for all pre-defined covariates and birth order of sibling. Only siblings with discordant exposure and outcome status would contribute to the estimates; thus, informative pairs are reported. Additional details on the sibling analyses, including the assumption test for carryover effects, are available in supplementary appendix 1. 29

Subgroup and sensitivity analyses

We did several subgroup analyses. Firstly, we analysed the risk of study outcomes by antibiotic groups (broad spectrum or narrow spectrum antibiotics; supplementary table B), given that broad spectrum antibiotics are reported to have a greater effect than narrow spectrum antibiotics on the gut microbiota. Secondly, we assessed whether the risk differed by specific timing of exposure (first, second, third trimester for pregnancy cohort; 0 to <2, 2 to <4, 4 to <6 months for infant cohort). Thirdly, as boys are more likely to receive a diagnosis of neurodevelopmental disorders than girls, we evaluated the association by sex of the infants. 30 Fourthly, we analysed the duration-response relation and the risk of the top three most frequently prescribed antibiotic classes in each cohort. Lastly, we investigated the risk of study outcomes stratified by birth year (minimum follow-up period). As a post hoc analysis, we also estimated the risk of joint antibiotic exposure during pregnancy and early infancy.

We did multiple sensitivity analyses to test the robustness of our main findings. We accounted for potential exposure misclassification, outcome misclassification, and residual confounding, and we also evaluated whether our main findings from the propensity score matched cohorts were robust across different propensity scoring methods. Detailed information on subgroup and sensitivity analyses is given in supplementary appendices 2 and 3.

Patient and public involvement

The NHIS privacy policy and our institutional policy were not equipped to support patients or members of the public as partners. As study investigators, we honoured this policy. As a result, no patients were involved in this research although we are grateful for their data, which made the research possible.

Cohort characteristics

We identified 3 665 246 children eligible for the pregnancy cohort, of whom 1 649 300 (45.0%) were exposed to antibiotics in utero. For the infant cohort, we identified 3 944 731 children, of whom 1 976 472 (50.1%) were exposed to antibiotics during early infancy ( fig 1 ). After one-to-one propensity score matching, we identified 980 872 and 804 887 pairs for the pregnancy and infant cohorts, respectively. We observed substantial baseline differences between the exposed and unexposed groups (for example, indication) before propensity score matching, but all characteristics were well balanced (absolute standardised mean difference <0.1) after matching in both cohorts ( table 1 ) All characteristics before and after propensity score matching are shown in supplementary tables C and D.

Selected baseline characteristics of pregnancy and infant cohorts stratified by antibiotic exposure after propensity score matching. Values are numbers (percentages) unless stated otherwise

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Antibiotic exposure during pregnancy and early infancy: propensity score matched analyses

The median follow-up time for each outcome ranged around seven years in both pregnancy and infancy cohorts (supplementary table E). For the pregnancy cohort, the rate difference was 0.15 per 1000 person years for autism spectrum disorder (exposed versus unexposed: 1.25 v 1.10), 0.09 for intellectual disorder (0.62 v 0.53), 0.21 for language disorder (2.59 v 2.38), and 0.09 for epilepsy (1.12 v 1.03) ( table 2 ). Exposure to antibiotics during pregnancy was associated with increased risks of all study outcomes, with adjusted hazard ratios ranging from 1.08 for epilepsy to 1.17 for intellectual disorder ( fig 2 , top).

Incidence rate of autism spectrum disorder, intellectual disorder, language disorder, and epilepsy stratified by antibiotic exposure after propensity score matching

Risk of autism spectrum disorder, intellectual disorder, language disorder, and epilepsy following exposure to antibiotics during pregnancy and early infancy. CI=confidence interval

We observed similar incidence rates and rate differences in the infant cohort (autism spectrum disorder: 0.05 (1.25 v 1.20); intellectual disorder: 0.13 (0.68 v 0.55); language disorder: 0.13 (2.71 v 2.58); epilepsy: 0.22 (1.01 v 0.80)) ( table 2 ). Likewise, antibiotic exposure during early infancy was associated with increased risks of all study outcomes, with adjusted hazard ratios ranging from 1.04 for autism spectrum disorder to 1.27 for epilepsy ( fig 2 , top).

Antibiotic exposure during pregnancy and early infancy: sibling analyses

The sibling analyses comprised 843 412 and 1 082 417 exposure discordant children for the pregnancy and infant cohorts, respectively. Their baseline characteristics and informative exposure-outcome discordant pairs are shown in supplementary tables F and G. In contrast to the propensity score matched analyses, we found that all estimates were attenuated in the sibling analysis and showed no substantial associations (hazard ratio for autism spectrum disorder 1.06, 95% confidence interval 1.01 to 1.12; intellectual disorder 1.00, 0.93 to 1.07; language disorder 1.05, 1.02 to 1.09; epilepsy 1.03, 0.98 to 1.08) in the pregnancy cohort ( fig 2 , bottom). Similarly, in the infant cohort, we observed no associations (hazard ratio for autism spectrum disorder 1.00, 0.96 to 1.03; intellectual disorder 1.07, 0.98 to 1.15; language disorder 1.04, 1.00 to 1.08), except with epilepsy, which remained slightly increased (1.13, 1.09 to 1.18) ( fig 2 , bottom). Additional results from the sibling analyses are described in supplementary appendix 1 and tables H-K.

We observed no notable differences in the association between antibiotic exposure during pregnancy or early infancy and all outcomes in the subgroup analyses, except for a slightly higher risk among infants who used antibiotics in the first two months of life and those who used antibiotics for longer than 15 days ( fig 3 ; fig 4 ; supplementary tables L-S). In the post hoc analyses, we observed increased risks of autism spectrum disorder and epilepsy among children who were exposed to antibiotics during both pregnancy and early infancy (supplementary table T).

Subgroup analyses on risks of autism spectrum disorder, intellectual disorder, language disorder, and epilepsy following antibiotic exposure during pregnancy. CI=confidence interval. Estimates of forest plot are those from sibling cohort

Subgroup analyses on risks of autism spectrum disorder, intellectual disorder, language disorder, and epilepsy following antibiotic exposure during early infancy. CI=confidence interval. Estimates of forest plot are those from sibling cohort

Sensitivity analyses yielded estimates generally consistent with those from the main findings (supplementary tables U-X). Additional analyses to account for potential outcome misclassification also showed similar results (supplementary appendix 3 and table Y). The E value for the point estimate of epilepsy associated with antibiotic exposure during early infancy was 1.51.

In this large nationwide cohort study, exposure to antibiotics during pregnancy or early infancy was not associated with increased risks of autism spectrum disorder, intellectual disorder, or language disorder in children. Although we observed small increased risks in the overall population, these associations were all attenuated and pointed towards the null in the sibling analysis, suggesting that the observed associations may have been confounded by shared familial factors. However, the risk of epilepsy associated with antibiotic use during infancy remained slightly elevated even after we accounted for the shared familial factors. Results from various subgroup and sensitivity analyses were largely consistent with our main findings, except for slightly increased risks observed among children who used antibiotics during very early life and those who used antibiotics for more than 15 days.

Comparison with other studies

A systematic review reported that available data on the association between prenatal or infant antibiotic exposure and autism spectrum disorder are conflicting and inconclusive. 12 A later cohort study based on the Swedish population found an increased risk of autism spectrum disorder after use of antibiotics both during pregnancy and during infancy, with an odds ratio of 1.16 (95% confidence interval 1.09 to 1.23) and 1.46 (1.38 to 1.55), respectively. 13 However, the authors noted that confounding by indication or genetics could not be ruled out. Likewise, a recent meta-analysis showed that an increased risk of autism (pooled odds ratio 1.13, 1.07 to 1.21) associated with antibiotic use in early life was no longer apparent when only the sibling matched studies were pooled (1.04, 0.97 to 1.11). 31 In line with previous evidence, our study further supports a lack of association between antibiotic use during pregnancy or infancy and autism spectrum disorder after control for many confounders including indications and genetic/familial factors.

Our study did not observe an association between prenatal or infant antibiotic use and intellectual disorder or language disorder, which to our knowledge have not been investigated to date. Given that intellectual disorder and language disorder are increasingly recognised as another common type of neurodevelopmental disorder, 32 further studies on the evaluation of these disorders are needed. Meanwhile, on the basis of the estimates observed in the comparison of the siblings, our study suggests no substantial association between prenatal or infant antibiotic use and intellectual disorder or language disorder.

By contrast, antibiotic use during infancy was modestly associated with epilepsy, even after control for familial factors in the sibling analysis, which indicates that familial confounding could not fully explain the observed increased risk. This increased risk was consistently observed across all subgroup analyses. Although several studies have investigated the risk of seizure or epilepsy in children associated with exposure to antibiotics during pregnancy, no previous studies have assessed this risk after antibiotic use in infants. 14 15 33 One hypothesised mechanism explaining the link between antibiotics and epilepsy is interference with gut microbiota, which can influence the interaction between the gut and the nervous system. 34 In support, emerging evidence from case reports are indicating intestinal dysbiosis in patients with epilepsy. 35 Because gut microbiota compositions are known to develop extensively during early life, antibiotic use during infancy may play a role in subsequent development of epilepsy. 11 Another plausible mechanism is central nervous system toxicity of antibiotics. Several antibiotics have been suspected to provoke acute seizure, and animal studies have also shown that β-lactam associated seizures may arise from its γ-aminobutyric acid A receptor binding property. 36 37 Although the acute symptomatic seizures provoked by antibiotics do not necessarily result in chronic epilepsy, a potential negative effect on the developing brain may exist. Nevertheless, our study is the first epidemiological study to have investigated the association between antibiotics and epilepsy in infant populations and report increased risk; thus, additional studies are needed to confirm our findings. While awaiting future studies, the small but potential risk of epilepsy should be taken into account when weighing the benefits and risks of using antibiotics in infants.

Strengths and limitations of study

Antibiotics are increasingly used during pregnancy and infancy, with parallel concerns indicating that alterations in the microbiome may be associated with neurodevelopmental disorders; thus, our study tackles an important question. The major concern in investigating the potential role of antibiotics in neurodevelopmental outcomes is confounding by indication and familial factors. To minimise the possibility of these confounding, we included a wide range of covariates in the propensity score model, such as indications and related healthcare utilisation (for example, proxies for the severity of indication), and also implemented sibling designs to disentangle the effects of underlying infection and familial factors. Another strength of our study is the large sample size, which enabled us to have sufficient statistical power and also to do various clinically relevant subgroup analyses. In addition, by using the nationwide longitudinal database, adequate follow-up was possible to identify the risk of neurodevelopmental disorders along with no risk of selection or recall bias.

This study also has several limitations. Firstly, exposure misclassification is possible as we defined exposure on the basis of prescription of an antibiotic not the actual use. Secondly, outcome misclassification is possible. Although the algorithm for defining epilepsy in our study has been validated with high positive predictive values in young children, 25 other outcomes have not been validated. Thus, we did a sensitivity analysis in which we redefined the outcomes by incorporating data from Korean Developmental Screening Test for Infants and Children, 38 a validated tool to detect neurodevelopmental disorders in Korea, and the results were consistent with those of our main analyses (supplementary appendix 3). Thirdly, although we considered a broad range of covariates, we cannot rule out the possibility of residual confounding. For instance, paternal characteristics (for example, paternal age and comorbidities), which may be associated with the development of neurodevelopmental disorders, were unavailable in our database. The data on maternal smoking status and body mass index were also incomplete and thus not included in the propensity score model or adjustment. Fourthly, the indicators that we included in our study as proxies for the severity of infection are not direct measures of severity. The inclusion of the number of inpatient visits or emergency department visits with infection diagnoses and the number of distinct infection diagnoses was based on the assumption that the inpatient and emergency department visits typically necessitate a higher level of medical care (for example, close monitoring and intensive treatment) and that multiple infections suggest a greater level of severity compared with a single infection. However, they do not provide a direct assessment of the severity itself; thus, future studies incorporating direct measures of severity would be valuable. Fifthly, although sibling analyses are useful in controlling for familial factors that are not easily captured in the administrative database, time variant confounders are still of concern. To tackle this concern, we additionally adjusted for time variant characteristics; however, potential residual confounding from non-shared factors may still exist. Sibling comparison designs are also susceptible to carryover effects 29 ; however, our analyses ruled out potential types of carryover effects. Lastly, as our study period included the early covid-19 era (2020-21), potential information bias on exposure, outcome, and covariate assessment due to delayed healthcare encounters may exist during this period.

Implications

In this study, the prevalence of antibiotic use during pregnancy and early infancy was 45.0% and 50.1%, respectively. Although antibiotics are essential for treating bacterial infections, concern is growing about their inappropriate use, which can contribute to antibiotic resistance. 39 40 Many countries, including South Korea and the UK, are actively working to reduce unnecessary prescription of antibiotics, especially for respiratory tract infections. 41 42 43 Despite the fact that many respiratory tract infections are viral and do not require antibiotics, studies have shown a substantial number of antibiotic prescriptions for such cases. 44 45 The challenge lies in the difficulty of distinguishing between bacterial and viral respiratory infections in primary care settings, a limitation also present in this study. 46 Nevertheless, a considerable number of antibiotics were prescribed with respiratory infections as the primary diagnosis during pregnancy and infancy in our study. Furthermore, our additional analysis indicates that 117 572 pregnancies and 742 823 infants were treated with antibiotics for 15 days or longer for respiratory tract infections, of which 21 118 pregnancies and 167 404 infants had no other diagnoses of infection. Of note, the recommended treatment durations for most respiratory tract infections are below 15 days. 44 Overall, clinicians should adhere to the recommended guidelines when prescribing antibiotics to pregnant women and infants to improve antibiotic stewardship.

Our study suggested no substantial association between prenatal or infant antibiotic exposure and autism spectrum disorder, intellectual disorder, and language disorder, but elevated estimates observed in several subgroups warrant further attention. Specifically, long term use of antibiotics (≥15 days) and antibiotic use during the first two months of life showed slightly increased risk even after control for familial factors. Moreover, in the post hoc analysis, antibiotic exposure both during pregnancy and during infancy was associated with autism spectrum disorder and epilepsy. Although residual confounding due to unfavourable health conditions cannot be completely ruled out, further investigation may be warranted. In the meantime, clinicians should carefully weigh the benefits and potential harms of antibiotics when prescribing antibiotics to pregnant women and infants.

Conclusions

In this large cohort study, exposure to antibiotics during pregnancy or early infancy was not associated with an increased risk of autism spectrum disorder, intellectual disorder, and language disorder in children. However, elevated risks were observed in several subgroups such as antibiotics use during very early life and long term antibiotic use, which warrants attention and further investigation. Moreover, antibiotic use during early infancy was modestly associated with epilepsy, even after control for indications and familial factors. When prescribing antibiotics to pregnant women and infants, clinicians should carefully balance the benefits of their use against potential risks.

What is already known on this topic

Antibiotics, which are known to disturb the microbiome composition, are commonly used during pregnancy and infancy to treat infections

Growing evidence indicates that early life microbiome disruption is associated with childhood neurodevelopmental disorders

What this study adds

The findings of this large cohort study suggest no association between maternal or infant antibiotic use and neurodevelopmental disorders

An exception was a modest association between exposure to antibiotics during infancy and epilepsy

Elevated risk observed in several subgroups such as antibiotic use during very early life and long term antibiotic use warrants attention and further investigation

Ethics statements

Ethical approval.

The study protocol was approved by the institutional review board of Sungkyunkwan University; informed consent was waived as anonymised claims data were used (2022-04-011).

Data availability statement

No additional data available.

Contributors: AC and HL contributed equally to the paper as joint first authors. AC conceived and designed the study. AC and HL did statistical analyses and drafted the article. All authors interpreted the data, revised the article critically for important intellectual content, and gave final approval of the manuscript. JYS is the guarantor. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted.

Funding: This work was supported by a grant (21153MFDS607) from the Ministry of Food and Drug Safety of South Korea in 2021-25 and by the National Research Foundation of Korea grant funded by the Korea government (No RS-2023-00208978). AC was supported by the Health Fellowship Foundation (2022). The funders had no role in the study design; the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the article for publication.

Competing interests: All authors have completed the ICMJE uniform disclosure form at https://www.icmje.org/disclosure-of-interest/ and declare: this work was supported by the Ministry of Food and Drug Safety of South Korea and by the National Research Foundation of Korea grant funded by the Korea government; JYS received grants from the Ministry of Food and Drug Safety, the National Research Foundation of Korea, the Ministry of Health and Welfare, and pharmaceutical companies including Pfizer, UCB, and LG chem, outside the submitted work; no other relationships or activities that could appear to have influenced the submitted work.

Transparency: AC, HL, and JYS affirm that the manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

Dissemination to participants and related patient and public communities: The study results will be disseminated to the public through press releases, social media, and presentations at conferences.

Provenance and peer review: Not commissioned; externally peer reviewed.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ .

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