autism essay pdf

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• v.25(1); 2016 Feb

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).

Educating Children with Autism (2001)

Chapter: 1 introduction.

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1 Introduction FEATURES OF AUTISM Autism is a disorder that is present from birth or very early in devel- opment that affects essential human behaviors such as social interaction, the ability to communicate ideas and feelings, imagination, and the estab- lishment of relationships with others. It generally has life-long effects on how children learn to be social beings, to take care of themselves, and to participate in the community. Autism is a developmental disorder of neurobiological origin that is defined on the basis of behavioral and de- velopmental features. Although precise neurobiological mechanisms have not yet been established, it is clear that autism reflects the operation of factors in the developing brain. As yet, known direct links between pathophysiology and behavior in autism are still rare and have not yet had great influence on treatments or diagnoses (see Rumsey et al., 2000). Nevertheless, current biologic research, such as in genetics, may already have important implications for families of children with autistic spec- trum disorders. Autism is best characterized as a spectrum of disorders that vary in severity of symptoms, age of onset, and associations with other disorders (e.g., mental retardation, specific language delay, epilepsy). The manifes- tations of autism vary considerably across children and within an indi- vidual child over time. There is no single behavior that is always typical of autism and no behavior that would automatically exclude an indi- vidual child from a diagnosis of autism, even though there are strong and consistent commonalities, especially in social deficits. 11 

12 EDUCATING CHILDREN WITH AUTISM A number of years ago, the concept of pervasive developmental dis- order (PDD) was introduced to provide an umbrella term for autism and other disorders that include similar impairments in basic social skills but vary in severity or the presence of communication delay and repetitive behaviors. Because of the continuity across autistic disorders, this report addresses both the more narrowly defined disorder of autism and the broader range of autistic spectrum disorder including pervasive develop- mental disorder—not otherwise specified (PDD-NOS), Asperger’s disor- der, and childhood disintegrative disorder. Autistic spectrum disorders are unique in their pattern of deficits and areas of relative strengths. Be- cause of the special characteristics of Rett’s syndrome (i.e., its onset and pattern of deficits), it is not specifically considered in this report. Chil- dren with Rett’s syndrome, however, may require similar services to chil- dren with autism in some circumstances. THE CHALLENGE OF EDUCATING CHILDREN WITH AUTISM Education, both directly of children, and of parents and teachers, is currently the primary form of treatment in autism. For the purposes of this report, education is defined as the fostering of acquisition of skills or knowledge—including not only academic learning, but also socialization, adaptive skills, language and communication, and reduction of behavior problems—to assist a child to develop independence and personal re- sponsibility. Education includes services that foster acquisition of skills and knowledge, offered by public and private schools; infant, toddler, preschool and early education programs; and other public and private service providers. Young children are defined here as children 8 years or younger. Because children with autism are at high risk for other impair- ments, educational planning must address both the needs typically asso- ciated with autistic spectrum disorders and needs associated with accom- panying disabilities. Education of children with autism was accepted as a public responsi- bility as part of the Education Act of All Handicapped Children in 1975. Yet today, 25 years later, despite the federal mandate for appropriate education and intervention services, the goals, methods, and resources available vary considerably from state to state and from school system to school system. In the last few years, courts have become increasingly active forces in determining the methods applied and the resources allo- cated by school systems for the education of children with autistic spec- trum disorders. Although there is a very substantial body of research on the treatment and education of these children (Rumsey et al., 2000), this work has not often been clearly integrated into educational decision-making and policy at local or state levels. For example, many treatment approaches and 

INTRODUCTION 13 demonstration projects have disseminated information, yet most have not yet provided appropriate, scientifically rigorous documentation of effec- tiveness and efficiency. While research in developmental psychology, child psychiatry, and pediatric neurology has become increasingly well integrated, there is a need for more effective communication between professionals in these disciplines and the educators and other profession- als who carry out the bulk of treatment and intervention-oriented re- search. THE COMMITTEE’S WORK Charge At the request of the U.S. Department of Education’s Office of Special Education Programs, the National Research Council formed the Commit- tee on Educational Interventions for Children with Autism and charged the committee to integrate the scientific, theoretical, and policy literature and create a framework for evaluating the scientific evidence concerning the effects and features of educational interventions for young children with autism. The primary focus of the charge was early intervention, preschool, and school programs designed for children with autism from birth to age 8. The charge included specific suggestions to examine sev- eral issues pertaining to education of children with autism: early inter- vention, diagnosis and classification, the rights of children with autism under IDEA, mainstreaming, and assistive technology. To carry out its charge, the committee examined the scientific litera- ture; commissioned papers addressing science and policy issues; exam- ined solicited reports provided by leaders of model intervention pro- grams; and conducted two workshops at which researchers, educators, administrators, practitioners, advocates of individuals with autism, and other interested participants presented to the committee information and perspectives on approaches to address the educational needs of children with autism. The committee also solicited and reviewed written state- ments, provided by individuals and organizations, summarizing their perceptions of the educational needs of young children with autism. The committee also addressed a specific charge to survey the developing field of assistive technology for young children with autism. Thus, the committee’s activities served as a forum for interdisciplinary discussion of theory and scientific research concerning the evaluation of educational needs of, and methods used with, young children with autism. The committee conceptualized its task as the integration and evalua- tion of existing information from multiple sources in order to provide recommendations regarding educational policies affecting families with young children with autism. These policies are carried out in school 

14 EDUCATING CHILDREN WITH AUTISM systems and state and federal programs. The committee applied strict standards to assess the quality of the large body of information that it assembled. The committee considered arguments of legal rights and documentation of public policy, and current practices in well-established programs, as well as empirical data concerning the effectiveness of vari- ous techniques. Within its evaluation of the current scientific literature, the committee’s goal has been to interpret findings as broadly as possible in terms of their implications for early educational practices, while retain- ing scientific integrity and perspective in considering the strengths and limitations of various bodies of work. Committee’s Process for Evaluating Evidence Science is a systematic way of gathering, analyzing, and assessing information. One of the strengths of the field of autism is the many disciplines and areas of scientific inquiry within which it has been ad- dressed. The committee’s approach was to gather information from as wide a range of sources as possible, to assess the strengths and limitations of different sources of information, and to assess the results with an eye toward convergence, particularly from independent sources, of descrip- tive data, inferential data, and theory. For example, within the field of autism, there are many approaches to intervention that are widely disseminated but little researched. Some approaches have been greeted with great enthusiasm initially, but have relatively quickly faded out of general use, in part because of their failure to demonstrate worthwhile effects. Other approaches have withstood the test of time across sites and the children and families they serve, though they continue to be largely supported by clinical descriptions of effective- ness, rather than by formal evaluations. Yet wide use and respect cannot be interpreted as clear evidence of effectiveness; therefore, the committee elected to consider information about these approaches in light of more empirically oriented studies. To achieve a systematic and rigorous assessment of research studies, the committee established guidelines for evaluating areas of strength, limitations, and the overall quality of the evidence; these guidelines are presented in Box 1-1. They are based on approaches used by scientific societies and in recent publications, including: the American Academy of Neurology (Filipek et al., 2000); the American Psychological Association (American Psychological Association, 2000; Barlow, 1996; Chambless and Hollon, 1998); the Society for Clinical Child Psychology (Lonigan et al., 1998); and the New York State Department of Health (1999). A number of comprehensive reviews concerning early intervention in autism also pro- vided examples of ways to systematize information (Dawson and Osterling, 1997; Howlin, 1998; Rogers, 1998; Rumsey et al., 2000). These 

INTRODUCTION 15 BOX 1-1 Guidelines Used to Evaluate Studies Every research report considered by the committee was assigned to one category (I-IV) for each area (A, B, and C). A. Internal Validity: Control for nonspecific factors, such as matura- tion, expectancy, experimenter artifacts I. Prospective study comparing the intervention to an alternative in- tervention or placebo in which evaluators of outcome are blind to treat- ment status II. Multiple baseline, ABAB design, or reversal/withdrawal with mea- surement of outcome blind to treatment conditions or pre-post design with independent evaluation III. Pre-post or historical designs or multiple baseline, ABAB, reversal/ withdrawal not blind to treatment conditions IV. Other B. External Validity/Selection Biases I. Random assignment of well-defined cohorts and adequate sample size for comparisons II. Nonrandom assignment, but well-defined cohorts with inclusion/ exclusion criteria and documentation of attrition/failures; additionally, ad- equate sample size for group designs or replication across three or more subjects in a single-subject design III. Well-defined population of three or more subjects in single-subject designs or sample of adequate size in group designs IV. Other C. Generalization I. Documented changes in at least one natural setting outside of treatment setting (includes social validity measures) II. Generalization to one other setting or maintenance beyond exper- imental intervention in natural setting in which intervention took place III. Intervention occurred in natural setting or use of outcome mea- sures with documented relationship to functional outcome IV. Not addressed or other guidelines were used by both committee members and commissioned paper authors in their reviews of the literature. Figures 1-1, 1-2, and 1-3 present summarized data from journal articles cited within the areas ad- dressed during the workshops (communication, social development, problem behaviors, intervention methods, and sensorimotor develop- 

16 EDUCATING CHILDREN WITH AUTISM 100 90 80 Level I 70 Level II 60 Percent Level III 50 Level IV 40 30 20 10 0 Social Communication Problem Intervention Sensory-Motor (N = 47) (N = 60) Behavior Methods (N = 22) (N = 9) (N = 13) FIGURE 1-1 Internal validity. NOTES: Level I represents the strongest methodological controls and IV the least strong (see Box 1-1); N is the number of studies. SOURCES: For social studies, McConnell (1999); for communication studies, Goldstein (1999); for problem behavior studies, Horner (2000); for intervention studies, Kasari (2000); for sensory-motor studies (Baranek, 1999). ment), in terms of percentages of studies falling into different levels of rigor with respect to internal validity, external validity, and generaliza- tion. This information is discussed in more detail in Chapter 15 and in the chapters describing those content areas. (For details on the coding of individual studies, see the appendices of the papers cited in the figures.) One of the difficulties in interpreting research, particularly longitudi- nal studies, is that standards for scientific research within different theo- retical perspectives have changed enormously in the last 20 years, and they continue to evolve. Twenty years ago, behavioral researchers were not as concerned with rigorously standardizing measures or diagnoses, maintaining independence between intervention and assessment, or ana- lyzing the effects of development. Similarly, group designs based on a clinical trials model were not expected to monitor treatment fidelity, equate participants for intellectual or language level, address generaliza- tion or maintenance of effects, or justify measures by their clinical value. Therefore, particularly when depicting outcomes from longitudinal stud- ies, reviewers of the literature often have to piece together information 

INTRODUCTION 17 100 90 80 Level I 70 Level II Percent 60 Level III 50 Level IV 40 30 20 10 0 Social Communication Problem Intervention Sensory-Motor (N = 47) (N = 60) Behavior Methods (N = 22) (N = 9) (N = 13) FIGURE 1-2 External validity. NOTES: Level I represents the strongest methodological controls and IV the least strong (see Box 1-1); N is the number of studies. SOURCES: For social studies, McConnell (1999); for communication studies, Goldstein (1999); for problem behavior studies, Horner (2000); for intervention studies, Kasari (2000); for sensory-motor studies (Baranek, 1999). fragmented across studies. Today, that information would have been an expected component of a research design from the start. Clinical research always involves compromises based on such factors as access to populations and acknowledgment of clinical needs; often, expense is also considered. Even today, there are very different standards across journals and across research communities as to what are consid- ered unacceptable compromises and what is deemed a necessary part of dealing with complex questions. One of the goals that arose from this review was to identify ways of bridging gaps between perspectives in setting guidelines for research about autism. The committee recognized that a range of emphases and designs is important for different questions. Because of the varied nature of the research, the guidelines presented in Box 1-1 were used to characterize the research reviewed. In this way, the strengths and limitations of individual studies could be considered when deriving conclusions based on the consistencies and inconsistencies ob- served across investigations and theories. Evidence concerning the effectiveness of instructional and compre- hensive programs, strategies, and approaches to intervention for young 

18 EDUCATING CHILDREN WITH AUTISM 100 90 Level I 80 Level II 70 Level III Percent 60 50 Level IV 40 30 20 10 0 Social Communication Problem Intervention Sensory-Motor (N = 47) (N = 60) Behavior Methods (N = 22) (N = 9) (N = 13) FIGURE 1-3 Generalization. NOTES: Level I represents the strongest methodological controls and IV the least strong (see Box 1-1); N is the number of studies. SOURCES: For social studies, McConnell (1999); for communication studies, Goldstein (1999); for problem behavior studies, Horner (2000); for intervention studies, Kasari (2000); for sensory-motor studies (Baranek, 1999). children with autism was considered. The committee’s strategy in assess- ing the effectiveness of components of intervention programs and ap- proaches was to consider, along with the findings of individual research papers, the methodological challenges that many clinical studies face in attempting to control for nonspecific factors, selection biases, and the difficulty in measuring meaningful, generalizable outcomes. Some as- pects of interventions, particularly short-term, problem-focused treat- ments, are much more easily researched than longer-term interventions aimed at more multifaceted concerns (American Psychological Associa- tion, 2000). The committee summarized results across areas of interest and approaches to intervention, taking these factors into account. The goal was to integrate this information into a coherent picture of appropri- ate educational interventions for young children within the autism spec- trum, and to acknowledge points of convergence and points of contro- versy to be addressed in future educational research, practice, and policy. There are no strong studies that compare one comprehensive intervention program with another. Because programs are evolving (and better ap- proaches may be developed in the future), the committee chose to focus on discussion of the effective components and features of each program— 

INTRODUCTION 19 identified on the basis of theory, empirical reports, and consensus across representative programs—rather than to attempt any ranking of specific programs. There are several related areas the committee hoped to address but, because of limited resources and time, did not. Two issues we did not address are the feasibility and costs of various programs and treatments. Because feasibility and cost-effectiveness formulations involve not only short-term costs to school systems but also short- and long-term costs to health systems and society as a whole, and this information and its analy- sis are not readily available, it was felt that it would be inappropriate for us to analyze these questions in a superficial way. However, this infor- mation is much needed. We were also interested in more directly ad- dressing ways of implementing the changes we recommended, but we were unable within the constraints of this project to acquire sufficient information and expertise about strategies for educational change. Be- cause discrepancies in the kind of programs provided are so great across the United States (Hurth et al., 2000; Mandlawitz, 1999), questions con- cerning implementation are also crucial. ORGANIZATION OF THE REPORT The report is organized according to relationships among issues that, the committee believes, represent the key areas pertaining to educational interventions for young children with autism. Part I addresses the gen- eral issue of goals for children with autistic spectrum disorders and their families. Within Part I, Chapter 2 describes how autistic spectrum disor- ders are diagnosed and assessed and prevalence estimates, Chapter 3 considers the impact on and the role of families, and Chapter 4 discusses appropriate goals for educational services. Part II presents the characteristics of effective interventions and edu- cational programs. Chapters 5 through 10 discuss fundamental areas of development and behavior that must be addressed by such programs: communication; social, cognitive, sensory and motor development; and adaptive and problem behaviors. Chapter 11 analyzes the characteristics of representative instructional strategies, and Chapter 12 analyzes the features of ten model comprehensive programs and approaches to inter- vention. Part III examines the policy and research contexts within which inter- ventions are developed, implemented, and assessed: Chapter 13 presents an overview of public policy and legal issues pertaining to education for children with autism, Chapter 14 addresses the needs for personnel prepa- ration to implement policies, and Chapter 15 identifies the experimental design and methodological issues that should be considered by future researchers in educational interventions for children with autism. 

20 EDUCATING CHILDREN WITH AUTISM Our final chapter summarizes the committee’s findings and presents conclusions about the state of the science in early intervention for chil- dren with autism and its recommendations for future intervention strate- gies, programs, policy, and research. 

I Goals for Children with Autism and Their Families 

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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Autism Spectrum Disorder (ASD) Essay

• To find inspiration for your paper and overcome writer’s block
• As a source of information (ensure proper referencing)
• As a template for you assignment

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.

• Tourette’s syndrome: Causes and Treatments
• Understanding the Linkage between Aggression & Personality Disorders: A Critical Analysis
• Emerging Adults With ASD and the Importance of Close Relationships
• Autism Spectrum Disorder: Diagnosis, Impact, Treatment
• Autism Spectrum Disorders: Testing and Measurement
• Mental Illnesses History and Treatment
• Psychopathologies: Co-occurring Diagnoses
• The Identification of Bipolar Disorders
• How Do People Labelled With a Mental Illness Deal With Their Stigmatization?
• Attention Deficit Hyperactivity Disorder Causes
• Chicago (A-D)
• Chicago (N-B)

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Guest Essay

My Son and Gus Walz Deserve a Champion Like Tim Walz

By Tina Brown

Ms. Brown is the author, most recently, of “The Palace Papers: Inside the House of Windsor — the Truth and the Turmoil."

The sight at the Democratic convention on Wednesday night of Tim Walz’s 17-year-old son leaping to his feet, with streaming eyes, a hand to his chest with a cry of “That’s my Dad” was heart piercing.

As the mother of Georgie, a 38-year-old on the spectrum who still lives with me, I recognized him immediately as one of “ours,” a sweet, unfiltered, slightly bewildered-looking young man who wasn’t quite sure what was expected of him in this epic moment of political adulation.

Gus Walz has, according to his parents, a nonverbal learning disorder, A.D.H.D. and an anxiety disorder, all of which they regard not as a setback but as his “secret power,” that makes him “brilliant” and “hyperaware.”

I know exactly what they mean. One of the joys of my life in the social churn of New York is living with a son whose inability to read the room makes him incapable of telling anything but the truth. Once, as my husband, Harry Evans, and I left a pretentious social gathering in the Hamptons, Georgie told the host sunnily: “Thank you very much. No one spoke to me really, so it was a very boring evening. The food was OK. I doubt I will come again.”

“I have never been prouder of you in my life!” shouted my husband in the car. How many times have all of us wanted to say that as we gushed about the fabulous time we just hadn’t had? Then there was the moment he went up to Anna Wintour at one of my book parties and asked if she was Camilla Parker Bowles. And the time at the intake meeting for a supported work program, when the therapist asked Georgie, “Has anyone ever molested you?” “Unfortunately not,” he replied. Georgie teaches me every day how much we depend on social lies to make the world go round. His sister — his forever best friend — and I feel so lucky to have him in our lives. So did his dad, who died in 2020.

And yet for people who are different and have no support, the world can be bleak. Their loneliness can be agonizing. Some people assume the school days are the hardest, but it’s the years after that are the social desert. Having a friendly, forgiving workplace to go to is critical. It’s often their only taste of community and what makes them such reliable and rewarding employees. The work from home movement has been a killer for people with special needs, often depriving them of the only social connections they have.

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