Autistic Disorder

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REPORT

Topic: "Autistic Disorder"

Contents

Statement of the problem

1. Autism spectrum disorders

2. Causes of autism

3. Autism therapies

Conclusion

References

Statement of the problem

Autism is a life-long developmental disability for which there is no cure. In fact, research into this condition has not yet reached a primary precondition (if not prerequisite) for finding a cure: consensus among those researching the disability concerning what causes autism. There are various suggestions, but as yet, no clearly supported generalizations.

While much time and effort have been devoted to the treatment of autistic symptoms, or managing autistic behaviors, comparatively little has been written about its cause or causes. Even less bibliometric work has been compiled concerning autism's etiology, and this research has tended toward a narrow focus and year span to highlight a specific autism cause. However, a broader view of autism etiology research reveals many causes under investigation . If autism is caused by genetic, environmental, and brain development malfunctions coming together at some unfortunate opportunity, the research should reflect this mix. On the other hand, if autism is caused by any one of the three (or some other single biological, psychological, or autoimmune cause), this distinction should be borne out in the literature. While clarifying the relationships among suggested causes of autism and tracking their origins and growth will not necessarily lead the way to a cure, it is a fundamental step which could at least ease the way by clarifying the range of what has been said and done. For these reasons, the focus of this research is on the changing nature of autism etiology literature as it has followed the varying research being done into the possible causes of autism.

1. Autism spectrum disorders

Autism spectrum disorders (ASDs) are a group of developmental disabilities that can cause significant social, communication and behavioral challenges. People with ASDs handle information in their brain differently than other people.

ASDs are "spectrum disorders." That means ASDs affect each person in different ways, and can range from very mild to severe. People with ASDs share some similar symptoms, such as problems with social interaction. But there are differences in when the symptoms start, how severe they are, and the exact nature of the symptoms [5; 694].

There are three different types of ASDs:

- Autistic Disorder (also called "classic" autism)

This is what most people think of when hearing the word "autism." People with autistic disorder usually have significant language delays, social and communication challenges, and unusual behaviors and interests. Many people with autistic disorder also have intellectual disability.

- Asperger Syndrome

People with Asperger syndrome usually have some milder symptoms of autistic disorder. They might have social challenges and unusual behaviors and interests. However, they typically do not have problems with language or intellectual disability.

- Pervasive Developmental Disorder - Not Otherwise Specified (PDD-NOS; also called "atypical autism")

People who meet some of the criteria for autistic disorder or Asperger syndrome, but not all, may be diagnosed with PDD-NOS. People with PDD-NOS usually have fewer and milder symptoms than those with autistic disorder. The symptoms might cause only social and communication challenges.

Signs and Symptoms are next. ASDs begin before the age of 3 and last throughout a person's life, although symptoms may improve over time. Some children with an ASD show hints of future problems within the first few months of life. In others, symptoms might not show up until 24 months or later. Some children with an ASD seem to develop normally until around 18 to 24 months of age and then they stop gaining new skills, or they lose the skills they once had.

Table 1: Early Symptoms of Autism [10; 415]

A person with an ASD might:

- Not respond to their name by 12 months;

- Not point at objects to show interest (point at an airplane flying over) by 14 months;

- Not play "pretend" games (pretend to "feed" a doll) by 18 months;

- Avoid eye contact and want to be alone;

- Have trouble understanding other people's feelings or talking about their own feelings;

- Have delayed speech and language skills;

- Repeat words or phrases over and over (echolalia);

- Give unrelated answers to questions;

- Get upset by minor changes;

- Have obsessive interests;

- Flap their hands, rock their body, or spin in circles;

- Have unusual reactions to the way things sound, smell, taste, look, or feel.

Diagnosing ASDs can be difficult since there is no medical test, like a blood test, to diagnose the disorders. Doctors look at the child's behavior and development to make a diagnosis [5; 695-696].

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

There is currently no cure for ASDs. However, research shows that early intervention treatment services can greatly improve a child's development. Early intervention services help children from birth to 3 years old (36 months) learn important skills. Services can include therapy to help the child talk, walk, and interact with others. Therefore, it is important to talk to your child's doctor as soon as possible if you think your child has an ASD or other developmental problem.

Even if your child has not been diagnosed with an ASD, he or she may be eligible for early intervention treatment services. The Individuals with Disabilities Education Act (IDEA) says that children under the age of 3 years (36 months) who are at risk of having developmental delays may be eligible for services. These services are provided through an early intervention system in your state. Through this system, you can ask for an evaluation [3].

Reviews tend to estimate a prevalence of 6 per 1,000 for autism spectrum disorders as a whole however prevalence rates vary for each of the developmental disorders in the spectrum. Autism prevalence has been estimated at 1-2 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, childhood disintegrative disorder at 0.02 per 1,000, and PDD-NOS at 3.7 per 1,000. These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder [6; 417-418].

While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys being affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1, [2; 594] affecting 1 in 70 males, but only 1 in 315 females.[1; 7-8] Females, however, are more likely to have associated cognitive impairment. Among those with an ASD and mental retardation, the sex ratio may be closer to 2:1. [7; 141] Prevalence differences might be accounted by gender differences in the expression of clinical symptoms, with females showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis. [12; 803-808]

2. Causes of autism

Now many risk factors have been identified in the research literature that may contribute to the development of autism. These risk factors include:

- genetics,

- prenatal and perinatal factors,

- neuroanatomical abnormalities,

- environmental factors.

Genetic risk factors

The results of family and twin studies suggest that genetic factors play a role in the etiology of autism and other pervasive developmental disorders. Studies have consistently found that the prevalence of autism in siblings of autistic children is approximately 15 to 30 times greater than the rate in the general population. In addition, research suggests that there is a much higher concordance rate among monozygotic twins compared to dizygotic twins. These studies suggest a strong genetic component in autism. It is estimated that autism involves 5-10 genes and possibly more. It appears that there is no single gene that can account for autism. Instead, there seems to be multiple genes involved, each of which is a risk factor for part of the autism syndrome through various groups. Possible susceptibility regions include chromosomes 1p, 2q, 7q, 13q, 16p, and 19q [8; 495-500].

Prenatal and perinatal risk factors

A number of prenatal and perinatal complications have been reported as possible risk factors for autism. These risk factors include maternal gestational diabetes, maternal and paternal age over 30, bleeding after first trimester, use of prescription medication during pregnancy, and meconium in the amniotic fluid. While research is not conclusive on the relation of these factors to autism, each of these factors has been identified more frequently in autistic children compared to their non-autistic siblings and other normally developing youth [3; 344-348].

Neuroanatomical findings

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

In neuroanatomical studies, it has been shown that for autistics there is reduced activation in the primary and secondary somato-sensory cortices during Theory of Mind and facial emotion response tasks when compared to control. This is consistent with reports of patterns of abnormal cortical thickness and grey matter volume in those regions in autistics. In normal children, there is a bias of the left lateralized network that is essential for language development, as shown by magneto-encephalography. Specifically, there was a left dominance of parieto-temporal coherence in the theta band that was correlted with higher performance on language related tasks. This was not correlated with head circumference or chronological age [2].

Environmental risk factors

A wide variety of environmental risk factors have been proposed as contributing to autism. These include gastrointestinal or immune system abnormalities, allergies, and exposure of children to drugs, vaccines, infection, certain foods, or heavy metals. The evidence for these risk factors is anecdotal and has not been confirmed by reliable studies.[10; 2-15] The subject remains controversial and extensive further searches for environmental factors are underway.

There has been a great deal of controversy over the years surrounding various theories of the etiology of autism spectrum disorders. In the 1950s, the "refrigerator mother theory" emerged as an explanation for autism. This theory was based on the idea that autistic behaviors stem from the emotional frigidity, lack of warmth, and cold, distant, rejecting demeanor of a child's mother.[4; 420] Naturally, parents of children with an autism spectrum disorder suffered from blame, guilt, and self-doubt, especially as the theory was embraced by the medical establishment and went largely unchallenged into the mid-1960s. While the "refrigerator mother theory" has been rejected in the research literature, its effects have lingered into the 21st century. Another controversial theory suggests that watching extensive amounts of television may cause autism. This theory is largely based on research suggesting that the increasing rates of autism in the 1970s and 1980s were due to the growth of cable television at this time. This theory has not been supported in the research literature. Probably the biggest and most widely circulated controversial theory of autism etiology is the "vaccine theory". This theory suggests that autism results from brain damage caused either by

(1) the measles, mumps, rubella (MMR) vaccine itself, or by

(2) thimerosal, an MMR vaccine stabilizer that is 50% ethylmercury.

The current scientific consensus is that no convincing scientific evidence supports these claims, based on various lines of evidence including the observation that the rate of autism continues to climb despite elimination of thimerosal from routine childhood vaccines.[13; 275] Major scientific and medical bodies such as the Institute of Medicine and World Health Organization as well as governmental agencies such as the Food and Drug Administration and the CDC reject any role for thimerosal in autism or other neurodevelopmental disorder.

3. Autism therapies

autism disorder risk factor

Over the past two decades, there has been increasing attention to the development of evidenced-based interventions for young children with ASDs. Additionally, many unresearched alternative therapies have also been implemented (e.g., vitamin therapy and acupuncture). Although evidenced-based interventions for autistic children vary in their methods, many adopt a psychoeducational approach to enhancing cognitive, communication and social skills while minimizing problem behaviors. It has been argued that no single treatment is best and treatment is typically tailored to the child's needs. Available approaches include Treatment and education of autistic and related communication handicapped children (TEACCH Structured Teaching, Picture Exchange Communication Systems (PECS) an Augmentative and Alternative Communication system, Pivotal Response Training (PRT), Discrete Trial Training (DTT), Incidental Teaching, Positive Behavior Supports, Verbal Behavior Analysis (VBA) all of which have roots in applied behavior analysis (ABA); speech and language therapy, social skills therapy, occupational therapy, and parent-communication training. [7; 62-70] One of the most empirically supported intervention approaches is ABA, particularly in regard to early intensive home-based therapy. It is recommended that children receiving early intervention ABA therapy receive approximately 40 hours of therapy per week for about two years. This intensive approach underlies the UCLA Young Autism Project, originally developed by Lovaas and colleagues, and children in these programs have demonstrated gains in IQ that are maintained until adolescence. [6; 7] Although ABA therapy has a strong research base, other studies have found that this approach may be limited by diagnostic severity and IQ. [9; 10]

Early Intensive Behavioral Intervention, through the use of Applied Behavioral Analysis, has been researched for over 40 years in its effectiveness. Most EIBI programs recognize that all skills appropriate for each specific age are teachable and should be taught. General curriculum areas that are addressed are language, social skills, play skills, motor skills, pre-academic and academic skills, and independent living skills. ABA models of intervention for preschool age include two main approaches to teaching. "Discrete Trial Teaching" or DTT, includes multiple discrete opportunities that are presented across the day or session. A discrete trial consists of the therapist presenting an instruction, the child responding, and the therapist responding to that by presenting a consequence. If the child responds incorrectly, the reinforcer is not given and the therapist will follow up with a error correction procedure, followed by another trial. A strength of this way of teaching is the child receives a large number of trials in a short time, allowing for a large amount of learning opportunities. A potential weakness may be that the skills learned in this structured setting are not easily generalized in less strict settings. "Natural Environment Teaching" consists of maximizing naturally occurring learning opportunities. It involves a more child-directed format that allows for the child to initiate learning, and the therapist to recognize this and follow it by prompting the child for a desired behavior before giving the reinforce.

All successful early intervention programs should focus on the TRIAD of impairments in ASDs. This includes:

a) Joint attention and communication,

b) Social understanding and relationships,

c) Flexibility in thinking and behavior [18; 42].

It also includes a strong, positive partnership with parents, siblings, and co-therapists to keep consistency throughout the childs day. Research for more effective treatments should focus on the extent to which E.I Programs are adapting to the child's pattern of strengths and weaknesses and take into account all family circumstances. The importance and effectiveness of treatment (especially ABA formatted treatment) relies heavily on both child and family circumstances. At the child's level the age at entry into treatment and the severity of impairment on a cognitive, language, and behavioral level are crucial. At the family level, Socio-Economic status, level of income, presence of parents and proximity to outside family and resources, organization, extent of stress of the parents and ability to work alongside the therapist are most important for success.[23; 390]

The Early Start Denver Program integrates applied behavior analysis with relationship and developmental based approaches. Autistic children who participated in the Early Start Denver Program showed significant increase in IQ, adaptive behavior and diagnostic status when compared to community interventions.

Many popular therapies including auditory integration training, GFCF diets, and chelation are not considered evidence-based practices. Notably, research suggests that children with ASDs on GFCF diets do not differ from control groups in terms of their symptoms. [1; 225]

Conclusion

Autism remains an intriguing disorder that is only partially understood. No theory can claim to be the most widely accepted and each has its own difficulties. "Theory"-theory needs to find ways to deal with much of the new research on where and how certain tasks are performed in the brain. Some of this research, as Goldman (2006) notes, seems to violate the modularity basis that "theory"-theory requires. Further, the "theory"-theorists' like Baron-Cohen have retreated from their theoretical commitments and offered alternative views of the autistic disorder (Baron-Cohen, 2002). Simulation theory and Executive Control theory often rely on the claim that the executive control abilities are dysfunctional in persons with autism and some recent research calls this into question (Ozonoff, S., and Strayer, D., 2001; Hughes, C., 2002).

Some recent research has tried to blend together the theoretical tenets of all of the approaches (Cundall, 2006; Keenan, 2000) forming a hybrid version of the theories and often a detente between "theory"-theory and simulation theory can be found. Researchers like Goldman think theoretical reasoning about other's mental states is likely, but not the basic form of socio-cognitive thought. "Theory"-theorists often note that something like simulation is used, but it is only a later developmental ability in social cognition. Other researchers, Rittscher, et al, (2003) are avoiding some of the more theoretical disputes and have simply begun to investigate how socio-cognitive information is processed in the brain. Autism still presents any researcher interested in explaining socio-cognitive development an interesting challenge and any theory that purports to explain socio-cognitive structure and development will need to offer an explanation of the disorder.

References

1. Autism and Developmental Disabilities Monitoring Network Surveillance Year 2006 Principal Investigators (2009). "Prevalence of autism spectrum disorders-Autism and Developmental Disabilities Monitoring Network". MMWR Surveillance Summary 58: 1-20

2. Fombonne, E (2009). "Epidemiology of Pervasive Developmental Disorders". Pediatric Research 65 (6): 591-598

3. Gardner, H; Spiegelman, & Buka (2011). "Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis". Pediatrics 128 (2): 344-355

4. Kanner, L (1949). "Problems of nosology and psychodynamics in early childhood autism". American Journal of Orthopsychiatry 19 (3): 416-426. http://online library.wiley.com/doi/10.1111/j.1939-0025.1949.tb05441.x/ abstract; jsessionid= CB8D015B339A3E0E5F8848FA598A5D1A.d02t03

5. Lord C, Risi S, DiLavore PS, Shulman C, Thurm A, Pickles A. Autism from 2 to 9 years of age. Arch Gen Psychiatry. 2006 Jun; 63(6): 694-701

6. Mash & Barkley (2003). Child Psychopathology. New York: The Guilford Press. pp. 409-454

7. Myers SM, Johnson CP, Council on Children with Disabilities. Management of children with autism spectrum disorders. Pediatrics. 2007;120(5): 62-82

8. Risch, Neil, Spiker, Lotspeich, Nouri et al. (1999). "A genomic screen of autism: Evidence for a multilocus etiology". American Journal of Genetics 65 (2): 493-507

9. Rogers SJ, Vismara LA (January 2008). "Evidence-based comprehensive treatments for early autism". J Clin Child Adolesc Psychol 37 (1): 8-38

10. Rutter, M (2005). "Incidence of autism spectrum disorders: Changes over time and their meaning". Acta Paediatrics 94: 2-15

11. Sickelmor, Pam. "Triad of Impairments". Autism Training and Support. Retrieved February 20, 2011

12. Tsakanikos, E., Underwood, L., Kravariti, E., Bouras, N., & McCarthy, J. (2011). Gender differences in co-morbid psychopathology and clinical management in adults with autism spectrum disorders. Research in Autism Spectrum Disorders, 5: 803-808

13. Waterhouse, Lynn (2008). "Autism overflows: Increasing prevalence and proliferating theories". Neuropsychological Review 18 (4): 273-286

14. Webster, Alec; Anthony Feiler, Valerie Webster (2003). "Early Intensive Family Intervention and Evidence of Effectiveness: lessons from the South West Autism Programme". Early Child Development and Care 173 (4): 383-398

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