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Definition and Background of Approaches to Autism - Essay Example

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In this current paper under the title "Definition and Background of Approaches to Autism", the author will make an earnest attempt to explore and discuss how autism may be explained at the following levels: genetic, physiological, and psychological. …
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Definition and Background of Approaches to Autism
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RUNNING HEAD: APPROACHES TO AUTISM An Overview of Autism School An Overview ofApproaches to Autism In this paper we will look at how autism may be explained at the genetic, physiological and psychological levels. Describing important factors in these areas, I will attempt to bring together various existing approaches, theories and speculations regarding autism, and thus try to show how an integration of these can be used to effectively understand autism. Also, such juxtaposition will help us break free from singular and exclusive understandings of this complex disease, aiding more fruitful advances in addressing it. Definition and Background The term autism was first applied by Dr. Leo Kanner, a psychiatrist in John Hopkins University, to describe a group of children who were self-absorbed and had severe behavioural, social and communication problems. Based on large-scale surveys conducted in England and the United States, a general statistics of 4.5 out of 10,000 live births is widely accepted as the prevalence rate of autism. Recent statistics have included a range of autism spectrum disorders (term first suggested by Wing and Gould in 1979) like PDD (Pervasive Developmental Disorder) and Asperger syndrome along with autism in determining autism prevalence statistics, indicating incidence higher rates of % to % of the population. There are many more children with autistic-like disorders than there are children with autism itself. Thus it is difficult to say that this or that symptom will establish an individual as autistic beyond doubt. Autistic individuals may exhibit several behaviours that are common to disorders that are classified separately such as Angelman Syndrome, Asperger Syndrome, Attention Deficit Disorder, Fragile X Syndrome, Landau-Kleffner Syndrome, Pervasive Developmental Disorder, Prader-Willi Syndrome, Rett Syndrome and Wills Syndrome. Let us look at some of these. Though not considered a sub-type of autism, individuals suffering from Angelman Syndrome may exhibit characteristics that are similar to that of autism, often leading to a secondary diagnosis of autism, like hand-flapping, little or no speech, attention deficits, hyperactivity, feeding and sleeping problems, delays in motor development, biting and hair pulling. Individuals suffering from Asperger Syndrome usually hold conversations which are mostly about themselves, with the voice tending to be flat and emotionless and the speech becoming stilted and repetitive. They are found lacking common sense and an ability to think abstractly in addition to displaying inappropriate reciprocity in terms of social interaction, in addition to engaging in odd-forms of self-stimulatory behaviour. Though it is widely assumed that high-functioning autistics have Asperger Syndrome, it may be noted that there are several other forms of autism that are high-functioning as well and that Asperger Syndrome and autism are clinically separate categories (Rinehart, Nicole J., Bradshaw, John L., Brereton, Avril V., Tonge, Bruce J., 2002) Approximately 15% to 20% of those with Fragile X Syndrome exhibit autistic-type behaviours, such as poor eye contact, hand-flapping or odd gesture movements, hand-biting, and poor sensory skills. Behaviour problems and speech/language delay are common features of Fragile X Syndrome. A common characteristic of Landau-Kleffner Syndrome, which is often diagnosed in conjunction with autism is the failure to respond to sounds. Thus, parents may suspect their child of hearing loss. Autistic characteristics seen in Landau-Kleffner Syndrome individuals include pain insensitivity, aggression, poor eye contact, insistence on sameness, and sleep problems. Some suggested causes have been a dysfunctional immune system, exposure to a virus, and brain trauma; anticonvulsant mediations, corticosteroids and brain surgery being used for treatment. Prader-Willi Syndrome is a disorder which is sometimes associated with, but not a subtype of, autism. Some of the behaviours which are common to both Prader-Willi Syndrome and autism is: delays in language and motor development, learning disabilities, feeding problems in infancy sleep disturbances, skin picking, temper tantrums, and a high pain threshold. The most effective form of treatment for people suffering from Prader-Willi Syndrome is behaviour modification. Children afflicted with Rett Syndrome often exhibit autistic- like behaviors, such as repetitive hand movements, prolonged toe walking, body rocking, and sleep problems. Many people with Williams Syndrome exhibit autistic behaviors. This includes: developmental and language delays, problems in gross motor skills, hypersensitivity to sounds, being picky eaters, and perseverating. Causes of Autism The causal factors of autism and an established list of its symptoms are yet to be scientifically determined beyond doubt. Its symptoms vary and many of the symptomatic characteristics associated with autism may or may not be exhibited by some autistic individuals. Although there is no known unique cause of autism, there is increasing evidence regarding the fact that autism can be caused by a variety of problems. Various theories postulating genetic evidence for the occurrence of autism is available (Veenstra-VanderWeele, Jeremy, Christian, Susan L. & Cook Jr., Edwin H. , 2004). For example, there is a greater likelihood that two monozygotic twins (i.e., identical twins) will have autism than two dizygotic twins (i.e., fraternal twins). In the case of monozygotic twins, there is a 100% overlap in genes; whereas in dizygotic twins, there is a 50% overlap in genes, the same overlap as in non-twin siblings. Currently, a great deal of research has focused on locating the 'autism gene;' however, many researchers speculate that three to five genes will likely be associated with autism. There is also evidence that the genetic link to autism may be a weakened or compromised immune system. Other research has shown that depression and/or dyslexia are quite common in one or both sides of the family when autism is present. There is also evidence that a virus can cause autism. There is an increased risk in having an autistic child after exposure to rubella during the first trimester of the pregnancy. The Cytolomegalo virus has also been associated with autism. Additionally, there is also a growing concern that viruses associated with vaccinations, such as the measles component of the MMR vaccine and the pertussis component of the DPT shot, may cause autism. We find a growing concern that toxins environmental agents, toxins, drugs, viruses and poisonous substances such as lead and mercury(Parsell, Diana, 2004) may be additional causes of autism apart from strictly genetic reasons. Brain and Bio-chemical Abnormalities Autistic individuals often display insensitivity to physical pain. This has been explained as being caused by elevated levels of endorphins, which are endogenous opiate-like substances, in the body. A possible reason for such elevated levels of endorphin in the body is attributed to the ingestion of food items containing proteins like gluten and casein which have configurations similar to that of endorphins. Intestinal tract problems, such as leaky gut (small holes in the intestine), yeast overgrowth, low levels of secretin, infections resulting from viruses or toxins such as metals are also often found to be present in autistic individuals. For most people, it takes a short period of time, less than a second or two, to redirect attention from one stimulus to another in the environment. In contrast, autistic individuals continue to attend to a stimulus even when prompted for redirection, and they may take three to five seconds or longer to shift their attention. Hyperplasia, the reduction in size of lobules VI and VII of the cerebellum and hyperplasia, the enlargement of these lobules is attributed to the inability to shift attention in normal time in autistics. Though this theory is not verified in autopsy studies, autopsy studies have shown a dramatic reduction in Purkinje cells in the cerebellum in autistics. These cells are rich in the neurotransmitter serotonin. Abnormal levels of serotonin are well-documented in individuals with autism and may be linked to faulty arousal and problems in mood regulation. Autistic individuals typically have problems processing auditory information, hearing speech sounds but not perceiving the meaning of the sounds. For example, when someone says 'butter' though the person hears the speech sound, they do not understand the meaning of the sound. On the other hand, autistic individuals are often seen as having a very high or exclusively visual thinking. Thus, Temple Grandin, a 44 year-old autistic woman says, All my thinking is visual As a young child I had visualizations to help me understand the Lord's Prayer. The "power and the glory" were high-tension electric towers and a blazing rainbow sun. The word "trespass" was visualized as a "No Trespassing" sign on the neighbour's tree I still have problems handling long strings of verbal information. If directions from a gas station contain more than three steps, I have to write them down. Condon (1985) Additionally, Condon (1985) found that autistics and, to a lesser extent, dyslexics and stutterers have a defective orienting response. One ear hears a sound sooner that the other. The asynchrony between ears is sometimes over one second. Many autistics also have problems with modulating sensory input (Ornitz, 1985). They either overreact or under-react. Ornitz (1985) suggesting that some cognitive deficits could be caused by distorted sensory input. Autistics also have profound abnormalities in the neurological mechanisms that control the capacity to shift attention between different stimuli (Courchesne, 1989). Cerebellar abnormalities may play a role in increased sound sensitivity. Research on rats indicates that the vermus of the cerebellum modulates sensory input (Crispino & Bullock, 1984). Stimulation of the cerebellum with an electrode will make a cat hypersensitive to sound and touch (Chambers, 1947). Though the underlying reasons for auditory processing problems in autism are still not known, autopsy research by Doctors Bauman and Kemper have shown that an area in the limbic system, the hippocampus, is neurologically immature in autistic individuals (Bauman & Kemper, 1994). The hippocampus is responsible for sensory input as well as learning and memory. Information is transmitted from the auditory sensory organ to the hippocampus which processes this information and transfers it to specific parts of the cerebral cortex for long-term storage. Thus, since the hippocampus is underdeveloped, the function of long-term memory is hampered since the hippocampus cannot process and transfer the auditory signals efficiently. Interestingly, those individuals who do not have auditory processing problems are often auditory learners. These children do very well using the Applied Behaviour Analysis (ABA) approach, whereas those who are visual learners do not do as well with this approach. Given this, one might suspect that many visual learners have auditory processing problems and that visual learners will do quite well with a visual communication/instruction approach. It is also possible to provide visual support with ABA programs that have an auditory component. In this way, the visual learner can process the auditory information more easily. Important findings indicate specific damage in the limbic system, particularly in the amygdala and hippocampus as possible cause for extreme aggression or passivity in autistic individuals. Much of this research has been conducted by Dr. Margaret Bauman, (Dept. of Neurology, Harvard Medical School), and Dr. Thomas Kemper, (Depts. of Neurology, Anatomy, and Pathology, Boston University School of Medicine). They report densely packed neurons in the amygdala and hippocampus of persons with autism and that these neurons are smaller than in normal persons. The amygdale controls our aggression and emotions. In addition, the amygdala is responsive to a variety of sensory stimuli, such as sounds, sights, and smells; as well as emotionally or fear-related stimuli. Dr. Rimland theorized that autistic children had difficulty relating new information to previously stored information due to damaged hippocampus. Also, damage to the hippocampus can result in stereotypic, self-stimulatory behaviours and hyperactivity, which are displayed by autistic children. Autistic individuals are also often found engaging in self-injurious behaviour. This has been explained by the theory that such behaviour releases beta-endorphins in the person's brain providing a kind of internal pleasure. Sudden episodes of self-injury may also be caused by sub- clinical seizures, characterized by abnormal EEG patterns. It may be that due to some dysfunctional system in the brain or periphery, the body craves stimulation; and thus, the person engages in these behaviours to excite or arouse the nervous system. Some forms of self-injury can also be a result of over-arousal or self-stimulatory, stereotypic behaviours. .Self-injury and self-stimulatory behaviours may act as a release by blocking out the over stimulating environment, lowering sensory overload and calming the person. Social theories explain self- injury in terms of seeking-attention or seeking to escape or avoid an assigned task. There is also the possibility that these behaviours could be related to hypersensitivity to certain sounds in the environment. Self-injurious behaviour may also be instigated by easily treatable causes like middle-ear infections. Another problem found in autistic individuals is the incompatibility of their social- emotional age with the corresponding, normally expected intellectual age. Margaret Bauman, M.D. has found neurological evidence that indirectly supports the relationship between brain functioning and social-emotional age determining that immaturities in the amygdala and hippocampus in autopsies, responsible for emotions, aggression, sensory processing and learning, memory, and the integration of sensory information respectively. People with autism are more susceptible to allergies and food sensitivities than the average person; and this is likely due to their impaired immune system. Food sensitivities may be responsible for numerous physical and behavioural problems, such as headaches, stomach-aches, feeling of nausea, bed-wetting, appearing 'spaced out,' stuttering, excessive whining and crying, sleeping problems, hyperactivity, aggression, sound sensitivity, temper tantrums, fatigue, depression, intestinal problems (i.e., gas, diarrhoea, constipation), muscle aches in the legs, ear infections and possibly seizures. There is growing evidence that the gut or intestinal tract of autistic children are impaired. Researchers have documented yeast overgrowths (Candida albicans), low levels of phenyl sulphur transferees, and measles virus in their intestinal tract. A dysfunctional immune system has also been associated with autism. It is thought that a viral infection or an environmental toxin may be responsible for damaging the immune system. As mentioned above, there is also evidence of a genetic association to a compromised immune system. Researchers have found that many autistic individuals have a decreased number of helper t-cells which help the immune system fight infection. Autistic individuals sometimes have difficulty with the transition to puberty. Approximately 25% have seizures for the first time during puberty which may be due to hormonal changes. In addition, many behaviour problems can become more frequent and more severe during this period. However, others experience puberty with relative ease. Cognition One of the most characteristic symptoms of autism is a dysfunction in social behaviour. The social problems can be classified into three categories: socially avoidant, socially indifferent, and socially awkward. Socially avoidant individuals avoid virtually all forms of social interaction. The most common response is tantrumming and/or 'running away' when someone tries to interact with him/her. As infants, some are described as 'arching their back' from a caregiver to avoid contact. For many years, it was thought that this type of reaction to their social environment indicated that autistic individuals did not like or were fearful of people. Another theory, which is based on interviews with autistic adults, suggests that the problem may be due to hypersensitivity to certain sensory stimuli. For example, some state that a parent's voice hurt their ears; some describe the smell of their parents' perfume or cologne as offensive, and others describe pain when being touched or held. Socially indifferent individuals who are described as 'socially indifferent' do not seek social interaction with others (unless they want something), nor do they actively avoid social situations. They do not seem to mind being with people; but at the same time, they do not mind being by themselves. It is thought that this type of social behaviour is common in the majority of autistic individuals. One theory is that autistic individuals do not obtain 'biochemical' pleasure from being with people. Since the chemical responsible for this, beta-endorphins are normally elevated in autistics, they do not need social interaction to obtain pleasure. Socially awkward autistics may try very hard to have friends, but they cannot keep them. One reason for their failure to make enduring social relationships with others may be the lack of reciprocity in their interactions and inability to learn social skills and taboos by observation. In addition to the above three types of social deficits, the social cognition of autistic individuals may also be dysfunctional. Recent research has shown that many autistic individuals do not realize that other people have their own thoughts, plans, and points of view. They also appear to have difficulty understanding other people's beliefs, attitudes, and emotions. As a result, they may not be able to anticipate what others will say or do in various social situations. This has been termed as a lack of 'theory of mind', an idea which has received much attention lately. Many autistic individuals appear to have 'tunnel vision', or stimulus over-selectivity, a phenomenon whereby a person focuses on only one aspect of an object or environment while ignoring other aspects. It is argued by some that this is the reason why parents often suspect their child of being deaf. One theory states that these individuals are born with 'too much' concentration; and as a result, it is very difficult for them to expand or widen their attention span. Another theory states that these individuals cannot process or attend to the environment as a whole because it may become overwhelming, i.e., lead to over- arousal. As a result, they may try to simplify their life by focusing on only a small part of their world The autistic savant is one of the most intriguing and remarkable phenomena in cognitive psychology where an autistic person who is debilitated in several areas of capacities such as memory and speech displays extraordinary abilities in specific tasks. The most common forms involve mathematical calculations, memory feats, artistic abilities, and musical abilities Thus some can multiply and divide large numbers in their head and can also calculate square roots and prime numbers in a similar manner whereas musical savants can pick up the exact pitch of a melody they heard only once as well as remember the music. "Throughout elementary school my speech was still not completely normal. Often it took me longer than other children to start getting my words out. Singing, however was easy. I have perfect pitch and I can effortlessly hum back the tune of a song I have heard only once or twice", says Grandin. Sensory over-stimulation has been the major mode of explaining the phenomenon of autistic savant. Conclusion I have in this paper described the major theories on brain and bio-chemical dysfunctions causing autism. It will be important for future researchers to examine the relationship between these two types of abnormalities. I have also listed out sensory impairments in autism and cognitive deficits as well as particularities in autistic individuals. Autism is a very complex disorder; and the needs of these individuals vary greatly. After years of extensive research, traditional and contemporary approaches are enabling us to understand and treat these individuals. It is also important to mention that parents and professionals are beginning to realize that the symptoms of autism are treatable--there are many interventions that can make a significant difference. Given time researchers will unravel the mystery of autism. References Bauman, M., & Kemper, T.L. (1985). Histoanatomic observations of the brain, in early infantile autism. Neurology, 35, 866-874. Bauman, M.L., & Kemper, T.L. (1994). Neuroanatomic observations of the brain in autism. In M.L. Bauman & T.L. Kemper (Eds.), The neurobiology of autism. Baltimore: Johns Hopkins UP Chambers, W.W. (1947). Electrical stimulation of the interior cerebellum of the cat. American Journal of Anatomy, 80, 55-93. Condon, W.S. (1985). Sound-film microanalysis: A means of correlating brain and behavior. In F.Duffy & N.Geschwind (Eds.), Dyslexia: A neuro-scientific approach to clinical evaluation. Boston: Little, Brown Courchesne, E. (1989). Implications of recent neurobiologic findings in autism, In Conference Proceedings; Autism Society of America, (pp. 8-9). Washington, DC: Autism Society of America. Crispino, L., & Bullock, T.H. (1984). Cerebellum mediates modality-specific modulation of sensory responses of midbrain and forebrain in rats. Proceedings: National Academy of Science - Neurobiology, 81, 2917-2920. Grandin, Temple. An Inside View of Autism. In Centre for the Study of Autism: Temple Grandin. Retrieved 11/21/2005 from http://www.autism.org/temple/inside.html McEachin, J.J., Smith, T., & Lovaas, O.I. (1993). Long-term outcome for children with autism who received early intensive behavioral treatment. American Journal of Mental Retardation, 97, 359-372. Ornitz, E. (1985). Neurophysiology of infantile autism. Journal of the American Academy of Child Psychiatry, 24, 251-162 Parsell, Diana. (2004) Abstract: Assault on Autism. In Science News. Vol. 166 Issue 20, p311- 312, retrieved 11/ 22/2005 from http://web28.epnet.com/citation.asptb=1&_ug=sid+3637520C%2DD31B%2D47B1%2D882D%2DE1890AEC87FB%40sessionmgr4+dbs+aph+cp+1+B1F4&_us=frn+1+hd+False+hs+True+cst+0%3B1%3B2%3B3%3B4+or+Relevance+ss+SO+sm+KS+sl+0+dstb+KS+mh+1+ri+KAAACBYC00048727+9635&_uso=hd+False+tg%5B0+%2D+st%5B0+%2Dautism+db%5B0+%2Daph+op%5B0+%2D+mdb%5B0+%2Dimh+3B01&fn=1&rn=4 Rimland, G., & Fein, D. (1988) Special talents of autistic savants. In L.K. Obler & D. Fein (Eds.), The exceptional brain. New York: Guilford. Rinehart, Nicole J., Bradshaw, John L., Brereton, Avril V., Tonge, Bruce J. Dec 2002. A clinical and neurobehavioural review of high-functioning autism and Asperger's disorder. Vol. 36 Issue 6, p762-770, retrieved 11/22/2005 from http://web28.epnet.com/citation.asptb=1&_ug=sid+3637520C%2DD31B%2D47B1%2D882D%2DE1890AEC87FB%40sessionmgr4+dbs+aph+cp+1+B1F4&_us=frn+1+hd+False+hs+True+cst+0%3B1%3B2%3B3%3B4+or+Relevance+ss+SO+sm+KS+sl+0+dstb+KS+mh+1+ri+KAAACBYC00048727+9635&_uso=hd+False+tg%5B0+%2D+st%5B0+%2Dautism+db%5B0+%2Daph+op%5B0+%2D+mdb%5B0+%2Dimh+3B01&fn=1&rn=1 Veenstra-Vander Weele, Jeremy, Christian, Susan L., & Cook Jr., Edwin H. (2004) Abstract: Autism As a Paradigmatic Complex Genetic Disorder. In Annual Review of Geonomics & Human Genetics, Vol. 5 Issue 1, p379-405, retrieved 11/22/2005 from http://web28.epnet.com/citation.asptb=1&_ug=sid+3637520C%2DD31B%2D47B1%2D882D%2DE1890AEC87FB%40sessionmgr4+dbs+aph+cp+1+B1F4&_us=hd+False+hs+True+cst+0%3B1%3B2%3B3%3B4+or+Relevance+ss+SO+sm+KS+sl+0+ri+KAAACBYC00048727+dstb+KS+mh+1+frn+11+455C&_uso=hd+False+tg%5B0+%2D+st%5B0+%2Dautism+db%5B0+%2Daph+op%5B0+%2D+mdb%5B0+%2Dimh+3B01&fn=11&rn=14. Read More
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