A Full Explanation of Autism Spectrum Conditions - Assignment Example

?A Report on “Cognitive theories do not provide a full explanation of autism spectrum conditions. Discuss.” of I. Introduction Reports of both adults and children with autism spectrum disorders (ASDs) have significantly increased and therefore have become more prevalent in the present age than it was before (Centers for Disease Control and Prevention 2012). Recognition of this condition as highlights of clinical and sociological research has produced awareness to our generation of the existence of such developmental disability. It is of utmost urgency and importance that local, national and worldwide level of discussions be given about this topic to mobilize mitigation actions and management. It is the goal of this paper to discuss autism spectrum conditions, cognitive theories which aim to provide an understanding of it, the failure to achieve this and the reasons for the failure that relate to the complex nature of autism. What is Autism Spectrum Disorder? Centers for Disease Control and Prevention (2012) defines Autism Spectrum Disorders as “a group of developmental disabilities characterized by impairments in social interaction and communication and by restricted, repetitive, and stereotyped patterns of behaviour”. Being a spectrum disorder or condition, this also implies that autism is manifested according to a range of degree of severity (Baron-Cohen 2008). ASDs are conditions that largely affect the social abilities of a person and consequently the progress to most aspects of developmental growth. ASDs are generally recognized through its main symptom which is reliably detected, that is the deficiency in verbal and nonverbal communication (Baron-Cohen et al. 1985). On one side, it may appear that an individual with ASD is completely deficient of social skills, language and key learning capabilities. In this case, this is diagnosed as classic autism (Baron-Cohen 2008). However on the other side, it is also possible that the ASD individual may have average or even above average IQ with advanced vocabulary albeit there is lack of interest in engaging in communications, and a distinctively peculiar social manner in a way that the ASD could be particularly one-sided or very self-centred. This is diagnosed as Asperger Syndrome (Baron-Cohen 2008). These two extremities are both recognized under ADS. Common characteristics of these diagnoses are the strong inclination of the individual to engage in routinary and repetitive activities, and that they can be exceptionally consumed in topics of their interest. It is reported that 1% of the population have autism (Baron-Cohen 2008; Gillberg 2004). Prevalence of Autism Spectrum Disorders It is alarming that the Centers for Disease Control and Prevention’s (2012) Autism and Developmental Disabilities Monitoring Network (ADDM) reports that one in 88 children in United States has been identified with ASD. ADDM was able to identify in their studies that ASD reaches its peak manifestation at age 8 while symptoms are typically revealing even before the age of 3 years old (Centers for Disease Control and Prevention 2012). Understanding the ASD by methods of research and regular discussions indeed shows necessity at this current time as not only individuals and their families are being affected by this phenomenon. It can be regarded as a national and worldwide issue. The rise of ASD cases is expected as projected by a simple model created from various sources of autism data. Rogers 2011 shows a forecast of adults with autism to increase by over 600% using any extrapolation assumption. The care, support and management of ASDs are costly. In the United States, it costs over $12,000 to educate students with disabilities annually while for adults, it costs about $50,000 to $100,000 to support in a living set-up. These figures still vary according to age range of autism and also life longevity. Thus, this poses an imperative area of research for more detailed knowledge and understanding on the occurrence and extending of ASD cases. “Theory of Mind” ASDs are believed to have a lack of the “theory of mind” (Baron-Cohen et al. 1985). The “theory of mind” is a hypothesis of autism that was introduced by Baron-Cohen et al. (1985) which identified the key social and communication symptoms of individuals with ASDs (Tager-Flusberg 2007). Baron-Cohen et al. (1985) further explains the theory of mind being the inability to represent mental states which therefore results to the inability to assign beliefs to others and consequently being unable to predict the behaviour of other people. This explains well why ASD individuals are unable to read on social cues on a group environment and as a result, they prefer to play or work alone. They lack the understanding of group communication because they cannot read the unspoken messages in a group interaction. This aspect can also be considered as a type of conceptual perspective-taking skill (Shantz 1983). Smukler (2005) however contradicts this theory arguing that it misrepresents autism. He employed a social constructionist perspective and arrived at a conclusion that the theorists of The Theory of Mind define autism as a form of insufficiency that requires fixing instead of accommodation. He proposed alternative narratives that encompass perspectives of individuals with autism who were labelled that way and this provided a significant counterbalance to the limitations of this view. The Cause of Autism Spectrum Disorders Happe and Ronald (2008) states that “autism is diagnosed on a base of combinations of triad impairments found in social interaction, communication and flexible imaginative functions that have restricted and repetitive behaviours and interests”. Having enough evidence to affirm the complexity of ASD, its integral aspects have been proven to have unique causes that coexist. Happe, Ronald and Plomin (2006) argues that no single genetic or cognitive cause exist for the diverse symptoms of autism. They presented evidences of non-overlapping genes responsible for symptoms of social impairment, communication problems, and rigid and repetitive behaviours (Happe et al. 2006). In fact, they defend that the single explanation of autism through the cognitive level was a failure. They therefore proved that there is no single cause for the occurrence of autism having three core aspects – genetic, neural and cognitive areas – that co-occur at above chance rates (Happe et al. 2006). Genetics of Autism Spectrum Disorders Geschwind (2011) describes ASD as a neurodevelopmental syndrome which is characterized by a combination of abnormalities recognized as language, social cognition and mental flexibility. He further explains that there are many ASD susceptibility genes that have already been identified to collectively contribute to the 10-20% ASD cases. Geschwind (2011) states that although it is established that ASD is diverse in origin, its source genes can provide important information about its pathophysiology. He supports the application of diverse genetic and genomic methods so that evidence can be gathered on coming together of disruption of key biological pathways which have implications in other similar neurodevelopmental disorders. With information of what genes are involved in ASD, Geschwind (2011) asserts that it is an important guide to identify the specificity of ASD and the shared neurobiological and cognitive features among those which are categorized as clinical disorders. And it could help achieve the goal of linking gene to the brain circuits and to cognition and behaviour. Genetic Variants of Autism The common symptoms of ASD are typified as a neurodevelopmental syndrome which are suggested from earlier discussions to have many causes and not only attributed to a single gene (Geschwind 2011; Happe and Ronald 2008; Happe, Ronald and Plomin 2006). In here, Klei et al. (2012) have adopted quantitative genetics techniques and contrast of ASD subjects as controls to estimate the portion of liability through additive genetic effects also known as narrow-sense heritability. They have found out that there is a myriad of common variants with very small effect that impacts ASD liability. This means that common genetic polymorphisms contribute significant additive genetic influence on ASD liability which then project varying impacts. Klei et al. (2012) concludes that there are many common variants that have small effects that affect liability to ASD. Thus, ASD must be a collective implication of the several small contributions of various genetic variants. Cognitive Theories of Autism Cognitive theories are used to explain the relationship between autism and the behaviour of the individual with autism. According to Rajendran and Mitchell (2007), there are three theories of autism recognized. These are: The Theory of Mind Deficit, Executive Dysfunction and the Weak Central Coherence. These theories have been rooted from decades of research in developmental psychology of which it was only during the mid-80s when it was known for autism to be a manifestation of primary cognitive deficit. Rajendran and Mitchell (2007) discuss each theory cited. The Theory of Mind Deficit as earlier explained in previous paragraph, identifies that individuals that have autism are not able to “impute mental states to themselves and others” (Premack and Woodruff 1978). This deficiency then translates to the inability of the individuals with autism to relate mentally or take into account the other person’s mental states. The often used test to determine the existence of Theory of Mind is called the unexpected transfer test of false belief, a test developed by Wimmer and Perner (1983). It was through this test that Baron-Cohen et al. (1985) discovered that about 80 percent of children with autism exhibit a deficit of theory of mind because they failed the unexpected transfer test. However, it was contested by Happe (1994) that having the 20% of individuals with autism to actually pass the test is problematic as it implies that the deficit is not universal. In response to this, Baron-Cohen (1985) adjusted his proposal that the Theory of Mind is in a delay rather than a deficit. From then, a series of questions and adjustments of the theory were set considering other influence such as developmental delay, verbal mental age and its relation to other factors (Happe 1995; Bowler 1992). However it is notably established in the Theory of Mind that individuals with autism exhibit difficulties in understanding both their own and others’ mind (Rajendran and Mitchell (2007). The Theory of Executive Dysfunction came from reports of researchers who observed that the symptoms shown by individuals with autism were similar to those with specific brain injury (Rajendran and Mitchell 2007). The authors establish that its “accounts of autism is that executive functions are intrinsically domain-general”. The Theory of Mind was not enough to explain symptoms exhibited by those of what we currently know as Dysexecutive Syndrome (DES) consisting of the need for sameness, difficulty to switch attention, tendency to perseverate and lack of impulse control (Rajendran and Mitchell 2007; Baddeley and Wilson 1988). Rajendran and Mitchell (2007) elaborate that these individuals are commonly challenged with executive function as a result of frontal lobe damage thereby directing researchers to propose a shortfall in Executive Function causes autism (Ozonoff et al. 1991a). The Executive Function reasoning may able to have explained the many features of autism however Rajendran and Mitchell (2007) suggest that it is limited to the fact that not every individuals with autism actually display Executive Function and if they did, there are differences in their Executive Function profiles. It meant that it is not a classifying feature and may be observed in other disorders as well. Lastly, the Weak Central Coherence Theory (WCC) is a domain general process and one of its important strengths include a justification on the non-social and social characteristics of autism like the attention to acute detail which can be from pedantry to obsession (Rajendran and Mitchell 2007; Firth 1989; Frith 2003; Frith and Happe 1994; Happe 1999). Rajendran and Mitchell elaborate that this theory practically implies that typically developing individuals process information by extracting a holistic sense or gist. Furthermore, Frith and Happe advise that individuals with autism process things in a detail-focused way by processing the constituent parts rather than the global whole. Thus they are dramatically keen to details and tend to ignore the whole. This view has brought autism research into areas of perceptual abilities. However more interpretations have been brought up for WCC and therefore needs more verification (Happe 1999; Happe and Frith 2006). In the end, Rajendran and Mitchell (2007) conclude that WCC has become specified by having delineated the boundaries of the theory’s areas of explanation. This includes the perception that WCC is a global processing deficit, instead WCC is a superior local processing. Rajendran and Mitchell (2007) therefore affirms the concept that autism in a multiple deficit. II. Discussion Cognitive theories do not provide a full explanation of Autism Spectrum Conditions Since the inception of autism spectrum conditions by initially diagnosing through behavioural criteria in the 1940s (Kanner 1943) with evident symptoms of impairment in verbal and nonverbal communication (Baron-Cohen et al.1985), research has been invigorated until it advanced into cognitive, neurological, genetics, genomics, pathological and also intervention science aspects. Our knowledge of ASDs has indeed significantly progressed with more accurate data on its natural history and likelihood of symptoms approaches. We also now know more statistics and have traced earlier manifestations when we have learned the convergence points from clinical records. This then allowed us to project the cost, severity and future impacts in our nation. Having mentioned all these impressive milestones on our familiarization with ASDs, our areas of difficulties still exist. Numbers of individuals with autism continue to rise in children while adults suffer from it in their lifetime. Its continued existence and prevalence seem to promote more responsibilities of medical attention to the individual and their families. What can be done to mitigate the circumstance is still unknown. This therefore proves that the cognitive theories that we currently adapt to intervene and manage ASDs, even as sophisticated and current as they are still do not solve the problem. They do not provide a full explanation of ASDs that would help to lessen if not to completely stop the conditions. There is no doubt of our gratitude of the most prized knowledge we now hold about ASD but still, it seems that only the tip of the iceberg has been exposed. There is more to explore underneath. And our current information are good leads to a must be greater issue relating to something bigger than physiological or genetic alterations in our body systems. I believe that there must be influential factors that would have induced such changes, but which are yet to be discovered. The interrelations of our environment and people may answer such questions as we are all part of a bigger world albeit each one is a tiny component of a giant system. Thus, the cognitive theories that we often refer to must be explored further as by themselves, they cannot explain fully the enigma of ASDs. More Cognitive Theories Apart from what have been discussed earlier by Rajendran and Mitchell (2007) about the three most recognized cognitive theories, there are more hypotheses that have been recently developed in the attempt to clearly explain ASDs. These are but indicators that the existing cognitive theories do not provide full explanation of ASDs. One interesting hypothesis of Kunda and Goel (2010) states that some individuals with autism make use of visual mental representations and processes to perform certain activities that are usually performed verbally by developing individuals. The authors call it “Thinking in Pictures” hypothesis. Kunda and Goel (2010) observe that individuals with autism are typically described as analogical in that they have structural correspondence to what they represent. This therefore is closely related to perceptual mechanisms (Kosslyn et al. 2006). The difference of Thinking in Pictures theory from other cognitive theories earlier discussed is that Weak Central Coherence (WCC) and Enhanced Perceptional Functioning (EPF) consider cognition, equating various representational modalities (visual, auditory, etc.) within each of these two types of processing (local vs. global or perceptual vs. high-level) (Kunda and Goel 2010). Contrastingly, Kunda and Goel (2010) elaborate that Thinking in Pictures theory consider cognition, equating various processing types (perception, working memory, long term memory) only within each of two particular representational modalities, visual vs. verbal. Whereas WCC and EPF explicitly consider autistic superiorities on some visual tasks, Thinking in Pictures currently does not consider an exact mechanism for such pattern albeit there are many possibilities to take note such as increased visual expertise both developmentally and cognitively. Thus Kunda and Goel (2010) urge that the theory that individuals with autism may “think visually” must be given attention as a cognitive model, and appropriate focus in behavioural and neurobiological experiments. Already mentioned in the above paragraph, Enhanced Perceptual Functioning (EPF), according to Kunda and Goel (2010) and Mottron et al. (2006) is another cognitive theory that explains that individuals with autism possess enhanced low level perceptual processing across a variety of modalities, as compared to cognitive processing that involves higher levels of neural integration. To demonstrate this, Kunda and Goel (2010) enumerate the numerous research that have found evidence of uniqueness and often superiorities in low-level visual perception in individuals with autism. Take the findings of Bertone et al. (2005) and Vandenbroucke et al. (2008). It has also been characterized by Ropar and Mitchell (2002) that autistic perception can be defined in some tasks as less influenced. It was said by Caron et al. (2006) that what makes superiorities in autism on visual tasks, is a combination of locally oriented processing and enhanced perceptual processing, as for those who share these two traits. Overlap of Cognitive Theories Apparently, overlapping characteristics can be observed from the theories mentioned above. As more observations and group tests on individuals with autism are conducted, more ASD reasonings make sense and are validated, while others are perceived to be needing more data validation. The complexity of systems involved and its complications on the convergence of affected systems make the explanation of ASD to be overwhelming. And also, taking into consideration the uniqueness of the system response of each individual with autism add more factor to be measured. It could be that ASDs are more than interrupted, altered or converged cognition patterns in the brain, but somehow there is this unique response by each individual with autism that is remarkably marked by the uniqueness exhibited in his own physical and genetic makeup. If this is so, it is certain that cognitive theories will not be enough to effectively explain the ASDs. Our Recent Progress in Understanding Autism Rutter (2011) highlights the scientific progress that we have achieved in terms of advances in our understanding of clinical characteristics, advances in genetics, development in environmental research and the status of operations on psychological treatments. All these benefit our current approach and management of ASDs. However, prevention and cure of autism itself remain intangible. The succeeding paragraphs report these milestones on different areas of ASDs as Rutter (2011) explains. It must be noted that it is indeed a puzzle that with all the scientific knowledge, validation of cognitive theories and research results, autism maintains its mysterious status in that we still do not have the data in order to avoid its occurrence neither to eradicate its symptoms. Temporary developmental regression notably connected to language and language-related skills is validated to be characterized in autism (Rutter 2011;Werner and Dawson 2005). It was found out by Baird et al. (2008a) and Pickles et al. (2009) that regression indeed was strongly associated with autism and rare in other neurodevelopmental disorders. Their research also imply that it was misleading to regard regression as a category of present or absent occurrence since the presence of minor degrees of regression still points to autism. Savant skills are comparable to regression as a lead to autism. It was proven that Savant skills represented true abilities. The study of Howlin et al. (2010) showed that about a third of individuals with autism had either Savant skills on the basis of parental report or a remarkable cognitive skill thereby confirming that it is not true that it is uncommon in individuals with autism. It therefore appears that Savant skills are specifically typically related with autism. Woodhouse et al. (1996) reports the increased brain size of individuals with autism. This was confirmed by the first structural brain imaging studies done by Piven et al. (1995). It was then proven that there is indeed a global increased brain growth although it is not confirmed whether this is due to an excess of neurons, and/ or decreased synaptic pruning (Keller and Persico 2003). Courchesne et al. (2003), (2007) and, Redcay and Courchesne (2005) report a fascinating finding about the brain size being normal at birth but it significantly grow in the early years just when it is the period when the first obvious signs of autism show. Furthermore Rutter (2011) elaborates the key value of the increase in brain growth in early years. It indicates a kind of neural process that only arrives in time of the toddler age period, albeit the genetic liability has been present from before birth. Rutter (2011) verifies that specific cognitive deficits have a significant role in the liability to autism. This has been possible through a wider application of experimental designs, eye-tracking methodology, use of functional brain imaging and the baby-sibling prospective studies (Klin et al. 2005, Frith and Frith 2008). Buitelaar (2003) and, Scahill and Martin (2005) discuss that autism stands out from all other psychiatric disorders in that it shows no measurable benefits of psychotropic medication on core symptoms like impaired social reciprocity and social communication. They have found out one potential answer to the question. It could be that the basic deficit does not involve neurotransmitters. A satisfactory answer is still being sought as it could provide an understanding on the neural basis of autism. Genetic findings in twin and family studies show that ASDs in general could be inherited at about 90% chance (Rutter 2005b). Pickles et al. (1995) and (2000) findings show that it is likely that there are at least three or four genes involved in susceptibility to autism although the number could actually be greater than that. Rutter et al. (1994) reports that ASDs were linked with chromosomal abnormalities or genetically determined medical conditions in at least 10% of cases. One important finding by Bailey et al. (1995) and Le Couteur et al. (1996) was that the genetic liability for autism is widespread to comprise a broader phenotype. There are studies exhibiting that autism is connected with rare pathogenic gene mutations such as neuroligins, neurexin and SHANK 3(Rutter 2011; (Persico and Bugeron 2006; Durand et al. 2007; Bourgeron 2007; Geschwind and Levitt 2007; Jamain et al. 2008). There are just areas of ambiguity in that albeit the clinical liabilities linked with these genes incorporate autism, what frequently dominates is intellectual disability. Rutter (2011) clarifies that genes certainly do not code for specific psychiatric categories and pleiotropic outcomes are to be anticipated. This lack of specificity weakens the theory to explain ASDs. Management of ASDs Like any other medical conditions, early detection of autism spectrum conditions in an individual helps significantly on management of the individual himself and his family in respect of health, emotional, social and intellectual aspects. Early diagnosis and seeking of medical attention on ASDs can make a difference on handling the situation. Baron-Cohen (2008) reports that the most effective interventions for children with ASDS include special education that incorporates teaching of social skills and Applied Behavioural Analysis (ABA) where proper skills and behaviours are taught by methods of principles of reinforcement (Koegel et al. 1998; Volkmar et al. 2004). The critical components for effective early intervention include that the methods to be highly structured, intensive and customized to each individuals (Baron-Cohen 2008). It is also advised that proper cognitive interventions be implemented for teenagers and adults (Golan et al. 2006b). Baron-Cohen (2008) states that medical treatments are not usual. He elaborates that we are still subject to the ethical issue of trying to “cure” autism. He mentions that it is undeniable though that there are ASD aspects that need medical help such as, empathy difficulties, while there are some that do not, such as the systemising talents. Seeking of information about ASD, its characteristics and management practices are critical actions about handling ASD cases. III. Conclusion Autism is associated with distinctively reduced ability to reproduce (Rutter 2011). We are however facing the dilemma of prevalence of ASDs. It tells us that autism keeps on spreading instead of dying out. This has yet to be answered but the findings propose that the genetic influences on autism may very well adapt mechanisms which are not like those that are applied in other mental disorders. Rutter (2011) further exposes that autism may possibly involve greater role for rare pathogenic gene mutations. Cognitive theories and even the scientific findings on autism provide insufficient explanation on the condition. All the sound reasoning and rationalization based on medical and social facts deem incomplete to end or to prevent the adversity of ASDs. Autism seems to be a vast condition confined in the complexity of the brain and the make-up of the individual with autism. Such a fascinating, overwhelming and mysterious case. On the other side, our progress on the knowledge of autism has significantly advanced and transformed. And it seems to be going to the direction of continuously being transformed as we unravel one component to another or when we have linked one character traits to another. Indeed it challenges our ability to ask questions and solve problems. It is essential that while we are yet in the process of seeking understanding, management of ASDs needs to be prioritized as well. Our current achievements are a cumulation of what we have learned from the past about ASDs and how we are putting all the pieces of the puzzle together. IV. Recommendations It is unquestionable that autism remains a big challenge for our generation that is waiting to be explored and understood further. Many efforts have been used to be able to gather the current findings that we have. Psychologists, social practitioners, clinicians, geneticists, molecular biologists, families and individuals with autism must all join forces in perseverance of data coordination and linkages in order to seek answers on ASDs. The cognitive theories that we take hold could somehow help us to respond to ASDs albeit they don’t provide full explanation of such cases. Current medical practices at least ease the symptoms and intervention programmes for management must be aggressively adopted to enable all of us to thrive above this dilemma. We are grateful that we have this hope for the discovery and clarity of ASD. V. References Baddeley A and Wilson B 1988, Frontal amnesia and the dysexecutive syndrome. Brain and Cognition, 7(2): 212–230, In Rajendran G and Mitchell P 2007, Cognitive theories of Autism, Developmental Review, 27: 224-260. 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