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Q. Discuss the theoretical explanations for autism in the light of research evidence
A. In order to be able to answer this question a brief description of autism shall be presented that highlights some of the symptoms central to the disorder and some concise statistics of its epidemiology. Following this, theoretical explanations for the disorder shall be discussed, with a particular focus on the contribution of recent research evidence. A second point to note is that for the purposes of this essay the word Autism shall be used to encompass all disorders under the umbrella of Autistic spectrum disorder.
Autism is a pervasive developmental disorder, meaning that it manifests itself in early childhood and lasts throughout the individual’s lifespan. It has been found to affect approximately 5-13 births out of 10,000, with the majority of these being male (Newschaffer, Croen & Daniels, 2007). Autistic individuals tend to have poor social interaction and communications skills, as is portrayed by their use of echolalia (i.e. meaningless repetition of another person’s spoken words) and pronoun reversal (i.e. referring to oneself as ‘he’, ‘she’, or ‘you’). Autistic individuals struggle with non verbal communication too, exhibiting impairments in eye contact and facial expression. Furthermore, individuals with autism tend to display stereotypical and often highly restricted patterns of interest (they may become preoccupied with a particular object, for example) that are often resistant to, and inflexible to, change in general. Now that autism has been succinctly described, explanations for the disorder will be focussed on, beginning with the contribution of genetics.
In identical twins, concordance rates for autism have been found to be between 60 - 90% (Lichtenstein, Carlstom, Rastam, Gillberg and Anckarstator, 2010). These researchers further suggested that genetic effects may even account for up to 80% of the variability of symptoms found in Autistic individuals. A number of other studies have yielded similar results that also emphasise the influence of genetics, (Ciuladaite et al 2011) found that a small deletion of around 25 genes in chromosome 16 is associated with Autism, whilst Burnside et al (2011), found that deletions and mutations in segments known as BP1-2 tend to also be associated with Autism, leading Schoaf and Zoghbi (2011) to assert that maybe even hundreds of genetic alterations contribute to Autism.
Whilst such studies provide a basis for the development of Autism they do not as such explain, structurally, what effect the genetic alterations have on the biology of the autistic individual. Other researchers have stepped in here, asserting that these genetic alterations disturb the process of synaptogenesis (i.e. the sprouting of new neurons and connections in first three years of life) and thus negatively impact upon the establishment of synaptic clefts leading to deficits in cell to cell connectivity (Klauch, Poutsha and Chiocchetti 2011). Not all theorists have agreed with this postulation, however. In opposition to this, Markram and Markram (2011) argued that rather than having deficits in cell to cell connections, autistics have neural circuits that are hyper-reactive (which explains why some autistics may have a very good memory or may become overly emotional). The researchers state that as the disorder progresses, these overly strong reactions to experiences drive the brain to a highly selective state that essentially traps the individual into secure routines with few surprises. Whilst engaged in such routines, the autistic does not experience everything quite so intensely.
This explanation for autism has become known as the intense world theory. Support for the theory was found by Markram, Markram, Rinaldi, Mendola and Saudi (2008) who found that rats (induced into an autistic type state) have a hyper-reactive amygdala, leading to hyper fear. Moreover, Courchesne, Redcoy, Morgan and Kennedy (2005) found that micro structural maladaptive development in the frontal cortex leads to over connectivity in that area but conversely to reduced reciprocal connectivity in other areas. This finding is important, as it can help merge the intense world theory with findings such as those by Klauch, Poutrcha and Chiocchetti, (2011) (that cell to cell connectivity is reduced), by allowing for certain areas of the brain to be over connected and for those particular areas to be under-connected to other parts of the brain. These research findings thus offer an explanation as to why autistics become stuck in rigid routines and fear anything outside of them.
Other researchers, such as, Azmita, Singh, Hou and Wegiel (2011), criticise the intense world theory for neglecting the atrophic (damaging) effects of serotonin that appear in dead autistic’s brains, which Nakamera et al (2010) states may occur because of serotonin transporter binding problems. Interestingly, the researchers do not note in which areas of the brain these binding problems occur. Perhaps these binding problems may in fact be related to Courchesne, Redcay, Morgan and Kennedy’s (2005) research that found reduced reciprocal connectivity from the frontal cortex to the rest of the brain. Hypothetically, the binding problems or atrophic effects of serotonin may be damaging areas between the frontal cortex and the rest of the brain leading to this reduced reciprocal connectivity and may therefore conversely support the intense world theory.
Either way, Courchesne, Redcay, Morgan and Kennedy’s (2005) research used a very small sample size, meaning the results may not have been representative of the autistic population in general (Lam, Aman and Arnold, 2006). Moreover, Cloury, Molnar and Rakic (2010) noted that many of these studies involved rats, and whilst they can be useful, there are many areas of the cerebral cortex that are uniquely human (in a genetic molecular and anatomical sense) and thus not all findings may be applicable to the human autistic population. It is worth noting that all of these aforementioned studies have, been orientated towards a biological explanation for autism, leaving other potential explanations thus far unturned.
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