Autism Spectrum Disorder: The Keys Thesis

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As noted in the located research, "individuals with autism may have an IQ at any level. By convention, if an individual with autism has an IQ in the normal range (or above), they are said to have 'high-functioning autism' (HFA)." (Baron-Cohen, 1) For a parent with a young child who exhibits signs of true intelligence or even of prominent and unique talents, the understanding of autism as a disorder becomes somewhat difficult to accept.

This leads us to consider a question which remains today up for ongoing debate in diagnosis and treatment perpsecitve. Namely, it is argued that the term disorder is improperly applied to those with symptoms of autism which might otherwise display the capacity for a healthy and full development as individuals. Accordingly, the research conducted here brings us into contact with an article which "considers whether Asperger Syndrome (AS) or high-functioning autism (HFA) necessarily lead to disability or whether AS/HFA simply lead to 'difference'. It concludes that the term 'difference' in relation to AS/HFA is a more neutral, value-free, and fairer description than terms such as 'impairment', 'deficiency' or 'disability'; that the term 'disability' only applies to the lower functioning cases of autism; but that the term 'disability' may need to be retained for AS/HFA as long as the legal framework only provides financial and other support for individuals with a disability." (Baron-Cohen, 1) This suggests primarily that balance is required in understanding Asperger's Syndrome and High Functioning Autism, which may subject individuals to unique perceptual challenges but which may not appropriately be understood as disorders. This suggests that autism and its related conditions occur in far too great a variety of symptomatic forms in order to be deconstructed effectively along the lines of such a distinction.

This type of debate, however, only further confutes the already difficult task of identifying the presence or absence of the condition in young potential subjects. Fortunately, symptoms are not the only element available for consideration in achieving a diagnosis. To the contrary, the discourse on autism has increasingly come to recognize that there are clear genetic forces which factor into the occurrence of autism and which might offer clues for diagnosis. Moreover, there is a recognition within the context of this discussion that there may exist a certain genetic makeup predisposing a normally developed or non-Pervasive Developmental Disorder (PDD) individual to a set of traits which correspond in their combined presence with symptoms and traits associated with autism and related PDDs.

This genetic makeup is referred to as the autism phenotype, which pertains to the proposition that amongst sufferers of PDD conditions or autism, genetic relatives to these sufferers and individuals living in developmental normalcy, there is a pool of potentially shared characteristics. Said characteristics, as further discussion will indicate, are correlated to behavior, emotional disposition, communication barriers, physical distinctions and some savant features. (Bishop et al., 1431)

Therefore, at the center of this discussion is the key definitional basis stating tha "the concept of the 'broad phenotype' of autism refers to the finding that relatives of people with autism often have mild forms of autistic-like characteristics, such as social and communicative difficulties" to name just a few. (Bishop et al., 1431) Thus, discussion on this subject has concerned the value of identifying the characteristics said to define the phenotype in both sufferers and their relations.

It is here appropriate to consider the pool from which relevant characteristics are drawn. The characteristics which define the severely handicapping neurological condition, autism, vary from one sufferer to the next. As stated in the above examination of its condition, the diagnosis and treatment of autism will vary considerably based on the severity and permutation of the conditions present in the subjected individual.

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Moreover, autism itself is deeply shrouded in mystery. There are a great many competing and complimentary theories relating to the presence of autism which suggest its causes may be some combination or diversity of factors causing the deleterious genetic mutation preventing proper neurological development.

One thing which is certain and which causes us to question with even greater intensity the true factorial basis for the occurrence of autism is its rising prominence in the United States. Indeed, the exponential nature of its rise in occurrence qualifies it for epidemic status. As of 2006, "autism in the United States ha[d] been increasing for two and a half decades, from one child in 10,000 to one in 500 or perhaps even 166 today." (Easterbrook, 1) This constitutes an alarming increase in occurrence of that which had generally been understood to be a genetic disease.

The discussion of the phenotypic conditions pertaining to autism require us to consider some of the genetic theories relating to autism, though these do little to address the issue of its epidemic rise in modern occurrence. A compelling finding on the subject dictates that there is a direct connection, nonetheless, between the presence of autism in the child and some string of this disorder in the genetic material of the family. To this end, "studies of families ascertained through a single autistic proband suggest that the genetic liability for autism may be expressed in nonautistic relatives in a phenotype that is milder but qualitatively similar to the defining features of autism." (Piven et al., 185) This suggests that there may be some correlation between the presence of autism in an individual and the genetic makeup of the individual's family. Moreover, we may suggest that where autism is already documented, a family may be believed to be in a category of higher susceptibility for a recurrence of this condition. This should serve as a point to highlight in attempting to diagnose its presence. Family history and the presence of developmental abnormalities in siblings or parents can help us to ascertain the likelihood that a developmental issue in the young child is a part of the autism spectrum disorder.

Conclusion:

The study conducted here above reinforces the initial presumption that there are core complexities in diagnosing the presence of autism because it is a spectrum disorder. This means that its manifestation might take on any number of symptoms described above, that the degree of its severity is likely to vary widely and that the nature of the treatment and therapy to be prescribed will vary considerably as well. The findings from our research indicate that diagnosis in sufferers from birth to age 6 will depend heavily on the familiarity which parents or guardians have developed with the potential symptoms of autism.

The study here provides a basis for understanding these symptoms, ranging from the array of possible indications of severe autism to those possibly more subtle symptoms of HFA or Asperger's. Further, the study denotes the presence of a broad phenotype for autism that helps to draw a connection between familial genetic patterns and the presence of autism. Therefore, parents who have a family history of development delay or otherwise could consider this a sensible imperative for investigating the possible symptoms that can help precipitate early diagnosis.

Fundamentally, we find that early diagnosis will improve the opportunity of young sufferers to mature into accommodating educational and familial conditions. Recognizing even those less salient clues as to the presence of the disorder can be the difference between realizing or missing this irreplaceable opportunity.

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