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The purpose of this assignment Is to outline the history, etiology and prevalence of Autistic Spectrum Disorder (SAD). Moreover, It will critically examine current legislation, cognitive and affective theories and will ultimately demonstrate the utility of such theory being put into practice in the writer’s given field of work. For the purpose of this assignment the words Autism and SAD will be used interchangeably and any names used will be pseudonyms. The field of Autism has developed significantly over the past few years and there has been much research since Its discovery over 60 years ago (Wolff 2004).
Nevertheless, It Is actually still In its Infancy and there Is a long way to go towards fully understanding the condition known as Autism, which to a great extent remains very much a mystery. As more children are diagnosed with Autism and with an augmented interest and awareness from professionals working within the field, this has ultimately led to a greater demand for information and knowledge, not only from professionals but also from parents and Individuals affected by Autistic Spectrum Disorder (SAD) (eager 2005).
SAD affects the way a person communicates and limits their ability to relate to others n a meaningful way; it is a lifelong developmental disorder that emerges in early childhood. It varies from person to person and many of the features will change with age and maturity (Bergman 2005). It is identified by three distinguishing primary impairments In language, social skills and behavioral flexibility, which are referred to as the Triad of Impairments (Casein & Barker 2009). Additionally. He primary characteristics that defend SAD are often compounded by a learning disability and associated features such as self-injury and/or aggression, repetitive traits, unusual ensure responses, abnormalities in eating, drinking or sleeping and a compelling need for routine (Bergman 2005). It is also often present in conjunction with a co morbid mental health condition such as depression or an anxiety disorder. Autism Is only one element of a wider spectrum of disorders of varying type and severity which includes Espalier’s Syndrome and Atypical Autism.
Although there is strong evidence that SAD is present from birth, it is generally not diagnosed until after two years of age (Shore and Bass 2010). An Increase In awareness and Incidence of SAD has raised such concern that It has owe reached the political agenda, The Scottish Executive published their report ‘The same as you” (2000) which reviewed services for people with learning disabilities. One of the recommendations of the report was to ensure that the interests of children and young people with learning disabilities and autism spectrum disorder were addressed.
The Scottish Government subsequently commissioned the Public Health Institute of The report was published in 2001 making thirty two recommendations to ensure services were meeting the needs of those accessing them. One of the main commendations was that the Scottish Intercollegiate Guideline Network (SIGN) should develop evidence based clinical practice guidelines on SAD. SIGN Guideline 98 was published in 2007 providing an evidenced based guideline for use by clinicians to inform their assessment process.
There is no doubt they have made a significant impact on clinical practice in Scotland (Scottish Government 2010 McClure and El Couture 2007). More recently they committed to continuing to strive to improve the lives of people affected by SAD and as such have developed a draft Scottish Autism Strategy Towards an Autism Strategy for Scotland” (Scottish Government 2010). The draft sets out what the government in conjunction with service users, careers and professionals proposes to do to meet the needs of people with SAD in response to the growing phenomenon that is Autism.
It recognizes that whilst there have been considerable advances in Scotland, much still needs to be done to meet the needs of people with SAD and their careers. Education is a key component and has a major impact on the lives of SAD sufferers and their parents. The Government acknowledged the need for parental consultation guarding the educational needs of their child with the introduction of their Education Additional Support for Learning Scotland Act (2004).
The bill aimed to offer support to children suffering hardship; which may be long- term support for disabilities or short term due to exceptional circumstances including bereavement or physical illness. It was reviewed in 2009 with the amended Act coming into force in November 2010. The term Autism is fairly new to the world of medicine and science: however, Autism itself is not a new condition. It didn’t suddenly appear in humans in 1943 following he publication of Leo Canner’s paper “Autistic disturbances of affective content” (cited in O’Brien and Tagged 2006).
Williams (1996) concurs suggesting that reference to SAD has been made in fairytale and ancient folklore and in old stories of “feral children”. The first use of the word “Autistic” which is derived it from the Greek word autos (meaning self), was in 1912 in the American Journal of Insanity (O’Brien and Tagged 2006). Eugene Bubbler, a Swiss psychiatrist used the term to describe a group of symptoms of schizophrenia, where he characterized his group of adult patients as Ewing self obsessed (Irritated).
However, the term became widespread in 1943 with the publication of Canner’s paper. Canner recognized a pattern of symptoms in his sample of eleven children and used the term Autism to describe their withdrawn acknowledged that these children were not typically mentally retarded or suffering from a psychiatric disorder but demonstrated intriguing traits and for this he used the term Early Infantile Autism (O’Brien and Tagged 2006). Just one year later Hans Aspirer, an Austrian doctor published his paper, which had striking similarities to Canner’s research (Happen 1994).
Although his work was published, it was not fully appreciated until Loran Wing translated it into English in 1981. It wasn’t until the sass’s that researchers began to have an understanding of Autism in children. However, treatment at this stage remained very much medically based with the emphasis greatly on cure of the “disease”. Treatments were very much bio chemically based with medications such as LSI: electric shock treatment was also widely used.
During the sass’s and sass’s there was an increased awareness from health, education and indeed the general public, leading to a recognition that although there is always a place for medication, the way forward was with cognitive and behavioral techniques such as intensive early intervention (Wolff 2004). If we go back thirty years, the prevalence of Autism was decidedly less as opposed to today where it is closer to 1 :OHIO (Baron-Cohen 2008). There are several theories as to why the incidence has risen; Harrison et al, (2006) suggest that the rise could be due to better diagnostic expertise.
Waterholes (2008) concurs with this suggestion, signifying that an increased awareness and services and changes to the diagnostic criteria have all had an influence in prevalence. Baron-Cohen (2008) also recognizes that as Autism is on a spectrum, “shades” of Autism or mild cases of Autism are now being included in prevalence numbers, where they may previously have been excluded. There are many debates as to the cause of Autism: it is however, generally accepted that there is no single unit cause but rather, a series of behaviors with multiple causes and neurological processes have been identified (Router 2005).
However, certain hypothesis or theories which have been purported to be causative, have proved to be highly controversial, with parents often wondering if they were in anyway to blame (Happen 1994). The thought process behind ‘Refrigerator Mothers’ theory was that their children had autism because of the mother’s frigidity. They were supposedly “cold” towards their child and didn’t interact, play with them or show affection (Satiric 2003). This was first noted by Leo Canner in his paper “Autistic disturbances of affective content” (cited in O’Brien and Tagged 2006).
Canner noted a “genuine lack of maternal warmth”. Satiric (2003) suggests that Canner overlooked the fact that the children in his study had siblings that were unaffected by the same parents affection or lack of it. The theory continued to gain credibility during the sass’s and sass’s particularly due to Bruno Fetishism’s articles which continued to promote this theory. Despite the theory being utterly discredited it continues to place a terrible burden on mothers already devastated by their child’s condition (Happen 1994). T al, (2001) and Satiric et al, (1998) it has to be acknowledged that genetics have a key role to play: there is consistent evidence from twin and family studies to support this. However, as yet, no specific gene has been identified. Research into the role of genetics in SAD is undoubtedly expanding rapidly (Guppy and State 2007). We could not mention causes without giving consideration to a hypothetical link with vaccines: in particular the Measles, Mumps and Rubella vaccine (MR..). It has been argued that the MR.. Vaccine causes intestinal problems leading to the development of autism.
The controversy was due to the publication of Dry Andrew Wakefield study in 1998. This work has since been discredited with suggestions that there was a monitory incentive behind it (Dear 2011). Despite this theory being strongly refuted by the medical fraternity, there remains a minority of parents and researchers who antique to pursue this link (Foment and Charities 2001). Unsung et al (2009) raise the question of a hormonal link, as Autism overwhelmingly affects more males than females, by 4:1 .
Kline (2009) suggests that this theory is supported by research into exposure of too much testosterone in utter which results in a masculine mind body. The findings come from an eight-year study relating to the development of 253 children according to levels of testosterone they were exposed to in the womb. As demonstrated, the struggle to understand SAD is ongoing, but researchers and linsang recognize that there is a cognitive process that may play a part. As such, one of the major goals of the research conducted over the past thirty or so years was to achieve a better understanding of these cognitive processes.
Consequently, various cognitive theories have been developed (Burnett et al 2005). There have been many theories put forward to explain SAD: however, there are three main cognitive theories popular with today’s researchers. They attempt to explain the social and non-social characteristics of SAD, namely: Theory of Mind; Executive Function and Central Coherence. Cognitive ability relates to how a person processes information influencing thinking, reasoning, remembering and imagining Amazon 2003).
Baron-Cohen (1989) purports that the ability to understand the thoughts and feelings of others is crucial in appreciating the social world in which we live. He further suggests that development of social cognition is fundamental to Autism and thus we have the Theory of Mind hypothesis. Burnett et al (2005) suggest that Theory of Mind (TOM) is perhaps the most well known of the cognitive theories. It can be explained as an ability to mind read, in there words being able to comprehend other people’s thoughts, beliefs and thoughts, beliefs and intentions to oneself.
Baron-Cohen (1989) suggests that these intentions are inferred, which requires a complex cognitive process. The Sally Anne test is a well known false belief test often used when assessing TOM: it focuses on the autistic child’s inability to put themselves in the mind of another. They could not consider that Sally could believe something that wasn’t true (Baron-Cohen 2008). He suggests that children with Autism suffer from “mindlessness”, that they are blind to another’s mental state.
The strength of the theory-of-mind hypothesis is that it is well placed to explain many of the behavioral symptoms of autism; however, people with autism also show distinctive strengths in certain areas that the theory-of-mind account cannot readily explain (Baron-Cohen 2008). Executive function refers to high-level abilities that influence more fundamental skills such as planning, attention, memory and motor skills. It is an essential skill necessary to facilitate daily living in an ever changing, unpredictable world, allowing us to adapt to unexpected situations and ultimately manage stressful situations.
This theory provides an insight into the restricted and repetitive behaviors, as well as some of the practical difficulties and challenges often exhibited in children with SAD (Pennington, et al 1997). Baron-Cohen (2008) elucidates that executive dysfunction is often observed in patients who have acquired damage to the prenatal brain area and suggests that although there has been no brain damage in Autism, there is perhaps an immaturity in the prenatal brain area of those affected by SAD.
He also suggests that executive dysfunction occurs in a large number of clinical disorders: thus is not exclusive to autism. One of the more widely known and accepted theories is the weak central coherence theory (Firth 2003). ATA Firth undoubtedly advanced this theory, surmising that autistic people typically think about things in the smallest possible parts. Her hypothesis is that children with autism actually perceive details better than non autistic people, but that “they cannot see the wood for the trees” (Firth 2003).
Happen and Firth (2006) and Happen and Booth (2008) suggest that current thoughts around Central Coherence theory propose that there is a range of cognitive styles within the general population: from strong coherence where there is a tendency to sis details while you concentrate on the meaning; to weak coherence where you tend to focus only on the detail whilst missing the meaning. Happen and Firth (2006) suggest that weak coherence lies at the root of SAD symptoms including the need for routine and sameness, paying particular attention to parts of objects and obsession preoccupations.
Happen and Firth (2006) also recognize a failure to use context in reading, for example: “l will lead the way’ and “it was like carrying lead”, although the word is spelt the context, whereas those with SAD would have difficulty in differentiating. Carroll and Russell (1997) concur, stating that when central coherence skills are measured with perceptual or verbal-semantic tasks, the results undoubtedly reveal that autistic individuals have a tendency for fragmented perception.
Moreover, Baron-Cohen (2008) questions if the Central Coherence theory could explain the existence of special skills (Savant syndrome) where people with SAD have one or more areas of expertise, ability, or brilliance that is in contrast with their overall limitations, perhaps due to a bias towards detail-focused processing (Baron- Cohen 2004). There are various tests used to measure central coherence such as the Embedded
Figures Test where you have to find common geometric shapes in a larger design and Block design Task where you are required to take blocks that have different designs and arrange them according to a pattern (Lott, Gomez & Happen 2008). Shah and Firth (1983) demonstrated that children with SAD were quicker at picking out hidden figures in the Embedded Figures Test than the children in the control group and also suggest that children with Autism performed above their mental age.
Booth and Happen (2010) imply that there is currently no consensus regarding the validity of the weak central coherence theory. Conversely, Carroll et al (2000), Burnett et al (2005), Eel (2007) and Lott, Gomez and Happen (2008) state unequivocally , that children and adults with SAD display weak central coherence. Baron-Cohen (2008) also questions the strength of this theory and suggests that for it to demonstrate utility, it requires to be used in conjunction with one of the neurological theories.
It must be acknowledge that theories are exactly that, only theories: which ultimately can and indeed, should be challenged and may be wrong: as demonstrated previously with the ‘Refrigerator Mother’s’ theory which has long been discredited Eastman 2003). As universal service providers, Health Visitors are often the first point of contact for parents concerned about their child’s development or lack of speech. In relation to the children I work with (mainly pre 5), I can best associate with Central Coherence Theory, as parents often present with concerns about their child’s odd obsession behaviors.
Weak Central Coherence explains the child’s inability to see the bigger picture and their need for routines and an acute attention to detail. Paul is three and a half and has an obsession with keys which has seen him start his father’s car and allowed him o escape from the house while everyone slept. Colic is seven and insists on the Evolve on his shoes being fastened nine times before he will leave the house, it scant be eight or ten, if they are accidentally fastened ten times he will take them off and interest with the cars he is given but could spend all day Just spinning the wheels.
Aiding is four and when drawing a face gives it only a mouth, no eyes and no nose. Having an increased understanding of the cognitive theories enables me to explain to parents why their children might be behaving in this manner and undoubtedly gives hem better insight into their child’s behavior. Over the past two years, my own awareness of SAD has grown greatly and as a result I became aware of the lack of peer support in my practice area. As a direct result of this I set up a parent support group “Little STARS” which has now been running for over a year.
The criteria for the diagnosis of Autism have been agreed internationally, through the publication of the International Classification of Disease version II(ICED 10) issued by the World Health Organization (WHO 2007) and the Diagnostic and Statistical Manual f Mental Disorders 4th edition (ADSM-lb). They have similar symptom criteria for diagnosis, based on the triad of impairments: social development; communication skills and restricted range of activities or interests/ repetitive behaviors. Hodge (2005) argues that diagnosis can, in fact be counter productive for parents as they become focused on a condition rather than their child.
In my practice I have experienced this and often highlight to, and reassure parents that their child hasn’t changed overnight, that they are still the same child they were without the ‘label’ of Autism. However, undoubtedly, early diagnosis is paramount to early intervention Jovanovich and Washman (2005), Riot (2006),Baron-Cohen (2008)). Indeed diagnosis is often the start of the magical mystery tour that is SAD; parents grieve not for their child, but for the hopes and aspirations they had for that child and they can certainly become frustrated by the ongoing demands placed on them by their child (O’Brien and Tagged 2006).
In conclusion, there is a vast support network for parents: central to this is the Health Visitor, who provides continual support to families. It has to be hoped that as political awareness increases regarding Autism, there will be a continued enhancement of service provision and support for families, which can only improve the lives of those affected by this debilitating condition.
Undoubtedly Autism is a developmental disorder, which will continue to captivate researchers, challenge the clinicians working in this field and ultimately continue to distress those affected by it. The debate on the increase in prevalence will no doubt continue; is the increase due to an environmental toxin, can it be attributed to diagnostic criteria and better education or is it due to the inclusion of milder cases of autism in the spectrum (Baron-Cohen 2008).