Analysis and Evaluation of Theoretical Perspectives in Autism

Date
1946

Theory
Kanner Interpersonally distant parents Bettleheim Cold detached mothers

Main Focus
Autism in children is a result of poor parenting including lack of emotion especially from the mother. The behaviours of mothers were seen as having a greater impact than the behaviours of fathers. The term refrigerator mothers was used by Bettleheim

Evaluation Strengths
Some success has been observed by treating children with increased warmth and acceptance.

Weakness
McAdoo & DeMyer (1978) and Bartak (1975) found no differences between mothers of autistic children and other mothers. The theory has been totally discredited. Many parents were left feeling guilty for over 20 years for the part they played in their childs condition. Advocates of Bettleheims theory remain despite it being discredited. Some autistic children pass the Sally Anne test when older. Theory of mind only accounts for the cognitive impairments in autism Theory of mind does not explain characteristics seen in savant autistics This focusing on detail rather than on the whole is not unique to autism. This theory does not explain other impairments associated with autism such as language skills.

Psychoanalytical Perspective

1967

1989 1990

Cognitive Perspective

Uta Frith Baron-Cohen Lack of a Theory of Mind or Mind Blindness

1994 2005

Uta Frith & F Happe Weak Central Coherence

Research suggests that children with autism lack a theory of mind, meaning they are unable to reflection on their own thoughts and those of others. The research used the Sally Anne test which required children to see a situation from another persons point of view. This theory suggests that individuals with ASD focus more on the parts or specifics rather than the whole or bigger picture. Research has shown that individuals with ASD could complete a visual/spatial block test more quickly than others. This difference was explained by their attention to detail and not being distracted.

In a sample of 41 neuro typical or Downs syndrome children 35 responded correctly to the test compared to 4 out of 16 children with ASD. Theory of Mind offers an explanation for the cognitive impairments in autism. Weak central coherence offers an explanation for a number of ASD traits: 1 Savant artists building up pictures from recalled detail. 2. Noticing tiny details or changes. 3. Some autistic children recognise faces through individual features rather than as a whole. 4. Unlike their peers some autistic children find it easier to memorise lists of words rather than sentences.

2005

Sally Ozonoff Impaired Executive Functioning

2003

Baron-Cohen Extreme Male Brain

1943

Genetic Perspective

Kanner genetic component Ritvo et al Twin studies

Executive Functioning controls our behaviour and thinking. It is allows us to use goal-directed behaviour, behave appropriately, filter sensory inputs, think in an abstract way and adapt our actions as necessary. This theory suggests that ASD is caused by impairment in this functioning, possibly related to damage in the frontal lobes of the brain. This theory suggests that the right brain hemisphere is more developed than the left in both males and females with autism. looks at the autistic strength of working with systems, often to the point of obsession, a behaviour controlled by the right brain hemisphere and the weakness in empathy towards others, a behaviour controlled by the left brain hemisphere. In his study of autism Kanner oserved that autism often ran in families.

This theory explains the need for routines and consistency in people with autism and the difficulty experienced when having to adapt to a new situation or in organising themselves

Some individuals with damaged frontal lobes show a lack of executive functioning but no other ASD traits.

When compared to the general population males and females with ASD exhibit strengths in the use and understanding of systems but weaknesses in empathy. Systems are controlled by the right hemisphere and empathy is controlled by the left hemisphere. Males are typically right hemisphere orientated and females left hemisphere. He recognised the need for a genetic component to autism to be explored.

This theory can explain Aspergers syndrome but does not explain characteristics of lower functioning autism.

Population Genetics

1985 1995

This theory is based on the heritability of autism.

Rutter et al Twin studies

A sample of 23 Monozygotic twins showed 96% concordance for autism A sample of 17 dizygotic twins showed 25% concordance for autism Monozygotic twins showed 60% concordance for autism and 90% concordance for significant problems related to autism

The knowledge of genetics at this time was in its infancy consequently Kanners suggestion was not followed up for many years. No single gene could account for all the characteristics of autism. The small size of these samples meant that 1 incidence of autism could significantly alter the concordance rates.

1994

Folstein
Shared Environmental Factors

No concordance for autism was found amongst the dizygotic twin sample. 30% parents with children on the autistic spectrum also showed autistic traits. This theory suggests that chromosomal Chromosomes including the Xabnormalities are responsible for chromosome and chromosomes 7,10 autism. and 15 have been linked to ASD as well as being a known cause of other rarer disabilities such as Fragile-X, Tourettes, Prader-Willi syndrome and Angelman The higher occurrence rates for autism in males than females could be partially explained by links to the X-chromosome. Irregularities in endorphin levels increase the characteristics of autism Individuals with autism show a reduction in autism characteristics when given endorphin blocking drugs. These wide ranging differences could account for the pervasive nature of Autism Syndrome. Brain size of autistic children is normal at birth and an increase is observed during the early years correlating with the appearance of ASD traits. Evidence suggests this change is specific to ASD. Unlike neuro typical brains, ASD brains show no difference between the frontal and temporal cortex lobes. Many reports were based on individual cases and so lack validity. As yet there is no conclusive evidence found to support these ideas. Some of these chromosome abnormalities are not specific to autism.

2008
Molecular Genetics

Abrahams Multiple chromosome involvement

1992

Biological / Neurological Perspective

Kalat Endorphin levels

1999

Happe Differences in Brain Function

Autism can be explained by differences in brain function between individuals with autism and the general populations. This cluster of theories includes: overall increase in brain size, increase in cerebellum size, abnormalities in blood flow, functioning of the amygdala, And variation in the activity in genes various functions.

Studies suggest a correlation between increased endorphin level and autism but non evidence to confirm this is a cause of autism. This theory offers an explanation of autism based on differences between brain function and growth but does not identify a reason for these differences.

2005

Ramachandran Mirror Neurons

Broken mirror neurons are thought to account for the difficulty in seeing things from anothers view point as observed in autism.

1996

Gupta Immune Deficiency Shaw High Yeast Levels

Autism is a response to problems with the immune system

Studies observed decreased activity in genes linked to brain functioning and increased activity in genes linked to immune or inflammatory functions. Mirror Neurons are activated when the individual is doing something or when they observe the actions of someone else. There is some evidence that mirror neurons do not activate when people with autism observe the actions of others. Some evidence points to improvement in autistic traits following intervention to boost the immune system. Animal studies show candida infection to produce toxins that could result in brain damage. Rimland proposed a 5-10% chance of ASD developing after candida infection. Children with autism often have elevated yeast levels. Yeast free diets have been reported to decrease autistic behaviours. This theory has been around for many years. Opiates produce effects that resemble some autistic characteristics including changes in motivation, emotional state, attachment behaviour and responses to stress and pain. Numerous cases have been documented to show an improvement

Connection between mirror neuron dysfunction and autism is yet to be proved conclusively.

1999

Biochemical Perspective

This theory looks at high yeast levels leading to leaky gut allowing toxins into the blood stream and consequently into the brain. Candida is a yeast like fungus that in high levels has been linked to the development of autism.

Research is, as yet inconclusive and does not show a direct relationship between immune deficiency and autism. There is no evidence to support a higher frequency of human ASD births related to candida infection. No controlled studies have been used to verify the candida theory. Mothers of autistic children do not show a higher frequency of candida infection than other mothers Most evidence comes from individual reports. There is a lack of conclusive evidence from controlled studies, although recent longitudinal studies promise to offer more reliable data. Health risks associated with gluten free

2002

Shattock & Whiteley Opioid-Excess Theory

Foods containing gluten and casein are not fully digested and leak opioid peptides through the intestinal wall into the bloodstream. This affects the central nervous system and neurotransmission resulting in autistic characteristics.

1998

Wakefield MMR Vaccines

2010

Price et al. Thimerosal

Environmental Perspective

This theory proposes increases in autism can be linked to the use of the MMR vaccine. The vaccine affects the intestinal tract. Thimerosal used as a preservative in some vaccines and is mercury based introduces neurotoxins into the blood and central nervous system. Exposure in the uterus to rubella infection, alcohol consumption, valporic acid ( used in the treatment of epilepsy, depression, migraine, bipolar and schizophrenia) and thalidomide (used in sleeping pills and as a preventative for morning sickness) have all been associated with development of autism. Difficulties at birth including: breech birth, complications with the umbilical cord, multiple births, maternal bleeding and foetal distress point towards a higher risk of developing autism.

in multiple autistic behaviours related to removal of gluten and casein from the diet. It is a course of action advocated by many parents and doctors and widely promoted on the web through You-Tube. The effect of opioid excess is worsened by testosterone so this could offer an explanation of higher occurrence of autism in males. Administration of the MMR vaccine occurs in the same time period in which autistic traits appear in infants Mercury is a known neurotoxin and thimerosal is also known to be toxic when inhaled, ingested or making contact with skin. Its effects can also be cumulative. Animal studies on rats have shown that exposure to valporic acid in the womb can produce ASD characteristics.

and dairy free diets.

The frequency of ASD in children receiving the MMR vaccine was no higher than in the general population. No studies confirm the effect of thimerosal on the development of ASD. ASD rates continued to rise after thimerosal was removed from many childhood vaccines. This type of exposure can only explain a few cases of autism and is not consistent from one case to another. Much of the evidence comes from individual cases and is based on recall of facts.

2007

Gardener et al. Prenatal Environment

2002

Hultman Perinatal Environment

Many of the events explored were related to lack of oxygen to the baby. Being aware of these risk factors may allow earlier diagnosis of autism and earlier intervention.

There is insufficient evidence to implicate one specific event as a cause of autism, more likely to be a combination of events. Much of the evidence comes from individual cases and is based on recall of facts.

2008

Schendel Premature or low weight babies

Babies born prematurely or with a low birth weight are more susceptible to developing autism.

2012

Kong et al Raised Parental Age

Increased parental age, especially of the father, may result in copy number variations (minute chromosomal deletions or replications) giving rise to a greater risk of ASD developing.

1978

Rimland Poor nutrition

Poor nutrition may result in autistic type characteristics.

2010

Rutter Quasi-Autism

Lack of environmental stimulation contributes to the development of characteristics similar to ASD.

Children born at 5.5 pounds or below show a 2.3-3 times increased risk of developing autism. The link between low birth weight and autism is stronger in girls than in boys offering an explanation for the gender variation in autism occurrence. Sperm, unlike eggs, are constantly produced so are susceptible to copy number variations, explaining why the increased age of fathers is a significant factor. At 20 a father can pass on 25 new genetic errors but at 40 the rate increases to 65 errors. Individuals with autism have shown an improvement in some behaviours after megavitamin supplements, especially Vitamin B6. Omega fish oils appear to be particularly effective in improving some autistic behaviours. A study of Romanian orphans adopted by UK families, suggest that 1 in 6 children who were institutionalised until older than 6 months showed some ASD traits. The design of the study eliminated other variables such as malnutrition and foetal alcohol syndrome.

Very small sample sizes. Autism is less likely to occur in low weight babies than many other developmental disabilities including vision, hearing and cerebral palsy. Most of these variations are not seen in the parents so do not account for ASD running in families.

No reliable evidence to support this theory.

Evidence suggests no link between neglect and abuse Could the 1-6 occurrence rate point to an additional genetic component.

References

Herbet, J. D., et al. (2002). Separating fact from fiction in the etiology and treatment of autism. The Scientific Review of Mental Helath Practice, 1(1). Rice, K. (n.d.). Causes of Autism. Retrieved from Keith E Rice: http://www.integratedsociopsychology.net/autism-causes.html Rudy, L. J. (2010). What Causes Autism. Retrieved from About.Com Autism Spectrum Disorder: http://autism.about.com/od/whatisautism/p/autismcauses.htm Rutter, M. L. (2011). Progress in understanding autism: 2007-2010. Journal of Autism Developmental Disorders, 41, 395-404. doi:10.1007/s10803-011-1184-2 What is Autism? (n.d.). Retrieved from Autism Speaks: http://www.autismspeaks.org/what-autism

Recommended Further Reading

Abrahams, B. S., & Geschwind, D. H. (2008). Advances in autism genetics: on the threshold of a new neurobiology. Nature Reviews Genetics, 9, 341-355. doi:10.1038/nrg2346 Baron-Cohen, S. (1989). The autistic child's theory of mind: A case of specific developmental delay. Journal of Child Psychology and Psychiatry, 30(2), 285-297. Baron-Cohen, S. (2002). The extreme male brain theory of autism. Trends in Cognitive Sciences, 6(6), 248-254. Bettelheim, B. (1967). The empty fortress. New York: Free Press. Doja, A., & Roberts, W. (2006). Immunization and autism: A review of the literature. The Canadian Journal of Neurological Sciences, 33(4), 341-346. Edelson, S.M. (2008). The candida yeast-autism connection. Salem, Oregan: Centre for the Study of Autism. Gardener, H., Speigelman, D., & Buka, S. (2009). Parental risk factors for autism: comprehensive mate-analysis. The British Journal of Psychiatry, 195(1), 7-14. Hallmayer, J., & et al. (2011). Genetic heritability and shared environmental factors among twin pairs with autism. Archives of General Psychiatry, 86(11), 1095-1102. Happe, F., & Frith, U. (1996). The neuropsychology of autism. Brain, 119(4), 1377-1400.

Happe, F., & Ronald , A. (2008). The 'fractionable autism triad': A review of evidence from bahavioural, genetic, cognitive and neuarl research. Neuropsychological review, 18(4), 287-304. Hultman, C., Sparen, P., & Cnattingius, S. (2002). Perinatal risk factors for infantile autism. Epidemiology, 13(4), 417. Kanner, L. (1946). Autistic disturbances of affective coontact. American Journal of Psychiatry, 103, 242-246. kong, A. (2012). Rate of de novo mutations and the importance of fathers age to disease risk. Nature(488), 471-475. doi:10.1038/nature11396 Mason-Brothers, A., Mo, A., & Ritvo, A. (1985). Concordance for the syndrome of autism in 40 pairs of afflicted twins. The American Journal of Psychiatry, 142(1), 74-77. Ozonoff, S., Rogers, S., & Pennington, S. (1991). Executive function deficits in high-functioning autistic individuals: Relationship to theory of mind. Journal of Child Psychology and Psychiatry, 32(7), 1081-1105. Ramachandan, V., & Oberman, L. (2006). Broken mirrors: A theory of autism. Scientific American, 295(5), 62-69. Rutter, M. (2000). Genetic studies of autism from the 1970's into the millenium. Journal of Abnormal Child Psychology, 28(1), 3-14. RS, G. (1996). Dysregulated immune system in children with autism. Beneficial effects of intravenous immune globulin on autistic characteristics. Journal of Autism Developmental Disorders(26), 439-452. Schendel, D., & Bhasin, T. (2008). Birth weight and gestational age characteristics of children with autism, including a comparison with other developmental disabilities. Pediatrics, 121(6), 1155-1164. Shah, A., & Frith, U. (1993). Why do autistic individuals show superior performance on the block design task? Journal of Child Psychology and Psychiatry, 34(8), 1351-1364. White, B., & M White. (1987). Autism from the inside. Medical Hypotheses, 24(13), 223-229. Whiteley, P., Rodgers, J., & Shattock, P. (2000). Feeding patterns in autism. Autism, 4(2), 207-211.