Summary
Summary Autism - Background and Diagnosis
- Module
- Autism Spectrum Conditions
- Institution
- University Of Reading (UoR)
These notes are a short summary of Autism and how it is diagnosed.
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Background and diagnosis- Autism symptoms and strengths
- Social model of disability
- Diagnosis
The SAGE handbook of developmental disorders
Autism spectrum disorders – general overview
Historical perspective
• Lane (1979) - likely autism has existed for a very long time
• First documentations were made in early 1940
• Leo Kanner (1943) - detailed descriptions of 11 children who shared qualities of aloofness,
insistence on sameness and language delays or oddities
• Hans Asperger (1944) - described 4 “little professors” with qualities of awkwardness and
circumscribed interests, strengths in vocab and syntactic aspects of language
o Compared by frith in 1989
• At the time autism was seen to develop as a result of social deprivation or poor parenting
(Bettelheim, 1967). Was believed to be a childhood form of schizophrenia
• Rutter and Lockyer (1967) - associations between autism and seizures and intellectual
disability – evidence that is was neurological
• Rutter and Schopler (1978) - language deficits were integral to autism
• Hermelin and O’Connor (1970) - carried out systematic experiments on cognitive processing
in autistic children. Showed autism could be understood by systematic testing around
cognition
• Schopler (1971) - wrote a paper working on the idea that autism is a neurobiological
disorder. Proposed that parents were blamed for causing autism but this was a scapegoat.
• Lovaas (1966) - behaviourist – belief that operant-learning principles could be used to teach
anything
o Beginning of ABA
• Folstein and Rutter (1978) - twin study. Greater concordance for autism in monozygotic.
Symptoms were not identical
• Wing and Gould (1979) - epidemiological study of children in London. Impairments in social
reciprocity, language comprehension and play.
• Parent advocacy organisations have been important
o Autism society of America
, o British national autism society
Epidemiology
• Earliest studies indicate prevalence of 4-5 in 10,000 1960 (Frombonne, 2007)
• Estimated to be 4 times more common in males
• Only about 20% of children with autism were estimated to have IQs outside range of
intellectual disability
• Late 1980s – higher prevalence – 10 in 10000 and higher
• Cdc (2007) - 1 in 150 children in us
• Baird et al (2006) - 1 in 100 in uk
Causes
• Not result of trauma or injury
• Genetics
• Limited data
• Bailet et al (1995) - concordance is 60-90% in identical twins
• Pickles et al (1995) - autism is polygenic
Neurological and biochemical studies
Neuroanatomical and imaging studies
• Post-mortem studies are unrepresentative and limited
o Show reduced cell size, increased cell packing density in the amygdala and other medial
temporal regions. As well as reduced number of Purkinje cells in the posterior inferior
cerebellar hemispheres
• Increased white and grey matter volumes during first years of life (Courchesne et al, 2001)
• Reports of increased head circumference and brain weight in children with asd( Bauman and
Keper, 2005)
• Brain overgrowth reaches a plateau or decreases during late childhood and adolescence
(Carper et al, 2006)
• Enlargement of the cerebellar hemispheres – Brambilla et al (2003)
• Increased and decreased volumed of hippocampus and amygdala reported in asd (Munson
et al, 2006)
o Inconsistencies due to age?
o Mosconi et al (2009) - longitudinal study of autistic toddlers. Enlargement of right
amygdala from age 2-4 correlated with joint attention deficits at age 4
• Functional imaging studies provide more direct measure – fMRI
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