Developmental disorders

Static & Dynamic approaches

Static approach to developmental disorders: neuropsychological model. One-to-one mapping between modular (genetic) impairment and disorder across development.

Dynamic approach: developmental model (atypical developmental trajectory). No one-to-one mapping between genes and disorder

Most developmental disorders will have some kind of genetic basis. One of the most striking examples of this discussion comes from Williams syndrome, which has a genetic basis (microdeletion of 24-30 genes on chromosome 7). Williams syndrome is a developmental disorder characterised by physical differences (heart defects, fphysical appearance), cognitive deficits, and cheerful disposition.

Paterson, Girelli, Butterworth & Karmiloff-Smith (2006) examined numerical impairments in typically developing (TD), williams syndrome (WS) and downs syndrome (DS) infants and children when discriminating small numbers. WS and TD infants performed better than DS infants. In childhood and adulthood, TD and DS children performed better than WS children. Patterns of impairment change over development

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Developmental dyslexia

Waddington's epigenetic landscape provides a useful way to understand how a disorder's manifestation can change over the course of development. What the epigenetic landscape shows is that the relation between genes and behaviour is complex and dynamic across development.

Developmental dyslexia: 3-6% prevalence, polygenic (moderate heritability). Historically characterised as "word blindness". Explanations include:

  • Difficulties making matches between sounds and visual patterns (Birch & Belmont, 1964)
  • Temporal processing deficit (Stein, 2001)
  • Phonological processing deficit (Pennington et al, 1991)
  • Difficulty with automatisation of movement and cognition (cerebellar deficit) (Nicolson & Fawcett, 1990)

The phonological account wins - although motor and temproal processing difficulties have been observed in some people with developmental dyslexia they are just not as prevalent as phonological difficulties (Ramus, 2003)

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Autism Spectrum Disorder

Prevalence of around 0.9%, but more in males than females. Polygenic (high heritability). Wing (1988) characterised Autism as a triad of impairments: social deficit, communicative deficit, and repetitive and stereotyped behaviours.

Theory of mind account: Baron-Cohen, Leslie & Frith (1985) found that ASD children were pretty bad at a variant of Wimmer and Perner's false belief task (80% failed), compared with 4 year old children and mental age-matched children with Down's syndrome (86% passed). Precursors to theory of mind are observable in infants (Onishi & Baillargeon, 2005) and toddlers. There is an absence of theory of mind in children autism.

Happe et al (2006): maybe there is no core deficit - symptoms of ASD can be pretty unrelated to each other, with poor correlations between different symptoms. Twin data suggests the various symptoms are coded by different genes.

Not all children who show atypical markers go on to develop ASD (Elsabbagh & Johnson, 2010). Risk of ASD is associated with the way the brain responds to dynamic stimuli.

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