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  1. Family genetics
    • parents/ siblings have an 8 fold increase in the risk for ADHD so genes are very important
    • BUT if whole family behaves chaotically/ badly then it appears to be genetic when actually it’s environmental
    • Twin studies reveal inheritability of 60-90%
    • when twin studies reveal inheritance then look at molecular genetics to see what genes are involved
  2. Molecular genetics
    polymorphisms of dopamine genes (e.g. DRD4) (polymorphisms = variations in genes which can be seen in the normal populations)
  3. FARAONE et al 2005
    serotonin/ receptor genes (e.g.SLC6A4)
  4. WILLIAMS et al 2010
    large rare CNVs (repeats of gene sequences) more common in those with intellectual impairments and implicated ASD
  5. Recurring theme in ADHD
    • high heritability
    • multiple genes act as risk factors (have small effects but none sufficient to begin the disorder alone like in FXS)
    • likely to have environmental cause factors
    • epigenetics (how genes are expressed not changed)
    • gene x environment interaction
    • risk factors increase the likelihood of disorder occurring
  6. Pre-natal risk factors
    • maternal lifestyle (drinking/smoking)
    • maternal stress (over secretion of cortisol)
    • maternal medication (asthma/anti-depressants
  7. Peri-natal risk factors
    • low birth weight = 2 fold risk increase
    • lesions in frontostriatal brain circuits
  8. Post-natal
    • food additives/allergies
    • exposure to lead and neurotoxins
  9. Social Environment
    • physical, cognitive and environmental deprivation
    • maternal depression (those who are drinking or smoking due to depression ultimately)
    • marital discord (would be stressful)
    • low parental warmth
  10. BROOKES et al 2010
    • gene x environment interaction
    • maternal drinking in pregnancy alone doesn’t cause ADHD but with the genetic risk it increases the likelihood the baby will have ADHD
  11. THAPAR et al 2010 aim
    is smoking during pregnancy associated with symptoms of ADHD
  12. THAPAR et al 2010 procedure
    • measured children's ADHD using parent and teacher ratings
    • maternal smoking
    • conduct disorder symptoms
    • family adversity
  13. THAPAR et al 2010 results
    • genetics accounted for most of the variance in ADHD
    • maternal smoking was found to be an environmental mediator of ADHD symptoms even when other confounds taken into account
  14. THAPAR et al 2010 conclusions
    maternal smoking is a risk factor of ADHD in addition to genetics
  15. Neurobiology
    these brain differences not really causally related but are just witnessed in those with ADHD
  16. ADHD is a fronto-striatal disorder
    • frontal lobes important for EF control and there are similarities between ADHD and individuals with frontal lobe lesions
    • evidence for reduced total brain volume up to 5%
    • evidence for alterations in dorsolateral pre-frontal cortex and neostriatum
    • marked cortical thinning in pre-frontal regions
  17. SOWELL et al 2003
    • children with lesser volumes of gray matter are more inattentive
    • those with larger frontal lobes were more hyperactive
  18. Neural Circuits
    • many brains circuits implicated in ADHD such as posterior-parietal (attention orientating and alertness)
    • real attempt to map cognitive profile to the brain
  19. ADHD as a catecholamine disorder
    • symptoms reduced by dopamine agonists (polymorphisms affect dopamine implicated) therefore neurochemistry important
    • mouse models which have catecholamine knocked out have behaviours which are identical to ADHD
  20. ADHD as an executive function disorder
    • longest standing and most evidence
    • deficits to high order cognitive processes that guide behaviour such as response inhibition, planning and working memory
    • poor on tasks that involve executive function e.g. tower of Hanoi
  21. BARKLEY’S MODEL 1997
    • core deficit in inhibition leads to problems in other areas of executive control e.g. working memory
    • some argue inhibition is not the core deficit as there can be problems in aspects of executive control without inhibition being impaired
  22. WILLCUTT et al. (2005)
    review: EF not sufficient to cause ADHD
  23. ADHD as a problem of motivation or reward DEMERIE et al 2011 aim
    how do kids respond to different kinds of reward (money vs. social praise)
  24. DEMERIE et al 2011 procedure
    • ADHD / ASD/ TD took part
    • reward size depended on task performance (how fast they could push a button)
    • reward varied between social and monetary
    • hypothesised kids with ASD not interested in social praise
    • ADHD equally happy with either reward
  25. DEMERIE et al 2011 results
    • found TD children happy with either reward
    • both clinical groups more motivated by money
  26. What is the implications of DEMERIE et al 2011
    • implication to intervention because kids want to please others with actions (hence why TD kids were happy with social praise)
    • if clinical groups don’t care about social praise have to think of something else to motivate them or their behaviour will not change
  27. ADHD as a problem of a delay aversion/ temporal processing PALOYELIS 2010
    • delay aversion, how long can they resist treat
    • Children were offered a low reward immediately or had to wait a few days for a larger reward e.g. £10 now or £100 next week?
    • ADHD cannot wait for reward while typical kids wait longer for reward
  28. Implications of PALOYELIS 2010
    • This has implications on rewarding good behaviour because children with ADHD do not have a concept of time and so offering a reward much later is not going to alter behaviour. The reward would have to immediate
    • may be due to poor temporal processing ability which is not only important for organisation but also related to working memory deficits
  29. ADHD as a multiple deficit disorder SJOWALL et al 2012
    • looked at executive function, delay aversion, reaction time variability (measure of sustained attention), emotion regulation and recognition and found that it predicted some unique variance in group function
    • no gender differences even though we would expect girls to have bigger problem with inattention
  30. SJOWALL et al 2012 criticisms
    • usually in this type of study, ADHD as a whole are compared to TD and their groups means are compared with ADHD generally have lower scores on whatever the measure is (i.e. attention)
    • however there is a lot of variation within ADHD so the categorical analysis takes an individual approach and asks if these children are impaired or not on each task
    • able to see what else each child is impaired on i.e. If you are impaired on delay aversion are you also impaired on executive function
    • authors believe that diagnosis should be based on behaviour and not on cognitive tests because ADHD does not always present itself
  31. Overt characteristics of ADHD
    • Inattentiveness: style of behaviour involving disorganisation/lack of persistence (disorganised, can’t get act together)
    • Hyperactivity: excess of movement, highly correlated with impulsivity (always on the go)
    • Impulsiveness: acting without reflecting (interrupting people)
  32. DSM IV definition of ADHD
    • 3 types: predominately hyperactive impulsive, predominately inattentive type and combined type
    • symptoms must be prevalent across situations (not just at school)
    • developed before 7 years of age
    • must lead to impaired functioning
    • Of course younger children not as organised as teens but there comes a point where this disrupts function = ADHD
  33. What are the risks of having ADHD
    • tend to think before they act so many with ADHD are at risk of:
    • school failure
    • teenage pregnancy
    • addiction
    • car accidents
  34. Co-morbidity
    • tends to be the rule rather than the exception
    • 30% have learning difficulties such as language impairment/dyslexia
    • 25% have mood disorders
    • 25 % have anxiety disorders
Card Set:
2013-05-25 16:55:33

Lecture 5
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