ADHD Flashcards
1
Q
DSM-V criteria for ADHD
A
- either 6 or more inattention symptoms or 6 or more hyperactivity.impulsivity symptoms
- at least 6 months and before 12 years of age
- persistent not situational
- must be a clinically significant impairment in social, academic or occupational functioning
2
Q
what are the three types of ADHD
A
- predominantly inattentive
- predominantly hyperactive/impulsive
- combined`
3
Q
demographic of ADHD
A
- peak onset between ages of 3 and 4
- 3%-5% of children
- higher in areas of low SES
- M:F ratios: 4:1 hyperactivity/impulsivity type, 2:1 for inattention type
- comorbidity: 50% also show another disorder e.g. ODD, dyslexia, dyspraxia, anxiety
- 30%-50% persists in adulthood
- as you age inattentiveness increases, hyperactivity decreases
- persistant ADHD more likely with comorbid disorders
- highly associated with criminal actibity, substance abuse, long-term unemployment
4
Q
Diamond 2005 and ADD/ADHD
A
- ADHD is a separate disorder than purely inattentive ADD
- different neuropsychological profiles: ADD workig memory and processing speed, ADHD, inhibitory control
- different neurobiolocal basis, ADD dopamine ADHD norepinepherine
- different patterns of social impairment and comorbidity
- but mixed evidence from other studies
5
Q
Genetics of ADHD
A
- increased risk for 1st and 2nd order relatives (Faraone 1995)
- siblings 3 to 5 times more at risk (Biederman 1992)
- Higher in monozygotic twins (50-80%) than dizygotic twins (33%)
7 candidate genes (esp. DAT-1 and DRD4, these are two of the 5 linked to the dopaminergic system. 2 are linked to serotoninergic system
- likely to have a complex genetic origin
6
Q
environmental risk factors for ADHD
A
- alcohol and nicotine (but people with ADHD more likely to smoke and drink and more likely to have a mother with ADHD than non ADHD childen so is this eve real)
- low birth weight, premature birth
- obstetric complications
- maternal stress
- exposure to lead during childhood
7
Q
Discuss executive function in ADHD
A
- inhibition (Barkley 1997)
- inhibition problems causes secondary deficits which causes symptoms of impulsiveness, inattention, hyperactivity
- weak inhibitory control leads to deficits in working memory, self-regulation
- behaviour of those with ADHD is controlled by immediate events and reinforcers due to impaired ability to represent goals plans and temporal sequences
- Nigg 2005, EF tasks, ADHD normally perform worse than controls, particularly on spatial working memory tasks (0.75), response suppression (0.61) and stroop (0.7)
8
Q
reward processing in ADHD
A
- sagvolden 1998
- reward processing deficits cause the symptoms
- Barkley 2001, reward discounting task e.g. £10 now, £100 in one year, ADHD went for lower rewards now than controls, delay aversive
-
9
Q
what brain areas involed in which type of reward processing
A
key brain areas in reward processing are the orbitofrontal cortex (all), ventromedial prefrontal cortex (drugs) anterior cingulate cortex (financial reward) striatum (cultural rewards e.g. art, desginer goods), amygdala, social rewar e,g, trust love
10
Q
reaction time and ADHD
A
- timing deficits cause symptoms
- Toplak 2006 says there is evidence that ADHD display poorer performance on duration perception, reproduction and finger tapping tasks
- RT (reaction time) variability
- also called intra-individual variability
- Tamm 2012 review
- tau as an index of lapses in attntion
- Epstein 2011, all of the 3 types of ADHD plus controls completed 5 RT tasks. Tau was the only RT variability indicator that showed differences between groups across all tasks
- children with ADHD had greater RT variability compared to controls, regardless of subject or task variables
- increased RT variability is a robust phenomenon in children with ADHD
11
Q
heterogeneity in ADHD
A
Nigg 2005
- usually less than half of ADHD children are impaired on EF
- a difference between ADHD and control does not mean all ADHD children are impaired
- so do deficits characerise ADHD if not all children are impaired in that area?
12
Q
ADHD and triple route model
A
- Sonuga Barke 2010,
- 9 tasks looking at 3 domains: inhibitory control, delay aversion, temporal processing
- ADHD children, their non ADHD siblings, and non ADHD controls
- 71% of ADHD displayed a deficit in one or more domans
- but 70% of these only had a deficit in 1 of the 3 domains
13
Q
Cognitive-energetic model of ADHD
A
- Sergeant 1985 originally most recent update 2005
- Cognitive function is due to computational and state factors
- specifies top down and bottom up factors
- ADHD deficits at lower levels explain dysfunction at higher, executive levels
- three levels
- 1 process (computational) factors
2 state (effort, arousal, activation) factors
3 - monitoring and evaluation factors
14
Q
ADHD and bottom-up/top-down models
A
ADHD consists of
- core deficit in state regulation, perceptual sensitivity and/or weak arousal mechanisms. this is reflectedi n RT variability. bottom-up process.
- non-causal exective function impairments that may be related to recovery from ADHD (top-down process)
- says a bunch of people including Halperin 2008 and Kuntsi 2010
15
Q
endophenotypes of ADHD
A
- heritable, vulnerability traits that mark a risk for the development of the disorder
- should co-occur with the disorder (but given the heterogeneity of ADHD its unlikely to be present in all)
- should be heritable (so identical twins should be more similar than non-identical twins)
- should show familial suceptibility (so non-affected relatives should exhibit the endophenotype to a greater degree than the avg member of general pop)
