ADHD 1 Flashcards
1
Q
characteristics of ADHD
A
- hyperactivity, impulsivity and attentional problems
- often has difficulty sustaining attention in tasks or play activities
- often fidgets with or taps hands or feet or squirms in seat
- several symptoms have to be present before age 12 and manifest in more than one context
2
Q
ADHD in DSM 5
A
- ‘A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development’
- recognises three ‘presentations’:
1. predominantly inattentive
2. predominantly hyperactive-impulsive
3. combined
2
Q
ICD 11 and ADHD
A
‘a persistent pattern of inattention and/or hyperactivity-impulsivity that has a direct negative impact on …. functioning’
3
Q
ADHD prevalence
A
- UK = ~5% of children/adolescents have a diagnosis of ADHD
- boy: to girl ratio = ~3:1
- symptoms continue into adulthood in 8-43% of cases (gender gap may narrow)
–> activity issues decline and attentional issues remain
4
Q
baseline treatment for ADHD
A
- in kids over 5, adolescents and adults
- DL-amphetamine
or - methylphenidate
- class B drugs
- drugs of abuse
- effective but addictive
5
Q
estimated cost of ADHD in the UK
A
- combined cost of children and adolescents is roughly £2.4 billion
- drugs and treatments
- cost of juvenile detention
6
Q
ADHD in 1902
A
- George Fredric Still (paediatrician)
- gave a series of lectures
- talked about a group of kids he has been studying
- described 20 cases of children with a “defect of moral control…. (don’t think about others) without general impairment of intellect and without physical disease”
- “the immediate gratification of self without regard either to the good of others or to the larger and more remote good of self”
-“fidgety….” - “a quite abnormal incapacity for sustained attention”
7
Q
ADHD 1917-1928
A
- Encephalitis lethargica epidemic
- less severe had cold symptoms, more severe were more rigid and statue like (eyes became almost paralyzed)
- many affected children who survived the encephalitis, subsequently showed abnormal behaviour
- “Postencephalitic behaviour disorder”
- children often became hyperactive, distractible, irritable, antisocial, destructive, unruly, and unmanageable in school
- first association of (now) ADHD with brain damage
- when adults recovered they often had Parkinson’s symptoms
8
Q
ADHD 1940s/50s Minimal brain damage
A
- assumption that minimal damage to the brain, even when it cannot be demonstrated objectively, causes postencephalitic-type behaviour disorder
- brain damage would be inferred just from looking at kid’s behaviour
–> not great
9
Q
ADHD 1960s
A
- Minimal brain dysfunction (MBD)
- became clear that this disorder (“hyperkinetic impulse disorder”) could occur in the absence of explicit brain damage
- the Oxford International Study Group of Child Neurology therefore advocated a shift in terminology by replacing the term “minimal brain damage” by “minimal brain dysfunction”
- certain behaviours are not always linked to brain damage
10
Q
ADHD 1968
A
- minimal brain dysfunction was eventually considered too broad
- leading to a focus on more specific symptoms… (especially hyperactivity)
- 1968 DSM II:
–> “Hyperkinetic Reaction of Childhood”
11
Q
ADHD in the 1970s
A
- throughout 70s, developing realisation that attentional problems were as significant, or more significant, than hyperactivity in this patient group
- inattention now seen as important
12
Q
ADHD 1980
A
- 1980 DSM III:
–> “Attention Deficit Disorder (ADD)”
–> with or without hyper-activity - hyperactivity was no longer an essential diagnostic criterion for the disorder
–> could just have issues with attention/inattention - developed three separate symptom lists for:
1. inattention
2. impulsivity
3. hyperactivity
13
Q
ADHD 1987
A
- DSM III-R:
–> “Attention Deficit Hyperactivity Disorder” - brought the symptom list together
- now could have attention issues, or hyperactivity issues OR BOTH
14
Q
ADHD 1994, 2000, 2013
A
- DSM IV 1994
–> first time ADHD was able to be seen in adults and children - DSM IV-TR 2000
–> ADHD in adults and kids - DSM 5 2013
–> ADHD in adults and kids
15
Q
impact of ADHD
A
- DSM 5:
–> there is clear evidence that the symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning - ADHD associated with:
–> poorer educational attainment
16
Q
impact of ADHD - Fleming et al. (2017) - education
A
- poor educational attainment
- 4 Scotland-wide NHS databases
- 4 Scotland-wide school databases
- school leavers 2009-13
- ADHD vs non-ADHD
- Likelihood (OR)
Sub-GCSE qualifications - poorer results in ADHD kids
–> slightly worse for boys than girls
17
Q
impact of ADHD - Klein et al. (2012) - employment
A
- poor occupational attainment
- adults (mean age 41) diagnosed with ADHD at 6 -12 years of age
- vs controls
- less employed with ADHD (84% vs 95%)
- lower salaries in ADHD
(60k vs 100k)
18
Q
impacts of ADHD - Hoza et al. (2005) - child classmate evaluations
A
- children with ADHD
–> 7.0-9.9 years - and their same sex classmates
- study where kids are asked about who they like the most/least
- less popular with ADHD
- more rejected with ADHD
- ADHD and control are equal for average rating
19
Q
impact of ADHD - Lange et al (2016) - physical health
A
- physical health problems
- accidents over the last 12 months requiring medical treatment in children with ADHD (10.4 years old) and controls were recorded
–> ADHD = 23%
–> control = 15.35 - higher in ADHD kids
20
Q
impact of ADHD - Larson et al (2010) - mental health
A
- mental health problems
- kids ages 6-17
- much higher anxiety and depression in ADHD kids compared to non ADHD kids
- also higher autism and tourette likelihood in ADHD kids
21
Q
impact of ADHD - Levy et al., (2014) - drugs
A
- drug addiction
- higher drug dependence in adults for those with ADHD compared to non-ADHD
22
Q
negative effects of ADHD on:
A
- academic achievement
- occupational achievement
- social integration
- physical health
- mental health
23
Q
summary of ADHD (consequence and symptoms)
A
- ADHD is characterised by hyperactivity, impulsivity and attentional problems
- it affects around ~5% of children/adolescents, and symptoms can continue into adulthood in up to one half of cases
- clinical awareness of the condition dates back to the early years of the 20th century
- term ‘ADHD’ first appeared in the DSM III-R (1987)
24
Q
2 classical theories of ADHD
A
- something to do with frontal cortex
- something to do with dopamine
25
Q
classical theory 1 of ADHD - frontal cortex
A
- has something to do with the frontal cortex
- 3 types of evidence:
1. neuropsychology
2. structural imaging
3. functional imaging
26
Q
neuropsychology evidence for frontal cortex damage and ADHD
A
- the symptoms of ADHD are similar to the changes following frontal cortex damage
- impulsivity measured using the ‘Iowa Gambling Task’
27
Q
Iowa Gambling Task
A
- different deck of cards
- some are advantageous
- some are disadvantageous
- in disadvantageous you gain more now but also lose more later on
–> net of 250 loss
–> short term gain - in advantageous you gain less now more also lose less later
–> net gain of 250
–> less reward immediately but greater later reward
28
Q
results of Iowa gambling task
A
- ADHD pick disadvantageous over advantageous
–> want short term reward
–> more impulsive choice - similar to those with brain damage to frontal cortex who are more impulsive
29
Q
delay aversion (reward)
A
- people with ADHD want immediate reward
- take it whilst its on offer
30
Q
Barkley’s ‘behavioural disinhibition’ theory of ADHD (executive)
A
- Professor of Psychiatry at the Medical University of South Carolina
- sees poor behavioural inhibition as the central deficiency in ADHD
- accounts for attentional and kinetic symptoms
- lack of ‘Self-control’
31
Q
Phineas Gage
A
- serious damage to his frontal cortex
- showed disinhibited behaviour
- similar to ADHD
32
Q
structural evidence for ADHD and frontal cortex damage
A
- frontal lobe grey matter volume is lower in those with ADHD
- 232.87 vs 260.07
33
Q
functional PET evidence for frontal cortex damage and ADHD
A
- a study that used PET scanning
- radioactive version of flourine used to emit positrons
- deoxy glucose injected into brain
- when brain is active it needs large supply for glucose
- radioactive area associated with glucose
–> those were the active areas - got kids to do a basic and boring task
–> less brain activity in ADHD kids in this task than non ADHD kids
–> frontal areas perform less well # - structural and functional issues in ADHD brains
34
Q
classical theory 2 in ADHD - dopamine
A
- it has something to do with dopamine
- 3 types of evidence:
1. medication
2. imaging
3. reward/reinforcement
35
Q
medication evidence for dopamine in ADHD
A
- drugs used to treat ADHD increase dopamine levels
- Microdialysis:
–> a small, semi-permeable probe is inserted into a specific brain site
–> fluid is perfused through the probe and chemicals in the extracellular fluid diffuse across the membrane and are collected
–> samples are then analyzed using chromatography methods (e.g. HPLC) - dopamine levels in the striatum after i.p. D-Amphetamine or methylphenidate increase
36
Q
imaging evidence for dopamine in ADHD
A
- ADHD is associated with an increase in dopamine reuptake
- can use SPECT scans
–> single photon emission tomography
–> more reuptake proteins for dopamine in ADHD individuals
37
Q
reward/reinforcement evidence for dopamine in ADHD
A
- ADHD is associated with changes in response to ‘reward’
–> increases in dopamine in response to food
–> increase in response to sex
38
Q
Disruption of learning by non-contingent reinforcement (Douglas and Parry, 1983)
A
- elementary school children (mean age around 9.5 years old)
- 33 with ADHD, 33 without
- had to release a response key when a stimulus light came on (reaction time task)
- 3 conditions:
1. rewarded on every trial when they got faster
2. rewarded on every other trial when they got faster
3. rewarded randomly (non-contingent) - reward = told they were “very good”, “excellent” or “very fast”
- non-contingent reinforcement schedule resulted in slower mean reaction times in the ADHD sample
–> harder to figure out reward schedule - also delay aversion
39
Q
classical theories suggest (summary)
A
- that the disorder has something to do with the frontal cortex
- that the disorder has something to do with dopamine
- in the case of the frontal cortex evidence comes from:
–> neuropsychology
–> structural imaging
–> functional imaging - in the case of dopamine, evidence comes from:
–> medication
–> imaging (SPECT)
–> reward/reinforcement
