TASK 1 - ADHD Flashcards
1
Q
ADHD
A
= attention-deficit/hyperactivity disorder
- neurodevelopment disorder
- difficulties learning to pay attention, control impulses, organise behaviours to accomplish long-term goals
2
Q
DSM-5
A.
A
persistent pattern of inattention and/or hyperactivity that interferes with functioning or development
- inattention: 6 symptoms have to be present for at least 6 months
- hyperactivity: 6 symptoms for at least 6 months
3
Q
A.
1. inattention
A
- overlooks or misses details, work is inaccurate;
- difficulty sustaining attention in tasks
- does not seem to listen when spoken to directly (mind is elsewhere)
- does not follow through on instructions, fails to finish work
- difficulty organising tasks, poor time management, disorganised work
- dislikes/avoids engaging in tasks requiring sustained mental effort
- loses things necessary for tasks/activities
- easily distracted by extraneous stimuli
- often forgetful in daily activities
4
Q
A.
2. hyperactivity + impulsivity
A
- often fidgets with/taps hands/feet or squirms in seat
- leaves seat in situations when remaining seated is expected
- runs/climbs in situations where it is inappropriate;
- unable to play or engage in leisure activities quietly
- often ‘on the go’, acting as if ‘driven by motor’
- often talks excessively, is very loud
- often blurts out an answer before question has been completed
- often has difficulty waiting his/her turn
- often interrupts or intrudes on others
5
Q
DSM-5
B.
A
several inattentive/ hyperactive-impulsive symptoms were present prior to 7-12 years
- age of onset
6
Q
DSM-5
C.
A
several inattentive/ hyperactive-impulsive symptoms were present in 2 or more settings
- pervasiveness: not circumstance driven
7
Q
DSM-5
D.
A
there is clear evidence that the symptoms interfere with/reduce quality of social-academic or occupational functioning
- impairment
8
Q
DSM-5
E.
A
symptoms do not occur exclusively during another psychotic disorder and are not better explained by another mental disorder
- uniqueness
9
Q
prevalence
A
onset: begins in childhood, mostly diagnosed in elementary school
- 3-5% of school-age children
- in 50% percent symptoms persist into young adulthood
- boys 2x more likely
- -> girls: primarily inattentive + have less disruptive behaviour –> under-identification
10
Q
co-morbidity risk
A
increased risk for:
- antisocial personality disorder
- substance abuse
- mood/ anxiety disorders
11
Q
ADHD inattentive type
A
= attention deficits
- 6 or more criteria (1)
12
Q
ADHD hyperactive/impulsive type
A
= constantly restless, without thinking about consequences
- 6 or more criteria (2)
13
Q
combined ADHD
A
= hyperactive + inattentive
- 6 or more criteria in (1) and (2)
14
Q
co-morbidities
1. co-occuring
A
- symptom domains/clusters + co-morbidities (anxiety disorders, conduct disorder)
- -> lead to - functional/psychosocial impairments
- self (low self-esteem); school (academic difficulties); family; social (socialisation deficits)
15
Q
co-morbidities
2. consequence of ADHD
A
- ADHD only (kindergarten)
- low self-esteem
- poor relations, learning delay (6)
- mood disorder, challenging, defiant behaviour (10)
- antisocial behaviour, ostracism, conduct disorder (14-16) …
16
Q
impairments
- childhood
A
- injuries
- academic achievements
- -> 20-25% have specific learning disorder = even harder to concentrate in school
- poor relationships (become aggressive if things don’t go their way)
17
Q
impairments
- adolescence
A
- low self-esteem
- substance abuse
- accidents
- relationships
18
Q
impairments
- adulthood
A
- under-employed + frequent job changes
- legal issues
- marital problems
19
Q
conduct disorder
A
= aggressive/antisocial behaviour in children
- 45-60% of ADHD children develop it
20
Q
causes
- biological
A
- PFC: smaller in volume, abnormal activation when inhibit responses (control, attention, planning)
- less connectivity between PFC and emotional, motor & memory areas
- cerebellum (motor behaviours)
- catecholamine neurotransmitters (esp. dopamine, norepinephrine) function abnormally: sustained attention, inhibition of impulses, processing of errors
- often history of prenatal and birth complications (e.g. drinking, smoking during pregnancy)
21
Q
causes
- genetic
A
- heritability is one of the highest
BUT not clear what aspects are inherited - gene-environment interactions
22
Q
causes
- psychological/social
A
- more likely to belong to families with frequent disruptions (moving, divorce)
- fathers: more prone to antisocial, criminal behaviour
- mother-child interactions: hostile, conflicting
23
Q
biological causes
- immaturity hypothesis
A
= brains are slower to develop than the brains of other children (neurologically immature)
- unable to maintain attention and control behaviour appropriate to age
24
Q
theories
1. poor inhibitory control
A
ADHD as poor inhibitory control + neuro-cognitive disorder
= problems of executive, higher order control functions
- lack of attentional, strategic flexibility, display of poor planning and working memory and failure to effectively monitor behaviour
- self-regulation deficits: related to impaired executive functioning (WM, response inhibition)
- standard stop signal task
25
theories
| 2. delay aversion
ADHD as delay aversion + motivational style
= motivation to escape/avoid delay
- unwillingness to wait for delayed rewards and events --> cause impaired performance
- abnormal sensitivity to reinforcement (rewards, punishment, feedback) --> preference for immediate over large delayed rewards
- inattention/hyperactivity result from delay aversion
- choice delay task
26
theories
| - dual pathway model (1 + 2)
- explains neuropsychological heterogeneity in ADHD as two more or less independent patterns of deficits, each affecting some ADHD’s
- ADHD as developmental outcome of two distinct psychological/developmental processes
27
dual pathway model
| - DTAP (1)
= dysregulation of thought + action pathway
- ADHD = disorder of the regulation of thought + action resulting from inhibitory disfunction
- brain: higher order cognitive control circuits are messed up --> (pre-)frontal regions and their connections to the basal ganglia and striatum (meso-cortical dopamine system)
- no direct pathway between inhibitory dysfunction & symptoms: mediated by secondary processes (cognitive + behavioural dysregulation)
- symptoms reduce the amount of time spent on the task which in turn worsens cognitive regulation (vicious loop)
28
dual pathway model
| - MSP (2)
= motivational style pathway
- ADHD = motivational style mediated by the emergence of delay aversion
- brain: reward circuits are messed up --> ventral-striatal network (incl. NAC) (meso-limbic branch of the dopamine system)
- children fail to effectively respond to contextual delay demands (impulsive due to messed up reward circuit) --> they start to dislike those situations --> start to avoid delay
- expression of delay aversion is context dependent
- moderated by culture: when parents are unforgiving & have high standards they likely create the context for the emergence of delay aversion
29
theories
| - triple pathway model
1. cognitive problem (6%) --> INHIBIT
a. dorsal fronto-striatal loop = inhibition/cognitive control
2. motivational/reward processing problem (19%) --> DELAY (AVERSION)
a. ventral fronto-striatal loop = delay aversion/reward processing
- -> many seem unaffected
3. time management problem (26%) --> TIMING
a. fronto-cerebellar loop = temporal processing deficit (TPD)
- implicates WM problems
- substantial subgroups of patients are affected in only one of the three domains --> diagnostic difficulties
30
triple pathway model
| - vigilance (zeeuw)
= slow responding + low target detection possibly related attention networks
- possible 4th pathway
- specially for inattentive type
- impairment frequently coincided with other impairments
31
treatment
| - medication (stimulant)
- ritalin, dexedrine, adderall
= increase levels of dopamine by inhibiting reuptake and enhancing release
√ decrease demanding, disruptive + non-compliant behaviour
√ increase positive mood, goal-directedness, quality of interactions
x side effects: increased frequency of tics, decreased growth rate, reduced appetite, insomnia, edginess, gastrointestinal upset
x use increased a lot (greater recognition vs. inappropriate overuse)
x often mis-prescribed (esp. for boys & younger kids)
32
treatment
| - medication (norepinephrine)
- atomoxetine, clonidine, guanfacine
= affect norepinephrine levels in non-stimulant ways
√ reduce tics + increase cognitive performance
x side effects: dry mouth, fatigue, dizziness, sedation
33
treatment
| - medication (antidepressants)
--> when accompanied by depression
- bupropion
= affect dopamine levels
- better cognitive performance BUT not as effective as stimulants
34
treatment
| - behavioural
= reinforce attentive, goal-directed & prosocial behaviour
- changing rewards and punishments (token policy: give chips as a reward and take them as punishment; exchange for fun activities)
--> learn to anticipate consequences of behaviour, make less impulsive choices, interact more appropriately
√ highly effective
35
treatment
| - combination
- more likely to produce short-term improvements than medication or BT alone
BUT no difference in the long-run to BT alone
36
treatment
| - computerised WM training
- building on executive function theory (1)
- automatically and continuously adapts difficulty level to the performance of the child to optimise the training effect
- span-board task (non-practiced measure of visuospatial WM)
√ improved performance not only on WM but also reasoning + response inhibition
√ decrease in parent-rated symptoms of ADHD
--> effects comparable to medication
37
computerised WM training
- overlapping neural systems for WM and executive functions explain generalising effect of the training
- -> WM can be improved by training in children with ADHD --> improves response inhibition and reasoning + reduction of parent-rated inattentive symptoms of ADHD
- inattentive + combined type benefit most
38
computerised WM training
| + game elements
- use multiple sensory modalities (e.g. colour, sounds, movement) + frequent immediate feedback
--> provides external motivating contingencies; heightened activation/ arousal state
√ directly enhances effect of training
√ more motivated (= reduced absence time during training + greater number of trials completed)
√ do better during training (= fewer incorrect trials)
√ significantly improved after training on an untrained WM task
--> heightened motivation + stimulation increases maintenance of concentration/attention + withholding of impulsive, inappropriate behaviours
39
training + transfer effects in pre-school children
| - WM training
√ improves cognitive functioning
√ significant effect on non-trained WM tasks
- significant transfer effects to attention
- increased activity in parietal & prefrontal cortex
x could not be generalised to inhibitory functioning or problem solving
--> could be valuable in treatment (as WM & ADHD are highly connected)
40
training + transfer effects in pre-school children
√ significant improvement on trained tasks
x no improvement on non-trained tasks --> neuropsychological basis for WM + inhibition are at least partly different
- not as easy to adjust difficulty for inhibition as it is for WM (= less training effect)
