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Flashcards in TASK 1 - ADHD Deck (40)
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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

  1. inattention: 6 symptoms have to be present for at least 6 months
  2. hyperactivity: 6 symptoms for at least 6 months
3
Q

A.

1. inattention

A
  1. overlooks or misses details, work is inaccurate;
  2. difficulty sustaining attention in tasks
  3. does not seem to listen when spoken to directly (mind is elsewhere)
  4. does not follow through on instructions, fails to finish work
  5. difficulty organising tasks, poor time management, disorganised work
  6. dislikes/avoids engaging in tasks requiring sustained mental effort
  7. loses things necessary for tasks/activities
  8. easily distracted by extraneous stimuli
  9. often forgetful in daily activities
4
Q

A.

2. hyperactivity + impulsivity

A
  1. often fidgets with/taps hands/feet or squirms in seat
  2. leaves seat in situations when remaining seated is expected
  3. runs/climbs in situations where it is inappropriate;
  4. unable to play or engage in leisure activities quietly
  5. often ‘on the go’, acting as if ‘driven by motor’
  6. often talks excessively, is very loud
  7. often blurts out an answer before question has been completed
  8. often has difficulty waiting his/her turn
  9. 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
  1. symptom domains/clusters + co-morbidities (anxiety disorders, conduct disorder)
    - -> lead to
  2. functional/psychosocial impairments
    - self (low self-esteem); school (academic difficulties); family; social (socialisation deficits)
15
Q

co-morbidities

2. consequence of ADHD

A
  1. ADHD only (kindergarten)
  2. low self-esteem
  3. poor relations, learning delay (6)
  4. mood disorder, challenging, defiant behaviour (10)
  5. 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
Q

theories

2. delay aversion

A

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
Q

theories

- dual pathway model (1 + 2)

A
  • 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
Q

dual pathway model

- DTAP (1)

A

= 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
Q

dual pathway model

- MSP (2)

A

= 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
Q

theories

- triple pathway model

A
  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
Q

triple pathway model

- vigilance (zeeuw)

A

= slow responding + low target detection possibly related attention networks

  • possible 4th pathway
  • specially for inattentive type
  • impairment frequently coincided with other impairments
31
Q

treatment

- medication (stimulant)

A
  • 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
Q

treatment

- medication (norepinephrine)

A
  • atomoxetine, clonidine, guanfacine
    = affect norepinephrine levels in non-stimulant ways
    √ reduce tics + increase cognitive performance
    x side effects: dry mouth, fatigue, dizziness, sedation
33
Q

treatment

- medication (antidepressants)

A

–> when accompanied by depression
- bupropion
= affect dopamine levels
- better cognitive performance BUT not as effective as stimulants

34
Q

treatment

- behavioural

A

= 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
Q

treatment

- combination

A
  • more likely to produce short-term improvements than medication or BT alone
    BUT no difference in the long-run to BT alone
36
Q

treatment

- computerised WM training

A
  • 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
Q

computerised WM training

A
  • 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
Q

computerised WM training

+ game elements

A
  • 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
Q

training + transfer effects in pre-school children

- WM training

A

√ 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
Q

training + transfer effects in pre-school children

A

√ 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)