HC4 Flashcards

1
Q

what are biomarkers for adhd? where are the genes located?

A

could be related to symptoms dopamine receptor and transporter genes involved in transport, re-uptake, receptor (DAT1; DBH; DRD4 and DRD5), serotonin receptor and transporter genes (5-HTT;HTRIB), noradrenaline- genes (ADRA 2A, ADRA 2C). Odds-ratio= together less than 1.5!! Results are inconsistent, depends on sample and effect sizes are usually very small

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2
Q

what are biomedical risk factors of ADHD?

A

antibiotics use in early life, insufficient omega 3 and 6 in the body which you receive through food, disruption of gut microbiota and irregular circadian rhythm/ sleeping disorders/ difficulty sleeping or waking early in the morning.

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3
Q

what are environmental risk factors of ADHD?

A

low birth weight (normal gestational age of 40 weeks but less than 2500 grams)/ prematurity, alcohol during pregnancy, exposure to lead (for example from drinking water), but very expensive to replace furniture or whatever that has lead in it), traumatic brain injuries.

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4
Q

what are social environmental risk factors of ADHD?

A

harsh discipline and authoritarian parenting and severe early deprivation

(group of children raised in orphanages in east-Europe like Romania, Ukraine, Russia in war between Russia and Europe. One of journalists found large building with many noises, large number of children without clothes and just one caretaker for 30 children, fed but not stimulated, no relationship with caretaker. Then they followed these children who were adopted by parents in Western countries; they found that in beginning almost all children had intellectual disabilities because of social deprivation (motor and language delays) but after few years IQ raised and motor developed normal, but some executive functions still lacked behind control groups, and kept on being oversensitive to specific noises, more anxious, and majority kept showing ADHD. Because prefrontal cortex is latest to develop, but they missed lots of experiences essential for developing prefrontal cortex ).

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5
Q

what are the 3 broader characterizations of adhd?

A
  • Emotion regulation difficulties (ERD)
    – anger susceptibility/ irritability or low distress tolerance
    – Present in 40-50% of ADHD population
    – ERD may delineate a diagnostic subtype.
  • Sluggish cognitive tempo (SCT)
    – a constellation of cognitive (e.g., excessive daydreaming, being ‘lost in a fog’) and motor (e.g., underactive, slow-moving) elements
    – Affects 25-40% of ADHD population
    – SCT appears to mediate ADHD-related academic difficulties.
    – New name: cognitive disengagement syndrome
  • Sleep problems is extremely common in people with ADHD
    – Poor or insufficient sleep could play a causal role in ADHD.
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6
Q

neuropsychological test battery

what ef need to be measured for adhd

A

motor inhibition

interference control

task switching or cognitive flexibility

selective and sustained a ttention

working memory

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7
Q

what tasks measure motor inhibition

A

go/no go

stop-signal (druk op a of b pijltje maar soms stop teken)

stroop (colours)

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8
Q

what tasks measure selective and sustained attention

A

visual selection task

continuous performance task

vigilance task

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9
Q

what tasks measure working memory

A

backwards digit span task

corsi block span task

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10
Q

what does the cognitive and motivational impairment model entail?

A
  • impaired signalling of delayed rewards (Delay aversion= preference for immediate rewards or a constant need for stimulation, difficulty imaging reward that is in the future) and neurocognitive dysfunctions, incl. working memory and executive functions (deficient inhibitory control)

– Working memory provides an interface between perception, attention, memory, and action. It is essential for recognition of externally presented stimuli. WM-impairment has been linked to inattentiveness in ADHD

– Impaired inhibitory processing: poor response inhibition capacity in patients with ADHD when performing Stop-Signal and Go/No-go tasks

  • However, executive dysfunctions cannot explain sufficiently the presence of ADHD
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11
Q

how much is brain development delayed for children with adhd and in what areas?

A

typically 3 years in cortical regions and 4/5 in prefrontal cortex

The peak of cortical thickness maturation delayed in ADHD children relative to typical controls by an average of 3 years across all cortical regions, with up to 4-5 years delay in frontal and temporal areas, respectively (Shaw et al., 2007)

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12
Q

what is seen in brain of adhd children only (not in adolescense or adulthood)?

A

smaller total intracranial volume, total cortical surface area, and volumes of subcortical nuclei, including amygdala and hippocampus, along with long implicated striatal regions

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13
Q

what is a trend in neuroimaging studies in adhd?

A

researchers are beginning to lean away from
investigations into regional abnormalities in favor of studying the effects of impairments in
communicatory connections between regions

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14
Q

what is brain structure network based on

A

connections between and within brain areas

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15
Q

what is brain function network based on

A

brain activity, co-activation (neural oscillations) of neurons within and between brain areas

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16
Q

what 3 brain networks are distinguished? how do they interact?

A

1) default mode network

(internal focus of attention, not from environment) this is dominant network
- when listening to prof speaking for 40 minutes you might lose focus and start wandering

: Resting-state fMRI: Default Mode Network (DMN)= active when you are ‘doing nothing in particular’

2) Until it is interesting again then:
salience network

directs attention to salient events

3) if it gets difficult then:

central executive network

17
Q

what happens in neural networks of children with adhd?

Differences in functional connectivity or identifying specific impairments in large scale neural networks in ADHD vs controls; what are results of this?

A
  • absence of a negative correlation
    between task positive (SN and CEN) and task negative (DMN) in the brain in ADHD. It looks
    like these networks do not function as separate networks – as no negative correlation is seen. Trouble navigating to other

– During the working memory task, reduced activation in task-positive and reduced deactivation in task-negative (i.e., default mode) areas were correlated with CBCL Attention Problems scores (Owens et al., 2022).

18
Q

default mode network

A

Recall of the past (autobiographical memory)
and imagination of the future, reflection on present mental states (esp. affective) and
‘mind-reading’ (social cognition).

19
Q

fronto-parietal or executive control network

A

Top-down signals for current task goals, exert control by flexibly biasing information
flow across multiple large-scale functional networks overcoming conflict from previous
habits. Also allows for novel task control

20
Q

(affective) salience network

A

Maintains a stable ‘saliency’ or priority
map of the visual environment – including surprising stimuli, and stimuli that are
pleasurable and rewarding, self-relevant, or emotionally engaging (both appetitive
and aversive such as threats).

21
Q

functional networks of brain

A

Cingulo-Opercular Network: Vigilance and sustained attention. Tonic alertness for working memory. Set maintenance in working memory related tasks. Response override after conflict detection

Dorsal Attention Network: selective attention

Ventral Attention Network: Bottom-up attentional processing

Auditory Network

Visual Network

Somatosensory-Motor Network

Subcortical Network: e.g., limbic system

22
Q

what is most effective adhd treatment

A

combination of medication and cognitive behavioral therapy
- psycho education of the family, coaching of teachers

23
Q

asd risk factor heretability is polygenetic, which means

A

a large number of candidate genes increase the risk. Common variants
and rare genetic variants (e.g. de novo variants)

24
Q

what is it called when you have : trouble communicating but not repetitive or other symptoms

A

social communication disorder

25
Q

what are environmental risk factors for asd

A

– Maternal conditions, complications of pregnancy, medications (use of antiepileptics, asthma medications), exposure to toxic substances (e.g. air pollution)
– Prematurity (vulnerable to forms of gray and white matter brain injury, anoxia, hypoglycaemia)
– Advanced parental age (both parents contribute to genetic risk)

26
Q

heretability in asd is high 60-95%

what are genetic risk factors for asd

A

– Damage of DNA: microdeletions (non-heritable genetic characteristics).
– Epigenetic processes: (micro)RNA (switching genes on or off, involved in the development of dendrites, vulnerable to environmental influences)
– Genetic susceptibility (oversensitivity to specific environmental influences, e.g. fine dust)

27
Q

what are neuropsychological symptoms of asd

A
  • Primary deficits in perception, e.g. face perception, perception and interpretation of emotional expressions, melodic aspects of auditory stimuli
  • Deficits in social cognition, e.g. changes in gaze direction from early age, joint attention, imitation (in particular non-intentional acts), theory of mind, empathy
  • Deficits in episodic memory (difficulty remembering and telling experiences in correct order)
  • Deficits in all executive functions
  • Motor problems (fine motor control, visuo-motor coordination, atypical handling of objects)
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