W7 - EF Flashcards

1
Q

What is cognitive control

A

Conscious internal goal take precedence over automatic processes

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2
Q

Three behaviors demonstrating cognitive control

A
  • Inhibitory Control - Impulse Control - Selective Attention
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3
Q

What is the neural network needed for cognitive control based on initial studies. What study did they use.

A

Stroop Task: 1.) Anterior Cingulate Cortex (ACC) 2.) Dorsolateral Prefrontal Cortex (DLPFC)

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4
Q

What is the brain areas in charge of cognitive control doing

A

ACC: Detects need for greater level of control DLPFC: Implement top-down control over performance

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5
Q

It isn’t clear how conflict resolutions is mediated as…?

A

Unclear whether mediated by: 1.) Task relevant information amplify neural representation 2.) Task irrelevant information inhibit neural representations 3.) Both

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6
Q

How did they resolve the questions regarding how the neural network on cognitive control resolves conflict

A

Stroop Task with congruent/incongruent face-name stimuli because faces are known to elicit BOLD response in FFA

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7
Q

In the face-name stroop task, what were the results and conclusion

A

1.) Faces = Target; Higher cognitive control performance associated with increased activity in FFA compared to low control trials 2.) Faces = Distractor; Control performance no associated with FFA activity > Better cognitive control performance associated with amplified processing of faces (when faces ere a target)

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8
Q

When tested on functional interactions between regions associated with higher cognitive control and FFA, what did they find

A

Psychophysiologic Interaction Analysis (PPI): Only functional coupling between DLPFC and FFA increased under high control in face target condition (not distractor)

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9
Q

What are common tasks examining inhibitory control. Why?

A

Go/No-Go and Stop Signal Task Requires participants to withhold a prepotent/automatic response, Ideal for neuroimaging as it allows events of interest (success/failed inhibition) c.an be isolated in time from on-going task-related activity

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10
Q

Inhibitory Control: What did fMRI find

A

1.) Right Inferior Frontal (Part of PFC) 2.) Right parietal 3.) Dorsal ACC (Note: fMRI only allows correlation)

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11
Q

Inhibitory Control: What did leision studies find

A

Right inferior frontal gyrus Correlated with SSRT (Volume of IFG damage increase, SSRT RT increase)

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12
Q

Inhibitory Control: What did TMS studies find

A

Right inferior frontal gyrus Correlated with SSRT (TMS of Right IFG impaired performance) - TMS of middle frontal/angular gyrus no effect

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13
Q

Based on fMRI, leision and TMS studies on IC, what is the overlapping region

A

Right Inferior Frontal Gyrus.

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14
Q

How is cognitive function is related to treatment success

A

Directly: Treatment to assist with cognitive dysfunction may directly assist with these difficulties Indirectly: Greater cognitive capacity through CBT

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15
Q

Results of self-control tasks (GNG/SST) from dependent drug users and gamblers. What are the neurological and behavior results. What is unclear

A

Neurological: Significantly lower activity in PFC and ACC Behavioural: Poorer performance on self-control tasks Unclear: Cognitive Dysfunction cause/caused by drug use?

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16
Q

Results from Cocaine Stroop Tasks

A

Active and abstinent drug users = slower RT’s for the drug-related words or pictures (Significant interference)

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17
Q

Why do drugs take up the evocative property?

A

Drugs > Dopamine > Overactivation of Limbic System Limbic System > Hippocampus > Repeated pairing of drug-induced euphoria with drug stimuli

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18
Q

Change blindness test in drug-users

A

Attentional Bias. Found relationship between alcohol intake and sensitive to change

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19
Q

What is attentional bias predictive of in drug-users

A

Predicts treatment outcomes and success

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20
Q

What happens to a child in a family of drug dysfunction

A
  • PFC deficits in drug-naive children > predictive of drug addiction?
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21
Q

What kind of behavior does PFC activity in IC predict?

A

Prefrontal Activity during Inhibitory Control: Predicted binge drinking Poor EF + Hypoactivity in brain areas: Predicted relapse More than 70% accuratey

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22
Q

What is ADHD characterised by

A

Inattention; Hyperactivity; Impulsitivity

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23
Q

What are neuropsychological deficits in ADHD

A

Involve higher order EFs: 1.) Response inhibition 2,) Motor timing

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24
Q

What symptoms are associated with poor inhibition in ADHD

A

Motor: 1.) Motor Clumsiness Response Inhibition: 2.) Reactive response in cognitive task 3.) Problems delaying response 4.) Poor protection of interference Social and Emotional: 5.) Disruptive Social Behaviour 6.) Emotional Dyscontrol

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25
Q

Improving control: Psychopharmocology

A

SST: Improved by atomoxetine (noradrenrgic) Reward Learning Tasks: Improved by citalopram (Serotonergic)

26
Q

Improving control: What psychopharmology has been shown to improve performance on attentional tasks. And brain area they correlatet with?

A

Consistently: 1.) Atomexotine (Noradrenegic) 2.) Methylphenidate (Ritalin) > Improvements were associated with significant increases in right IFG activity

27
Q

Dopemine in MA users

A

Low D2 receptor levels and depleted metabolsim

28
Q

What does level of dopamine metabolism depletion predicts:

A
  • Relapse Risk - Development of Parkinsonian Symptoms - Associated with 4x greater risk of developing Parkinson - Associated with greater reward impulse
29
Q

Improving control: What psychopharmology has been shown to improve performance on MA Users. And what were they correlated with?

A

Ritalin Improvement associated with VMPFC activity

30
Q

Do neuroenhancers improve treatment outcomes? Some examples

A

Generally not/mixed results Modafinil Methylphenidate/Ritalin

31
Q

What are recent trials demonstrating neuroenhancers improving treatment outcomes

A

Dexaamphetamnie

32
Q

What is the neuro behind ADHD and drug addiction

A

Low levels of dopemine

33
Q

What is the role of dopemine in response inhibition

A

Unclear. 1.) Transforming to-down inputs into context-dependent signal to faciliate behaviour 2.) Modulate between stimulation vs overstimulation

34
Q

What disease is a good example of the complex relationship between dopemine and cognitive control

A

Parkinson Disease - Associated with low inhibition and low dopamne - No evidence that dopemine replacement therapy > Cognitive control (Subset of PD patients who begin DRT develop impulse-compulsive behaviors)

35
Q

In the face-name stroop task, what were the hypotheses

A
  1. amplified processing of faces (when faces were target = larger bold with higher control) 2. suppressed processing of faces (when faces were distractor = smaller bold with higher control) 3. both
36
Q

Where is strength of reward craving reflect in neurobiology?

A

Strength of Craving = Cue-related limbic activity

37
Q

What cognitive deficits do MA users show

A

1.) Poor verbal memory 2.) Slowed Processing speed 3.) Executive function - Disinhibition - Selective attention - Decision making / Biased to immediate reward, ignore future consequences - Cognitive flexibility / Task switching

38
Q

What is the magnitude of cognitive deficits do MA users comparable to. vs cocaine users, marijuana users, AD

A

Higher than cocaine & marijuana; slightly lower/ comparable to Alzheimer.

39
Q

Does behaviour (frequency, duration and quantity) of MA use predict level of cognitive impairment?

A

No. It is unclear what predicts level of impairment. - Individual (potentially genetic) variation in susceptibility to MA toxicity - Age & Gender - Co-morbidity (other psychiatric conditions)

40
Q

D2 Levels. Which has been linked to vulnerability to addictions.

A

Lower D2 = Vulnerable to addictions. High D2 = Protective factor in siblings of drug dependent individuals

41
Q

What is the Inverted U-shaped curved in dopemine (Volkow). Compare low D2 and high D2

A

Optimal level of Dopamine stimulation = ‘pleasant’ - Low level of d2 receptors = Large drug-induced increases in DA result in optimal stimulation - High levels of d2 receptors = Large drug-induced increase pushes them to far and into the unpleasant range of the curve

42
Q

What is depleted in MA users. What does it predict?

A

Dopemine D2 levels and metabolism. Dopamine metabolism depletion predicts: 1.) Relapse 2.) Development of Parkinsonian symptoms 3.) 4x greater increase of PD (NOT COCAINE) 4.) Impulsive for reward

43
Q

What gene has been proposed to affect D2 receptors in the midbrain? What has possession of this gene been associated with

A

Taq1A allele. Possession of 2 copies associated with: Reduced D2 density = low dopaminergic Seek dopamine stimulation, which can be: direct (cocaine) indirect (risk-taking)

44
Q

What does Taq1A allele predict

A

1.) Risk of developing drug dependence 2.) Poor response to drug treatment/ High relapse

45
Q

What is ‘supersensitivtiy’ in Taq1A

A

‘Supersensitivity’: After abstinence, Taq1A experience more powerful euphoria upon taking their previously addicted substance, making them vulnerable to relapse

46
Q

What is the underlying principle of human learning

A

Prediction error (Magnitude of dopamine: Greater magnitude = More likely behavioral change/Learn) Brain monitors difference between what we expected to happen and the actual outcome.

47
Q

What does prediction error aim to maximize

A

Reward. Feedback indicating an outcome > More likely to be learnt

48
Q

Dopemine & Games: What is it sensitive to

A

1.) Difficulty - Game harder = Reward intermittent 2.) Probability - E.g. poker machines. Strategy of variable ratio schedule so won’t win, but entice sufficiently 3.) Satiation - Hedonic adaption is the effect that satiation has on dopamine release to intermittent rewards

49
Q

People who self-report high impulse has been associated with..?

A

Low D2.

50
Q

What does selective attention require

A

Selectively attending to stimuli in the presence of incongruent/salient stimuli requires top-down control

51
Q

High sensation seekers have been associated with…

A

Low reward sensitivity Poor inhibitory control

52
Q

How do we operatinalise impulsitivity

A

Baratt Impulsitivity Scale

53
Q

How does the limbic system reacts to reward/loss in alcoholics

A

Increased activation in reward Decreased activation in punishment

54
Q

Does the limbic system pattern of activation found in alcholic extend to children?

A

Yes in drug-naive children of alcoholics i.e. more sensitive to reward less sensitive to punishment

55
Q

How do we operationalise impulsiveness for reward

A

Delay discounting task - Immediate reward vs Large, delayed reward

56
Q

How do we operationalise decision making

A

Gambling Task - Good decks vs bad decks

57
Q

Gambling task in drug users ndividuals

A

Drug abusers showed impaired performance (bad decisions)

58
Q

Gambling task in cocaine individuals

A

Poorer decision making. - Less DLPFC and ACC activation - Greater orbitofrontal activity

59
Q

What is a cool way of treating substance use disorders

A

Contingency management. Provide tangible, positive, reinforcement for objective evidence of behaviour change.

60
Q

What does drug-related cue activation in limbic and frontal regions predict in alcohol dependent individuals

A

Magnitude of drug-related cue-induced activation of limbic and medial prefrontal regions predicts subsequent relapse