W7 - EF Flashcards by andy Sitoh

What is cognitive control

Conscious internal goal take precedence over automatic processes

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Three behaviors demonstrating cognitive control

Inhibitory Control - Impulse Control - Selective Attention

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

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

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What is the brain areas in charge of cognitive control doing

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

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

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

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

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

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

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

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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What are common tasks examining inhibitory control. Why?

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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Inhibitory Control: What did fMRI find

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

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Inhibitory Control: What did leision studies find

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

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Inhibitory Control: What did TMS studies find

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

Right Inferior Frontal Gyrus.

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How is cognitive function is related to treatment success

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

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

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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Results from Cocaine Stroop Tasks

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

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Why do drugs take up the evocative property?

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

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Change blindness test in drug-users

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

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What is attentional bias predictive of in drug-users

Predicts treatment outcomes and success

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What happens to a child in a family of drug dysfunction

PFC deficits in drug-naive children > predictive of drug addiction?

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What kind of behavior does PFC activity in IC predict?

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

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What is ADHD characterised by

Inattention; Hyperactivity; Impulsitivity

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What are neuropsychological deficits in ADHD

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

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What symptoms are associated with poor inhibition in ADHD

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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Improving control: Psychopharmocology

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

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

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

Dopemine in MA users

Low D2 receptor levels and depleted metabolsim

What does level of dopamine metabolism depletion predicts:

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

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

Ritalin Improvement associated with VMPFC activity

Do neuroenhancers improve treatment outcomes? Some examples

Generally not/mixed results Modafinil Methylphenidate/Ritalin

What are recent trials demonstrating neuroenhancers improving treatment outcomes

Dexaamphetamnie

What is the neuro behind ADHD and drug addiction

Low levels of dopemine

What is the role of dopemine in response inhibition

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

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

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)

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

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

Where is strength of reward craving reflect in neurobiology?

Strength of Craving = Cue-related limbic activity

What cognitive deficits do MA users show

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

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

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

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

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)

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

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

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

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

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

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

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

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

What does Taq1A allele predict

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

What is 'supersensitivtiy' in Taq1A

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

What is the underlying principle of human learning

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.

What does prediction error aim to maximize

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

Dopemine & Games: What is it sensitive to

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

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

Low D2.

What does selective attention require

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

High sensation seekers have been associated with...

Low reward sensitivity Poor inhibitory control

How do we operatinalise impulsitivity

Baratt Impulsitivity Scale

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

Increased activation in reward Decreased activation in punishment

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

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

How do we operationalise impulsiveness for reward

Delay discounting task - Immediate reward vs Large, delayed reward

How do we operationalise decision making

Gambling Task - Good decks vs bad decks

Gambling task in drug users ndividuals

Drug abusers showed impaired performance (bad decisions)

Gambling task in cocaine individuals

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

What is a cool way of treating substance use disorders

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

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

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