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Rob (Not Edited) 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 top-down cognitive control

A
  1. Inhibitory Control
  2. Impulse Control
  3. 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 in the stroop task?

A
  • Dorsal ACC
    • Detects response conflict present in an incongruent word
      • i.e. Greater level of control
  • DLPFC
    • Implement top-down control over performance
      • e.g. biasing visual system
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5
Q

How did they resolve the questions regarding how the neural network on cognitive control resolves conflict in the stroop task?

A

Egner and Hirsch (2005) fMRI study

  • Stroop Task with congruent/incongruent face-name stimuli
  • Faces are known to elicit BOLD response in FFA
    • Could test whether:
      • Amplified processing of face (Faces target)
      • Suppressed processing of face (Face distractor)
      • Both
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6
Q

Results and conclusion:

Face-name stroop task with fMRI

A

1.) When faces were target

  • Higher cognitive control performance associated with increased FFA activity compared to low control trials

2.) When faces were distractor

  • Control performance not associated with FFA activity

Conclusion

Better cognitive control performance associated with amplified neural representation of task-relevant information (In this case, amplified processing of faces)

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7
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,

but not in the face distractor condition

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8
Q

What are common tasks examining inhibitory control.

Why?

A

Go/No-Go and Stop Signal Task

  • Requires participants to withhold a prepotent, or automatic, motor response
  • Ideal for neuroimaging, EEG, TMS, as it allows events of interest (success/failed inhibition) to be isolated in time from on-going task-related activity
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9
Q

Inhibitory Control: What did fMRI find

A

Successful response inhibition involved:

  1. ) Right IFG
  2. ) Right parietal
  3. ) Dorsal ACC

(Note: fMRI only allows correlation)

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10
Q

Inhibitory Control: What did leision studies find

A

Volume of lesion damage to the right IFG exclusively, correlated with SSRT (Faster times = Better Control)

  • Right IFG
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11
Q

Inhibitory Control: What did TMS studies find?

A

SSRT

  • Right IFG
  • TMS of middle frontal or angular gyrus had no effect
  • TMS of all three sites did not significantly affect the speed or accuracy of go trial responses
    • Speed of responding is important in response inhibition studies, because the faster you respond the harder it is to inhibit
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12
Q

Based on fMRI, leision and TMS studies on IC, what is the critical region for inhibitory control?

What is the point of running so many different methods?

A

Right IFG

  • Combination of methods allows discrimination of the network of regions important to response inhibition
  • Which can then be tested with causation using either TMS or a lesion study
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13
Q

Disadvantage of leision studies

A

Inability to specify discrete neuroanatomical regions

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14
Q

What is the DSM Criteria for Substance Use Disorder. What is the key thing they are looking out for?

A
  • Larger amount or longer period than intended
  • Persistent desire or unsuccessful efforts to cut down
    • Relative, not absolute, loss of control.
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15
Q

Is cognitive function related to treatment success? Why?

How does treatment success assist with this?

A

Cognitive function is related to treatment success

  • Ability to inhibit the immediate pursuit of pleasurable stimuli
  • Development of adaptive patterns of behaviour
    • Key factors in drug dependence

Treatment

  • Assist directly, or
  • Indirectly through greater cognitive capacity from CBT
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16
Q

What is the evidence that dependent drug users and gamblers have poor self control (Results and Neurological Implications)? What is unclear?

A

Dependent drug users and gamblers: SSRT and GNG

Behavioural

  • Poorer performance on self-control tasks

Neurological

  • _​_Significantly lower activity in PFC and ACC

Unclear

  • Causal relationship between drug use and brain
    • To what extent dysfunction is caused by or causes drug use
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17
Q

What is the evidence that drug users suffer interference from drug-related stimuli? Results?

A

Drug-related Emotional Stroop

Results

Active and abstinent drug users:

  • Slower RTs for the drug-related words or pictures compared to neutral words or pictures
  • Cocaine users suffer significant interference from cocaine related words and pictures in comparison to controls
  • Both groups are distracted by evocative stimuli
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18
Q

How do drugs (natural or unnatural) attain salience?

A
  • Drugs (including natural rewards) produce euphoria
    • Overactivates limbic centres in the brain via dopamine release in nucleus accumbens (NAc)
  • Limbic system closely tied to hippocampus
    • Repeated pairing drug-induced euphoria with drug-related stimuli creates association
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19
Q

What is the evidence suggesting that drug users are attentionally biased towards drug stimuli

A

Change Blindness Task

Attentional Bias

  • Heavier alcohol users were more sensitive or attentional biased to alcohol-related stimuli
    • Required less latency to detect
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20
Q

What is attentional bias predictive of in drug-users

A

Predicts treatment outcomes and success (cocaine users and alcohol users)

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21
Q

What are evidences suggest that drug-naive children has poor control?

A

It was found that drug-naive children:

  • Prefrontal dysfunction
  • Poor cognitive control performance in drug-naïve children predicts risk for subsequent drug addiction
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22
Q

What kind of behavior does PFC activity in IC predict (Whelan)

A

PFC activity during IC task:

  • Predicted binge drinking
    • At age 16 using model of parameter at age 14
  • Predicted relapse
    • More than >89% accuracy
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23
Q

What is ADHD characterised by?

What are neuropsychological deficits in ADHD?

What are ADHD symptoms

A

ADHD

  • Inattention
  • Hyperactivity
  • Impulsitivity

Neruopsychological Deficits

  • Response inhibition
  • Motor timing

Symptoms

Response inhibition

  • Reactive responses + problems delaying
  • Poor protection of interference

Motor

  • Motor Clumsiness

Social and Emotional

  • Disruptive Social Behaviour
  • Emotional Dyscontrol
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24
Q

Improving control: Psychopharmocology.

What is the outcome variable (IC Tasks)

A
  • SST (Inhibitory Control) and Attentional Task
    • Improved by Noradrenrgic
    • Improved by MPH (Ritalin)
      • MPH associated with right IFG increases during stop trials
  • Reward Learning Task
    • Improved by Serotonergic

Outcome Variable: IC Task

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25
Q

What are the neurobiology behind MA users.

What are the 4 things it predict?

A

Depleted D2 receptor levels and metabolism

Level of depletion: Predicts

  • Relapse Risk
  • Development of Parkinsonian Symptoms
  • Associated with 4x greater risk of developing Parkinson
  • Associated with greater reward impulse
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26
Q

Can we improve control in diseases?

A

Cognitive enhancers have NOT generally improved treatment outcomes for psychostimulant users in RCTs, or have mixed results at best

  • Modafinil
  • Methylphenidate/Ritalin

Outcome: Relapse

TLDR: Improve task performance, not treatment outcome

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27
Q

What are recent trials demonstrating neuroenhancers improving treatment outcomes

A

Dexaamphetamnie

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28
Q

What is ADHD and Drug Addiction characterised by neurobiologically?

A

Low tonic levels of dopamine

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29
Q

What is the role of dopemine in response inhibition

A

Role for dopamine in response inhibition is unclear

  • Either
    • Transform top-down inputs into context-dependent signal; or
    • Modulate between seeking stimulation and avoiding overstimulation
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30
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 dopamine
  • No evidence that dopemine replacement therapy improves cognitive control
    • Subset of PD patients who begin DRT develop impulse-compulsive behaviors
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31
Q

What does showing drug-related stimuli do to drug users

A
  • Activate limbic regions associated with use of the drug
    • Strength of cravings reflected in cue-related limbic activity
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32
Q

What does drug-related cue activation in limbic and frontal regions predict?

A

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

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33
Q

What cognitive deficits do MA users show

A
  • Poor verbal memory
  • Slowed Processing speed
  • Executive function
    • Disinhibition
    • Selective attention
    • Decision making
    • Cognitive flexibility
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34
Q

What is the magnitude of cognitive deficits are MA users compared to cocaine users, marijuana users, AD

A

Significant magnitude across domains (Learning, EF, Memory)

  • Higher than cocaine and marijuana
  • Slightly lower/Comparable to Alzheimer.
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35
Q

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

A

Though MA use has been associated with impairment, use behaviour does not predict.

  • Individual (potentially genetic) variation in susceptibility to MA toxicity
  • Older participants
  • Men
  • Confounded by co-morbidity (other psychiatric conditions)
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36
Q

D2 Levels. Which has been linked to vulnerability to addictions or protetive factors?

A
  • Lower D2 = Vulnerable to addictions.
  • High D2 = Protective factor in siblings of drug dependent individuals
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37
Q

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

A

Optimal level of Dopamine stimulation to be ‘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
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38
Q

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

What is associated with greater dopamine stimulation?

And what do they benefit from?

What do they predict?

A

Gene

  • Taq1A allele. Possession of 2 copies associated with:
    • Reduced D2 density
      • Hypodopaminergic State
      • Low dopaminergic tone

Why

  • Positive reinforcement (euphoria) and negative reinforcement (stress reduction) associated with dopamine stimulation is linked to source of stimulation, giving it greater salience and desire
    • Limbic System
  • Benefits from external dopamine stimulation
    • Directly (cocaine) or indirectly (risk-taking)

Predicts

  • Predicts drug dependence (2-5x)
  • Predicts poor responses to treatment and high relapse
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39
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

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40
Q

What is the underlying principle of human learning. Elaborate.

A

Prediction error

  • Difference between what expectations and outcome
  • Size of difference (Prediction error) is represented in dopamine cell activity
    • Greater magnitude = More likely behaviour will change to move closer to perceived ‘succesful state’
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41
Q

What does prediction error system aim to maximize. What else influences the system?

A

Reward.

  • Feedback indicating an outcome much better than expected
    • More likely to be learnt
  • Individual differences and maturational changes in the desire to (a) seek reward or (b) avoid punishment also influence the prediction error system
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42
Q

Dopemine and Games: What is it sensitive to

A

Dopamine release is sensitive to:

  • Difficulty
    • Game gets harder, rewards more intermittent
  • Probability
    • E.g. poker machines
    • Never know when you win, but win just often enough to entice
  • Satiation
    • Hedonic adaption is the effect that satiation has on dopamine release to intermittent rewards
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43
Q

People who self-report high impulse has been associated with..? What does amphetamine help with and what hypothesis was it consistent with?

A

Low D2.

Small amount of amphetamine led to greater D2 release.

  • Consistent with hypothesis
    • Individuals with low D2 have enhanced response to D2 stimulation
    • Enhanced response associated with stronger subjective desire or ‘wanting’ of the drug
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44
Q

How do we operatinalise impulsitivity

A

Baratt Impulsitivity Scale

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45
Q

What does selective attention require

A

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

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46
Q

High sensation seekers have been associated with…

A
  • Low reward sensitivity
    • (Need high sensations to bump up)
  • Poor inhibitory control
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47
Q

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

A

Yes in drug-naive children of alcoholics

  • More sensitive to reward
  • Less sensitive to punishment
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48
Q

How do we operationalise impulsiveness for reward

A
  • Delay discounting task
    • Immediate reward vs Large delayed reward
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49
Q

How do we operationalise decision making

A

Gambling Task - Good decks vs bad decks

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50
Q

Gambling task in drug users individuals

A

Drug abusers showed impaired performance (bad decisions)

  • Cocaine users show poorer decision making
  • Less DLPFC and ACC activity
  • Greater Orbitofrontal activity
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51
Q

What is a cool way of treating substance use disorders

A

Contingency management.

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

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52
Q

What is the neuro and bio behind ADHD and drug addiction

A

Combination of

  • High drive for reward
  • Low ability to control reward impulse
  • Low sensitivty to punishment
    • Modulated by Dopamine (Low levels)
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53
Q

What is the key role of dopamine

A

Key: Reward Sensitvity

  • Vulnerability to drugs
  • Novelty-seeking
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54
Q

What is performance monitoring

A

Identification and correct differences between an intended and executed response

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55
Q

Neuropsychological symptoms of performance monitoring deficits

A
  • The difference between knowing and doing
  • Perseverative behaviour
    • i.e. no learning
  • Lack of insight
    • i.e. denial
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56
Q

What do many clinical group show neurologically in performance monitoring?

A

Hypoactive ERN/ACC after mistake

  • Cocaine users, SZ, AD, Alcohol, borderline personality disorder; medication-naïve adolescents with ADHD;
    • However, this could be due to a number of different explanations: task is too boring, doesn’t evoke enough emotion when a mistake is made etc.
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57
Q

What is the exception group which shows hyperactive ERN

A

OCD and OCD students

Heightened error-related ACC and ERN response

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58
Q

What is the ERN and what does it correlate with?

A
  • ERN in ACC (Medial Frontal Region) approx 50 to 100ms after making an error
  • ERN correlates with error awareness
    • Confident they made an error = Higher ERN
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59
Q

What is the “Rabbitt effect” and who shows it

A

“Rabbitt Effect”

Cautious, or slowing, of response times immediately following an error

  • SZ Patients, or any group with hypoactive ACC/ERN
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60
Q

What is the two-factor theory of delusion. What does it explain

A

Explains monoethetic delusions.

  • Factor 1
    • Depends on where brain has damaged cortex
  • Factor 2
    • Each share a common dysfunction in belief evaluation
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61
Q

What is the one-factor theory of delusion

A
  • Dynamic relationship between top-down and perception.
  • Impaired prediction error system to update beliefs.
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62
Q

What are the 3 hypotheses on what ERN represents?

A
  • Emotional impact of an error #1
  • Response conflict #2
    • Two competing responses
  • Reward less than expected #3
    • Relative outcome
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63
Q

The conflict monitoring theory of dorsal anterior cingulate cortex (dACC) function argues that it responds to the response conflict inherent to many executive function tasks, such conflict arises from what

A

Competition between two competing responses, which are typically congruent and incongruent to the task requirements

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64
Q

What is the evidence that ERN represent conflict monitoring (#2)

What is the caveat?

A

2 Evidence:

  • ACC activity during error correlates with slowing of response speed on the following trial
  • Greater ACC during an error thought to reflect response conflict in trials

Caveat

  • Separating the “response” from “accuracy feedback” results in greater ACC activity for the “feedback“ compared to “response”
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65
Q

What is the neurobiology behind ERN and the proposed role of ACC based on #2

A

#2

  • ERN in ACC
    • Decrease dopamine in Midbrain (Basil Ganglia)
  • Correct response
    • Increase dopamine in Midbrain (Basil Ganglia)

Proposed Role of ACC

Trasmit value of response to regions critical for behaviour

(.e.g DLPFC for inhibition; hippocampus for learning)

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66
Q

What is the underlying principle underlying human behaviour and how does it relate to prediction errors?

A

Prediction error

  • Greater magnitude of prediction error
  • Greater dopamine cell activity
  • Likely behaviour will be ‘successful’
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67
Q

The reward prediction model of error:

How does ERN represent outcome relative to expectation (#3)

A

Reward prediction model of error #3

ACC activity or ERN reflects outcome relative to prediction

Evidence: Gambling Task

ERN influenced more by relative loss or gain, than whether a participants was correct or incorrect

  • Gain + Correct / Loss + Error was greater than
  • Gain + Error / Loss + Correct
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68
Q

How does ACC lesion relate to prediction error based on animal studies?

What does it suggest?

A

ACC Lesion in Monkeys

  • No impairment in performance immediately after an error
    • Intact learning from immediate feedback
  • Unable to sustain rewarded responses
    • Impaired ability to integrate feedback over time

Suggests ACC integrates value of outcome information

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69
Q

Do PD Patients learn better from Reward or Punishment (Experiment)

A

Patients off-medication (Low Dopemine)

  • Better learning from punishment than reward

Patients on-medication (High Dopemine):

  • Better learning from reward than punishment

[Note: Uncommon weird pattern in PD as usually low dopamine means greater sensitivity to seek reward]

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70
Q

Taq1A and learning patterns: Rewards vs punishment

A
  • Low D2 receptors (Taq1A) learn better from reward
  • But ‘Typical’ pattern (Normal D2) learn better from negative feedback/punishment
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71
Q

How does ACC represent perceived and unperceived errors? Evidence from antisaccade task.

A

ERN represents both perceived and unperceived errors similarly (Unconscious detection)

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72
Q

What is Error Awareness Task

A

Simiar to stroop task

Incongruent: Repeat words or correct colour words, leading to many unperceived errors

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73
Q

What did the Error Awareness Task reveal?

A
  • ACC activity was necessary, but not sufficient, for awareness
    • ERN was similar, does not vary in whether participants were aware
    • ACC is important for awareness, but does not determine if we are aware
  • Insula and parietal activity predicted awareness.

(GSR reveals that they truly were unaware, not just forgetting to tell the experimenter)

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74
Q

What brain areas in drug-abusers/others are associated with poor awareness (independent of task perforamance)

A

Cocaine, Cannibis, ADHD, SZ, Traumatic Brain Injury, AD

Reduced activity in both ACC and insula are associated with poor error awareness, independent of task performance

  • Hypoactive ERN
    • Poor insight into their own symptoms
  • Poorer inhibitory control performance
  • Poorer awareness of inhibitory failures
    • Only in repeated trial errors
    • Conscious error perception in congruent trials comparable to controls
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75
Q

In cocaine-dependent users, what is the hypoactive ERN associated with and what did it predict?

A

Hypoactive ERN

  • Associated with reduced insight into effects of drug use
  • Predicted likelihood of relapse and extent of cocaine use following relapse
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76
Q

What does insula do?

A
  • Involved in all subjective feelings
  • Awareness/ Interoception, of afferent representations of the feelings from the body
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77
Q

Why do drug addicts not seek help

A

It is partly due to lower awareness = don’t realize need for help

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78
Q

What happened to smokers when the insula is damaged. Why

A

Likely to quit.

Insula critical to awareness of cravings > lost cravings

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79
Q

How does the insula and ACC work together

A
  • Insula
    • Limbic sensory
    • Site of awareness on basis of afferent representations
  • ACC
    • Motor cortices
    • Initiation of behaviour.
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80
Q

Why does Methylphenidate influence the magnitude of the error-related negativity?

A

Methylphenidate influences prefrontal dopamine release

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81
Q

Can we use drugs to enhance ERN (specifically ERN only). What is the underpinning physiological changes

A

Yes.

  • Single dose of MPH can improve error awareness without much change in response speed, accuracy, or inhibitory control
    • Underpinned by physiological changes in ACC (Or parietal in sustained attention)
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82
Q

Neural mechanisms of learning

A

Strengthening of synapses.

Learning must be associative (emotions, motor planning)

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83
Q

How to maintain durable and flexible encoding

A
  1. ) Meaningful encoding upon broader framework
  2. ) Retrieval Practice
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84
Q

What is the relationship between sensitivty to reward and dopamine

A
  • Less D2 = Increased sensitivty to reward
  • Less D2 = Decreased senstiivty to punishment
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85
Q

What is the monetary incentive GNG task

A

Adding a punishment factor into GNG task

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86
Q

Results of monetary GNG task in drug-abusers vs control (Include Brain Parts)

A

Punishment manipulation

Significantly improved performance for both groups

However,

  • Controls more sensitive to punishment
    • Greater post-error slowing
    • Insula: r = 0.40; dACC: r = 0.37
  • CD shows dimished response to punishment
    • Less post-error slowing
    • Hypoactvity in dACC and insula
    • Insula: r = 0.04 ; dACC: r = -.05
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87
Q

Why was paired-associative learning task developed?

A

Examine confound: Do gambllers perform badly because of failed learning or risk-taking?

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88
Q

Paired-associative learning in cannabis users - Behavioural and neural results

A
  • Reduced ability to correct
  • Reduced ACC and hippocampus
    • ACC trasmit value to hippocampus to learn
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89
Q

What is the outcome measure of paired-association learning task

A

Number of repeated errors

(Number repeats down the sequence. See whether they learn)

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90
Q

What were the results of the associative learning task - Brain Parts implicated

A

Mistake Learning/Corrected

ACC and hippocampus (learning)

ACC trasmit value to hippocampus to learn

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91
Q

What were the results of the associative learning task when punishment is involved - Neurological results

(What is the implication)

A
  • ACC not modulated by punishment/size of penalty
    • ACC detects how it should influence future behaviour
  • Insula modulated by punishment/size of penalty
    • Insula learn from adverse outcomes, and if no insula, we don’t learn from severity of outcome.
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92
Q

What is ACC related to in learning outcomes

A

ACC activity reflects the extent to current outcome should dictate future actions. It is NOT modulated by punishment.

  • Rmb: leisioned ACC in monkeys showed only last outcome affected and they are unable to integrate feedback over time
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93
Q

ACC and Insula: Summary

A

ACC

  • Detect error (conscious and unconscious)
    • Both perceived and unperceived errors.
  • Not modulated by severity of punishment.
  • Determines how current outcomes should predict future behaviour by transmitting information to other relevant regions

Insula

  • Afferent representations
  • Detect error (conscious)
    • Perceived erorrs
  • Modulated by severity of punishment

Both needed for learning

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94
Q

What are the main components in the original cognitive model (Baddeley and Hitch, 1974)

A

STM

  1. ) Phonological Loop
  2. ) Visuospatial Sketchpad
  3. ) Central Executive
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95
Q

What are 3 properties of the phonological loop

A

Phonological Loop

  • Hold memory traces for few seconds before they fade (7 +- 2)
  • Articulatory rehearsal process, like subvocal speech
  • Limited capacity because articulation occurs in real time
    • (as items increases, point reached when first item faded before latest item is rehearsed)
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96
Q

What are the 4 evidences to support existence of a phonological loop

A
  1. Phonological similarity effect
  2. Word-length effect
  3. Irrelevant sound effect
  4. Lesion
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97
Q

What is the task typically used in phonological loop and outcome factors

A
  • Digit span task
    • Examine how much load size
  • Backwards digit span
    • Central executive manipulation
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98
Q

What is the phonological similarity effect. Contrast this with LTM

A

Accurate recall:

  • Similarity of sound is more important than meaning of sound
    • vs LTM, where Meaning > Similarity
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99
Q

What is the word-length effect

A
  • Span declines as word length increases from one to five syllabus
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100
Q

What is the irrelevant sound effect. What is the crucial requirement

A
  • Impaired recall due to concurrent or subsequent presentation of irrelevant spoken material
    • Includes speech, music

Crucial requirement:

  • Fluctuation in state of irrelevant stimulus stream
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101
Q

What is lesion data evidence to support phonological loop

A

Patients with verbal deficit and broca area lesions in absense of an articulation deficit show:

  • No phonological similarity effect
  • No word length effect
  • Appear to avoid articulation
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102
Q

What are properties of the visuo-spatial sketchpad.

What is the typical task?

What does the visuos-spatial sketchpad account for?

A

Task: Corsi blocks

  • Limited capacity (4 +- 1 objects)
  • Capaciy to hold and manipulate visuospatial representations
  • Accounts for change blindness
  • No distinction between vision and spatial (How do we imagine vision without a space?)
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103
Q

Verbal and Spatial WM architecture

A

Shared hemispheric and neuroanatomical archiecture for both verbal and spatial WM.

No hemispheric specialisation

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104
Q

What are properties of the central executive. What is the task?

A

Concept of the Homonculus:

  • Divide, switch, focus attention
  • Connects working memory and LTM
    • Required for WM tasks that require manipulation of information held in storage

Tasks

  • Orientation Span Task
  • Backward digit span
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105
Q

Explain the orientation span task. Why is it used?

A

Orientation Span Task

  • Reads the equation aloud as soon as it appears
  • Indicate whether provided answer was correct and read the word at the end aloud
    • Do an operation (phonological/visuo-spatial)
  • Write down the five words in correct order
    • OSPAN score = Sum of recalled words for sets recalled in perfect order

Why?

  • Requires manipulation of information and storage in working memory
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106
Q

When do neurons fire in a WM task?

A

Cells in PFC specifically fired in the delay period of a delayed response test

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107
Q

Spatially selective DLPFC neurons in non-human primates show what pattern of activity

A

Persistent and location specific activity for a particular location in visual space during the delay period of a WM task

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108
Q

Persistent activity of PFC neurons in delayed period:

When does it persist (2 Things)

What happens if it does not?

A

When does PFC persist?

  • Persist during delay period
  • Persist during time epoch when representative is active
    • Activity dissipates when representation is no longer needed
  • If activity does not persist through retention interval, memory performance is compromised
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109
Q

Persistent activity of PFC neurons in delayed period:

Two more properties (2 things)

A

Properties:

  • Magnitude of persistent activity commensurate or correlated with memory load
  • Selective
    • Spatially selective (Specific visual space)
    • Subsequently identified PFC neurons selective for cues, delay, response
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110
Q

Does persistent activity represent maintainance of past stimulus?

What has it shown to represent?

And what does it suggest?

A

Persistent PFC activity for

  • Visual stimuli in absense of WM demands
    • Maintainance
  • Anticipation of future stimulus
  • Representing or Maintaining abstract information
    • e.g. rules, associations, told to maintain

(a) Maintainance; (b) Manipuation; (c) Selection

Not represent

  • Maintenance of physical stimulus presentation

Delay is Process of maintainance, not stimulus itself

111
Q

Describe the Sternberg. What did the Sternberg Task results reveal?

A

Sternberg

  • Hold some items before a delay
  • Ask which items come before the item flashed

Results

  • As number of items or WM load increases
    • Accuracy decrease
    • Reaction time increase
    • PFC activity increase
      • But we don’t know whether it’s maintainance, selection, or manipulation
112
Q

How have people tried to tease apart maintainance, selection, or manipulation? What are the results

A

Sternberg

  • Number of items is the case, but the structure is different

Results

  • Structural items had more PFC activity than unstructured items
  • Mean Span (Structured > Unstructured)
    • Suggest configuration is represented by PFC
113
Q

EEG studies/Oscillations of working memory

A
  • Theta (4-7Hz)
    • Organisation of sequentially ordered WM items
  • Alpha (8-13Hz)
    • Active inhibition of task-irrelevant information
  • Gamma (30-200Hz)
    • WM Maintenance

TAG

114
Q

What is the task combining WM and EF. What are the results (And implications)

A

Task requiring maintance of WM load while performing congruent or incongruent responses (EF Task).

Results

  • Longer RT for high WM load
  • PFC activity greater for high WM load
  • Greater processing in face-processing areas in high WM load
    • Greater distraction and obligatory processing of irrelevant information (Faces)
    • WM influence can be examined in level of FFA activity (Quantify)
115
Q

Response inhibition with a WM load in drug-dependent and depressed patients.

Why?

A
  • Inhibitory control affected by simultaneous working memory load of a craving
    • Cocaine
    • Depression/Anxiety
    • Eating Disorders
      • Thoughts are subvocally produced and rehearsed, loading on phonological loop capacity (Verbal memory load)
116
Q

When there is chocolate craving, what is impaired

A

Significant impairment in visuospatial WM

117
Q

When there is cigarette craving, what is impaired

A
  • Significant impiarment in verbal WM that worsened with longer periods of abstinence
  • Phonological loop
118
Q

As WM demands increases, what predicted better performance and differentiated groups among cocaine users?

A

Response inhibition with WM load

  • As WM load increases, inhibition performance usually worse
  • Increasing DLPFC activity predicted better performance and differentiated groups as WM demands increases
119
Q

What are other correlations of WM (other than EF)

A

Developmental type-ish

  • General fluid intelligence (gF)
  • Reading comprehension
  • Language
  • Non-verbal problems solving
120
Q

Is WM related to EF. Why? Which one (WM/EF) do clinical patients show deficits in?

A

WM and EF are highly related (Predictive one another)

Why?

  • WM is critical to goal-maintenance required for top-down EF control
  • Clinical patients often show impairments in both domains
121
Q

Why is low WM correlated with poor developmental type skills

A

Children with poor WM have failure to cope with simultaneous processing and storage demands (dual task, mental task)

122
Q

fMRI research has demonstrated a relationship between working memory and intelligence, which can be best described as

A
  • Efficiency with which DLPFC activity supports WM predicts IQ; or
  • “Efficiency with which DLPFC activity supported WM mediated the relationship between gF and WM”
123
Q

According to early behavioural research, does training WM improve performance?

A

Training WM significantly improved performance on standard WM tasks (those that have been trained), with some generalisations to other domains

124
Q

What are the 2 principles relating WM and training

A

Training WM Task:

1.) Increase WM Capacity

(physiological change)

or

  1. ) Increase efficiency of using WM capacity
    (via. strategy use such as chunking)
125
Q

Principle 1: Increase WM capacity. What should happen

  • 2 Outcomes
A
  1. ) Induce brain signatures observed in high-capacity individuals
  2. ) Benefits and pattern changes observed independent of specific task
126
Q

What is the task to train WM

A

N-Back Task

Remember each item and respond to each item that occurs 2 words before

127
Q

N-back task training results and caveat?

A

Results

  • Increases in PFC activity after training
  • Regions where brain activity correlated with increased WM capacity

However, they did not examine if:

  • PFC increase are associated with post-training increase in WM capacity
128
Q

What was argued as to how training increases WM? What might influence this benefit?

A

Increases efficiency (not capacity)

  • Induces plasticity in intraparietal-PFC network
    • Improves the control of attention
  • Individual difference in dopamine may influence training benefits
    • By influencing both WM performance and plasticity effects
129
Q

Does WM Training improve IQ

A
  • N-Back training shown to increase gF scores by about 4 Points
    • More training = More IQ
130
Q

What are some specific suggestions as to how WM training improves IQ? What do strategies include

A

WM-training increases strategy use. Strategies includes

  • Greater use of chunking
  • Automatisation of basic processes
    • Shorter times on the distractor task
    • More time for refreshing the memoranda
    • More time for removing interfering distractor representations from WM
131
Q

3 Criticisms of WM and Training Benefits

A
  • Cost-Benefit Analysis
    • Financial+Time Cost > Benefits
  • Genersaibility
    • No evidence of generalisation to other skills/tasks
  • Sustainability
    • Weak/mixed evidence after cessation of training
132
Q

WM training on ADHD children in a randomized-controlled trial.

Results.

What does it suggest.

A

Good:

  • Raters: Lower symptoms
  • Parental and Teacher rating: Increase in EF performance
  • WM Performance: Increase (Specific)

No Change

  • Independent Raters: No change
  • Lab Test: No Change
  • Academic performance: No change

Suggest strong placebo effect by parents

133
Q

Study: Neuroracer Descriptives and Results

A

N = 47, 67 years old

  • Both behavioural and neural support
  • Increases WM performance, supported by EEG
    • Midline theta power and theta coherence improved
  • Only WM performance, no evidence of far transfer
134
Q

Criticism of Neuroracer’s publications.

A
  • Most comparision are not significant but not reported
    • Far transfer did not occur
  • Multiple comparision not corrected
  • Competing financial interest (founder of company)
    • Publication Bias
  • Excluded many participants in screening
135
Q

Academic outcomes of WM Training in children

A

No outcomes.

In fact, Math scores were worse

136
Q

Does Far Transfer of WM Training occur?

Why/Why not?

And what is the implication?

A

No.

  • Placebo (Most far transfers observed is due to this)
    • Premorbid cognitive ability predicts engagement in cognitively demanding actvities
  • Skill acquisition rely on domain-specific information (e.g. chunking). Neural patterns observed in these people reflect change in domain-specific abilities

Implication

  • Neural plasticity and skill acquisition are related but domain-specific
  • Most effective way to acquire a new skill is to train that particular skill
137
Q

What is Papez Circuit and what is the problem

A

Circuit Theory of Emotions

  • More descriptive than functional
138
Q

What is ‘Psychic Blindness’ and what did the study show?

A

Animal Evidence

  • Damage to MTL
  • “Psychic Blindness” in monkeys
    • Lack of fear or tendency to approach objects normally eliciting a fear response
139
Q

Evidence of Amygdala Emotions: SM

A

SM

  • Lack of fear
  • Unable to facial decode emotions
  • Inappropriate social behavior
140
Q

How does amygdala damage block fear? What are the parts of the amygdala?

A

Function of Amygdala

  • Does not block exhibition of fear
    • e.g., startle
  • Block the ability to acquire and express conditioned response to neutral stimulus

Lateral nucleus

  • Convergence area for information from multiple brain regions
  • Allows formation of associations underlying fear conditions

Central nucleus

  • Initiate an emotional response if a a stimulus, after being analysed, is determined to represent threatening or dangerous
141
Q

How does information about an aversive stimulus reach the amygdala?

A

Low Road

  • Subcortical pathway in which sensory information about a stimulus is projected to the thalamus
  • Sends a crude signal to the amygdala
  • Indicating whether the visual stimulus roughly resembles an aversive (or conditioned) stimulus

High Road

  • Slower pathway
  • Provides more thorough processing to confirm the initial low road information
142
Q

Evidence for implict learning of fear

A

Implicit

Learning is expressed indirectly, through a behavioural or physiological response

  • Patients with amgydala damage fail to show an indirect fear response (e.g., +BP)
    • No implicit fear response via. physiological changes
  • Can report parameters of fear conditioning and essentially what is supposed to happen.
143
Q

Amygdala is critical to implicit fear learning, but is it explicit? How so?

A

Plays a role in emotional responses to stimuli whose emotional properties are learned explicitly

  • Amygdala activity enhance strength of explicit memories for emotional events by modulating storage of these events
    • Modulate arousal to emotional events, which in turn, modulate memory enhancement
  • Amygdala amygdala during emotional stimuli presentation correlated with arousal-enhanced recollection
144
Q

How does amygdala label a stimulus? What is it important to?

A

The amygdala doesn’t appear important to consciously label a stimulus as good, bad, arousing or neutral, but does appear to be important for normal responses to social stimuli, in particular facial expressions

145
Q

Amygdala and emotional faces? Which emotion is stronger? And what conditions does it enhance the response?

A
  • Anydala activity greatest for fearful expressions, in comparison to all other expressions
  • Even when stimuli is subliminal, there is a greater response, but is further enhanced when attention is directed to the face
    • Suggests amygdala is important for responses to social stimuli
146
Q

Why do we use faces as stimuli

A

Good control

  • can manipulate expression only
147
Q

What is a common problem with neruoimaging evidence like fMRi in facial emotion

A

Problems with fMRI in emotions

  • Imaging requires repetitive presentation of the same stimulus type in order to identify a reliable signal average
  • Repeated presentations of emotive stimuli produce habituation, with smaller self-report and physical responses to the stimulus over time
148
Q

Can we “train’ attentional bias such that fear is processed less, or Cognitive bias modificiation

A

Cognitive bias modificiation

  • Experimenetally, yes
    • Possibility of publiciation bias
    • Low quality trials
  • No significant clinically relevant effects.
149
Q

Other associations of brain and emotions

A

Angry

Orbitofrontal Cortex

  • Increases with attention

Disgust

Insula

  • Also involved in other emotions
150
Q

Role of Insula in emotions

A

Suggested to be involved in all subjective feelings

  • Represents current and predictive states allowing for learning of feeling states and uncertainity
  • Awareness/Introspection of afferent representations of the feelings from the body
    • Not just own body, but to represent emotional states of others
151
Q

What are the 3 types of frontotemporal dementia (FTD)

A

A progressive neurodegenerative brain disorder

  1. ) Semantic
  2. ) Progressisve Nonfluent
  3. ) Behavioural Variant
152
Q

Behaviour Variant Frontotemporal Dementia: Symptoms (BFTD)

A

“Handbrakes taken off”

  • Disinhibition
    • Socially impusive, dgaf
  • Apathy
  • Lack empathy
  • Perservative
  • Dietary Change/Hyperorality
  • EF Dysfunction
    • Lack of insight
153
Q

Diagnosis of possible, probable and definite BFTD

A

Possible: 3 or more symptoms

Probable: 3 or more symptoms + progression + MRI change

Definite: 3 or more symptoms + pathology

154
Q

Pathology of FTD: Brain and Genes

A

Brain

  • Grossly atrophied orbitofrontal and medial regions
    • Occasional temporal and basal ganglia
    • (opposite from AD, which originals from MTL to frontal)
  • Approximately 50% have tau protein

Genes

  • Some familial links (C9), but many FTD don’t have this type genes
155
Q

Which emotions recognition do FTD patients show deficits in. What are some circumstances which these patterns show

A
  • Negative emotions
    • Deficit
  • Happiness
    • Intact
  • Surprise
    • Equal
  • Not due to differences in task difficulty or modality (Visual, sound)
156
Q

What emotional reactivity like changes in physiological responses (blood pressure, etc) do FTD patients show deficits in

A

Basic stimuli (e.g. loud noise): impaired

Complex stimuli: variable

157
Q

Neuroimaging FTD

Facial, Emotional Evaluation and Socal Evaluation and how is amydala related?

A

Poor Facial Recognition

  • Amygdala damage correlated with negative facial expression

Poor Emotional Evaluation

  • Video vignettes
    • Poor recognition of negative emotions
    • Intact recognition of positive emotions

Poor Social Evaluation

  • Video vignettes
  • Poor recognition in sarcasm
    • Correlated with Amygdala damage more strongly than any other region, but still significant effects in other regions
158
Q

Neuroimaging FTD: Insight. Brain Parts implicated.

A

bvFRD has the poorest insight across domains compared to all other groups

Quality of insight (Judge reactions of others)

  • OFC and Frontopolar Grey Matter

Emotional insight (Recognising change in own emotions)

  • Frontopolar, Amygdala, and Hippocampal Grey Matter
159
Q

FTD vs Other disorders

A

FTDs are consistently worse on emotion recognition tasks, as well as worse on insight tasks

160
Q

What is the caveat with studies on FTD

A
  • Small samples of clinical studies
    • Prevented analysis of relationship between emotion processing problems and day-to-day functioning
    • Kipps et al. 2009 did not find a relationship between emotion recognition and activities of daily living (n = 28), despite deficits on both
161
Q

Amygdala: Function of lateral nucleus vs central nucleus

A

Lateral: Conveyance area, form associations underlying conditioning

Central: Initiate emotional response

162
Q

What emotions do FTDbv group show impairment with

A

Negative emotions (anger, disgust, fear)

163
Q

FTD: Summary of brain areas and implications

A

Amygdala: Negaitve Emotional, Social, Emotional Insight

OFC: Quality of Insight

164
Q

What is the treatment rates with depression. What defines treatment-resistant

A
  • 40% remission with first treatment
  • 10% treatment resistant (at least 4 medication failures), also predicts relapse after ECT
165
Q

Why is treatment depression difficult

A
  • Depression defined in DSM as behaviour, not pathology
  • Few animal models
166
Q

What are structural regions associated with depression, and key region discussed in this lecture

A

Cortical

  • Frontal

Subcortical

  • Caudate
  • Hippocampus
  • Cingulate
167
Q

What is the problem with structural imaging and its association with depression

A

Cause and effect unclear.

  • Possible that depression > less exercise > affects hippocampus (synaptic plasticity)
  • Cohen’s d show hippocampus most severe
168
Q

Across studies, when depression occurs in a clinical group, it is associated with?

A
  • Decreased activity in PFC
  • Increased activity in rostral anterior cingulate
    • Subcollosal cingulate gyrus, Brodmann Area 25
169
Q

What is the converging evidences on the role of Subcollosal Cingulate

A

Decrease sCg activity

  • Active Drug Floxetine
  • Successful Treatment

increased sCg activity

  • Inducing depressed mood
  • Treatment resistant patients

Treatment resistance results from sCg connectivity problems

170
Q

Is everyone with depression applicable to undergo DBS?

A

Only treatment-resistant group

171
Q

What are the results with open-label DBS treatment. What should one be concerned about.

A
  • Successful (66% and 50%)
    • 6 Patients and 20 Patients
  • No changes in neuropsych testing
    • Surprising

Should be concerned about placebo effect

172
Q

How fast do people respond to DBS treatment and what can we predict?

What kind of effects do people undergone DBS treatment claim to experience?

A

By 1mo, can predict responders from non-responders.

Introspective and Extrospective Awareness

173
Q

What is intention-to-treat. What is its utility

A

Include all participants, preserving randomization

  • Still has placebo effects
174
Q

What is the results in open-label intention-to-treat

A

Shows consistent positive treatment outcomes

175
Q

What are problems with open-label studies of DBS. There are 5.

A
  • Bias
    • Lack of blinding and randomization
  • Placebo
    • Lack of control
  • Ambiguous duplication
    • Competing interests
  • Small sample size
  • Heterogeneous outcome measures
176
Q

What are the results for DBS for treatment-resistant unipolar and bipolar depression

A

Good

177
Q

What are results form randomized-control DBS studies

A

BROADEN trial.

No dramatic change, where control group had even lower depression than active treatment group.

178
Q

What is the duration of randomized-control DBS studies

A

Active vs sham double blind

16 weeks, followed by open-label continuation phase. However, cessation after 16 weeks due to ineffectiveness.

179
Q

What are the problems with systematic controlled studies

A
  • Suboptimal patient selection
  • Inconsistent targetting of DBS sites
  • Insufficient current delivery
180
Q

What the task examining voluntary attention? What are other names of voluntary attention

A

Posner Cueing Task

  • Meaures Endogenous/Covert attention
    • covert = not moving eyes
181
Q

What is endogenous attention and why does posner cueing task examine this

A

Orientation of attention to the cue is

  • Driven by goals (internally)
  • Not due to environment/physical features
182
Q

What is unilateral spatial neglect

A
  • Symptom of patients behaving as though parts of objects, and or the world around them do not exist
  • They are largely unaware of this deficit
  • Show extinction (unlike heminaopia)
183
Q

What brain damage is associated with unilateral spatial neglect

A
  • Stroke
  • Brain injury to right parietal and frontal cortex
184
Q

Do patients with stroke always have unilateral spatial neglect. Why?

A
  • People with stroke largely loses this neglect.
  • Stroke = Pressure
    • So after stroke dissipates, pressure goes back to normal, neglect dissipates
185
Q

How do we examine unilateral spatial neglect.

At what spatial scales are these neglects

A

Line cancellation test

  • Neglect may arise at different spatal scales within the same patient
    • ​e.g. may ignore left page in book/left sided words
186
Q

What is extinction?

A

Failure to perceive a stimuli contralateral to leision when presented simultaenously with stimuli ipsilateral to lesion.

187
Q

How do we draw a distinction between spatial neglect and visual feild deficits?

A

Extinction

  • Spatial Neglect:
    • Will still repsond to unilateral presentation
  • Visual Field Deficits
    • Visual Field Damage
    • Will not respond to unilateral presentation.
188
Q

There are many studies showing different associations between neglect and brain regions. Why are there large variability?

A
  • Different methods (e.g., CT, fMRI, DTI)
  • How participants are selected, how long since stroke, what test used to measure neglect
  • Location of stroke (Naturalistic lesions)
    • Some patients die after stroke, can’t locate…
189
Q

What are the brain regions associated with neglect after confluence of imaging studies

A
  • Posterior parietal lobe
  • Temporoparietal junction (including STS)

PPL and TPJ (+STS)

190
Q

What are the results of primate studies on neglect?

A
  • Posterior pareital (by itself) does not cause neglect,
    • Both posterior paretal cortex, TPJ (includes STS) together causes it
  • Neglects are often temporary, not permanent
191
Q

In a lot of structural work, what do studies often miss out

A

They often ignored where white matter damager occur, that might have disconnected frontal, temporal and parietal cortices

  • Might be a disconnection syndrome
192
Q

Other than TPJ, STS, and Posterior Parietal Lobe, wich other region has been found to cause neglect? What is the caveat

A

Damage to subcortical nuclei (caudate, putamen).

  • Thought this might be due to disconnection: cortical hypoactivation to regions important for neglect like TPJ
193
Q

Is neglect more common after left/right hemisphere damage

A

Right hemisphere damage is more common

(far less common in left-handed participants)

194
Q

What are the models suggesting why neglect is more prominent after right-hemispheric damage?

A
  1. Representational Model
  2. Attentional Bias Model
195
Q

Elaborate on the representation model of unilateral spatial neglect

A
  • Right hemisphere represents right and left
  • Left hemisphere tepresents right only
  • Damage to left no neglect because right can maintain
196
Q

Elaborate on the attentional bias model of unilateral spatial neglect

A
  • Left and right have natural bias towards contralateral attention
  • Bias is assymmetrical with left hemisphere being more strongly biased towards right hemispace
    • that’s why we sit on the left
197
Q

Saliency in Neglect Patients. What does it suggest

A

Saliency of objects in neglected / contralesional field is impaired

  • Exogenous and endogenous (goal-driven) components of selective spatal attention are equally impaired
  • Abnormally high salience of ipsilesional stiuli can prevent them from being filtered when task-irrelevant but they are a minority of examples
198
Q

Saliency in dark room. Results and Implications?

A

Results

  • Patients in dark room without stimuli show spatial lateralised bias (Bias to look to the right/ ipsilesional hemispace/’good side’)
    • Eye movements reflect hemispatial bias. Gaze deviations are observed at rest

Implications

  • Not a reduced salience of contralesional spatial deficits alone
  • Also an imbalance in mechanism controlling in
    • (a) controlling gaze; and
    • (b) relevant to attention
199
Q

Is spatial lateralised bias related to early/late visual process

A

Bias does not reflect early visual mechanism

200
Q

There are 4 findings that supports inact early visual mechanism in neglect patients, which are

A
  1. Intact image segmentation of low-level visual features in the neglected visual field
    • e.g. figure ground illusions in neglected side
  2. Normal contrast sensitivity
  3. Occipital cortex responds to visual stimuli in the contralesional hemispace, even under extinction presentation
  4. Contralesional visual stimuli prime faster response times for subsequent stimuli
    • Unconscious processing
201
Q

What is the thrid model of unilateral spatial neglect

A

(Hence why frontal and temporal regions contribute to neglect syndrome)

Deficits is not spatial in nature. 3 non-spatial deficits to account for neglect:

  • Re-orienting of attentnion
  • Detection of heaviourally relevant stimuli
  • Difficult maintain arousal and vigilance
202
Q

Evidence for deficits not being spatial in unilateral spatial neglect

1.) Re-orienting of attention

A

In posner cueing task, even though invalid cues slowed reaction times (All patients)

  • Interaction effect where RTs significantly greater when invalid cue directed attention to ipsilesional hemsiphere (‘good’ side)
  • An example of not being able to shift attention from the ‘good’ side to the ‘neglect’ side
203
Q

Evidence for deficits not being spatial in unilateral spatial neglect:

2.) Detection of behaviourally relevant stimuli

A

1.) Other modalities

  • Show deficits in target detection in simple paradigms (auditory)
  • May reflect deficit in arousal and processing capacity

2.) Attentional Blink (not hemispheric)

  • RH stroke showed significant longer attentional blink than controls
  • RH stroke + neglect worsens the blink (See picture)
204
Q

Evidence for deficits not being spatial in unilateral spatial neglect: Arousal and sustained attention

A

RH and neglect patients deficits in

(a) Arousal
* Reduced GSR to electrical stimulation
(b) Sustained attention
* Elevator counting test / GNG / SST

Cognitive task but giving an arousal boost (non-lateralised thing) before that reduces the neglect (assumed to be lateralised)

205
Q

Neglect in left-handed patients is more common/less common

A

Less common

206
Q

Monkey lesion studies have indicated that the region most likely to cause neglect-like symptoms is ____

A

Temporal-parietal junction / TPJ

207
Q

The finding that neglect patients show deficits in non-spatial measures of attention has been argued to support what hypothesis?

A

The right hemisphere dominance of neglect reflects the laterality of mechanisms supporting reorienting, detection and arousal

208
Q

The Rees et al. (2000) study of neglect patients identified significant occipital cortex activity associated with the presentation of visual stimuli in the neglected hemifield, which demonstrated?

A

Neglect is not caused by abnormal visual processing at early stages of visual processing

209
Q

Localising the cortical mechanisms underlying neglect has been difficult because:

A

Neglect patients, especially those with enduring symptoms, typically have white matter damage which causes disconnection between cortical loci

210
Q

An extinction test helps to discriminate unilateral spatial neglect from hemianopia because?

A

Damage in the visual pathway will cause the patient to be non-responsive to all unilateral visual stimuli presentation

211
Q

Which type of visual deficit is most consistent with unilateral spatial neglect?

A

Fail to perceive a visual stimulus in the hemifield opposite (contralesionsal) to their brain lesion, when presented simultaneously with a stimulus in the ipsilesionsal hemifield

212
Q

Define selective attention. What kinds are there?

A

Cognitive processes that enable organisms to process relevant inputs, thoughts or actions while ignoring irrelevant or distracting ones

  1. ) Voluntary (Endogenous): Top-down / Goal-directed
  2. ) Reflextive (Exogenous): Bottom-up / Reflexive
213
Q

What is TBI

A

Traumatic Brain Injury

Brain damage by external mechanical force

214
Q

Given that attention is limited capacity, what must the system decide

A

Decide:

  • What is selected for extended processing
  • What gains access to awareness
215
Q

What are bottlenecks and what are the 2 theories

A

Bottleneck: Filtering of input that permit high priority information to gain access

  • Early
    • Stimuli need not completely perceptually analysed before selection for further processing or rejected as irrelevant
  • Late
    • Both attended and ignored inputs are processed equivalently and bottleneck occurs at higher level prior to awareness/further processing
216
Q

What are the results of posner cueing task in relation to cue period length. Explain.

A
  • RTinvalid > RTneutral > RTvalid
  • Benefit increases with cue period length
    • Because of internal shift in covert attention (‘mental spotlight’) to cued visual field
217
Q

What is the P1 ERP? What does it occur and not occur for?

A
  • 70-90ms after visual stimulus onset in occipital lobe
  • Larger when same stimuli appear at same location (Valid) compared to attention focused elsewhere (Invalid)
    • Does not occur for other features such as colour, spatial frequency, orientation, or properties
218
Q

What are fMRI findings in relation to posner cueing task

A

Stronger sensory processing of visual stimli when either covert or overt attention is applied to it (stronger when attended)

219
Q

What is the length of reflexive attention. What other properties you get with reflexive attention? Why?

A

Short lived (<300ms)

  • Inhibition of Return
    • Reflexively attended location become inhibitied over time, slowing responses in those areas
  • Necessary for coping with our dynamic environment, otherwise we’ll be constantly distracted during complex tasks…
220
Q

What are the pathways of voluntary and reflexive attention

A

Voluntary: Top-Down

  • Dorsal Pathway
    • Intraparietal cortex and superior frontal cortex

Reflexive: Bottom-Up

  • Ventral Pathway, lateralised to right hemisphere.
    • Temporoparietal cortex and inferior frontal cortex
  • Detecting behaviourally relevant or salient stimuli
  • Acts as cirucit breaker for Dorsal
221
Q

What is Balint’s syndrome. When does it occur?

A

Baliant’s Syndrome

  • Severe disturbance of visual attention and awareness
  • Perceive only one or a small subset of available ojects are perceived at any time
  • Typically occurs after stroke/CVA
222
Q

What are symptoms of balient syndrome

A
  • Simultagonsia
    • Deficit perceiving visual field as a whole
  • Ocular Aprexia
    • Deficit in eye movement to scan visual field
  • Optic atoxia
    • Deficit in visually guided hand movements
  • Bilateral occipitotemporal lesion:
    • Deficit in perceiving multiple objects in space
223
Q

Define Vigilance

A

Sustained Attention/Vigilance:

State of readiness to respond to rare, unpredictive stimumli

224
Q

Vigilance vs Selective Attention

A

Vigilance:

  • Neuroanatomically sepaarate
  • Basic attentional function that determines the efficacy of selective attention
225
Q

What is a property of sustained attained task

A

Has to be long.

Generally need to engage participants for 30 mins plus before seeing any decreament, even TBI patients

226
Q

What is the network for Vigilance/Sustained Attention. What is the evidence to support it? What NT is it sensitive to?

A

Right fronto-parietal network (IMPORTANT)

Reticular Activating System

  • Basal forebrain projects to prefrontal/parietal regions to facliatate top-down regulation of vigilance
    • Sensitivty to noradrenergic release

Evidence

  • Increased activty of right frontal and parietal regions in vigilance task
227
Q

What group of people is associated with vigilance deficits. Why?

A
  • TBI (Traumatic Brain Injury)
    • TBI affects frontal lobes and white matter
      • Affects sustained attention
    • Diffuse axonal injury disrupt reticular activating system
  • ADHD
228
Q

What is the first task used to examine vigilance and what is the problem

A
  • PASAT or CPT
    • Confounded with other cognitive domains such as processing speed
    • Vulnerable to rapid automatisation where limited attention still allow task performance
229
Q

What are more modern tasks to examine vigiliance. What do they examine

A

Standard SART and Fixed Sequence SART

  • Requiring inhibition of ongoing behaviour in context of a rare target
  • Test both IC and Vigilance
    • Distinction rest on whether vigilance is generated endogenously rather than exogenously
      • If IC poor, standard performance will be poor but fixed sequence will be ok
      • If TBI/vigilance poor, both will be poor
        • Inability to maintain a sufficient level of vigilance
        • Error rates at 25% or above despite sequence being entirely predictable
230
Q

What are some neurological and physiological features SART failures associated with physiologically and neurologically in TBI patients?

A

In TBI patients, SART failures are associated with…

  • Decreasd right frontal parietal
  • SCR
  • Alpha Band
231
Q

What are some neurological and behavioural SART failures associated with physiologically and neurologically in ADHD?

A

ADHD

  • Increase response variability
    • Rapid fluctuation in attention levels from trial-to-trial
  • Decreased right fronto-parietal
232
Q

What improves vigilance attention and what are other neurological associated outcomes in the task.

A

Methylphenidate

  • Improved SART
  • Increased right fronto-parietal activity
  • Decreased variabiltiy in response times
233
Q

MPH in TBI patients. What improves, and why?

A

Sustained attention, but also other cognitive domains

  • Sustained attention thought to be the ‘gate’ for other domains.
234
Q

Define Habit Performance

A

Habit Performance

  • Exhibition of learned behaviour
  • Insensitive to change in reward outcomes
235
Q

In humans (and animals), what are common features of habit learning.

What is an important distincton for humans?

A
  • Common features
    • Repeated responding which will form context-response associations in memory
    • Automatic habit performance is insensitive to value of outcome
  • In Humans
    • We engage in much more repetition (40% daily)
236
Q

When do habits typically arise and how? What is the difference between repetitious behaviour and habits

A
  • Habits typically arise due to an interface with goal-related behavior
    • Goals direct human action by providing a definition of a desired outcome

Repetition vs Habits

  • Repetitious Behaviour
    • Does not persist when value of repeated behaviour is absent
  • Habitual Behaviour
    • Persist when value of repeated behaviour is absent
237
Q

Are all habits automatic? Are all automatic responses habits? Give some examples

A
  • All habits are automatic
  • Not all automatic responses are habits
    • Priming
    • Classical conditioning
    • Non-assoicative learning
    • Reflexes
238
Q

When do implementation intentions or automated goals work?

A

Implmenentation intention (automated goals) will only influence behaviour if they are consistent with someone’s intention

239
Q

Is Habit automaticity is specific to a particular response or behavior? List down some cues.

A

Yes it is. Cues can be:

  • Physical environment
  • Other people
  • Preceding actions in a sequence
    • e.g. cigarette when at a bar or with alcohol
240
Q

Define habit response in context of representation

A
  • A habitual response is the cueing of mental representation that contains
    • Both the features of your response
    • And the features of perceptual information that cued the response
  • Vice versa, when habits are formed, perception of relevant context cue automatically activates mental representation of habitual response
241
Q

What are outcome-specific devaluation tasks and what did it show

A

What

  • Outcome-specific devaluation tasks
    • Associate cue and outcome
    • Devalue outcome by pairing it with something else

Results

  • Showed that it was associated with individual differences in self-control
    • Impusive (Low self-control) driven by stronger habitual cues
      • Devaluation effect was reduced in participants who scored high in motor impulsivity

Implication

  • Suggest that an interaction existed between habitual behaviour and indidvidual differences
242
Q

What is the consequence of choosing habitual, unwanted choices repeatedly

A

Repeated behaviour over time becomes more habitual and less goal dependent

243
Q

What is dual process models in habits. What do “Habits” exist?

A
  • Habit strength will interact with behavioural intentions
    • As habit strength increases, behvaioural intentions is less predictive of behaviour
    • As habit strength decreases, behvaioural intentions is more predictive of behaviour
  • Habits exist to allow greater efficiency by being a default setting, unless we are particularly motivated and able to engage in more deliberate and specific goal pursuit.
244
Q

How do habits develop (What kind of learning)

A
  • Instrumental learning
    • Reward response will be repeated
  • Everyday life is built upon repetition that provides multiple opportunities for habit formation
    • 40% of responses were performed daily, in the same context (but we are unaware)
245
Q

What are Pavlonian Context Cues (What did it show)? Give an example

A
  • Cues that are associated with reward that follows action
    • Motivational values of cues are unrelated to values of outcomes
    • Change likelihood of cues being expressed
  • Changes relationship between stimulus and reward
  • Shows that habitual responding continues to be influenced by motivational processess
  • Example: Interval schedules
246
Q

Interval schedules. Why does it allow automatisation?

A
  • Habits more likely to be formed when rewards are provided on an interval schedule
  • Forms assocation between context and response, without having to represent goal outcomes
    • Repeated response to stimulus results in repetition and automisation, with occasional and unpredictable rewards ensuring that the behavior doesn’t extinguish
      • e.g. cue + response = no goal (until repeated 10 times then goal)
247
Q

Does repetitiion always lead to habits? Why?

A

No.

  • Deliberate decision making will prevent/slow formation of habits
248
Q

In humans, is there a relationship between repetition and greater expression of habits? What does it imply?

A

Unlike animals, there is no relationship between repetition and expression of habits in humans.

Duration of stimulus-response training in reward-devluation paradigm was not associated with habit expression

Implication

  • In OCD and Drug-dependents, might be an interaction between
    • Propensity for habit learning (From training)
    • Impairment in goal-directed control
      • Poor impulse = Greater tendency to express
  • Suggest self-control mediates habit formation, unlike animals.
249
Q

What is the brain areas associated with habits

A
  • Basil Ganglia
  • Associative cortico-basal ganglia loops support goal-directed and habitual behaviour.
    • Dorsomedial straitum: Goal-Directed Control
      • Prefrontal cortex links
      • Caudate nucleus and Anterior putamen
    • Dorsolateral straitum: Acquiring new habits
      • Sensorimotor loop links
      • Medial and posterior putamen
      • More relevant to habits

(Proposensity for acquiring new habits + impaired goal directed control) (Imbalance in 2 systems?)

250
Q

Habits vs Goals. What are some situational factors affecting habits vs goal pursuit. When does habit trumpt goals?

A
  • Situation factors
    • (Poor) Self control
    • (Lack of) Task ability
    • Time pressure
    • Distraction
      • Acute and chronic stress, which have bidirectional relationship with these factors, increasing reliance on habits
  • Habits > Goal
    • If individuals lack motivation for deliberate decision making
251
Q

Are people aware of their habits? What often happens

A
  • Aware of habitual response
  • Unaware of cueing mechanisms
    • Tendency to infer behaviour was guided by goals, instead of preceding it
252
Q

What are challenges of habit change

A

Beahvioural changing techniques: Effective for sporadic (occasional) behaviours not habits

  • Responses do not reflect a person’s desire
  • Habitual behaviour activated automatically by environmental cues
253
Q

What aspects do behaviour change in practice focus on

A
  1. Impeded automatic cueing of old habits
  2. Encourage repeated use of new behaviours till habitual
254
Q

Behaviour Change 1: Impede unwanted habits. What are some techniques

A
  • Invoked thinking
    • Conscious deliberate thoughts and monitoring failures
  • Inhibitory plans
    • Specific inhibitory plans to cues linked to habits
  • Exposure Management / Habit dscontinutity
    • Reduce environmental cue
    • Life transitions
255
Q

Behaviour Change 2: Encourage desired habit. What is the problem and why is it limited?

A
  • Techniques have not built upon concepts of habit formation (Repetition, Stable Context, Reward Schedules)

Limited because:

  • Repetition can be extensive
  • Reminders can reduce automaticity
    • Disrupt automaticity
    • Encourage more deliberate thinking instead.
256
Q

Define Anxiety and how it is different from fear

A

Share many common physiological features

  • Anxiety
    • Sustained state of fear
    • Experienced in absense of direct physical threat and persist over longer period of time (6 months)
  • Fear
    • Fear response elicited by specific stimuli and short-lived
    • Fear response decreases when threat is removed
257
Q

What are some DSM diagnostics of GAD

A
  • Sustained
    • 6 Months
  • Physiological Responses
    • Restlessness
    • Fatigure
    • Sleep Disturbances
    • Muscle tension
258
Q

How is conditioned fear diminshed. When can we classify “Treatment Success”.

A

Graded Desensitization Training

  • Based on exctinction principles
    • Replace anxiety or fear response with relaxation response through classical conditioning
  • Gradually associate, through repeated pairings, a fear-arousing stimulus with a state of relaxation, in a series of graded steps.
    • Treatment success is defined when phobia is not hindering daily life
259
Q

Can fear disappear after successful training? What are the 3 effect to describe this?

What is it interpreted as…?

A

Fear can return AFTER successful extinction training

  • Time
    • Spontaneous recovery
  • Context
    • Renewal effect
  • Stress
    • Reinstatement effect

During extinction, “Fear memory” is interpreted as

  • Not deleted/erased; but
  • Inhibited
260
Q

Define “active coping”. What does “active coping” involve?

A

Definition

Actions that result in positive emotional outcomes and as a result, avoid negative consequence of fear

Involves:

  • Awareness of stressor
  • Attempt to reduce negative outcome
261
Q

What is reconsolidation?

How does it diminish conditioned fear expressions?

A

Alteration of original CS-US association stored in lateral amygdala

Consolidation

  • Actively seek to disrupt formation of memory

Post-Consolidation

  • Modify/inhibit (not eliminate) memory by actively retrieving
    • Reconsolidation period​: Act of retrieval makes the underlying memory trace fragile again, which provides another opportunity to disrupt memory, potentially allowing to block the memory completely
262
Q

What did animal studies demonstrate in regard to consolidation

A
  • Blocking reconsolidation period with protein synthesis inhibitors
    • Specifically blocked reactivation of fear memories
    • While leaving other memories intact
  • Fear memories did not return with time, context, or stress
263
Q

What did human studies demonstrate in regard to consolidation

A
  • No safe drug (protein synthesis inhibitors) to block human reconsolidation
  • Propanalol was the first drug used for experimental reconsolidation blocker
    • Unclear mechanisms
    • Most studies failed to show clear beneficial effecs in human studies
264
Q

What is suggested to be underlying Anxiety Disorder. And what are the brain parts implicated?

What else does anxiety impair?

A

Dysregulation of neurocircuitry of conditioned fear

  • Heightened amygdala activation
  • PFC control of amygdala disrupted

What else

  • Anxiety also impairs extinction learning and retention, as well as the regulation of emotional responses via cognitive strategies
    • e.g. anxious patients exhibit reduced PFC during or before fear extinction, and require heightened PFC to successfully reduce negative emotion with cognitive reappraisal
265
Q

What are the two key cognitive information processing bias, charactersitics of people with anxiety.

A
  1. Bias to threat-related information
  2. Bias to negative interpretation of ambiguous stimului
266
Q

1: Bias to threat-related information

A

Selective Attention Task:

  • Hyperactive Amygdala
  • Reduced PF control over amygdala response
    • Remember, training was clinically non-significant
267
Q

2: Bias to negative interpretation of ambiguous stimuli (what are some stimulis)

A

Stimulus: Not specific

  • Faces
  • Face-Voice Pairings
  • Verbal Homophones
    • Dye/Die
  • When evaluating future life events, anxiety overestimate the likelihood of negative outcomes
268
Q

What are the nerual mechanisms underlying cognitive biases of anxiety

A
  • Amygdala hyperactivity while attending and evaluating negative stimuli
    • Heightened cognitive and affective responses to potential threats
  • Prefrontally mediated cognitive and affective regulation processes also appear to be impaired in anxiety, reducing the ability to modulate these pre-existing tendencies

(Both Amygdala and PFC)

269
Q

What is uncertainity and how does it relate to anxiety. What is the study

A

​Uncertainity

  • Elicits greater anxiety
  • People with anxiety show threat-related information processing bias, altering their decision-making

Task: Risk (Dohnmen, 2011)

  • Anxiety correlated with greater risk aversion/avoidance for themselves.
    • When evaluation of a response includes increase in physiological response (BP, HR), anxious pariticpants are even more risk averse
  • When anxious participants made choice for another, they are less risk averse
270
Q

In Dohmen’s risk study, he examined gender, height, age, and parental academic achivement. What is the association with risk?

A

Gender

  • Women less risky

Height

  • Taller more risky

Age

  • Older less risky

Parental Academic Achivement

  • Having a mother, and lesser extent father, with academic achivement more risky
271
Q

What is ambiguity and how does it relate to anxiety?

A

Ambiguity

  • Ambiguity elicits greater anxiety
  • People with anxiety will show greater avoidance of ambiguous decisions
    • Overestimate probabiity of negative outcomes and their subjective cost
      • Car vs Train (Will choose car, even though car is more risky)
      • Visible and Opaque Urn
272
Q

What are the neural systems involved in decision making biases (In relation to anxiety)

A
  • Insula cortex
    • Detect own physiological response arousal
    • Insula:
      • Increased loss aversion (Physiological arousal heightened = Scared)
      • Leision impaired risk decision performance on tasks such as the Balloon Analogue Response Task
  • Prefrontal cortex (Dorsolateral and Ventromedial)
    • TMS stimulation will also stimulate this pattern of risky decision making
273
Q

What is framing effect and what does it relate to? How does anxiety fit into it?

A

Framing

  • Anxiety associated with greater framing effects because they are driven by loss aversion
    • e.g. Keep 20/50 or lose 30/50

Loss Aversion

  • Degree to which avoiding losses is priortised to achieving equivalent gains
  • Anxious associated with increased loss aversion
    • Increased sensitivty to loss
    • Avoid responses where there is a greater risk
    • Increasing risk taking behaviour

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