1
Q
What is cognitive control
A
Conscious internal goal take precedence over automatic processes
2
Q
Three behaviors demonstrating top-down cognitive control
A
- Inhibitory Control
- Impulse Control
- Selective Attention
3
Q
What is the neural network needed for cognitive control based on initial studies. What study did they use.
A
Stroop Task:
- ) Anterior Cingulate Cortex (ACC)
- ) Dorsolateral Prefrontal Cortex (DLPFC)
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
- Detects response conflict present in an incongruent word
- DLPFC
- Implement top-down control over performance
- e.g. biasing visual system
- Implement top-down control over performance
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
- Could test whether:
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)
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
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
9
Q
Inhibitory Control: What did fMRI find
A
Successful response inhibition involved:
- ) Right IFG
- ) Right parietal
- ) Dorsal ACC
(Note: fMRI only allows correlation)
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
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
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
13
Q
Disadvantage of leision studies
A
Inability to specify discrete neuroanatomical regions
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.
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
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
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
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
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
20
Q
What is attentional bias predictive of in drug-users
A
Predicts treatment outcomes and success (cocaine users and alcohol users)
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
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
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
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
25
What are the neurobiology behind MA users.
What are the 4 things it predict?
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
26
Can we improve control in diseases?
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*
27
What are recent trials demonstrating neuroenhancers improving treatment outcomes
Dexaamphetamnie
28
What is ADHD and Drug Addiction characterised by neurobiologically?
Low tonic levels of dopamine
29
What is the role of dopemine in response inhibition
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
30
What disease is a good example of the complex relationship between dopemine and cognitive control
_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
31
What does showing drug-related stimuli do to drug users
* Activate limbic regions associated with use of the drug
* Strength of cravings reflected in cue-related limbic activity
32
What does drug-related cue activation in limbic and frontal regions predict?
Magnitude of drug-related cue-induced activation of limbic and medial prefrontal regions predicts subsequent relapse
33
What cognitive deficits do MA users show
* Poor verbal memory
* Slowed Processing speed
* Executive function
* Disinhibition
* Selective attention
* Decision making
* Cognitive flexibility
34
What is the magnitude of cognitive deficits are MA users compared to cocaine users, marijuana users, AD
Significant magnitude across domains (Learning, EF, Memory)
* Higher than cocaine and marijuana
* Slightly lower/Comparable to Alzheimer.
35
Does behaviour (frequency, duration and quantity) of MA use predict level of cognitive impairment?
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)
36
D2 Levels. Which has been linked to vulnerability to addictions or protetive factors?
* Lower D2 = Vulnerable to addictions.
* High D2 = Protective factor in siblings of drug dependent individuals
37
What is the Inverted U-shaped curved in dopemine (Volkow). Compare low D2 and high D2
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
38
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?
_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
39
What is 'supersensitivtiy' in Taq1A
‘Supersensitivity’:
After abstinence, Taq1A experience more powerful euphoria upon taking their previously addicted substance, making them vulnerable to relapse
40
What is the underlying principle of human learning. Elaborate.
_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'
41
What does prediction error system aim to maximize. What else influences the system?
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
42
Dopemine and Games: What is it sensitive to
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
43
People who self-report high impulse has been associated with..? What does amphetamine help with and what hypothesis was it consistent with?
_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
44
How do we operatinalise impulsitivity
Baratt Impulsitivity Scale
45
What does selective attention require
Selectively attending to stimuli in the presence of incongruent or salient stimuli requires top-down control
46
High sensation seekers have been associated with...
* Low reward sensitivity
* (Need high sensations to bump up)
* Poor inhibitory control
47
Does the limbic system pattern of activation found in alcholic extend to children?
Yes in drug-naive children of alcoholics
* More sensitive to reward
* Less sensitive to punishment
48
How do we operationalise impulsiveness for reward
* Delay discounting task
* Immediate reward vs Large delayed reward
49
How do we operationalise decision making
Gambling Task - Good decks vs bad decks
50
Gambling task in drug users individuals
Drug abusers showed impaired performance (bad decisions)
* Cocaine users show poorer decision making
* Less DLPFC and ACC activity
* Greater Orbitofrontal activity
51
What is a cool way of treating substance use disorders
Contingency management.
Provide tangible, positive, reinforcement for objective evidence of behaviour change.
52
What is the neuro and bio behind ADHD and drug addiction
Combination of
* High drive for reward
* Low ability to control reward impulse
* Low sensitivty to punishment
* Modulated by Dopamine (Low levels)
53
What is the key role of dopamine
Key: Reward Sensitvity
* Vulnerability to drugs
* Novelty-seeking
54
What is performance monitoring
Identification and correct differences between an intended and executed response
55
Neuropsychological symptoms of performance monitoring deficits
* The difference between knowing and doing
* Perseverative behaviour
* i.e. no learning
* Lack of insight
* i.e. denial
56
What do many clinical group show neurologically in performance monitoring?
_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.
57
What is the exception group which shows hyperactive ERN
OCD and OCD students
Heightened error-related ACC and ERN response
58
What is the ERN and what does it correlate with?
* 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
59
What is the "Rabbitt effect" and who shows it
"Rabbitt Effect"
Cautious, or slowing, of response times immediately following an error
* SZ Patients, or any group with hypoactive ACC/ERN
60
What is the two-factor theory of delusion. What does it explain
Explains monoethetic delusions.
* Factor 1
* Depends on where brain has damaged cortex
* Factor 2
* Each share a **common dysfunction** in belief evaluation
61
What is the one-factor theory of delusion
* Dynamic relationship between top-down and perception.
* Impaired **prediction error** system to update beliefs.
62
What are the 3 hypotheses on what ERN represents?
* Emotional impact of an error #1
* Response conflict #2
* Two competing responses
* Reward less than expected #3
* Relative outcome
63
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
Competition between two competing responses, which are typically congruent and incongruent to the task requirements
64
What is the evidence that ERN represent conflict monitoring (#2)
What is the caveat?
#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"
65
What is the neurobiology behind ERN and the proposed role of ACC based on #2
**#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)
66
What is the underlying principle underlying human behaviour and how does it relate to prediction errors?
_Prediction error_
* Greater magnitude of prediction error
* Greater dopamine cell activity
* Likely behaviour will be 'successful'
67
The reward prediction model of error:
How does ERN represent outcome relative to expectation (#3)
_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
68
How does ACC lesion relate to prediction error based on animal studies?
What does it suggest?
_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
69
Do PD Patients learn better from Reward or Punishment (Experiment)
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]
70
Taq1A and learning patterns: Rewards vs punishment
* Low D2 receptors (Taq1A) learn better from reward
* But ‘Typical’ pattern (Normal D2) learn better from negative feedback/punishment
71
How does ACC represent perceived and unperceived errors? Evidence from antisaccade task.
ERN represents both perceived and unperceived errors similarly (Unconscious detection)
72
What is Error Awareness Task
Simiar to stroop task
Incongruent: Repeat words or correct colour words, leading to many unperceived errors
73
What did the Error Awareness Task reveal?
* 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)
74
What brain areas in drug-abusers/others are associated with poor awareness (independent of task perforamance)
_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
75
In cocaine-dependent users, what is the hypoactive ERN associated with and what did it predict?
_Hypoactive ERN_
* Associated with reduced insight into effects of drug use
* Predicted likelihood of relapse and extent of cocaine use following relapse
76
What does insula do?
* Involved in all subjective feelings
* Awareness/ _Interoception_, of *afferent representations* of the feelings from the body
77
Why do drug addicts not seek help
It is partly due to lower awareness = don't realize need for help
78
What happened to smokers when the insula is damaged. Why
Likely to quit.
Insula critical to awareness of cravings \> lost cravings
79
How does the insula and ACC work together
* Insula
* Limbic sensory
* Site of awareness on basis of *afferent representations*
* ACC
* Motor cortices
* *Initiation* of behaviour.
80
Why does Methylphenidate influence the magnitude of the error-related negativity?
Methylphenidate influences _prefrontal_ dopamine release
81
Can we use drugs to enhance ERN (specifically ERN only). What is the underpinning physiological changes
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)
82
Neural mechanisms of learning
Strengthening of synapses.
Learning must be associative (emotions, motor planning)
83
How to maintain durable and flexible encoding
1. ) Meaningful encoding upon broader framework
2. ) Retrieval Practice
84
What is the relationship between sensitivty to reward and dopamine
* Less D2 = Increased sensitivty to reward
* Less D2 = Decreased senstiivty to punishment
85
What is the monetary incentive GNG task
Adding a punishment factor into GNG task
86
Results of monetary GNG task in drug-abusers vs control (Include Brain Parts)
_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
87
Why was paired-associative learning task developed?
Examine confound: Do gambllers perform badly because of failed learning or risk-taking?
88
Paired-associative learning in cannabis users - Behavioural and neural results
* Reduced ability to correct
* Reduced ACC and hippocampus
* ACC trasmit value to hippocampus to learn
89
What is the outcome measure of paired-association learning task
Number of repeated errors
(Number repeats down the sequence. See whether they learn)
90
What were the results of the associative learning task - Brain Parts implicated
_Mistake Learning/Corrected_
ACC and hippocampus (learning)
ACC trasmit value to hippocampus to learn
91
What were the results of the associative learning task when punishment is involved - Neurological results
(What is the implication)
* 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.
92
What is ACC related to in learning outcomes
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
93
ACC and Insula: Summary
_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**
94
What are the main components in the original cognitive model (Baddeley and Hitch, 1974)
**_STM_**
1. ) Phonological Loop
2. ) Visuospatial Sketchpad
3. ) Central Executive
95
What are 3 properties of the phonological loop
_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)
96
What are the 4 evidences to support existence of a phonological loop
1. Phonological similarity effect
2. Word-length effect
3. Irrelevant sound effect
4. Lesion
97
What is the task typically used in phonological loop and outcome factors
* Digit span task
* Examine how much load size
* Backwards digit span
* Central executive manipulation
98
What is the phonological similarity effect. Contrast this with LTM
Accurate recall:
* Similarity of sound is more important than meaning of sound
* vs LTM, where Meaning \> Similarity
99
What is the word-length effect
* Span declines as word length increases from one to five syllabus
100
What is the irrelevant sound effect. What is the crucial requirement
* Impaired recall due to concurrent or subsequent presentation of irrelevant spoken material
* Includes speech, music
_Crucial requirement_:
* Fluctuation in state of irrelevant stimulus stream
101
What is lesion data evidence to support phonological loop
_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
102
What are properties of the visuo-spatial sketchpad.
What is the typical task?
What does the visuos-spatial sketchpad account for?
_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?)
103
Verbal and Spatial WM architecture
Shared hemispheric and neuroanatomical archiecture for both verbal and spatial WM.
No hemispheric specialisation
104
What are properties of the central executive. What is the task?
_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
105
Explain the orientation span task. Why is it used?
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
106
When do neurons fire in a WM task?
Cells in **PFC** specifically fired in the delay period of a delayed response test
107
Spatially selective DLPFC neurons in non-human primates show what pattern of activity
*_Persistent_* and *_location specific_* activity for a _particular_ location in visual space during the _delay period_ of a WM task
108
Persistent activity of PFC neurons in delayed period:
When does it persist (2 Things)
What happens if it does not?
_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
109
Persistent activity of PFC neurons in delayed period:
Two more properties (2 things)
_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
110
Does persistent activity represent maintainance of past stimulus?
What has it shown to represent?
And what does it suggest?
_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
Describe the Sternberg. What did the Sternberg Task results reveal?
_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
How have people tried to tease apart maintainance, selection, or manipulation? What are the results
_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
EEG studies/Oscillations of working memory
* 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
What is the task combining WM and EF. What are the results (And implications)
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
Response inhibition with a WM load in drug-dependent and depressed patients.
Why?
* 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
When there is chocolate craving, what is impaired
Significant impairment in **visuospatial** WM
117
When there is cigarette craving, what is impaired
* Significant impiarment in **verbal WM** that **worsened with longer periods of abstinence**
* Phonological loop
118
As WM demands increases, what predicted better performance and differentiated groups among cocaine users?
_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
What are other correlations of WM (other than EF)
_Developmental type-ish_
* General fluid intelligence (gF)
* Reading comprehension
* Language
* Non-verbal problems solving
120
Is WM related to EF. Why? Which one (WM/EF) do clinical patients show deficits in?
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
Why is low WM correlated with poor developmental type skills
Children with poor WM have failure to cope with simultaneous processing and storage demands (dual task, mental task)
122
fMRI research has demonstrated a relationship between working memory and intelligence, which can be best described as
* 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
According to early behavioural research, does training WM improve performance?
Training WM significantly improved performance on standard WM tasks (those that have been trained), with some generalisations to other domains
124
What are the 2 principles relating WM and training
Training WM Task:
1.) Increase WM _Capacity_
(physiological change)
or
2. ) Increase _efficiency_ of using WM capacity
(via. strategy use such as chunking)
125
Principle 1: Increase WM capacity. What should happen
- 2 Outcomes
1. ) Induce brain signatures observed in high-capacity individuals
2. ) Benefits and pattern changes observed _independent_ of specific task
126
What is the task to train WM
_N-Back Task_
Remember each item and respond to each item that occurs 2 words before
127
N-back task training results and caveat?
_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
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What was argued as to how training increases WM? What might influence this benefit?
_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
Does WM Training improve IQ
* N-Back training shown to increase *gF scores* by about 4 Points
* More training = More IQ
130
What are some specific suggestions as to how WM training improves IQ? What do strategies include
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
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3 Criticisms of WM and Training Benefits
* Cost-Benefit Analysis
* Financial+Time Cost \> Benefits
* Genersaibility
* No evidence of generalisation to other skills/tasks
* Sustainability
* Weak/mixed evidence after cessation of training
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WM training on ADHD children in a randomized-controlled trial.
Results.
What does it suggest.
_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
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Study: Neuroracer Descriptives and Results
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
Criticism of Neuroracer's publications.
* 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
Academic outcomes of WM Training in children
No outcomes.
In fact, Math scores were worse
136
Does Far Transfer of WM Training occur?
Why/Why not?
And what is the implication?
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
What is Papez Circuit and what is the problem
_Circuit Theory of Emotions_
* More descriptive than functional
138
What is 'Psychic Blindness' and what did the study show?
_Animal Evidence_
* Damage to MTL
* "Psychic Blindness" in monkeys
* Lack of fear or tendency to approach objects normally eliciting a fear response
139
Evidence of Amygdala Emotions: SM
_SM_
* Lack of fear
* Unable to facial decode emotions
* Inappropriate social behavior
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How does amygdala damage block fear? What are the parts of the amygdala?
_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
How does information about an aversive stimulus reach the amygdala?
_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
Evidence for implict learning of fear
_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
Amygdala is critical to implicit fear learning, but is it explicit? How so?
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
How does amygdala label a stimulus? What is it important to?
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
Amygdala and emotional faces? Which emotion is stronger? And what conditions does it enhance the response?
* 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
Why do we use faces as stimuli
Good control
* can manipulate expression only
147
What is a common problem with neruoimaging evidence like fMRi in facial emotion
_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
Can we "train' attentional bias such that fear is processed less, or Cognitive bias modificiation
Cognitive bias modificiation
* Experimenetally, yes
* Possibility of publiciation bias
* Low quality trials
* No significant clinically relevant effects.
149
Other associations of brain and emotions
_Angry_
**Orbitofrontal Cortex**
* Increases with attention
_Disgust_
**Insula**
* Also involved in other emotions
150
Role of Insula in emotions
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
What are the 3 types of frontotemporal dementia (FTD)
A progressive neurodegenerative brain disorder
1. ) Semantic
2. ) Progressisve Nonfluent
3. ) Behavioural Variant
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Behaviour Variant Frontotemporal Dementia: Symptoms (BFTD)
"Handbrakes taken off"
* Disinhibition
* Socially impusive, dgaf
* Apathy
* Lack empathy
* Perservative
* Dietary Change/**Hyper**orality
* EF Dysfunction
* Lack of insight
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Diagnosis of possible, probable and definite BFTD
Possible: 3 or more symptoms
Probable: 3 or more symptoms + progression + MRI change
Definite: 3 or more symptoms + pathology
154
Pathology of FTD: Brain and Genes
_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
Which emotions recognition do FTD patients show deficits in. What are some circumstances which these patterns show
* Negative emotions
* **Deficit**
* Happiness
* **Intact**
* Surprise
* **Equal**
* Not due to differences in **task difficulty** or **modality** (Visual, sound)
156
What emotional reactivity like changes in physiological responses (blood pressure, etc) do FTD patients show deficits in
Basic stimuli (e.g. loud noise): **impaired**
Complex stimuli: **variable**
157
Neuroimaging FTD
Facial, Emotional Evaluation and Socal Evaluation and how is amydala related?
_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
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Neuroimaging FTD: Insight. Brain Parts implicated.
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
FTD vs Other disorders
FTDs are consistently worse on emotion recognition tasks, as well as worse on insight tasks
160
What is the caveat with studies on FTD
* 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
Amygdala: Function of lateral nucleus vs central nucleus
Lateral: Conveyance area, form associations underlying conditioning
Central: Initiate emotional response
162
What emotions do FTDbv group show impairment with
Negative emotions (anger, disgust, fear)
163
FTD: Summary of brain areas and implications
Amygdala: Negaitve Emotional, Social, Emotional Insight
OFC: Quality of Insight
164
What is the treatment rates with depression. What defines treatment-resistant
* 40% remission with first treatment
* 10% treatment resistant (at least 4 medication failures), also predicts relapse after ECT
165
Why is treatment depression difficult
* Depression defined in DSM as behaviour, not pathology
* Few animal models
166
What are _structural_ regions associated with depression, and key region discussed in this lecture
Cortical
* Frontal
Subcortical
* Caudate
* Hippocampus
* Cingulate
167
What is the problem with structural imaging and its association with depression
Cause and effect unclear.
* Possible that depression \> less exercise \> affects hippocampus (synaptic plasticity)
* Cohen's d show hippocampus most severe
168
Across studies, when depression occurs in a clinical group, it is associated with?
* Decreased activity in PFC
* Increased activity in rostral anterior cingulate
* Subcollosal cingulate gyrus, Brodmann Area 25
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What is the converging evidences on the role of Subcollosal Cingulate
_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
Is everyone with depression applicable to undergo DBS?
Only treatment-resistant group
171
What are the results with open-label DBS treatment. What should one be concerned about.
* Successful (66% and 50%)
* 6 Patients and 20 Patients
* No changes in neuropsych testing
* Surprising
Should be concerned about *placebo* effect
172
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?
By 1mo, can predict responders from non-responders.
Introspective and Extrospective Awareness
173
What is intention-to-treat. What is its utility
Include all participants, preserving randomization
* Still has placebo effects
174
What is the results in open-label intention-to-treat
Shows consistent positive treatment outcomes
175
What are problems with open-label studies of DBS. There are 5.
* Bias
* Lack of blinding and randomization
* Placebo
* Lack of control
* Ambiguous duplication
* Competing interests
* Small sample size
* Heterogeneous outcome measures
176
What are the results for DBS for treatment-resistant unipolar and bipolar depression
Good
177
What are results form randomized-control DBS studies
BROADEN trial.
No dramatic change, where control group had even lower depression than active treatment group.
178
What is the duration of randomized-control DBS studies
Active vs sham double blind
16 weeks, followed by open-label continuation phase. However, cessation after 16 weeks due to ineffectiveness.
179
What are the problems with systematic controlled studies
* Suboptimal patient selection
* Inconsistent targetting of DBS sites
* Insufficient current delivery
180
What the task examining voluntary attention? What are other names of voluntary attention
Posner Cueing Task
* Meaures Endogenous/Covert attention
* covert = not moving eyes
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What is endogenous attention and why does posner cueing task examine this
Orientation of attention to the cue is
* Driven by goals (internally)
* Not due to environment/physical features
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What is unilateral spatial neglect
* 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
What brain damage is associated with unilateral spatial neglect
* Stroke
* Brain injury to right parietal and frontal cortex
184
Do patients with stroke always have unilateral spatial neglect. Why?
* People with stroke largely loses this neglect.
* Stroke = Pressure
* So after stroke dissipates, pressure goes back to normal, neglect dissipates
185
How do we examine unilateral spatial neglect.
At what spatial scales are these neglects
_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
What is extinction?
Failure to perceive a stimuli contralateral to leision when presented simultaenously with stimuli ipsilateral to lesion.
187
How do we draw a distinction between spatial neglect and visual feild deficits?
_Extinction_
* Spatial Neglect:
* Will still repsond to unilateral presentation
* Visual Field Deficits
* Visual Field Damage
* Will not respond to unilateral presentation.
188
There are many studies showing different associations between neglect and brain regions. Why are there large variability?
* 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
What are the brain regions associated with neglect after confluence of imaging studies
* Posterior parietal lobe
* Temporoparietal junction (including STS)
PPL and TPJ (+STS)
190
What are the results of primate studies on neglect?
* 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
In a lot of structural work, what do studies often miss out
They often ignored where white matter damager occur, that might have disconnected frontal, temporal and parietal cortices
* Might be a disconnection syndrome
192
Other than TPJ, STS, and Posterior Parietal Lobe, wich other region has been found to cause neglect? What is the caveat
Damage to subcortical nuclei (caudate, putamen).
* Thought this might be due to disconnection: cortical hypoactivation to regions important for neglect like TPJ
193
Is neglect more common after left/right hemisphere damage
Right hemisphere damage is more common
(far less common in left-handed participants)
194
What are the models suggesting why neglect is more prominent after right-hemispheric damage?
1. Representational Model
2. Attentional Bias Model
195
Elaborate on the representation model of unilateral spatial neglect
* Right hemisphere represents right and left
* Left hemisphere tepresents right only
* Damage to left no neglect because right can maintain
196
Elaborate on the attentional bias model of unilateral spatial neglect
* 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
Saliency in Neglect Patients. What does it suggest
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
Saliency in dark room. Results and Implications?
_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
Is spatial lateralised bias related to early/late visual process
Bias does not reflect early visual mechanism
200
There are 4 findings that supports inact early visual mechanism in neglect patients, which are
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
What is the thrid model of unilateral spatial neglect
(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
Evidence for deficits not being spatial in unilateral spatial neglect
1.) Re-orienting of attention
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
Evidence for deficits not being spatial in unilateral spatial neglect:
2.) Detection of behaviourally relevant stimuli
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
Evidence for deficits not being spatial in unilateral spatial neglect: Arousal and sustained attention
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
Neglect in left-handed patients is more common/less common
Less common
206
Monkey lesion studies have indicated that the region most likely to cause neglect-like symptoms is \_\_\_\_
Temporal-parietal junction / TPJ
207
The finding that neglect patients show deficits in non-spatial measures of attention has been argued to support what hypothesis?
The right hemisphere dominance of neglect reflects the laterality of mechanisms supporting reorienting, detection and arousal
208
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?
Neglect is not caused by abnormal visual processing at early stages of visual processing
209
Localising the cortical mechanisms underlying neglect has been difficult because:
Neglect patients, especially those with enduring symptoms, typically have white matter damage which causes disconnection between cortical loci
210
An extinction test helps to discriminate unilateral spatial neglect from hemianopia because?
Damage in the visual pathway will cause the patient to be non-responsive to all unilateral visual stimuli presentation
211
Which type of visual deficit is most consistent with unilateral spatial neglect?
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
Define selective attention. What kinds are there?
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
What is TBI
_Traumatic Brain Injury_
Brain damage by _external_ mechanical force
214
Given that attention is limited capacity, what must the system decide
Decide:
* What is selected for extended processing
* What gains access to awareness
215
What are bottlenecks and what are the 2 theories
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
What are the results of posner cueing task in relation to cue period length. Explain.
* RTinvalid \> RTneutral \> RTvalid
* Benefit increases with cue period length
* Because of internal shift in covert attention ('mental spotlight') to cued visual field
217
What is the P1 ERP? What does it occur and not occur for?
* 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
What are fMRI findings in relation to posner cueing task
Stronger sensory processing of visual stimli when either covert or overt attention is applied to it (stronger when attended)
219
What is the length of reflexive attention. What other properties you get with reflexive attention? Why?
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
What are the pathways of voluntary and reflexive attention
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
What is Balint's syndrome. When does it occur?
_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
What are symptoms of balient syndrome
* 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
Define Vigilance
Sustained Attention/Vigilance:
State of readiness to respond to rare, unpredictive stimumli
224
Vigilance vs Selective Attention
_Vigilance:_
* Neuroanatomically sepaarate
* Basic attentional function that determines the efficacy of selective attention
225
What is a property of sustained attained task
Has to be long.
Generally need to engage participants for 30 mins plus before seeing any decreament, even TBI patients
226
What is the network for Vigilance/Sustained Attention. What is the evidence to support it? What NT is it sensitive to?
_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
What group of people is associated with vigilance deficits. Why?
* TBI (Traumatic Brain Injury)
* TBI affects frontal lobes and white matter
* Affects sustained attention
* Diffuse axonal injury disrupt reticular activating system
* ADHD
228
What is the first task used to examine vigilance and what is the problem
* PASAT or CPT
* Confounded with other cognitive domains such as processing speed
* Vulnerable to rapid automatisation where limited attention still allow task performance
229
What are more modern tasks to examine vigiliance. What do they examine
_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
What are some neurological and physiological features SART failures associated with physiologically and neurologically in TBI patients?
In TBI patients, SART failures are associated with...
* Decreasd right frontal parietal
* SCR
* Alpha Band
231
What are some neurological and behavioural SART failures associated with physiologically and neurologically in ADHD?
ADHD
* Increase response variability
* Rapid fluctuation in attention levels from trial-to-trial
* Decreased right fronto-parietal
232
What improves vigilance attention and what are other neurological associated outcomes in the task.
Methylphenidate
* Improved SART
* Increased right fronto-parietal activity
* Decreased variabiltiy in response times
233
MPH in TBI patients. What improves, and why?
Sustained attention, but also other cognitive domains
* Sustained attention thought to be the 'gate' for other domains.
234
Define Habit Performance
_Habit Performance_
* Exhibition of learned behaviour
* **Insensitive** to change in **reward outcomes**
235
In humans (and animals), what are common features of habit learning.
What is an important distincton for humans?
* _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
When do habits typically arise and how? What is the difference between repetitious behaviour and habits
* 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
Are all habits automatic? Are all automatic responses habits? Give some examples
* All habits are automatic
* Not all automatic responses are habits
* Priming
* Classical conditioning
* Non-assoicative learning
* Reflexes
238
When do implementation intentions or automated goals work?
Implmenentation intention (automated goals) will only influence behaviour if they are consistent with someone's intention
239
Is Habit automaticity is specific to a particular response or behavior? List down some cues.
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
Define habit response in context of representation
* 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
What are outcome-specific devaluation tasks and what did it show
_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
What is the consequence of choosing habitual, unwanted choices repeatedly
Repeated behaviour over time becomes more habitual and less goal dependent
243
What is dual process models in habits. What do "Habits" exist?
* 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
How do habits develop (What kind of learning)
* 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
What are Pavlonian Context Cues (What did it show)? Give an example
* 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
Interval schedules. Why does it allow automatisation?
* 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
Does repetitiion always lead to habits? Why?
No.
* Deliberate decision making will prevent/slow formation of habits
248
In humans, is there a relationship between repetition and greater **expression** of habits? What does it imply?
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
What is the brain areas associated with habits
* 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
Habits vs Goals. What are some situational factors affecting habits vs goal pursuit. When does habit trumpt goals?
* 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
Are people aware of their habits? What often happens
* Aware of habitual response
* Unaware of cueing mechanisms
* Tendency to infer behaviour was guided by goals, instead of preceding it
252
What are challenges of habit change
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
What aspects do behaviour change in practice focus on
1. Impeded automatic cueing of old habits
2. Encourage repeated use of new behaviours till habitual
254
Behaviour Change 1: Impede unwanted habits. What are some techniques
* 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
Behaviour Change 2: Encourage desired habit. What is the problem and why is it limited?
* 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
Define Anxiety and how it is different from fear
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
What are some DSM diagnostics of GAD
* Sustained
* 6 Months
* Physiological Responses
* Restlessness
* Fatigure
* Sleep Disturbances
* Muscle tension
258
How is conditioned fear diminshed. When can we classify "Treatment Success".
_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
Can fear disappear after successful training? What are the 3 effect to describe this?
What is it interpreted as...?
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
Define "active coping". What does "active coping" involve?
_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
What is reconsolidation?
How does it diminish conditioned fear expressions?
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
What did animal studies demonstrate in regard to consolidation
* 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
What did human studies demonstrate in regard to consolidation
* 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
What is suggested to be underlying Anxiety Disorder. And what are the brain parts implicated?
What else does anxiety impair?
_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
What are the two key cognitive information processing bias, charactersitics of people with anxiety.
1. Bias to threat-related information
2. Bias to negative interpretation of ambiguous stimului
266
#1: Bias to threat-related information
Selective Attention Task:
* Hyperactive Amygdala
* Reduced PF control over amygdala response
* Remember, training was clinically non-significant
267
#2: Bias to negative interpretation of ambiguous stimuli (what are some stimulis)
_Stimulus_: Not specific
* Faces
* Face-Voice Pairings
* Verbal Homophones
* Dye/Die
* When evaluating future life events, anxiety overestimate the likelihood of negative outcomes
268
What are the nerual mechanisms underlying cognitive biases of anxiety
* **Amygdala hyper**activity 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
What is uncertainity and how does it relate to anxiety. What is the study
_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
In Dohmen's risk study, he examined gender, height, age, and parental academic achivement. What is the association with risk?
_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
What is ambiguity and how does it relate to anxiety?
_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
What are the neural systems involved in decision making biases (In relation to anxiety)
* 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
What is framing effect and what does it relate to? How does anxiety fit into it?
_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
NoM
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