W10 - Emotions Flashcards

1
Q

What is Papez Circuit and what is the problem

A

Circuit Theory of Emotions

  • More descriptive than functional
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2
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
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3
Q

Evidence of Amygdala Emotions: SM

A

SM

  • Lack of fear
  • Unable to facial decode emotions
  • Inappropriate social behavior
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4
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
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5
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
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6
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.
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7
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
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8
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

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9
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
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10
Q

Why do we use faces as stimuli

A

Good control

  • can manipulate expression only
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11
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
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12
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.
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13
Q

Other associations of brain and emotions

A

Angry

Orbitofrontal Cortex

  • Increases with attention

Disgust

Insula

  • Also involved in other emotions
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14
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
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15
Q

What are the 3 types of frontotemporal dementia (FTD)

A

A progressive neurodegenerative brain disorder

  1. ) Semantic
  2. ) Progressisve Nonfluent
  3. ) Behavioural Variant
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16
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
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17
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

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18
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
19
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)
20
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

21
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
22
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
23
Q

FTD vs Other disorders

A

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

24
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
25
Q

Amygdala: Function of lateral nucleus vs central nucleus

A

Lateral: Conveyance area, form associations underlying conditioning

Central: Initiate emotional response

26
Q

What emotions do FTDbv group show impairment with

A

Negative emotions (anger, disgust, fear)

27
Q

FTD: Summary of brain areas and implications

A

Amygdala: Negaitve Emotional, Social, Emotional Insight

OFC: Quality of Insight

28
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
29
Q

Why is treatment depression difficult

A
  • Depression defined in DSM as behaviour, not pathology
  • Few animal models
30
Q

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

A

Cortical

  • Frontal

Subcortical

  • Caudate
  • Hippocampus
  • Cingulate
31
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
32
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
33
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

34
Q

Is everyone with depression applicable to undergo DBS?

A

Only treatment-resistant group

35
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

36
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

37
Q

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

A

Include all participants, preserving randomization

  • Still has placebo effects
38
Q

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

A

Shows consistent positive treatment outcomes

39
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
40
Q

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

A

Good

41
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.

42
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.

43
Q

What are the problems with systematic controlled studies

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