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PSYC30018 - Neuroscience > W10 - Emotions > Flashcards

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

First evidence of Amygdala and Emotions

A

Animal Evidence: MTL > Lack of fear response

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3
Q

Evidence of Amygdala Emotions: SM

A

SM: No fear; unable to facial decode emotions; inappropriate social behavior

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4
Q

How does amygdala block fear

A

Does not block exhibition of fear (startle), blocks fear conditioning & learning (CR + neutral)

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5
Q

Pathways and brief description of amygdala

A

Low road: Sensory > Thalamus > Amygdala > Is it adversive?

High road: More thorough, confirms initial low road.

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6
Q

Is fear learning implicit/unconscious? What evidence do I have to claim this

A

Implicit/Unconscious

  • Expressed via. behavioural/physiological response (e.g., SCR).
  • Can report parameters of fear conditioning and what is supposed to happen
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7
Q

Fear Learning in faces. fMRI Evidence for implicitness. When is amygdala response stronger?

A

There is evidence to faces with “fear” expression even subconsciously.

But it is stronger with attention

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8
Q

Amygdala and explicit fear learning

A

By modulating storage of emotional events, Amygdala enhance strength of explicit memories. [Indirect: arousal to emotional events > modulate memory]

Amygdala activity in emotional stimuli correlated with arousal-enhanced recollection

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9
Q

Why do we use faces as stimuli

A

Good control (can manipulate expression only)

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10
Q

What is the problem with neruoimaging evidence like fMRi in facial emotion

A

Slow hemodynamic Changes. Repeated presentation of emotional stimuli = Habituation

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11
Q

Can we “train’ attentional bias such that fear is processed less

A

Experimenetally, yes. But there is no-significant clinically relevant effects.

Possibility of publiciation bias

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12
Q

Other associations of brain and emotions

A 
Angry = Orbitofrontal (increases with attention)
Disgust = Insula (also involved in other emotions)
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13
Q

Role of Insula in emotions

A

Suggested to be involved in all subjective feelings: Introspection and afferent representations.

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14
Q

What are the 3 types of frontotemporal dementia (FTD)

A
  1. ) Semantic
  2. ) Progressisve Nonfluent
  3. ) Behavioural Variant
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15
Q

Behaviour Variant Frontotemporal Dementia: Symptomps (BFTD)

A

1) Disinhibition
2) Apathy
3) Lack empaty
4) Perservative
5) Dietary Change
6) EF Dysfunction

“Handbrakes taken off”

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16
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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17
Q

Pathology of FTD: Genetic Markers

A

Gene: C9ORF72 (affects 7-12%). That means many FTD has no gene

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18
Q

Pathology of FTD: Brain

A

Grossly atrophied orbitofrontal and medial regions (opposite from AD, which originals from MTL to frontal)

19
Q

Pathology of FTD: What kind of protein

A

Tau Protein 50%

20
Q

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

A

Deficits in Negative emotions
Intact in happiness
Equivocal findings in surprise

  • Not due to task difficulty
  • Across modalities (face/voice/etc)
21
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

22
Q

Neuroimaging FTD (Emotional Evaluation and Socal Evaluation and how is amydala related)

A

Amygdala damage correlated with negative facial expression

Emotional Evaluation: Poor recognition of negative emotions; Intact recognition of positive emotions

Social Evaluation: Poor recognition in sarcasm

23
Q

Neuroimaging FTD: Correlation between sarcasm and amygdala

A

Poor sarcasm detection correlated with lower amygdala volume (stronger than all other cortical damage)

24
Q

Neuroimaging FTD: Insight (in their own impairment)

A

Poor insight across domains

  • Quality of insight correlated with OFC and Frontopolar Grey Matter
  • Emotional insight correlated with Frontopolar, Amygdala, and Hippocampal Grey Matter
25
Q

Emotional Recognition: FTD vs Other disorders

A

FTDs are consistently worse at processing emotions

26
Q

What is the caveat with studies on FTD

A

Small sample size

27
Q

Amygdala: Function of lateral nucleus vs central nucleus

A

Lateral: Conveyance area, form associations underlying conditioning

Central: Initiate emotional response

28
Q

What emotions do FTDbv group show impairment with

A

Negative emotions (anger, disgust, fear)

29
Q

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

A

40% remission with first treatment

10% treatment resistant (4 medication failures), also predicts relapse after ECT

30
Q

Why is treatment depression difficult

A

Depression defined in DSM as behaviour, not pathology

31
Q

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

A

Cortical: Frontal (key)
Subcortical: Caudate, Hippocampus, Cingulate (key)

32
Q

What is the problem with region and association with depression

A

Cause and effect unclear. Possible that depression > less sleep and exercise > affects hippocampus (synaptic plasticity)

33
Q

Specifically, what is the key region in depression

A

Increased activity in rostral anterior cingulate (area 25)

34
Q

What has been correlated in area 25: Treatment

A

Successful drug & treatment = Decrease RAC activity

Treatment resistant = Increased RAC activity

35
Q

Is everyone with depression applicable o undergo DBS?

A

Only treatment-resistant group

36
Q

What are the results with open-label DBS treatment

A

Successful (66% and 50%)

No changes in neuropsych testing (Surprising)

37
Q

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

A

By 1mo, can predict responders from non-responders

38
Q

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

A

Include all participants and limit bias by preserving randomization

39
Q

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

A

Shows consistent positive treatment outcomes

40
Q

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

A
  1. ) Bias (Lack of blind and random)
  2. ) Placebo (Lack of control)
  3. ) Ambiguous duplication (Competing interest)
  4. ) Small sample size
  5. ) Heterogeneous outcome measures
41
Q

What are results form randomized-control DBS studies

A

No dramatic change.

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

43
Q

What happened in the randomized-control DBS study after 16 weeks

A

Cessation due to ineffectiveness.

PSYC30018 - Neuroscience (14 decks)

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