W10 - Emotions Flashcards
What is Papez Circuit and what is the problem
Circuit Theory of Emotions. More descriptive than functional
First evidence of Amygdala and Emotions
Animal Evidence: MTL > Lack of fear response
Evidence of Amygdala Emotions: SM
SM: No fear; unable to facial decode emotions; inappropriate social behavior
How does amygdala block fear
Does not block exhibition of fear (startle), blocks fear conditioning & learning (CR + neutral)
Pathways and brief description of amygdala
Low road: Sensory > Thalamus > Amygdala > Is it adversive?
High road: More thorough, confirms initial low road.
Is fear learning implicit/unconscious? What evidence do I have to claim this
Implicit/Unconscious
- Expressed via. behavioural/physiological response (e.g., SCR).
- Can report parameters of fear conditioning and what is supposed to happen
Fear Learning in faces. fMRI Evidence for implicitness. When is amygdala response stronger?
There is evidence to faces with “fear” expression even subconsciously.
But it is stronger with attention
Amygdala and explicit fear learning
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
Why do we use faces as stimuli
Good control (can manipulate expression only)
What is the problem with neruoimaging evidence like fMRi in facial emotion
Slow hemodynamic Changes. Repeated presentation of emotional stimuli = Habituation
Can we “train’ attentional bias such that fear is processed less
Experimenetally, yes. But there is no-significant clinically relevant effects.
Possibility of publiciation bias
Other associations of brain and emotions
Angry = Orbitofrontal (increases with attention) Disgust = Insula (also involved in other emotions)
Role of Insula in emotions
Suggested to be involved in all subjective feelings: Introspection and afferent representations.
What are the 3 types of frontotemporal dementia (FTD)
- ) Semantic
- ) Progressisve Nonfluent
- ) Behavioural Variant
Behaviour Variant Frontotemporal Dementia: Symptomps (BFTD)
1) Disinhibition
2) Apathy
3) Lack empaty
4) Perservative
5) Dietary Change
6) EF Dysfunction
“Handbrakes taken off”
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
Pathology of FTD: Genetic Markers
Gene: C9ORF72 (affects 7-12%). That means many FTD has no gene
Pathology of FTD: Brain
Grossly atrophied orbitofrontal and medial regions (opposite from AD, which originals from MTL to frontal)
Pathology of FTD: What kind of protein
Tau Protein 50%
Which emotions recognition do FTD patients show deficits in. What are some circumstances which these patterns show
Deficits in Negative emotions
Intact in happiness
Equivocal findings in surprise
- Not due to task difficulty
- Across modalities (face/voice/etc)
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
Neuroimaging FTD (Emotional Evaluation and Socal Evaluation and how is amydala related)
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
Neuroimaging FTD: Correlation between sarcasm and amygdala
Poor sarcasm detection correlated with lower amygdala volume (stronger than all other cortical damage)
Neuroimaging FTD: Insight (in their own impairment)
Poor insight across domains
- Quality of insight correlated with OFC and Frontopolar Grey Matter
- Emotional insight correlated with Frontopolar, Amygdala, and Hippocampal Grey Matter
Emotional Recognition: FTD vs Other disorders
FTDs are consistently worse at processing emotions
What is the caveat with studies on FTD
Small sample size
Amygdala: Function of lateral nucleus vs central nucleus
Lateral: Conveyance area, form associations underlying conditioning
Central: Initiate emotional response
What emotions do FTDbv group show impairment with
Negative emotions (anger, disgust, fear)
What is the treatment rates with depression. What defines treatment resistant
40% remission with first treatment
10% treatment resistant (4 medication failures), also predicts relapse after ECT
Why is treatment depression difficult
Depression defined in DSM as behaviour, not pathology
What are regions associated with depression, and key region discussed in this lecture
Cortical: Frontal (key)
Subcortical: Caudate, Hippocampus, Cingulate (key)
What is the problem with region and association with depression
Cause and effect unclear. Possible that depression > less sleep and exercise > affects hippocampus (synaptic plasticity)
Specifically, what is the key region in depression
Increased activity in rostral anterior cingulate (area 25)
What has been correlated in area 25: Treatment
Successful drug & treatment = Decrease RAC activity
Treatment resistant = Increased RAC activity
Is everyone with depression applicable o undergo DBS?
Only treatment-resistant group
What are the results with open-label DBS treatment
Successful (66% and 50%)
No changes in neuropsych testing (Surprising)
How fast do people respond to DBS treatment and what can we predict?
By 1mo, can predict responders from non-responders
What is intention-to-treat. What is its utility
Include all participants and limit bias by preserving randomization
What is the results in open-label intention-to-treat
Shows consistent positive treatment outcomes
What are problems with open-label studies of DBS. There are 5.
- ) Bias (Lack of blind and random)
- ) Placebo (Lack of control)
- ) Ambiguous duplication (Competing interest)
- ) Small sample size
- ) Heterogeneous outcome measures
What are results form randomized-control DBS studies
No dramatic change.
What is the duration of randomized-control DBS studies
Active vs sham double blind 16 weeks, followed by open-label continuation phase
What happened in the randomized-control DBS study after 16 weeks
Cessation due to ineffectiveness.
