W10 - Emotions Flashcards
What is Papez Circuit and what is the problem
Circuit Theory of Emotions
- More descriptive than functional
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
Evidence of Amygdala Emotions: SM
SM
- Lack of fear
- Unable to facial decode emotions
- Inappropriate social behavior
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
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
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.
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
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
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
Why do we use faces as stimuli
Good control
- can manipulate expression only
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
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.
Other associations of brain and emotions
Angry
Orbitofrontal Cortex
- Increases with attention
Disgust
Insula
- Also involved in other emotions
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
What are the 3 types of frontotemporal dementia (FTD)
A progressive neurodegenerative brain disorder
- ) Semantic
- ) Progressisve Nonfluent
- ) Behavioural Variant
Behaviour Variant Frontotemporal Dementia: Symptoms (BFTD)
“Handbrakes taken off”
- Disinhibition
- Socially impusive, dgaf
- Apathy
- Lack empathy
- Perservative
- Dietary Change/Hyperorality
- EF Dysfunction
- Lack of insight
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: 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
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)
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
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
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
FTD vs Other disorders
FTDs are consistently worse on emotion recognition tasks, as well as worse on insight tasks
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
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)
FTD: Summary of brain areas and implications
Amygdala: Negaitve Emotional, Social, Emotional Insight
OFC: Quality of Insight
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
Why is treatment depression difficult
- Depression defined in DSM as behaviour, not pathology
- Few animal models
What are structural regions associated with depression, and key region discussed in this lecture
Cortical
- Frontal
Subcortical
- Caudate
- Hippocampus
- Cingulate
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
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
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
Is everyone with depression applicable to undergo DBS?
Only treatment-resistant group
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
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
What is intention-to-treat. What is its utility
Include all participants, preserving randomization
- Still has placebo effects
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 blinding and randomization
- Placebo
- Lack of control
- Ambiguous duplication
- Competing interests
- Small sample size
- Heterogeneous outcome measures
What are the results for DBS for treatment-resistant unipolar and bipolar depression
Good
What are results form randomized-control DBS studies
BROADEN trial.
No dramatic change, where control group had even lower depression than active treatment group.
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.
What are the problems with systematic controlled studies
- Suboptimal patient selection
- Inconsistent targetting of DBS sites
- Insufficient current delivery
