Emotions, Stress, and Executive Function Flashcards
Lecture 10
1
Q
what are emotions? how do they differ from mood?
A
subjective, conscious experience that is characterized by psychophysiological expressions, biological reaction and mental states
- emotions influence how we act while moods influence how we perceive
2
Q
are emotions irrational? why or why not?
A
they are not irrational
- emotions are preserved among mammalian lineage, there is must be an adaptive value
- parts of the brain responsible for emotion are also responsible for decision making
- emotion is critically linked to how we value things
- disruptions that impair emotion also impair judgement and decision making
- ex. psychopaths are worse at making decisions, don’t consider the right things when making decisions
3
Q
what are the two theories for emotion lateralization
A
- right hemisphere model of emotion - right cerebral hemisphere is specialized for emotional processing
- valence model - the two hemispheres govern different valences of emotion
- left = positive emotions
- right = negative emotions
- neither theory holds up well but we see small differences between hemispheres
4
Q
why do we sometimes think of emotions as discrete?
A
- paul ekman argued we have 6 primary emotions that are universal
- anger, fear, surprise, disgust, happiness, sadness
- in reality we found little consistency in how cultures rank emotions (except happiness)
5
Q
how do we think of emotions in terms of dimensions?
A
- think of emotions based on the dimensions of valence (pleasant vs. unpleasant) and intensity
- dimensions are thought to guide perception and action (approach/avoid)
- but, we sometimes approach unpleasant things (sad music) and are ambivalent about some things
6
Q
what are the brain regions of emotion?
A
- brain areas responsible for emotion are diffuse and overlapping
- population coding - one neuron can’t represent the emotion, the population of neurons firing represents the emotion/feeling
- it is hard to know if a brain area encodes a value or arousal or emotion
7
Q
what is kluver-bucy syndrome?
A
- removed the amygdala and part of temporal lobe of animals (anterior temporal lobectomy)
- animals presented very different behaviour
- lack of fear - would approach instead of avoid
- hyperorality - explored items by putting them in their mouths (problems with vision and recognition)
- misdirected hyper-sexuality
8
Q
how is the amygdala important in emotional learning?
A
- amygdala monitors the association between two different things (classical conditioning)
- is a coincidence detector
- there is a high and low road to fear
- high road is responsible for learning fear
- low road
9
Q
how do the high and low roads to fear function?
A
- high road goes from thalamus to cortex before the amygdala
- low road goes straight from the thalamus to the amygdala
10
Q
how does damage to the amygdala affect fear (depending on location)?
A
- damage to lateral amygdala → impairs learning of fear association
- damage to central amygdala → impairs expression of learned fear
11
Q
who is patient SM and how did they experience fear?
A
- had a disorder where they had complete bilateral amygdala loss
- had no experience of fear and no learned fear conditioning
- often approached fear stimuli instead of avoiding
- interpreted arousal as excitement instead of fear
- could still experience fear under the right conditions, like when exposed to CO2 inhalation
12
Q
why could patient SM experience fear during CO2 inhalation but not under any other condition?
A
- amygdala is used to trigger a state of fear when we encounter threatening stimuli in the external environment
- fear induced by internal stimuli are not controlled by the amygdala
- brain stem is responsible for introceptive fear-inducing stimuli
13
Q
how does patient SM represent the negative consequences of not experiencing fear?
A
- she had difficulty detecting threats and learning to avoid dangerous situations
- fear is adaptive, the amygdala promotes survival by compelling the organism away from danger using fear
- learned fear also helps us not make the same mistakes repetitively
14
Q
is the amygdala negatively valenced?
A
no
- in primate/rodent electrophysiology, the same amount of neurons that fire for aversive stimuli in amygdala, also fire for appetitive stimuli
- the amygdala is important in changing our values
- during stimulus de-valuation (satiation) - if you get a good thing repeatedly, we start to de-value it
- we evaluate appetitive vs. aversive stimuli differently
15
Q
what other parts of the brain are responsible for fear?
A
- PAG - periacqueductal grey
- part of the midbrain, tegmentum
- one of the main recipients of the activity from amygdala
- fear and shrieking behaviours
- ACC - anterior cingulate cortex (white matter?)
- runs next to corpus collusum
- activated during fear
- insula - hidden piece of cortex
- can be seen inside the lateral fissure
16
Q
what is anger driven by?
A
- anger is largely driven by inequality
- when fairness is compromised
- anger is prosocial, ensures people are treated fairly
- capuchin monkey gets angry after they see that the partner gets a grape while they get cucumber
17
Q
what is the ultimatum game and what does it tell us about anger and prosociality? how do we see this reaction in the brain?
A
- two player game where one play (actually a computer) divides money between themselves and another player, and the other player must accept or reject the offer and neither of them gets money
- as the split becomes more uneven, people reject the offer more often
- people say they want to punish the other person in hopes of better behaviour in the future, even at a cost to themselves (altruism)
- insula and anterior cingulate becomes more activated as more people reject offers (BOLD response)
18
Q
what is a homoeconomist?
A
- the economic human, we don’t correspond to rational economic behaviour
- we waste money and do things that don’t lead to best economic outcome
19
Q
what is the purpose of frustration?
A
to motivate us to try to go harder and further in the future
20
Q
what is the near miss effect?
A
- when you fail but are almost successful
- results in the largest frustration we can feel
21
Q
how does the near miss effect change behaviours on a slot machine task?
A
- when you have control of the arm of the slot machine, the near miss makes you more likely to play again (33%)
- makes us feel we are in control
- a full miss makes you less likely to play again
- irrational overall because in a casino, having a near miss doesn’t necessarily mean we are getting closer
22
Q
what does brain activity look like during a near miss?
A
- anterior cingulate cortex activity goes up more for near misses vs. full misses
- anterior insula activity is correlated with subjective effects of near miss
- responses are enhanced in individuals with pathological gambling disorder
23
Q
what is a prefrontal lobotomy?
A
- procedure previously done to “reduce disruptive behaviour”
- usually done on people in psychiatric and prison institutions, women, and children
- put a orbitoclast into the prefrontal cortex and moved it around
- did not improve disruptive behaviour - some people had drastic changes and others had less
24
Q
what are some executive functions?
A
planning, organization, flexible thinking, monitoring performance, multi-tasking, self-awareness, motivation, determining and exhibiting appropriate behaviour, regulating emotion
25
Q
how does bilateral damage to the ventral prefrontal cortex affect executive function?
A
- vmPFC is known to regulate emotions
- lots of other executive dysfunction but most intellectual ability is preserved
- problems with prioritization, emotional dysregulation, repeating mistakes, planning, rigidity in thoughts/actions, attention and concentration
26
Q
how does unilateral damage to the ventral prefrontal cortex affect executive function?
A
- most detrimental dysfunction when damage is in the right side
- disturbances associated with bilateral damage
- more executive dysfunction
- people with damage to the left side will lead more normal lives
- typical social and interpersonal behaviour
- stable employment
- personality relatively unchanged
- decision making ability relatively intact
27
Q
who was phineas gage?
A
- medial prefrontal cortex had been damaged
- previously thought that damage was bilateral, but there is more substantial damage in the left side
- lost fundamental aspects of his personality but still could maintain a job
- a decade after his injury, he developed severe epilepsy that ultimately led to his death
28
Q
what is passive vs. active stress?
A
- passive stress - something we need isn’t provided
- active stress - something happening to us
29
Q
how does controllable vs. uncontrollable stress affect us differently?
A
- stress immunization - exposure to controllable stress results in more resiliency to stress
- learned helplessness - exposure to uncontrollable stress results in less resiliency to stress in the future, even if it’s controllable
30
Q
what are the two physiological responses to stress?
A
- stress is a sympathetic response - controlled by nervous system signal, moves fast and leaves fast
- stimulates adrenal medulla and release norepinephrine into the body
- causes heart to raise faster and blood vessels to dilate
- stress is controlled by the HPA axis -controlled by hormones in the bloodstream, slower response that lasts longer
- hypothalamus signals to pituitary gland that releases hormones
- adrenal gland releases cortisol
31
Q
is stress beneficial or costly?
A
- stress is an adaptive response to threat
- mild levels of stress are beneficial but higher levels of stress have both costs and benefits
- when under high stress, we perform better in skills that are well-known but worse in skills that are new to us or not well-known
32
Q
what are the benefits and costs associated with high stress?
A
- benefits: improves implicit memory, simple tasks, habitual and well-rehearsed tasks, and short-term immune system suppression
- costs: compromises cognitive flexibility, working memory, executive functions
33
Q
how does catecholamine release relate to stress and arousal on the prefrontal cortex?
A
- there is a linear relationship between how stressed we are and how much catecholamines are released
- the affects of catecholamine release on performance look like the yerkes-dodson curve (based on arousal)
- with low levels of catecholamines, the prefrontal cortex fires less, is less likely to work together for a task, and is less discriminatory for what to fire for (easily distractible)
- at optimal levels of catecholamine release, the neurons create networks to work together and discriminate what to fire for
- in high stress, prefrontal cortex is suppressed and fires less while other parts of the brain (amygdala/basal ganglia) take on bigger roles
- striatum is responsible for habitual behaviour and amygdala learns associations
- high stress improves habitual behaviour
34
Q
what is chronic stress and how does it affect us?
A
- stress that is constant
- compromises immune functioning, mental health
- reduces hippocampal volume, thins PFC
- reduces performance on hippocampal- or PFC-dependent tasks
- requires more PFC activity to have same level of performance
- sends us further to the left of the yerkes-dodson scale
- shifts more reliance to subcortical structures (amygdala)
- may decrease baseline dopamine function
- effects often more pronounced in women
35
Q
what is burnout?
A
- loss of motivation and pleasure in things that were once enjoyable
- problems with irritability and looking ahead
- effects of chronic stress are reversible (restitution)
36
Q
what is the effect of the chronic stress of poverty?
A
- chronic stress of poverty affects executive functions, cost/benefit decision making, and ability to look ahead
- poverty affects cognitive performance on unrelated tasks
- exposure to irregular reward intervals guides individuals to act impulsively
- even people with high baseline self-control
- poverty disproportionately affects children and their brains → less grey matter volume
- poverty is chronic exposure to uncontrollable stress → has an effect on the brain and learned helplessness
37
Q
what is ADHD? what affects diagnosis?
A
Attention Deficit/Hyperactivity Disorder (ADHD)
- extreme inattention, hyperactivity, impulsivity
- intersects with development, maturity, and societal norms (2x more boys than girls)
- girls and women more often the inattentive subtype and potentially underdiagnosed
- youngest children in class are 40% more likely to be diagnosed with ADHD because they’re more immature compared to peers (overdiagnosed)
- diagnoses have increased more than 100% since 2007
38
Q
how do we treat ADHD?
A
- psychostimulants (amphetamine, methylphenidate) improve symptoms
- medications block DAT and NET, increasing functioning of these systems
- are stimulants but somehow improve hyperactivity
39
Q
how can we explain why psychostimulants improve symptoms of ADHD? what parts of the brain look different in people with ADHD?
A
- people with ADHD sit further on the left of the Yerkes Dodson curve
- low levels of catecholamine activity in PFC, firing less often, less integrated, and less discriminatory (more distractible)
- PET studies suggest DA system is hypoactive, but there are no changes to norepinephrine
- many studies suggest changes to PFC, DA system, and basal ganglia
- symptoms of ADHD relate directly to executive function
40
Q
how can we differentiate adult ADHD from chronic stress and burnout?
A
- all three result in less catecholamine release and sitting further left on yerkes dodson curve
- symptoms also overlap - ADHD may also increase risk of burnout
- requires nuanced diagnosis
