L8: Deconstructing fear memory Flashcards

1
Q

what are the 2 main treatments for people with anxiety disorders?

A

extinction & reconsolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what can you say about the prevalence of anxiety disorders?

A
  • leading form of mental illness worlwide
  • 60m in europe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are anxiety disorders? what lies at their core?

A
  • conceptualized as irrational and learned fears
  • associative fear memory lies at core
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

in what paradigms did emotional memory play a big role? in which didnt it?

A

big role: psychoanalysis, CBT
tiny role: behaviourism, biological psychiatry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how does fear conditioning work?

A

when a conditional stimulus (something neutral) is associated with an unconditional aversive stimulus (like a shock) which then leads the neutral something to always elicit that fear
- fear memory is strong - generalizes over time, context and stimuli
- “normal” fears have similar neurobio processes as irrational fears
- strong fear memory is functional and taps into one of the most important survival circuits (we want to predict)
- but can become irrational -> ADs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

do people w ADs realize their fears are irrational?

A

usually yes!
except when theyre actually confronted with the “threat”, then they fully believe they’re in danger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the principle of extinction?

A

learning not to fear!
its unassociating the conditioned stimulus (spider) from the unconditinal stimulus (shock) so that conditioned fear response to CS dissapears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the spontaneous recovery response?

A

that if you induce extinction learning in an animal/hulman you need to repeat it shortly after, otherwise the fear will come back
if you leave too much time between extinction sessions and then you give the unconditioned stimulus again, the US - CS association will come back strong again (person will immediately go back to becoming scared from CS again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is fear relapse explained by biology?

A

during extinction, inhibitory memory is formed in hippocampus, vmPFC
but fear memory stored in amygdala remains intact and may resurface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does traditinional vs modern learning theory explain fear?

A

Traditional: Habituation, CS (sound) -> no CR (fear)
Modern: Learning, CS (sound) -> no US (shock) . feel, think and act is the feared stimulus (sound) is followed by a catastrophe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does traditional vs contemporary theory explain exposure therapy?

A

traditional: habituation! (CS-> no CR)
contemorary: learning (CS-> no US) (basically you stop feeling, thinking, and acting as if the feared stimulus is followed by a catastrophe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

According to lecture, how can you optimize exposure treatment?

A
  • design exposure that violate expectancies: like probability of expected negative outcome (US), intensity of anticipated catastrophe, extent to which catastrophe is manageable all these expectations need to violated
  • focus on learning (mismatch, prediction error), condolidation, and retreival
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How effective is exposure therapy?

A
  • many patients benefit
  • but long term effects are weak:only 38% profit at long term
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is exposure therapy?

A
  • a way of reduceing conditional fear reaction
  • clinical equivalent of extinction: CS (the thing you’re afraid of that was initially neutral, like a dog) is repeatedly presented in the absence of the associated aversive event (the US)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

briefly explain the classical conditioning model

A

a neutral stimulus is conditioned (so it becomes the CS) by always associating an unconditioned stimulus with it (like an aversive sound). the unconditioned response that initially comes after exposure to the unconditioned stimulus, starts to automatically come after the CS as well, meaning it becomes a conditioned response to the CS.
for this the CS, or the neutral stimulus like a blue square, needs to be a reliable predictor of the US, aversive sound, so that there is an association between the memory representation of the CS and US (presentation of the blue square, CS, always activates the memory of the aversive sound, US, which then elicits fear (CR))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the inhibitory learning model?

A
  • central to extinction and exposure therapy
  • mean that the original CS-US (dog - biting) association learned during fear conditioning is not erased, rather its left intact as new, secondary inhibitory learning about the CS-US develops - specifically that the CS no longer predicts the US
  • after exctinction: the CS (dog) posesses 2 meanings: its original excitatory meaning (CS-US) as well as an additional inhibitory meaning (CS-no US)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can conditioned fear response come back?

A
  • passage of time = spontaneous recovery
  • leaving the therapeutic context = renewal
  • re-exposure to aversive event = reinstatement
  • new learning experience - rapid reacquisition

basically extinction does not generalize over time & context (as opposed to acquisition) !

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the cons of the inhibitory learning in exposure therapy?

A

even though fear subsides with enough trials of the CS followed by no US (the inhibitory meaning), there is retention of at least part of the original (CS-US) association (its not forgotten so to say)
this can lead to:
- spontaneous recovery: passage of time
- renewal: changing of context. if surrounding context is changed between extinction & retest then renewal of conditional fear. aka fear extinction appears to be specific to the context in which extinction occurs (so if exposure therapy is completed in only one or a few limited contexts, then fear is likely to return when the CS is encountered in a different context)
- reinstatement: if re-exposure to aversive event
- rapid reacquisition of the CR: if new learning experience with CS-US pairings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what do habituation models state about exposure therapy?

A
  • rests upon fear reduction during exposure trials as a critical index of therapeutic change
  • posit that fear reduction during an exposure trial is a necessary precursor to subsequent, longer lasting cognitive changes in the perceived harm associated w the phobic stimulus
  • while inhibitory learning models do not emphasize fear reduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

why does the inhibitory model on extinction not emphasize fear reduction to measure therapeutic change?

A

because fear reduction at completion of exposure therapy does not seem to predict the amount of fear expressed at the follow up extinction retest
this is because outward expression of fear and conditional automatic associations may not always change in concordance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the 8 exposure therapy optimization techniques that enhance inhibitory learning?

A
  1. expectancy violation
  2. deepened extinction
  3. occasional reinforced exctinction
  4. removal of safety signals
  5. variability
  6. retrieval cues
  7. multiple contexts
  8. affect labeling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the expectancy violation optimization technique?

A
  • premise: mismatch between expectancy & outcome is critical for new learning & for dev of inhibitory expectancies that will compete w excitatory expectancies (CS-US expectancy)
  • the more expectancy can be violated by experience, the greater the inhibitory learning
  • client has to identify the US (aversive sound, biting, humiliation) when predicting the expectancy to be violated
  • end of exposure trial determined by conditions that violate expectancies (social situation where there is no rejection), not by fear recdution
  • so you ask participants to judge what they leared regarding the non-occurence of the expected feared event (US) and how violated their expectations were (aka you’re mentally rehearsing the inhibitory CS-no US association by asking the patient to reflect on it)
  • key aspect: bring attention to both the CS (social interaction) and the non-occurence of the US (social rejection)
  • graduated exposure may be used (like longer trials each time ex for fear of heights u may ask the client to stay 5 sec longer on the balcony each time, even though fear may not reduce each time. u do it based on time not based on fear reduction)
  • cognitive strategies that reduce expectancy prior to extinction can negatively impact extinction learning (things like reducing probability overestimation (eg i am unlikely to be bitten by a dog)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the deepened exctinction technique?

A
  • either multiple fear CSs are first extinguished separetly before being combined during extinction, or a previously extinguished cue is paired with a novel CS
  • both feared stimuli must predict the same US (ex: one type of spider and another type of spider are both associated with the US of being bitten)
  • been shown to reduce spontaneous recovery & reinstatement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the occasional reinforced extinction technique?

A
  • involves occasional CS-US (dog - biting) pairings during extinction training
  • works because expectancy violation effect (if CS sometimes leads to US and sometimes not so ur less likely to expect the next CS to predict the US)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the removal of safety signals technique?

A

safety signals should gradually be phased out over the course of exposure therapy, if willing immediate removal of safety signals is preffered
cause safety signals can interfere with extinction but this depends on the number and strenght of inhibitory stimuli vs the number and strenght of excitatory stimuli (stimuli that predict the US, like social rejection) (how likely the social rejection seems)

26
Q

what are some common safety signals or behaviours for clients with anxiety?

A
  • presence of another person
  • therapists
  • cellphones
  • food
  • reduction of fear itself (for ppl who have fear of fear, try to reduce anxiety so it wont be seen by others which would cause more fear)
27
Q

what is the role of safety behaviours? how do they do this?

A

role: they allevaite distress in the short term, but when they are no longer present, the fear returns
how do they do this: interference with the development of inhibitory associations

28
Q

what is the variability technique?

A
  • enhances retention of learning & is more realistic of real world encounters of the feared stimulus (so offsets renewal effects)
  • in terms of timing between exposure sessions, in terms of stimuli used (from least scary to most scary hierarchy, stimuli are randomly picked, not in order), length of exposure etc
  • better long term effects but higher in the moment arousal
29
Q

what is the retrieval cues technique?

A
  • enhances retrieval of extinction learning & offsetting context renewal
  • include retrieval cues (of the CS-no US association) during extinction training to be used in other contexts once extinction is over
  • (ex: therapists office where previous exposure sessions were conducted can act as retrieval cue for new exposure)
  • instructional retreival cue can also help (make patient remember what was learned during last exposure session, or carry a bracelet that they bring to every exposure session)
  • this technique best used as relapse prevention skill, so not early in therapy
30
Q

what is the con of the retrieval cues technique?

A

they may acquire an inhibitory value and become a safety signal in that they are directly associated with the non-occurence of the US

31
Q

what is the multiple contexts technique?

A
  • offsets context renewal issues (that the fear returns when its encountered in a different context then the one in which therapy was conducted)
  • use interoceptive, imaginal, and in vivo exposures in multiple different contexts
32
Q

What is necessary for the transformation from short term to long term memory?

A

this process is also called consolidation
its mediated by protein synthesis dependent synaptic changes

33
Q

what is a therapeutic strategy for enhancing inhibitory regulation?

A
  • involves linguistic processing, for ex: affect labeling (stating an irrelevant but negative word everytime feared stimulus is presented (if u see spider, you say war)
  • linguistic processing, or genearl exectuvie functioning, reduces amgyala activity so reducing anxiety
34
Q

how can inhibitory exposure therapy be used for OCD?

A

S1: discussion on how avoidance prevents fear reduction since it doesnt allow for any violation in expectancy. focus on startegies that would lead to long term reduction
S2-5: in vivo exposure, starting with moderately difficult exercises, and then variability in difficulty of exercises, while gradually removing safety behaviours. eventually bring to mind the full intrusive violent images to mind
S6-11: in vivo exposure while incorporating several extinction enhancement strategies, used deep extinction & occasional reinforced extinction
Post: discussed context dependent nature of extinction learning, and suggested several relapse prevention strategies

35
Q

what are the differences between inhibitory based exposure therapy vs hiabituation based/cognitive based exposure therapy for OCD?

A
  1. inhibitory makes clients describe their feared outcome, their expected outcome in order to facilitate expectancy violation
  2. inhibitory involves lenghty discussions regarding the non occurence of the feared event after the exposure exercise
  3. in inhibitory the client is instructed to continue with a given exposure until their expectancy has been violated, or he has reached the agreed upon bheavioural goals, regadless of his level of distress/fear arousal
  4. cognitive restructing is not used before or during exposures, since this could reduce the expectancy of an anversive outcome thus reducing the exctinction learning
36
Q

how can inhibitory exposure therapy be used for PTSD?

A

S1: psychoeducation & make list of avoided situations & associated feared outcomes.
S2-4: in vivo exposures centered on expectancy violation while decreased use of safety behaviours. prior to exposures client is aksed to state the feared negative outcomes & to track their non-occurence each time
S5-12: in vivo exposure & incorporating imaginal exposure to the trauma. Set small goals to counter your expectations of what would happen if faced with the trauma images. repeated exposure to the images can help distinguish between the memory and the event itself.

37
Q

what are the differences between inhibitory based exposure therapy vs hiabituation based/cognitive based exposure therapy for PTSD treatment?

A

inhibitory
- targets aspects of expectancy violation & stimulus discrimination
- uses affective labeling
- ties exposure completeion to behavioural goals rather than fear level
- doesnt use cognitive restructuring prior to or during exposure

38
Q

How has perspective on memory changed?

A

new learning (active) -> consolidation -> stored memory (inactive) -> memory reactivation -> labile memory (active) -> reconsolidation -> updated memory (inactive)

39
Q

what are the differences between inhibitory based exposure therapy vs hiabituation based/cognitive based exposure therapy for social phobia treatment?

A

inhibitory differences w cognitive therapy
- no cognitive structuring prior to exposures (to maximise violation of the expectancy)
- cognitive restructuring in midst of exposures discouraged
inhibitory differences w habituation based approach
- emphasis on expectancy violation, rather than fear levels
- exposures are tailored to increase variability of fear induced both within and accross exercises (order wasnt based on increasing fear)
-

40
Q

how come exctintion therapy doesn’t seem to work for everyone? what can we do about it?

A

deficits in extinction learning, or more specifically, in deficits in inhibitory learning seen in ppl w ADs
-> optimize inhibitory learning during exposure therapy

41
Q

How can inhibitory exposure therapy be used for social phobia?

A

S1: psychoeducation & treatment planning
S2-5: creating an inventory of feared social situations & together creating corresponding exposure exercises & carrying them out. focus on what was learned in each exercise, rather than fear levels were measured. (this also determined order of exercises). clients expectations measured & compared to what acutally happened (consolidation)
S6-12: together design augmented exposure. first, safety beahviours were identified and eliminated. second, therapist works w client to counter tendency to imaginally replay perceived negative aspects of social encounters (post event processing). third, client did exposures that had very high probability of negative social feedback

42
Q

How can inhibitory exposure therapy be used for specific phobia?

A

S1: asssessment of situational avoidance behaviours & how exposure therapy could help clients life
S2-5: repeated practice & tracking of in vivo exposure. hypothesize wat client thought would happen in each situation & compare it to what actually happens. stop when hypothesis aka expactancy is violated, not when fear subsides
S6-12: augmented exposures w additional strategies (like multiple contexts).

43
Q

How can inhibitory exposure therapy be used for panic disorder?

A

S1: discussions about associative learning, how avoidance prevents extinction learning, and importance of exposures for eventual fear reduction. incorporate 3 extinction enhancement strategies throughout treatment: violation of expectancies, deepened exctinction, and removal of safety signals
S2-7: interoceptive exposure through induction of dizziness, shortness of breath, and racing heart. note what client expected to happen & what actually happened. starting at S4, gradual removal of safety signals.
S8-14: deepened extinction: combine ++ feared stimuli that have been extinguished in isolation.

44
Q

How does inhibitory exposure therapy for panic disorder differ from habituation & cognitive models?

A

difference from habituated
- therapist encouraged strategies that continually increased expectation & fear in order to facilitate extinction learning
difference from cognitive
- no cognitive reappraisal until after exposure

45
Q

What is meant by labile period?

A

period during which previously consolidated memories are sensitive to change and in need of restabilization

46
Q

How can maladaptive memories be tackled through reconsolidation?

A

memory reactivation can induce a labile period of under 6h, during which previously consolidated maladatpvie memories are sensitive to change (through protein synthesis inhibitors like anisomycin), and in need of restabilization
this is called reconsolidation

47
Q

How can consolidation be prevented?

A

by administering PSIs (Protein Synthesis Inhibitors) shortly after learning
once consolidated, memories appear insensitive to protein synthesis inhibition so cant be modified. BUT after reactivation of a memory, they can be changed again (using protein synthesis inhibition for ex)
ex: prponanolol or anisomycin (animals)

48
Q

what is the reconsolidation technique?

A
  • retreiving already stored memory and potentially changing them by doing so if done within the reconsolidation time frame
  • new info presented during this time frame may be incorporated into the memory and change it, could neutralize the fear memory itself (and the fear memory was shown to usually not come back with renewal, reinstatement, spontaneous recovery or rapid re-acquisition) -> so memory is not extinguished, its alltogether ‘deleted’. so effects of reconsolidation are stronger than normal exctinction training
  • so extinction during a reconsolidation time window may weaken the fear memory itself!
  • present CS 30min before extinction trials
49
Q

Is reconsolidation an option for PTSD treatment? what about for phobias?

A

PTSD: it has potential but more still needs to be realized
Phobia: propanolol give after feared stimulus exposure was shown to reduce fear

50
Q

What is the adaptive purpose of reconsolidation?

A
  • update memories to maintain their relevance in changing environments.
51
Q

what are prediction errors?

A

discrepancies between what we expected to happen & what actually happens
play role in reconsolidation

52
Q

How do prediction errors during memory reactivation affect susceptibility to protein synthesis blockade?

A

prediciton errors INDUCE supsceptibility to protein synthesis blockade aka amnestic effects like reconsolidation

53
Q

What are some prediction errors?

A
  • temporal: exposure happens during reactivation at different time than what was learned during training
  • contingency: exposure did not occur within time frame that it would be expected to occur
    so these things during reactivation make reconsolidation alteration possible
54
Q

What role do NMDA receptor activation and AMPA receptors play in fear memory?

A

NMDA receptor activation is necessary for labilization (unstabliziation) of a fear memory upon reactivation
AMPA receptors were crucial for the expression of that memory

55
Q

Are memory retrieval & expression necessary for memory reconsolidation?

A

no!

56
Q

What triggers memory destabilization during fear conditioning? how can we operationalize this?

A

Prediction error (could include violation of expectations, but also the learning of additional info if learning has not reached decreased so like novel experiences w feared stimluli can also destabilize the target memory), not absence of reinforcement!
so we shold tailor prediction errors to patients fears and expectations

57
Q

Are reactivation and reconsolidation the same?

A

no

58
Q

is prediction error during reactoin always sufficient for the induction of reconsolidation?

A

no

59
Q

How can we predict whether reconsolidation or exctinction will be the result of reactivation when prediction error occurs?

A

look at
length of reactivation: longer reactivation tend to lead to extinction rather than reconsolidation
amount of prediction error during reactivation

60
Q

What is a “limbo” period in the context of memory processes?

A

transitional state between reconsolidation and extinction, where neither process is domination

61
Q

What makes the induction of reconsolidation such a “balancing act”?

A

because without prediction error, memory is not labilized (destabilized) and made vulnerable to amnestic agents (modifiction), but with extended reactivation & multiple prediction errors, destabilization doestn take place and extinction may occur instead

learning history & temparement of individual whose memory is being targeted also play a role

62
Q

What criteria need to bet to use reconsolidation effectively in humans?

A
  1. presence of an interaction between memory reactivation (ie a brief reminder cue) and the experimental manipulation (ie administration of propanolol)
  2. time dependent effects if the manipulation
  3. memory specificity (the manipulation should only affect the reactivated memory)
  4. a dissociation of immediate & delayed effects of the intervention