Lecture 10 - theoretical frameworks and new directions Flashcards

1
Q

what is the importance of theoretical frameworks in psychopathology

A

provides further insight into mechanisms and processes that contribute to the emotional disorders
provides directions for future research

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2
Q

explain Beck’s model and the issue with it

A

Beck’s schema theory (also bower’s network model)

proposed mechanism of action but did not differentiate between depression and anxiety

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3
Q

cognitive schemata

A

relatively enduring characteristics of a person’s cognitive organization of representations of previous experience
importance for encoding and classifying stimuli, reasoning and retrieval
part of beck

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4
Q

dysfunctional schemata

A

this is what results in psychopathology according to Beck

content of the schemata varies by disorder but mechanism of action does not

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5
Q

how evidence did not support beck’s framework

A

depressoina nd anxiety result in different profile of biases for attention and memory

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6
Q

why did william et al 1988 develop their model and what is it called

A

integrative model

developed to explain why there should be a different pattern of results in anxiety vs depression

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7
Q

integrative model principles

A

key processing components - priming vs elaboration
main source of bias in anxiety is initial automatic priming towards detection of threat related material and subsequent elaborative processing away from processing of threat
in contrat in depression main biases result from resource demnading elaborative processing

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8
Q

some problems with integrative model

A

attention - evidence depression can result in attentional biases not consistent with integrative model
memory - anxiety patients can exhibit explicit memory biases - not consistent with integrative model

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9
Q

name an example of multi-level models ad why we need them

A

interacting cognitive subsystems

experimental findings seem best able to fit into modesl that posit different representational levels or sub-systems

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10
Q

common features of multi-level models

A

sub-systems or levels representing higher-order meaning and ones which reflect basic propositional and analogical properties of the information space
models differ in way that this is accomplished

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11
Q

explain the interacting cognitive subsytstems (teasdale and barnard 1993)

A

3 sensory-proprioceptive subsystems
2 intermediate structural subsystems
2 meaning subsystems
2 affecter subsystems

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12
Q

explain the propositional subsystem

A

propositions (factual statements) that are the lowest level semantic units in the system. facts are wither true or false

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13
Q

explain the implicational subsystem

A

schematic models that are comprised of information from multiple subsystems - visual, body state and propositional

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14
Q

combination of proposition and implicational subsystems produce…

A

emotion

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15
Q

interpretation of process from clinical example

A

propositional belief that i am a failure at work is rejected
implicational belief that i am always wrong and can not figure things out for self is confirmed and therefore more depression results

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16
Q

a limitation of interacting cognitive subsystems

A

distinction between propositions and implications is not always clear
more empirical evidence needed although some evidence exists (eg teasdale, taylor, cooper, hayhurt and pykel 1995)
teasdale et al 1995 found that depressed patients completed sentence stems with positive words or phrases that mapped onto high level schematic models rather than offering simple negative sentence completions

17
Q

key difference between single and multi-level theories

A

cognitive therapy - can challenge beliefs and negative thoughts at a propositional level
client rejects negative propositions but validates higher level model resulting in more depression
difference between intellectual beliefs and emotional beliefs (implicational level)

18
Q

ICS vs cognitive therapy

A

beck’s model - emotional consequence of thought (negative thought-depression)
in ICS, negative automatic thoughts consequence rather than cause of a depressive schematic model but negative thoughts can lock the system into a depression-maintaining vortex

19
Q

CARFAX model

A

model to explain mechanisms underlying OGM
functional avoidance
capture of retrieval by abstract ruminative structure
reduced executive resources

20
Q

explain functional avoidance of the CARFAX model

A

basic premise - the retrieval of general descriptions may produce less affect than the recollection of specific episodic memories
evidence - hermans et al 2005, found that individuals who retrieved memories in a less specific way also displayed a more avoidant style with respect to thoughts and feelings in general
problem - see overgeneral memory recall to positive and negative cues

21
Q

explain rumination as part of the CARFAX model

A

predominance of conceptual self-relevant infor in early stages of memory search may lead to difficulties in accessing specific memories
can view these self-representations as negative schemata
when emotional cue words used on the AMT, more likely to activate conceptual abstract info in individuals where this info is already highly accessible
therefore AMT words capture people, particulrly for those who ruminate
evidence - manipulations of rumination result in more OGM retrieval (Watknis and teasdale, 2001)

22
Q

explanation of reduced executive resources in the CARFAX model

A

generative retrieval requires use of limited executive resources
ability to retrieve specific memories in anrrative is associated with development of supervisory control functions (Fivush and Nelson, 2004)
evidence against executive account - williams and broadbent 1986 found OGM not associated with semantic fluency performance

23
Q

evidence for inhibition and OGM retrieval

A

Dalgleish et al 2007 - the key problem in retrieval of specific autobio memories is the failure to inhibit irrelevant infor leading to capture errors
demonstrated that OGM retrieval of autobio memories was correlated with errors on tasks where irrelevant material needed to be inhibited such as the emotional stroop but no tasks requiring general levels of executive resource like explicit memory tests

24
Q

vulnerability and depression - biological and cognitive factors

A

booji et al 2007 investigayed the relaptionshpi between acute tryptophan depletion (ATD) and cognitive reactivity (CR)
most models of emotionl disorders are stress-diathesis models
pre-existing vulnerability interacts with stress to produce disorder
need to look at relationship between cognitive and biological markers of vulnerability

25
Q

biological markers of depression

A

response to pharmacological challenges such as the dexamethasone/corticotropin releasing hormone (DEX-CRH) test
response to ATD (moreno et al 2000)

26
Q

psychological markers of depression

A

cognitive reactivity (segal et al 1999)
rumination (Kuehner and weber 1999)
information-processing indicies (elliot, 1998)

27
Q

actute tryptophan depletion explained

A

temporarily lowers serotonin (5-HT)
studies using this method have shown
- impaired memory consolidation (Riedel et al 1999)
- impaired emotional processing in healthy (Tunbridge et al 2003) and remitted depressed individuals (Booji et al 2005)

28
Q

serotonin (5-HT)

studies which aim to increase serotonin have shown…

A

it can facilitate the recall of positive information while impairing the detction of facial expressions of anger and fear in healthy volunteers (Harmer et al 2004)

29
Q

procedure to induce acute tryptophan depletion

A

aims to reuce Trp, a precursor to 5-HT
day 1: low Trp diet
ingestion of a mixture of all essential amino acids except Trp
results - Trp levels are reduced by 75-90%, 5-7 hours after administration and consequently 5-HT is impaired

30
Q

research from ATD studies

A

a high-dose of ATD deteriorates symptoms in around 50% of remitted depressed patients (Van Der Does, 2001)
responses to ATD may predict a recurrence of depression within 1 year (moreno et al 2000)

31
Q

cognitive reactivity

A

relates to dysfunctional schemas
it is argued that dysfunctional schemas do not dissapear during remission but become inactive
may be reactivated when a sad mood deepens
represents a feedback loop (Beck, 1967)

32
Q

how to induce cognitive reactivity

A

activate dysfucntional schemas
take dysfucntional attitude scale (DAS) at baseline
sad mood induction
DAS post induction
remitted depressed patients display higher DAS change score

33
Q

what is compassion

A

neff (2003) “ being touched by and open to one’s own suffering, not avoiding or disconnecting from it, generating their desire to alleviate one’s suffering and to heal oneself with kindness
self-compassion also involves offering non-judgemental understanding to one’s pain, inadequacies and failures, so that one’s experience is seen as part of the larger human experience

34
Q

explain the basis of MBCT

A

trains people to become more aware of body sensations, thoughts and feelings associated with depressoin
trains people to focus on here and now instead of those feelings, sensations and thoughts
acknowledge feelings but let them go

35
Q

why is an alternative to anti-depressents (paritcularly maintenance ones) important

A

adverse reactions to medications
preference not to take medications
non-adherence to taking medications
not building skills for developing resilience

36
Q

exposure therapy for phobias and anxiety disorders

A

derived from learning theory
involves designed experiences with feared stimuli
individual who has a fear of contaminated faucets guided to touch faucets without engaging in compulsive cleaning rituals

37
Q

what is being learnt in exposure therpy

A

the feared stimulus is not as harmful as expected
by repeatedly encouraging touching of feared stimulus (faucet) without safety behaviours and also the unconditioned stimulus

38
Q

problems with exposure therapy

A

half the people with OCD do not respond to exposure therapy (Homles et al 2014)
extinction learning not robust - eg may fail to generalize to new context
fear extinction - may involve inhibitory pathways from ventromedial prefrontal cortex to the amygdala
insights for treating this group may come from neuroscience and bio
using D-cycloserine (originally and anti-biotic) to enhance response to exposure therapy