problem 5 - panic disorder Flashcards
what is a panic attack
- consists of intense feeling of apprehension or impending doom
- sudden onset & associated with a wide range of distressing physical sensations
- Fearful sensations are seemingly unprovoked, unexplained & out of the blue
criticisms for Fava & Morton’s views of theories of PTSD
learning theory
fava & morton: does not figure prominently their model
evidence suggests:
* accounts of panic using classical conditioning describe a learning history → the experience of panic attacks is a CS for anxiety = potentiates the likelihood of future panic episodes
* an association is formed between aversive interoceptive stimuli and emotional response to these stimuli
criticisms for Fava & Morton’s views of theories of PTSD
cognitive theories
fava & morton: reviewed the 4 theories, combined them & attributed panic disorder to them - equal weight given to all theories
evidence suggests:
* there is unequal support for the models
* recent evidence has indicated that anxiety sensitivity (AS) may actually play a central role in the development of PD
criticisms for Fava & Morton’s views of theories of PTSD
psychodynamic theory
fava & morton: PD is viewed as stemming from an initial appraisal of an event as dangerous, followed by imagining that situation afterwards
evidence suggests:
* empirical support is limited
* there is absence of controlled or case data of successful treatment
criticisms for Fava & Morton’s views of theories of PTSD
biological theories
fava & morton:
* focus mainly of SFA (Klein) & neuroanatomical hypothesis (Gorman)
evidence suggests:
* Klein’s theory has been largely unsupported; research has reported that respiratory symptoms were not linked to panic disorder, but that a “fear of dying” was the strongest predictor
* it is unclear how a neurocognitive deficit would lead to cog misinterpretations of particular stimuli - Gorman does not explain
* F&M also fail to discuss emerging science on the neurobiology of panic disorder
criticisms of composite model by Fava & Morton
- fails to provide a causal model of panic disorder - dont describe the mechanisms through which treatment is effective
- there is an overall neglect of the use of empirical findings to weight the various components
- model focuses on SFA theory and neurocognitive deficits, both of which have not been empirically supported
- authors overgeneralize the imp of adverse life events; there is very little empirical data to support this hypothesis
- role of anxiety sensitivity (AS) is limited in the composite theory despite a large amount of evidence implicating its role in panic disorder
the mammalian defense system (PD)
Emotions like panic and anxiety can be conceived as action dispositions associated w efforts to escape/avoid danger or pain + are rooted in the survival circuits of the brain
defense circuits of the brain feed back to the sensory systems facilitating the detection of threatening & potentially harmful stimuli + prompting defensive reflexive, autonomic and motor responses to counter threats
conditioned anxious apprehension in ppl w PD
- After the first panic attack: mild body symptoms become CS, to previously harmless mild interoceptive stimuli, that engage a CR = anxious apprehension
- anxious apprehension can trigger acute panic attacks strengthening the association between CS and US
- potentially dangerous context
- anxious apprehension
- acute panic
modulation of acoustic startle response & PD
the acoustic startle response is augmented during fear conditioning + this activation is reduced in patients with unilateral lesions of the amygdala
Infliction of startle reflex varied with the proximity of the threat
- Anticipated threat more distant: startle responses were activated
- Anticipated threat closer: inhibition of the startle responses as well as strongly increased autonomic arousal
dynamics of defensive reacitivity in patients with PD
- When a remote threat is encountered (being entrapped in a narrow dark room) → anxious apprehension is engaged - associated with freezing and startle potentiation
- When the threat becomes more imminent (i.e., when interoceptive symptoms become more intense) → active flight behavior is initiated - associated with strong increase in autonomic arousal
intensity of the initial panic attack & PD
- Acquisition & resistance to extinction of conditioned associations increase as function of US intensity = predict that intensity of unconditioned threat should be imp for the development of anxious apprehension
- not a lot of info on this
what is interoceptive exposure?
systematic exposure to the bodily sensations that occur during a panic attack - e.g. head shaking, running in place, breath holding, hyperventilating
* exercises can be completed within-session or as hw assignments
* exercises presented at a mild intensity level to provide exposure without creating undue anxiety
* typically do not use graded hierarchies and appear to be most effective when strong sensations are evoked
* completion of an interoceptive exposure session often causes patients to realize that the feared outcome will not occur + that avoidance behaviours are not necessary
in vivo exposure for PD
focus of in vivo exposure - systematic and repeated contact with avoided situations
* first step in the treatment process: involves creating an exposure hierarchy where the patient identifies a variety of avoided situations that produce a range of distress when confronted
* exposure sessions can vary in intensity and whether they are therapist-directed or self-directed, massed or spaced
barriers to effective exposure therapy for PD
- client perceptions that interoceptive exposure is not effective
- session length - cant end too early
- resistance & treatment avoidance
- overly eager therapist or patient - not move too quickly through process
- novice therapists
- pharmacotherapy - if clients attributr reduction in symptoms to medication not exposure = wont want to continue w exposure
- acceptance of psychological factors - may not comply if they dont believe they have a psych problem
efficacy of CBT for PD
results from diff studies:
- large effect sizes found for cognitive-based interventions without significant exposure components
- CBT interventions that include a combination of cognitive restructuring and exposure elements appear to be the most effective
- these treatments produced large effect sizes for pre changes to postchanges, in order from best to least; cognitive restructuring, panic education, exposure, relaxation
