Problem 5: Panic disorder Flashcards
Clark’s theory for PD:
trigger stimulus –> perceived threat –> apprehension –> bodily sensations –> interpretations of sensations as catastrophic
-trigger can be internal or external
-criticism: model only explains what happens during panic attack
focus on catastrophic misinterpretations
-repetition of panic attack is what distinguishes clinical from non clinical patients
fava & Morton’s composite cognitive theory:
3 conditions in patients with PD: lower-self efficacy (ability to cope with threat), high anxiety sensitivity, learned threat
-panic attack cycle
-criticism: not empirically supported, no-cause effect relationship, does not describe mechanisms through which treatment would be effective
Gorman neuroanatomical hypothesis of PD
-biological predisposition + event –> lower threshold for fear system activation –> quicker physiological response –> more sensitive fear network
-contextual associations are stored in hippocampus and trigger fear network
-neuroendocrine activation
-you inherit susceptibility for PD, not the disorder itself
-early life event + attachment issues can be cause because they cause a sensitive fear network
Klein’s suffocation false alarm theory
-misinterpretation of stimulus
-there’s a correct cognition but the biological signal is wrong
-there’s an opiodergic dysfunction –> suffocation alarm (threshold reduced) –> biological responses –> cognitive responses –> Panic attack
-respiratory signals are key
threat imminence model (new neurobiological model of PD)
-pre-encounter (hyper vigilance to potential threat)
-post-encounter (threat detected: increased selective attention + freezing)
-circa strike (active defensive behaviour + escape )
-when organism is in context with predator and the predator has been encountered before –> triggers pre-emptive behaviour
-Evidence: startle response, dorsal PAG, ventral PAG, V1 PAG (directs freezing), dorso-lateral PAG directs escaping behaviour
-hyperventilation: low CO2 –> use paper bag to get more CO2 in the blood
startle reflex study in threat imminence model
when threat was distant –> startle response is activated –> alert to surroundings
when threat was imminent –> startle response shuts down, fight or flight is activated (circa strike zone)
room study for threat imminence model
-avoiders; refuse to enter chamber
-Escapers: entered chamber but left during 10 minutes
–> during initial exposure they showed strong startle potentiation + increased heart rate, shortly before they escaped, heart rate went up + significant inhibition in startle reflex
-completers: people that completed the whole exercise
–> strong startle potentiation + increase in autonomic arousal + strong anxious apprehension
what about high anxiety sensitivity
for people with high AS, their fear can be comparable to people with PD,
this was shown in a hyperventilation experiment in which a panic attack was triggered, they showed equal symptoms
treatment approaches for PD
-interoceptive exposure
-in vivo exposure
-panic control treatment (learning how to deal with symptoms)
-cognitive therapy (changing misinterpretations of somatic symptoms
-CBT and exposure were most effective
criticism on fava and Morton
-they don’t weigh the various theories according to how well supported they are in their model
-biological factors are included that have not been supported yet (should be treated as correlates)
-overgeneralize the importance of adverse life events (no data)
-role of anxiety sensitivity is too limited
revised composite theory
-more emphasis on AS
-biological factors and early childhood experiences are modeled to be the cause
-for people that had a PA, those that maintain catastrophic cognitions and aversive respiratory experience are more likely to develop PD
