Problem 5 - PD Flashcards
Panic Disorder (DSM, symptoms)
The recurring and unexpected panic attacks.
At least 1 panic attack is followed yay one month or more of the person fearing that they will have more attacks.
Avoidance behaviour is a hallmark criteria.
Symptoms 4+:
- Palpitations, sweating, trembling, sensations of shortness of breath, choking, nausea, dizzy, derealisation, losing control etc.
Cognitive models: Clark’s
- The misinterpretation of correct bodily sensations - ex: palpitations perceived as a heart attack.
- Stimuli can be internal (sensations, thoughts, images) or external (environmental factors)
- Cycle: trigger > perceived threat > apprehension > body sensations > interpretation of sensations as catastrophic.
Causal model:
- Biological: internal trigger > bodily sensations
- Cognitive: misinterpretation > threat (learned threat too) > apprehension
- Behavioural: panic attack
Criticism:
- Too simplistic, no epistemological reasoning, doesn’t account for difference between 1 attack and the disorder.
Cognitive models: Composite model (3)
- The 3 antecedent conditions:
- Low self-efficacy: from early attachment issues and leads to higher anxiety sensitivity.
- High anxiety sensitivity: from genetic predisposition and attachment issues.
- Learned threat: from early critical threat.
- System susceptibility:
- The 3 antecedents contribute vulnerability.
- Externally/internally triggered by a combination of learned threats and triggers or by low self-efficacy leading to increased arousal and bodily sensations.
- Vicious cycle from Clark’s model.
Causal model
Criticism:
- Lack of empirical support for some of the integrated theories.
- Descriptives
- Does not focus enough on anxiety sensitivity as a causal factor.
- No way to tell if one causes the other, if one is enough or if all of them do.
Biological models: Gorman (6)
- Fear network - centred in the amygdala and includes PFC, insula, thalamus and hypothalamus.
- Low threshold for fear network activation - bodily sensations lead to cognitive misinterpretations that trigger the fear network, releases neurotransmitters and autonomic and behavioural responses of PD occur, further amplifying bodily sensations.
- Inherited susceptibility - not conclusive.
- Conditioned learning/phobic avoidance - contextual information from threatening situations stored in the hippocampus which creates fast responding to similar stimuli.
- Adverse life events
- Trauma - contributes to lowering the threshold of activation of the fear network.
Causal model
Criticism:
- Unclear about the interpretations of internal stimuli.
- Not all neuro-cognitive deficits were observed.
Biological models: Klein’s
It is the correct interpretation of an incorrect physical signal.
- The body tricks you and not the mind.
The threshold for the suffocation false alarm is reduced by epidermic dysfunction.
- Misinterpretations of bodily sensations leads to low threshold for intensity of the feeling.
Causal model:
- Unspecified trigger
Criticism:
- Short and vague with low empirical support.
Neuroscience perspective - mammalian defence system
The amygdala plays crucial role in integrating sensory information and initiating appropriate defensive responses in the face of perceived threats.
Neuroscience perspective - threat imminence of defensive reactivity (3 stages + anxious apprehension)
Pre-encounter defence:
- Predator not seen yet but encountered before
- Pre-emptive behaviour: threat-nonspecific vigilance is engaged.
Post-encounter freeze:
- Predator is identified = organism freezes
- Increased selective attention towards the threat.
Circa-strike defence:
- Strong autonomic arousal and escape behaviour => can be triggered by the dorsal periaqueductal gray electrically/chemically.
- Activated when threat is imminent.
The pathway to induce escape behaviour: sensory transmission ⇒ lateral amygdala ⇒ basolateral amygdala ⇒ hypothalamus ⇒ dPAG ⇒ escape behaviour.
- Damage to this area disrupts defensive freezing.
Conditioned anxious apprehension: the initial attack serve as a conditioned trigger => can trigger acute panic attacks, reinforcing the association between the conditioned and unconditioned stimuli.
Empirical evaluations of the
- Modulating the acoustic startle response: assesses the activation of amygdala-dependent defence circuits to understand defensive behaviour - supports threat imminence model.
- Defensive reactivity: individual differences in reactivity => avoiders, escapees, and completers - supports acute threat model.
- The intensity of the first panic attack: crucial role in the development of PD - supports conditioning theories.
- Learning perspective: conditioned stimuli from first panic attack - supports conditioned anxious apprehension.
Neural networks of PD
Mild physical symptoms lead to the anticipation of a possible panic attack => associated with stronger activation of the:
- Insula
- Dorsal anterior cingulate cortex / dorsomedial prefrontal cortex (dACC/dmPFC)
Treatment for PD - Interoceptive exposure
- Exposing individuals to bodily sensations similar to those experienced during panic attacks.
- Exercises (shaking, running etc) that are tailored to the individuals, starting at a mild intensity.
- No use of hierarchies.
- Effective when strong sensations are evoked.
Treatment for PD - in-vivo exposure
- Focus is on systematic and repeated contact with avoided situations in person.
- Exposure hierarchy is created .
- Varies in intensity and whether it’s therapist-directed or self-directed.
Treatment for PD - Panic control treatment (4)
- Psycho-educational exercises: understanding the physiological reactions associated with PD.
- Cognitive restructuring: identify and challenge beliefs and thoughts related to panic.
- Breathing retraining: to counteract the effects of hyperventilation.
- Interoceptive exposure: provide evidence of somatic sensations being safe.
Treatment for PD - CBT
- Psycho-education
- Cognitive Restructuring - emphasis = to modify misinterpretations of somatic sensations.
- Behavioural techniques: induced feared sensations through hyperventilation - focus on body and word pairs that describe the sensation/catastrophes.
- Response prevention: facilitate disconfirmation of negative predictions regarding effects of symptoms - ex: no clinging on safety objects when feeling dizzy.
- Very effective with exposure therapy (72% panic free).
- Better than medication alone in all aspects but medication can be a good addition.
Treatment for PD - innovations
- Computers
- Biofeedback (measuring sensations and physical symptoms)
- Computerised self-help
- Virtual reality
- Internet-assisted therapy
- Teleconferencing
- Video conferencing
Treatment for PD - barriers
- Client’s face validity
- Length of the sessions
- Resistance and treatment avoidance
- Overenthusiastic patient/therapist
- New untrained therapists
- Pharmacotherapy could take over even though it’s not effective on its own.
- Acceptance of psychological factors.
- What if’s
