GAD, Panic Disorder, Agoraphobia

Question 1

GAD: DSMV criteria

Answer 1

A. Excessive anxiety and worry; more days than not, for at least 6 months.
B. Person finds it difficult to control worry.
C. Anxiety and worry are associated with 3+ or the following:
- restlessness or feeling on edge.
- easily fatigued.
- difficulty concentrating.
- irritability.
- muscle tension.
- sleep disturbance.
D. Anxiety, worry or physical symptoms cause distress or impairment of functioning.
F. Disturbance not due to effects of substance abuse or other medical condition.
G. Not better explained by another mental disorder.

Question 2

GAD prevalence

Answer 2

Wittchen et al (2011): EU 12 month prevalence= 1.7-3.4%.
- F/M ratio: 2.1.
Kessler et al (2005): Lifetime prevalence in USA = 5.7%.

High co-morbidity between GAD and other diagnoses, particularly SAD and depression.
High levels of co-morbidity between GAD and physical diagnoses (eg. gastrointestinal problems).

Question 3

GAD aetiology: Psychoanalytic theories (Freud)

Answer 3

Unconscious unresolved conflict between ego and id impulses.

• Punished for expression of id impulses?
• Defence mechanisms not strong enough to cope with levels of anxiety?

Theorists see roots of GAD in an adequate relationship between child and parents (Sharf, 2012).

Question 4

GAD aetiology: Biological theories

Answer 4

Evidence of reductions in neurotransmitters- serotonin (Mogg et al, 2004).
GABA- usually inhibits anxiety under stress.
HPA axis- controls reactions to stress; may play less significant role than it does in other anxiety disorders.
Genetic factors (Hettema et al, 2001)- significant role of genetic heritability for GAD; twin studies= .32 heritability; strong evidence of predisposition but clear role of environment too.

Question 5

GAD: biological treatments

Answer 5

BZs: increase availability of GABA, show some short term benefits, but should be avoided long term; show good efficacy vs placebo; side effects; dependence.
TCAs: better long term efficacy than BZs; greater evidence of side effects, but less serious.
SSRIs: paroxetine licensed for GAD treatment; RCTs have shown effective treatment; some side effects, eg. nausea, fatigue.
SNRIs: also useful.

Question 6

Worry & GAD

Answer 6

Several of these models have both cognitive and behavioural aspects.
Behaviour- tends to address avoidance.
Cognitive- tend to address worry, generally seen as central feature of GAD.

Question 7

GAD contemporary cognitive models

Answer 7

Metacognitive model of GAD (Wells, 1995; 2007)- two types of worry.

Type 1: active strategy for coping with anticipated danger; triggered by external events and non-cognitive experiences such as physical symptoms; once triggered, positive beliefs lead those with GAD to consider a series of danger related questions; until they feel they have generated coping strategies.

Type 2: During the course of type 1, negative beliefs about worry are activated; attempts then made to avoid worry; type 2 distinguishes between GAD and non-clinical worry.

Question 8

GAD: psychological interventions

Answer 8

Most difficult to treat anxiety disorder (Robichaud & Dugas, 2009).
First appeared in DSM 3- residual diagnosis; people with sig anxiety who did not meet criteria for other diagnoses.
Until recently people with GAD were offered CBT type interventions and relaxation.
Starting to see model-based interventions.

Question 9

GAD: psychological interventions cont.

Answer 9

Behavioural: initial treatments sought to target specific fear but finding specific cause in GAD not easy.
But some relaxation techniques successful.

Cognitive-behavioural:
CBT most common treatment.
Cognitive restructuring and relaxation- tackle distorted thoughts and information processing, reducing tension etc.

Question 10

Specific treatments for GAD

Answer 10

General CBT might focus on challenging content of type 1 worry but this can result in resistance and worry substitution.

Metacognitive therapy (Wells, 2007)- emphasises importance of examining the patient’s meta-cognitions (type 2 worry) that drive the implementation of maladaptive coping.
5 key components:
- case formulation.
- socialisation to the treatment.
- modifying negative beliefs about uncontrollability of worry.
- modifying beliefs about the danger of worry.
- modifying positive beliefs about worry.

Question 11

Evaluating treatments for GAD

Answer 11

Despite success, CBT/cognitive therapies are still less common than pharmacotherapy (Dinan, 2006)- probably changed through IAPT in the UK.
Evidence joint therapy has additional benefits (Gosselin et al, 2006)- CBT/drugs successful in tapering GAD patients off BZs.

Question 12

Panic attacks: DSMV

Answer 12

Not psychological condition but present with many anxiety disorders. 
"Abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, with four or more of the following symptoms. Can occur from a calm state or anxious state.
- palpitations, pounding heart
- sweating
- trembling
- sensations of shortness of breath
- feeling of choking
- chest pain or discomfort
- nausea or abdominal distress
- feeling dizzy, faint etc
- chills or heat sensations etc...

Question 13

Panic attacks: Basic facts

Answer 13

Kessler et al (2006): US life time prevalence: 22.7% (without meeting criteria for anxiety disorder).
F/M ratio: 1.4
Mean age of onset: 22.7

Panic attacks can occur with all anxiety disorders (and others):

• cued/expected: recognisable triggers (eg. making a speech in SAD).
• not cues/unexpected: panic disorder (experience unexpected attacks, but might also experience expected ones).

Question 14

Panic attacks: origins

Answer 14

General biological & psychological vulnerability.
70% + with panic disorder report significant stressors around the time of their first panic attack (Craske, Miller, Rotunda & Barlow, 1990).
These include illness, death of loves ones, break up of relationships etc.
Often people say it came out of the blue but when exploring their recent history there are significant stressors.

Question 15

Panic disorder: DSMV criteria

Answer 15

A. Recurrent unexpected panic attacks.
B. At least one of the attacks has been followed by one month of either:
- persistent worry about additional panic attacks or consequences.
- significant maladaptive change in behaviours related to attacks (eg. avoidance).
C. Disturbance is not due to physiological effects of substance abuse or illness.
D. Disturbance not better explained by other mental disorder.

Question 16

Panic disorder: facts

Answer 16

Wittchen et al (2011): EU 12 month prevalence: 1.8% of population (14 years old +).

• 7.9 mil.
• FM ratio: 2.5.

Kessler et al (2006): lifetime prevalence in USA- 3.7%.

Question 17

Panic disorder

Answer 17

Anyone can get panic attcks- around 25% of us will have one at some stage.
Panic disorder much less common.
Features: frequent, recurrent, unexpected attacks associated with:
- persistent concern of attacks.
- worry about implications.
- significant change in behaviour.

Question 18

Relationship between agoraphobia and panic

Answer 18

Until DSMV both were linked diagnoses:
- PD with A.
- PD without A.
- A without history of PD.
In response to repeated panic attacks, some people start to avoid specific situations for fear of panic occurring = agoraphobia.

Question 19

Agoraphobia: DSMV criteria

Answer 19

A. Marked fear and anxiety about two or more of the following:
- using public transport.
- being in open spaces.
- being in enclosed spaces.
- standing in line or being in a crowd.
- being outside or the home alone.
B. Individual fear or avoids these situations because of thoughts that escape might be difficult or help might not be available in the event of developing panic-like symptoms.
C. Agoraphobic situations almost always provoke fear or anxiety.
D. Agoraphobic situations are actively avoided, require presence of a companion, or endured with intense fear.
E. Anxiety is out of proportion to actual danger posed.
F. Persistent lasting 6 + months.
G. Anxiety or avoidance causes significant distress or impairment in social, occupational or other areas of functioning.
H. No other medical condition present.
I. Not better explained by symptoms of other disorder.

Question 20

Agoraphobia: basic facts

Answer 20

Wittchen et al (2011): EU 12 month prevalence: 2.0% of pop. (14+ years).

• 8.8 mil
• F/M ration: 3.1

Agoraphobia tends to increase as history of panic lengthens (Kikuchi et al, 2005).
Not related to age of onset or frequency of panic attacks (Arch & Craske, 2008).
Occupational status predicts avoidance- eg. have to leave house for work, less likely to develop agoraphobia.
Strongest predictor is gender: as severity increase, proportion of females increases. Socialised sex role expectations may contribute.

Question 21

Panic and agoraphobia models: behavioural

Answer 21

Barlow (1988) characterises panic attacks as “false alarms”,.
Panic disorder developed because exposure to panic attacks causes conditioning of anxiety to exteroceptive and interoceptive cues (Bouton, Mineka, and Barlow, 2001).
Model emphasises interoceptive conditioning: eg. raised heart rate becomes conditioned stimulus due to association with intense fear.
Leads to ‘learned alarms’- triggered by natural increases in feared bodily sensation (eg. exercise, caffeine).
This can happen without individual being aware of shift in bodily sensation, although those with PD often monitor their bodily sensations.

Question 22

Panic/agoraphobia: Biological theories

Answer 22

Genes: twins and family studies indicate moderate heritability = .43.
Children of PD parents at increased risk- “runs in families”.
Neurotransmitters: panic attacks may be due to dysfunction but no substance has been implicated.

Question 23

Panic/A: biological treatment

Answer 23

BZs:

• Alprazolam rapidly improves panic symptoms; sig. long term effects. Similar efficacy with clonazepam and diazepam.
• Tolerability is a problem- sedation reported in most studies.
• Slurred speech, memory and sexual problems.
• Up to 1/3rd of patients develop dependence.

TCAs:

• Imipramine effective in PD patients- but effect slower than BZs.
• Some side effects but reduce over time.

SSRIs:

• Paroxetine more effective than placebo and CBT for reducing panic attacks.
• Some side effects.

Question 24

Panic/A: psychological treatment

Answer 24

Panic control treatment- PCT (Barlow):

• clients taught about nature of anxiety.
• taught how to control breathing.
• taught hot to identify faulty automatic thoughts in panic- learn how to de-catastrophise.
• clients exposed to feared situation and body sensations (interoceptive exposure)- told to induce and evaluate.

Question 25

Evaluating treatments: panic/A

Answer 25

Several studies support benefit of PCT:

• produce lower levels of panic severity and phobic avoidance.
• more likely to achieve and maintain clinically significant change.

Some evidence CBT better than medication:

• but recent review suggest combination is best.
• no difference between CBT alone vs. SSRI alone (Van Apeldoorn et al, 2008).