Phobias & SAD and GAD & PD

Worry as cognitive avoidance Borkovec et al. 1994, 2004

• Worry has an important function for people with GAD

helps people avoid experiencing negative emotions

• Does not allow deeper emotional processing

• Worry is thought to be a linguistic process that does not tap into deeper mental

images

• People can avoid negative emotions associated with the worry is processed

without mental imagery

• Studies

people who were worrying did not create imagery; rather worry was experienced

as negative verbal/linguistic activity (e.g. Borkovec&Inz, 1990)

people verbally articulating fear material created much less heart rate activity

than when imagining the situation (Vrana et al.1986)

verbal processing impedes environmental and experiential information from being

process, preventing learning of nonthreatening associations (e.g. Roemer &

Orsillio, 2002)

• Worry can help someone anticipate and plan for the future

• For people with GAD worry helps

- avoid or prevent bad events

People with GAD find it more difficult to tolerate and accept uncertainty than

people without GAD (Dugas et al. 1998)

- motivate oneself to get things done

- prepare for the worst

- problem-solve

- distract oneself from even more emotional topics

- and superstitiously lessen the likelihood of bad events

• Processing bias to threat plays an important role in development and maintenance of anxiety

(Mogg & Bradley, 2005)

• attention bias: for threatening words and pictures

Person with GAD hypervigilant in detecting particular threats, leading to worry

• Interpretation bias: interpreting ambiguous stimuli as threatening

(e.g viewing news->personal threat)

• People with GAD display both biases (Mogg & Bradley, 2005)

• worry about worry

• For people with GAD often belief that worry is associated with going crazy or

uncontrollability of worry

->start to worry about how much they are worrying

• Metaworry good discriminator between GAD and other anxiety disorders

• During CBT therapists attempt to reduce low level of processing by having patients

“worry out “ their negative emotions -> exposure therapy to help processing worry

on a deeper level

• Although GAD mostly characterized by cognitive avoidance, behavioral avoidance

of situations (e.g. social situations) is seen in over half of the individuals

(Butler et al. 1987)

• CBT helps to reevaluate:

- the positive benefits of worrying

- interpretation biases of ambiguous stimuli

- their intolerance of uncertainty

- metaworry

• Most frequently studied, evidence-based, psychological strategies for treating GAD

include:

- Cognitive strategies

- Exposure-based strategies

- Acceptance based strategies

• CBT has been shown to be very effective for the treatment of GAD, with long term

effects

• Clinical improvement in 38-63% of individuals who complete treatment

(Waters & Craske, 2005)

-> this number not as high as CBT for other anxiety disorders

(80% clinical improvement in panic disorder, Campbell & Brown, 2002)

• Adding of mindfulness components leads to improvement of existing CBT treatments,

clinical improvement in 78% of individuals (Roemer et al.2008)

• Evidence for pharmacological treatments:

large randomized placebo-controlled trials with GAD have been conducted with

Benzodiazepines and antidepressants

• Compared to placebo, benzodiazepines provide effective and rapid symptomatic relief

(Galenberg et al. 2000)

-> should not be used for more than 2-4 weeks

-> side effects: dependency, sedation and increased risks of neonatal and infant mortility when

used while breastfeeding or late pregnancy

• SSRI are the recommended treatment

-> pharmacological treatments reduce physical symptoms rather than worry

(Anderson & Palm, 2006)

-> works also for co-morbidities

-> long term efficacy of antidepressant with follow-up of years required

->efficacy over 6 months follow-up periods: greater remission rates than placebo at 6 months

(69% vs. 42-46%)

• Very few studies compared effectiveness CBT with medication treatments for GAD

• Redmond (1981): stimulation locus coeruleus produced fear response in

monkeys

• Efferent axons of locus coeruleus that project to the hypothalamus are of

special significance for panic disorder (Charney & Heiniger, 1986)-

>influence on HPA-axis

• Administration of the noradrenergic antagonist yohimbine produced panic

attacks in panic disorder ( Abelson et al. 1992)

• Dysregulation (hyperactive) of noradrenergic system in panic disorder

(Coplan et al., 1997)

• Desynchronization of noradrenergic system and HPA axis possible but not

completely successful (Coplan et al. 1995)

• Dysfunctional neurotransmission at the serotonin receptors (5HT1A) may result in

anxiety or avoidant behavior (Deakin 1996)

• Activation of HPA Axis in panic disorder, may contribute to disruption of

hippocampal 5HT1A

neurotransmission (Lesch and Lerer 1991)

• Aberrant noradrenergic- serotonergic function (Boyer 1995)

• Serotonin depletion resulted in increased minute ventilation in panic disorder

patients

unaltered ventilatory function in controls (Kent et al., 1996)

• GABA = inhibitory neurotransmitter

• Benzodiazepines increase function of GABA

• global decrease in benzodiazepine binding

• with a peak decrease in orbitofrontal cortex, and insula, hippocampus in panic

disorder patients compared to healthy controls (Malzia et al., 1998)

• Injection of sodium lactate (panicogen) led to panic-like response in

GABA-blocked rats only (Shekhar 2006)

• Interaction GABA-glutamate interrupted in panic disorder

= substances that can induce panic attacks

• substances that influence HPA Axis

Yohimbine (noradrenaline increase)

coffein: adenosinergic (inhibitory) receptor antagonist

• Substances that influence lactate metabolism

sodium lactate, sodium bicarbonate, carbon dioxide

• Twin studies have attributed 30-40% of the variance for the liability to develop

panic disorder to genetic factors (Kendler et al., 2001; Scherrer et al. 2000)

• highly significant association between panic disorder in probands

and first degree relatives (Hettema et al. 2001)

• cholecystokinin, adenosine 2A, MAO A, and COMT genes.

• Dynamic Model:

panic attack = expression of an intense unconscious conflict (Bush et al. 1999)

core conflict of depencency and inadequacy (Shear et al. 1993)

Contemporary dynamic models: integration of biological and developmental stressors

(Milrod et al. 2004)

• Cognitive Behavioral Models

• Anxiety Sensitivity

• Core fear toward anxiety and its associated somatic symptoms

• Measured by anxiety sensitivity index

(Reiss et al. 1986)

• Significant predictor of the onset of panic in different patient populations

(e.g Ehlers 1995, Hayward et al. 2000; Maller and Reiss 1992)

• Ley (1985): hyperventilation theory : hyperventilation causes panic attacks

• Klein (1993): false suffocation alarm model: hyperventilation avoid panic

attacks

Person is hypersensitive to carbon dioxide levels ⇒ Minor drops in Oxygen result in false alarm "person is suffocating" ⇒ Panic Attack

First line treatments

• SSRI (Selective Serotonin Reuptake Inhibitors)

effective in many controlled studies ( e.g. Wade et al. 1997; Michelson et al 1998, 2000)

anxiolytic effect latency of 2-4 weeks

• Serotonin Norepinephrine Reuptake Inhibitors

effective in double blind placebo controlled studies (Bradwejn et al. 2005; Pollack et al. 1996)

Second line treatments

• Tricyclic antidepressants

frequency of adverse events is higher than for SSRI (Amore et al. 1999)

Third line treatments

• Benzodiazepines

anxiolytic effects immediately after oral intake, risk of dependency (Bradwejn 1993)

Cognitive behavioral therapy

“Panic control treatment”

(PCT, Craske et al., 2000, Hofmann & Spiegel, 1999)

Elements

• Education about anxiety and panic development

• Cognitive restructuration: identification and correction of thoughts /

false cognitions about anxiety and its consequences

• Training (reduction arousal, hyperventilation)

• Exposition, controlled hyperventilation

11-12 sessions, 3-4 months

Classical CBT Methods

• Hyperventilation

• Triggering bodily symptoms

• Deep breathing

• External focus

• mindfulness

Interoceptive exposure

Feared sensations become safe sensations:

• in the office with the therapist

• at home

• independent of the treatment context

Panic Cycle

Uh oh!

What if:

• This gets worse?

• I lose control?

• This is a stroke?

I have to control

this!

Relative Comfort

• Notice the sensation

• Do nothing to control it.

• Relax WITH

the sensation

Head rolling – 30 seconds - dizziness, disorientation

Hyperventilation – 1 minute - produces dizziness

lightheadedness, numbness, tingling, hot flushes, visual

distortion

Stair running – a few flights – produces breathlessness, a

pounding heart, heavy legs, trembling

Full body tension – 1 minute – produces trembling, heavy

muscles, numbness

Chair spinning – several times around – produces strong

dizziness, disorientation

Mirror (or hand) staring – 1 minute – produces derealization

• Efficacy between 87% and 75%

• Greater efficacy than relaxation therapy or control groups

• Greater efficacy than certain medicaments (e.g. alprazolam) and

similar to imipramine

• Long-term treatment with PCT is more effective than pharmacological

treatment

• Evidence of superiority from combined approach towards single treatment

not conclusive

• New developments: combination with self-help modules, therapy via

internet, electronic auto-observation