Transcript Generalized anxiety disorder - The Cambridge MRCPsych Course

Generalized anxiety disorder
Dr Joanna S Woodger
Generalized Anxiety Disorder (GAD)
• Excessive, uncontrollable worry often
disproportional
• GAD affects 2% of population
• GAD is chronic
History of GAD
• 20th century- distinction between fear and
anxiety
• Freud
• Jaspers
• Roycroft
Definition of GAD
• Controversial
• Debate whether GAD is:
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-free standing primary disorder
-prodromal or residual phase of other
disorders
-personality trait
-co-morbid condition that modifies the course,
treatment response and outcome of other
diseases
WHO ICD-10 classification of GAD
primary symptoms of anxiety most days, for at
least several weeks at the time
The symptoms should involve elements of:
• Apprehension
• Motor tension
• Autonomic over-activity
• Can be associated with transient other
symptoms e.g. depression
DSM-III 1980 first Classification of GAD
• Recognized GAD as a separate disorder with
symptoms as per ICD-10
• Since 1980 number of further modificationsin GAD symptoms must be present for at least
6mts
Prevalence and diagnosis of GAD
• DSM III vs DSM IV
Europe 1.7% (DSM IV)
Co-morbidity of GAD
• Anxiety disorders
• Psychiatric disorders (e.g. Depression)
• Medical conditions
Functional impact of GAD
• Social
• Employment
• Emotional
• Physical
Associated with increased risk of suicide
Biological basis of GAD
• GABA
• Serotonin
• Noradrenaline
GABA
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3 receptor types
GABAa most relevant
GABAaligand gated ion channel
Subunits: 2alfa,2 beta,1delta
Binding of GABA to GABAa receptor leads to
central channel opening, Cl- ions entering the
cell reduction of brain excitability resulting in
decrease of anxiety
GABA agonists
• Benzodiazepines
• Barbiturates
• Alcohol
Bind to various sites on the receptor to provide
anxiolytic effect
Benzodiazepines binding to GABA
receptor
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Unique site
Indirect channel opening- safer
Dose dependant affinity
Different bdz different affinity
Modeling of GAD
• Inhalation of 7.5% CO2 for 20 min
• Symptoms of GAD significantly decreased with
prior administration of bdz
Serotonin in GAD
• Several different drugs used in treatment of
anxiety disorders, act on 5HT systems
Mechanism of 5HT action in GAD
• SSRI likely to cause 5HT2c activation
• Anxiety decrease associated with 5HT2c
receptor de-sensitization
Relationship between GABA and 5HT
in GAD
• Speculation
• Mice lacking 5HTa receptor are more anxious
and have reduced expression of GABA/BZD
alpha-1 subunit
Treatment guidelines for GAD
British Ass of Psychopharmacology 2005
Take account of clinical features, patients preference,
availability
Choose evidence based treatment
Use treatment known to be efficacious in preventing relapse
Treatment of up to 12/52 may be necessary to assess efficacy
Continue treatment for at least 6 mts in patients who
responded
Monitor efficacy and tolerability during long term treatment
Consider SSRI as first line treatment
Routine combination of psychological tx is NOT recommended
After non response to initial treatment
consider:
• Switches to another evidence based tx
• Combining drug tx with CBT
• Combining drug tx only if there are no
contraindications
• Ref to specialist services in refractory patients
Predicting response
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Good predictors are:
-short duration of symptoms
-hx of depression or panic disorder
-psychiatric co-morbidity
Bad predictors are:
-lower symptom severity
-BZD use
Social phobia
• Definition:
• -inappropriate anxiety experienced in social
situations, often leads to avoidance
Sy of social phobia
• Anxiety
• Blushing
• Trembling
Co-morbidity of social phobia
• Depression
• Alcohol misuse
Onset and development of SP
• Starts early in life (before age of 18)
• 1st episode in public place
• Lasts for at least 6 mts (DSMIV)
Epidemiology, course and prognosis
• 3.7%
• M=F
• Symptoms last at least 20-25 years
Treatment for Social Phobia
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CBT
Relaxation training
Pharmacotherapy
-paroxetine
-sertraline
-fluoxetine
-phenelzine
-BZD for short term
Beta blockers for blushing, trembling, palpitations
The end