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Chapter 4: Generalized
Anxiety Disorder (GAD)
Karen Rowa
Heather K. Hood
Martin M. Antony
Diagnosis: Central Features
 Excessive worry occurring about a number of
different topics
 Symptoms of physiological or psychological
hyperarousal
DSM-5 Diagnostic Criteria for
Generalized Anxiety Disorder (GAD)
 Excessive anxiety and worry
 More days than not for at least 6 months; multiple topics
 Difficult to control
 Anxiety and worry are associated with ≥ 3 of following:
 Restlessness or feeling keyed up or on edge
 Being easily fatigued
 Difficulty concentrating or mind going blank
 Irritability
 Muscle tension
 Sleep disturbance
Diagnosis: Comborbidity
 Worry is a common feature of mood disorders
 ~80% of people with GAD also had a comorbid mood
disorder
 GAD cannot be diagnosed if the worry occurs exclusively
during a mood disorder, PTSD, a psychotic disorder, or
PDD
 GAD is highly comorbid with:
 Panic disorder with or without agoraphobia (41%), social
phobia (42%)
Diagnosis: Assessment
 Comprehensive assessment of GAD should cover:
 Beliefs about worry, intolerance of uncertainty, anxiety,
symptoms of hyperarousal, comorbid conditions, goals,
areas of behavioral inactivation, and emotional avoidance
 Self-report measures of GAD can help assess for
presence of diagnostic criteria, severity of worry,
and content of worry topics
Symptoms: Worry
 GAD worries are indistinguishable in content from
“normal” worries
 GAD worries differ from normal worries in that:
 Increased frequency and intensity
 Perceived inability to control the worry
 Distinguishable from cognitions seen in social
anxiety disorder and panic disorder
 More future-oriented
Symptoms: Avoidance and
Checking
 Many individuals with GAD engage in behaviors
intended to avoid or reduce distress or anxiety
 Individuals with GAD endorse similar degrees of
checking behavior compared to individuals with
OCD
 Checking in GAD is predominantly interpersonal (e.g.,
seeking reassurance from others)
Symptoms: Functioning
 Some individuals with GAD report severe disability
across domains
 Particularly romantic relationships
 Significantly lower overall quality of life and life
satisfaction in wider range of areas
 Self-esteem, work, health, and social relationships
Prognosis
 Chronic and relapsing with some fluctuation in course
 Probability of full remission at some point over 5 years is ~38%
 Probability of partial remission is ~47%
 Predictors of a negative clinical course
 Comorbid Axis I disorders
 Personality disorders
 Decreased life satisfaction
 Difficult family relationships
 GAD onset is equally likely to be before or after a
major depressive episode, indicating that GAD is not
simply a secondary condition
Epidemiology
 Current point prevalence = ~1.6%, lifestime prevalence = ~5%
 Median point prevalence in primary care settings is 5.8%:
 More likely to seek medical attention than individuals with other
disorders
 Median age of onset = ~31 years old
 Earlier onset associated with higher symptom severity, comorbidity, and
vulnerability to other disorders
 Women almost twice as likely to meet diagnostic criteria for GAD
 Men have higher rates of comorbid alcohol and substance use
 Women have higher rates of comorbid mood and anxiety disorders, and
greater degree of disability
 Different cultural groups may demonstrate differences in both the
content of worries and focus of GAD symptoms
Etiology: Problem-Solving Ability
 Worrying conceptualized as an attempt to anticipate or
solve real-life problems (i.e., constructive problemfocused coping)
 In GAD, the worry process breaks down and becomes
pathological
 Individuals with chronic worry do not have deficits in
problem-solving ability. They have…
 Less confidence about their problem-solving abilities
 A negative problem orientation
 Negative problem orientation and intolerance of
uncertainty predicts worry and symptom severity
Etiology- Probability Overestimation
and Catastrophizing
 People with GAD exhibit cognitive errors of:
 Probability overestimation: Thinking a feared consequence
is more likely to occur than it really is
 Catastrophizing: Assuming that an outcome will be much less
manageable than it actually is
 Estimates of the cost of one’s worry (i.e., negative
consequences of worrying) correlate with worry
severity
 Also catastrophize about positive aspects of their lives
and hypothetical situations
Etiology- Information-Processing
Theories
 Greater attention to threatening stimuli,
preferentially encode them, interpret ambiguous
stimuli as threatening, and memory biases for
threatening events
 Attentional biases include selective attention
toward, difficulty disengaging from, and attentional
avoidance of threatening stimuli
 Attentional bias remains when stimuli are masked;
processing of threat cues may not be at a conscious level
 Treatment modifies bias, for example, color-naming
interference is ameliorated by CBT
Etiology: Avoidance Theories
 Worry is cognitive avoidance, similar to behavioral
avoidance
 Verbal worry distracts from full experience of fear (e.g., feared
imagery, sensations of arousal)
 Reduction in distress and arousal in the short term
 Worry is negatively reinforced
 Instruction to worry in response to an anxiety-
provoking trigger increases threat duration and
decreases perceived control
 Opposite effect of imaginal processing or relaxation/distraction
Etiology: Intolerance of
Uncertainty Theory
 Tendency to react negatively to uncertain or
ambiguous situations
 Sometimes prefer a negative outcome to an uncertain
one
 Causes people to feel less capable of effectively solving
problems
 Leads to pathological worry instead of problem solving
 Intolerance of uncertainty correlated with worry in
GAD and controls
 In CBT for GAD, changes in intolerance of uncertainty
preceded changes in time spent worrying
Etiology: Metacognitive Model of
GAD
 Metacognition: Thinking about one’s thought
processes
 Type 1 worry: Worry triggered by everyday events
(e.g., worries about health, safety, or relationships).
 Type 2 worry: Worry about worry
 Positive beliefs: Belief that worry is useful
 Negative beliefs: Belief that worry is uncontrollable or
dangerous
 GAD individuals hold both positive and negative beliefs
 More metaworry than individuals with social phobia, panic
disorder, depression, and OCD
Etiology: Metacognitive Model
 Negative beliefs
 Clusters: Worry disrupts performance, worry
exaggerates the problem, and worry causes
emotional distress
 Associated with pathological worry, even when
other kinds of worry and anxiety are controlled
 Positive beliefs
 Clusters: Worry helps motivation and worry helps
analytical thinking
 Uniquely predict pathological worry above and
beyond negative beliefs
Etiology: Emotional Regulation
Model
 GAD individuals find it difficult to regulate
emotional experience
 Difficulty naming and understanding emotions, difficulty
accepting emotional experience, difficulty regulating
negative emotions
 Heightened intensity of emotion strong predictor of
GAD
 Differentiates GAD from social anxiety and major
depressive disorder
Etiology: Emotional Regulation
Model
 Negative mood states may prevent GAD
individuals from using “stop rules” to know when to
stop worrying
 Example of stop rule: “I will think of as many
possible responses as I can to the situation”
 When the “as many as I can” is paired with negative
mood, person feels she has not generated as many
responses as possible after reasonable effort, leading to
perseveration
Biological Etiology: GABA Theory
 GABA plays inhibitory role in the brain, aiding
inhibition of subcortical circuits stimulated by threat
 GABA receptors dense in frontal cortex, hippocampus,
and amygdala
 GAD individuals have decreased GABA activity
and less inhibition of these threat-activated
structures
 Also, reduced benzodiazepine receptor sensitivity:
important because binding of a benzodiazepine receptor
facilitates GABA binding
 Benzodiazepines effective treatment for GAD
Biological Etiology:
Neuroanatomical
 Larger amygdala and superior temporal gyrus
volumes, hypometabolisim in the basal ganglia,
and hypermetabolism in the prefrontal cortex
 Disrupted connectivity of the amygdala with
cortical and subcortical regions important for
anticipatory anxiety and emotional processing
 Activation in the prefrontal cortex regulates activation in
subcortical structures
 Problems in circuit may lead to GAD emotional
processing deficits
Biological Etiology- Other
Neurotransmitters Hormones
 Neuroephrine (NE): No differences between clinical and
control groups found on baseline levels even though
selective NE reuptake inhibitors are effective treatment
 Serotonin (5-HT): Low levels of serotonin and serotonin
receptor dysfunction linked with increased anxiety
 Cholecystokinin (CCK): Linked to panic attacks
sometimes seen in GAD. CCK agonist induces panic
attacks in ~71% of participants with GAD, ~14% of control
participants
 Cortisol: Levels significantly reduced following SSRI
treatment for GAD, and reduced cortisol associated with
reduced anxiety
Biological Etiology: Physiological
Signs
 Chronic worry associated with reduced autonomic
variability during stressful tasks
 Lower heart rate variability and decreased
parasympathetic activity during periods of worry and rest
 Heart rate variability is associated with symptom severity
in GAD, but not in other anxiety disorders
 Autonomic rigidity leads to less adaptive
behavioral and emotional responses to stressful
events
Risk Factors: Stress and Family
Environment
 Stressful life events increase risk of onset and
relapse
 Men with more than three stressful life events
have 8x greater rate of GAD
 GAD individuals experience more unpleasant,
negative, and rejecting family environments with
parent-child boundary problems
 Perceived parental alienation and rejection
correlated with GAD symptoms in adolescents
Treatments: CBT
 Most commonly used components
 Psychoeducation
 Relaxation training
 Monitoring of cues and triggers for worry
 Imaginal exposure
 In vivo exposure
 Cognitive restructuring
Treatments: CBT Efficacy
 CBT superior to wait-list controls and nonspecific
alternative treatments
 Effective for symptoms of worry, anxiety, and depression
 CBT and pharmacotherapy’s effect sizes are
similar
 CBT has advantage in long-term maintenance of
treatment gains, patient acceptability, and tolerability
 CBT is also useful in helping individuals discontinue
benzodiazepine medication
Treatments: Recent Advances
in CBT
 CBT variants targeting intolerance of uncertainty
and related cognitions
 Effective in group and individual formats
 Lasting improvements in GAD symptoms
 Gains maintained longer than with relaxation therapy
 CBT therapy derived from Wells’s metacognitive
model
 Lasting improvements in GAD symptoms
 Greater reductions than CBT targeting tolerance of
uncertainty
Treatments: Recent Advances
in CBT
 CBT augmented with other treatment strategies
(e.g., motivational interviewing) may reduce
treatment resistance and enhance efficacy
 Unclear which components of CBT are most useful
and whether new variants are reliably better than
standard CBT
 Large percentages of clients continue to experience
significant symptoms at posttreatment and follow-up.
Treatments: Pharmacological
 Response of GAD to placebo is particularly high (> 40%)
 More difficult to demonstrate significantly better effects for specific
medications
 Serotonin reuptake inhibitors (SSRIs) are the first-line
therapy for GAD
 CBT and pharmacotherapy similarly effective
 Benzodiazepines reduce both somatic and cognitive
symptoms
 Potential tolerance, dependence, and withdrawal symptoms
 Only recommended for short-term treatment (i.e., less than 4 weeks),
as an adjunct to antidepressant medication, or for severe, treatmentresistant GAD symptoms
Treatments- Alternative
Pharmacological Treatments
 Buspirone: Partial agonist of presynaptic serotonin receptors
 Moderate effect size
 Less well tolerated in clinical practice and less effective than SSRI treatments
 Selective Neuroepinephrine Reuptake Inhibitors (SNRIs)
 Venlafaxine has moderate effect size (similar effects to paroxetine)
 Demonstrated effectiveness over longer treatment trials
 Concerns about its safety in overdose and cardiac implications
 Pregabalin: Analogue of the neurotransmitter GABA
 Small to moderate effect sizes (not approved for GAD in United States)
 Greater efficacy for treating psychological distress relative to somatic symptoms
 Second Generation Antipsychotics
 Not effective as augmentation in treatment refractory GAD
 Quetiapine effective as monotherapy. Significant side effects limit clinical utility