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Summary Anxiety and Related Disorders GGZ2024 (English) tasks + lectures
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  • Course
  • Anxiety and Related Disorders (GGZ2024)
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  • Maastricht University (UM)

This document consists of a summary of the course Anxiety and Related Disorders GGZ2024 and can be used to prepare for the tutorials and for the exam.

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Document information

  • June 7, 2024
  • 97
  • 2023/2024
  • Summary

Subjects

  • social anxiety disorder
  • panic disorder
  • specific phobia
  • ocd
  • ptss
  • classical conditioning
  • exposure therapy
  • generalised anxiety disorder

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  • Maastricht University (UM)
  • Gezondheidswetenschappen
  • Anxiety and Related Disorders (GGZ2024)
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Task 1: GAD, SAD, and PD
How does the stress response work?
Immediate physical reactions: rapid breathing, increased heart rate, sweating, tremors, > part of the fight-flight
response/syndrome > prepares the body to face or flee an immediate threat

Long-term stressors -> first reactions are the beginning of a longer series of
physical/psychological reactions: physical reactions to stress occur in a consistent
pattern = Selye's model of general adaptation syndrome (GAS):

1. Alarm response = a version of fight-or-flight syndrome > generate
emergency energy
o Controlled by the sympathetic ANS via the sympatho-adreno-medullary
(SAM) system:
 Stressor -> hypothalamus activates sympathetic ANS ->
stimulation of the medulla (inner part) of the adrenal gland
secreting catecholamines (adrenaline + norepinephrine) ->
activation of various organs by adrenaline and norepinephrine ->
increased blood pressure, increased muscle tone, increased blood
sugar and other physical changes to provide energy to cope with
the acute stressor
 The pituitary gland also triggers the release of
endorphins, the body's natural painkillers.
 Also activation of the HPA system: hypothalamus stimulates the pituitary gland which then secretes
ACTH -> ACTH stimulates the cortex (outer surface) of the adrenal glands -> the adrenal glands secrete
corticosteroids that release the body's energy stores and fight inflammation
2. Resistance phase (if stressors persist): clear signs of the alarm response fade, so the dissipation of adaptive energy is
slower here, but the body is still working hard to deal with it > it is using up the body's reserves of adaptive energy
3. GAD stage/exhaustion: signs of physical wear and tear, especially in organ systems that were weak to begin with or
that were heavily involved in the resistance process.
o If adrenaline and cortisol remain at high levels, they can damage the heart and blood vessels and suppress the
functioning of the body's disease-fighting immune system -> adaptation diseases = diseases
caused/exacerbated by stressors

Selye's model underestimates the role of psychological factors in stress > development of psychobiological models that
emphasize the importance of psychological and biological factors. Psychological reactions:

1. Emotional changes: often disappear quickly after the stressors subside, but if stressors persist for a long time or occur in
tight succession, emotional stress reactions can persist and can lead to a tense, irritable, sad, or anxious feeling. In some
cases, these reactions can become severe enough to be diagnosed as GAD, MDD, or other stress-related problems.
2. Cognitive changes:
a. Reduction in the ability to concentrate, think clearly, or remember accurately:
i. Ruminative thinking = repeated intrusion of thoughts about stressful events
ii. Catastrophizing = putting too much emphasis on possible consequences of negative events
b. Narrowing attention > can increase the number of problem-solving errors
i. Functional fixedness = the tendency to use objects for only one purpose
c. Impaired judgment and decision-making > acting impulsively and sometimes foolishly
3. Behavioral reactions: expressions, shaky voice, etc., but also reaching for alcohol, sleeping too much, eating too much,
sometimes quitting work/school, or even committing suicide. Aggression is also common
o May provide temporary relief, but can also have negative health consequences + escape tactics and avoidance
tactics deprive people of the opportunity to learn more adaptive ways of coping with stressful environments

,Mediating factors help determine how much impact a stressor will have:

1. Perception of stressors: Stressors rated as threats > greater impact than stressors rated as challenges
o Influence of cognitive factors weakens as stressors become more extreme
2. Unpredictable and uncontrollable stressors are more impactful, especially when stressors are intense and relatively
short
3. Inadequate coping tools and methods > stronger responses to stressors
o Resources for coping include money and time to deal with stressful events
o Coping methods can be classified as problem-oriented or emotion-focused
 Problem-focused coping involves efforts to change or eliminate a source of stress
 Emotion-focused > aimed at regulating the negative emotional consequences of the stressor



What is Anxiety?
Fear = innate, adaptive mechanism that prepares us for action and protects us from expected threat

Biological aspects: increased sympathetic activity
Anxious individuals, both clinical and non-clinical, often exhibit heightened arousal characterized by increased activity of the
sympathetic nervous system, associated with the fight-or-flight response

 Hyperarousal has been demonstrated in normal subjects who have become anxious in the laboratory.
 In anxious patients, an anxiety-inducing situation is not necessary to produce
hyperarousal, but it appears to be chronic.

Terrifying gait study (Holden & Barlow) > chronically elevated heart rate in anxious
individuals:

 The average heart rate for agoraphobia was higher on each walk than that of the
controls
 HR decreased/habituation in both groups over the 7 walks, but on the last walk,
agoraphobias showed an increase in HR that differed from the continuing habituation
in the control subjects > perhaps the patients knew it was the last walk and responded with a "final exam effect".
 No difference between the 2 groups in HR response (HR during walk - baseline HR)
during the walk > indicates that higher HR during the walk for the patients was due
to the fact that they came in with a higher HR > reflects that patients are chronically
overaroused, whether they were engaged in an anxiety-inducing task or not.

Results of other studies:

 EEG Procedures: less Alpha and More Beta Activity in anxious patients versus controls
o Alpha activity -> relaxation: indicates that anxious patients are less relaxed
 Harmonic driving was much higher in anxious patients than in non-anxious controls

Results Loader & Wing:

 Habituation to GSR (galvanic skin response) was much slower in patients than in
control groups
 Patients had a higher frequency of spontaneous skin conductance fluctuations +
heart rate that was 15 beats per minute higher than the control group
 The more anxious the patient, the slower the habituation and the faster the
fluctuations

Results of the Lader study (as a result of the Lader & Wing study):

,  Normal check-ups and patients with specific phobias both quickly became habituated and had fewer spontaneous skin
fluctuations
 Patients with specific phobias are not in the same state of overarousal/readiness as other anxiety disorders.
Nevertheless, the anxiety states, as well as social phobia and agoraphobia, clearly show chronic overstimulation.

Coping Response: Autonomic Inflexibility of the Body
Study Borkovec and Hoehn-Saric:

 Anxiety, especially chronic, can be characterized by some degree of sympathetic impairment and autonomic inflexibility
o Autonomic inflexibility appears to be specifically associated with the worrying process and may represent a
coping response that arises when anxiety becomes chronic, rather than a biological marker of anxiety itself

Resulys Lyonfields, Borkovec and Thayer:

 GAD analog patients show very little HR variability throughout the experiment and significantly less variability than the
control group at baseline. In contrast, the control subjects showed more variability during the baseline, but significant
reductions in variability from baseline to aversive images and to worrisome thinking
 Conclusion = the worrying process is thus directly associated with a reduced parasympathetic control of cardiovascular
functioning > explains the autonomic inflexibility

Thayer Study > examined people who met all the criteria

 GAD patients showed increased HR and less vagally mediated HR variability in all conditions
 Concerns were characterized by decreased cardiac parasympathetic activity in both patients and controls - > care
process is directly associated with decreased parasympathetic control of cardiovascular functioning
 Anxiety + the worrying process may be associated with unresponsive ANS activity associated with decreased
parasympathetic activity, but this situation can be modified with successful treatment
o Study Borovec: The autonomic inflexibility found in anxious patients is related to the fact that the stimuli feared
by these patients are not produced by external environmental stressors, but are chronically present internally
generated thoughts about possible future threats.
 Patients with GAD showed a significant increase in HR variability and parasympathetic tone after CBT

Autonomic inflexibility appears to be a hallmark of anxiety disorders in general, not a psychophysiological trait associated with
just one disorder.



What is panic disorder?
Panic = intense fight or flight response, emotional arousal > can be the result of a malfunctioning alarm system

 Panic attack = a discrete period of intense anxiety/discomfort that peaks within minutes and is accompanied by four or
more somatic and/or cognitive symptoms
o Most commonly associated with panic disorder and agoraphobia

The essential characteristic of PD is the presence of recurrent, unexpected panic attacks, along with significant panic-related
worries

 The panic attacks cannot stem from the direct physical effects of a substance or medical condition alone
 The panic attacks cannot be caused by any other mental disorder

At least 4 symptoms must occur at the same time for the panic attack to be a full-symptom panic attack:

 Somatic symptoms: palpitations and chest pain, dizziness, nausea, feeling of heat or chills, shortness of breath, tingling,
sweating, feelings of unreality and trembling
 Subjective/cognitive symptoms: fear of dying and fear of losing control

, While panic attacks are required for a PD diagnosis, experiencing panic is not enough to justify this diagnosis > 28% of people will
experience a panic attack in their lifetime, but less than 5% develop PD.

Panic attacks usually develop in adolescence or early adulthood and are classified into three types in the DSM-5 intro:

1. Unexpected = not associated with any particular situation or internal cue -> required for PD!
2. Cued/situationally bound = almost always occurs when exposed to or in anticipation of a particular situation
3. Situationally predisposed = linked to a certain situation, but do not always occur
 Panic attacks with limited symptoms are also common in PD > attacks that are identical to seizures with full symptoms,
except that it is associated with less than 4 of the 13 panic symptoms

Many people with recurrent panic attacks significantly change their behavior (e.g., quitting a job) in response to the attacks.

 Worries about the next attack, or its implications, are often associated with the development of avoidant behaviors that
may meet the criteria for agoraphobia (AG).
o Originally, it was suggested that AG was a phobic disorder that stemmed from fears of public places that may
or may not occur in panic attacks > DSM-3: AG is a phobic disorder that can occur without panic attacks,
whereas PD was a separate class of anxiety disorders called anxiety states or anxiety neuroses.
o However, research recognized that AG is often a consequence of panic attacks > DSM-3-R and DSM-4: AG is
secondary to PD, it was a specification of a PD diagnosis indicating the severity of phobic avoidance behaviors
in PD
o DSM-5: AG is a codable disorder distinct from PD > patients may receive a PD diagnosis, an AG diagnosis, or a
diagnosis of comorbid PD and AG as AG exists in some cases without any prior indication of panic or panic-like
symptoms

Epidemiology
 Panic attacks: 28.3% (lifetime) and 11% (12 months)
 PD: 4.7-5.1% (lifetime) and 2.1-2.8% (12 months)
 PD without AG: 3.7-4.0% (lifetime) and 1.6% (12 months)
 PD with AG: 1.1% (lifetime) and 0.6% (12 months)
 AG:
o Total: 5.3%
o With PD: 1.9%
o Without PD: 0.6-0.8%
o Prevalence rates at 12 months for AG without PD vary between studies > highest in South Africa, lowest in
China

Effect of age, gender, race, and culture:

 Women are twice as likely to develop PD as men
 The 18-29 age group appears to be slightly below average prevalence at 3.9%, with 30-64 year olds being the most
affected at just over 6%. The least common group is 65+ (2.8%).
 Culturally bound differences can be seen in the presentation and interpretation of specific panic symptoms

PD is a common anxiety condition that affects about 2% of the population in the U.S. at any given time:

 The more severe variant with AG is less common than PD alone
 Compared to the U.S., PD rates are lower internationally, > PD is relatively uncommon in non-Western countries.

Start and course
The age of onset usually occurs in the mid-twenties:

 Bimodal distribution: two peaks in the beginning of PD and AG -> one from 15-24 and the other from 45-54 years
o A small proportion of individuals > early-onset variant of PD and AG in early adolescence
 The literature suggests a difference in the age of onset of PD and AG as a function of gender.

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