Anxiety Disorders 🫨

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Anxiety is a spectrum of experience – not always pathological.

Last updated 3:50 PM on 4/14/26
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43 Terms

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State anxiety

Transient experience with a temporarily increased sympathetic nervous system response and feelings of intense tension, worry and apprehension. Short term

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Trait anxiety

Personality trait. Stable across time and situations – people have a predisposition to respond in an anxious way.

Long term - shapes way process and make decisions

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Brain area for state anxiety

Anterior cingulate gyrus, precuneous cortex

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Brain area for trait anxiety

Superior frontal gyrus

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Anxiety is clinically relevant when…

  1. Disproportionate

  2. Severe/enduring

  3. Linked with functioning impairments

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Anxiety sensitivity

Fear of experiencing anxiety-related sensations and symptoms, based on the idea that you perceive them as psychologically/socially/physically harmful.

Linked to onset of anxiety disorders.

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GAD Criteria A

Excessive anxiety/worry on more days than not for >6 months, about several events or activities.

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GAD Criteria B

Difficult to control the worry.

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GAD Criteria C

Anxiety/worry linked with >3 symptoms. At least some present for more days than not, for at least 6 months.

i.                    Restless/keyed-up or on edge

ii.                   Easily fatigued

iii.                 Difficulty/concentrating/mind going blank

iv.                 Irritable

v.                   Muscle tension

vi.                 Sleep disturbance

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GAD Criteria D

Clinically significant distress or functional impairment.

  • 20% have more severe impairments.

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Panic attacks

Sudden and intense episodes of extreme fear/discomfort – 20% of people with GAD experience panic attacks.

Last 5-20 minutes, de-esculate themselves - in the moment, they genuinely think something catastrophic is happening.

1/3 of us will experience at least 1 panic attack in our lives

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PD Criteria A

Recurrent, unexpected panic attacks = abrupt surge of intense fear/discomfort that peaks within minutes.

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PD Criteria B

At least one attack has been followed by >1 month of:

i. Persistent concern about additional panic attacks or their consequences.

And/or

ii. Sig maladaptive behaviour change related to the attacks e.g. avoidance of situations, activities that believe triggered PD, performing safety behaviours (things think will stop another one happening).

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How many people with anxiety fulfil criteria for 2+ disorders.

40-70%

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Kessler et al. (2005)

Tetrachoric correlations show relationships between conditions for past 12 months (highest GAD-MDD, PD-dysthymia)

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Remes et al. (2016)

Review. Anxiety range 3.8-25%, most estimates 4-11%

Rates higher in women, young adults, people with chronic diseases, LGB, been/currently pregnant

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Millet et al. (2016)

Review anxiety prevalence in trans - 17-68%, higher in trans men

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Javaid et al. (2023)

Total number of people worldwide with an anxiety disorder increased 1990-2019. BUT after adjusting for changes in underlying population age structure, prevalence rates over the same time period appeared to be relatively stable.

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Baxter et al. (2013)

Review in 44 countries. Prevalence in Euro-Anglo cultures, non-western appear to have lower rates.

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Women with anxiety disorder are…

More likely to be diagnosed with MDD or BN over lifetime

Less likely to be diagnosed with a substance use disorder, ADHD or intermittent explosive disorder.

Sig higher proportion of women (44.8%) with a lifetime incidence of anxiety disorder met criteria for an additional anxiety disorder than men (34.2).

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Women/men internalising/externalising co-morbid disorders

·       Women more likely to have co-morbid internalising disorders – symptoms focused on self e.g. depression, ED.

·       Men more likely to have co-morbid externalising disorders – symptoms more outward focused e.g. aggression, impulsivity, substance-use.

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De Lijster et al. (2017)

14 studies. Mean age of onset is 21 years, similar for all genders.

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Bruce et al. (2005)

Followed MH people over 12 years. PD has higher remission than GAD. PD and GAD have similar recurrence rates until 8 years since recovery, where PD has increase in recurrence rates.

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Penninx et al. (2011)

Followed anxiety for 2 years. Median duration of illness 16 months.

42% showed chronic course

7% switched to depression

16% developed co-morbid depression

Presence of anxiety and longer duration episodes predicted by:

a)      Severity and duration of baseline episode

b)      Co-morbid depression-anxiety

c)      Earlier age of onset

d)      Older age overall

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Meier and Deckert (2019)

If have a first degree relative with an anxiety disorder, are 4-6x more likely to get one.

Heritability 30-50%

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Lawrence et al. (2019)

People whose parents have an anxiety disorder are more likely to have anxiety, depressive disorders (greater for anxiety).

If have a family member with anxiety disorder, not at risk for that specific disorder, but for an anxiety disorder in general.

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Ohi et al. (2020)

Shared genetic risk between anxiety disorders and Sz, ADHD and depressive disorders.

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Temperament in anxiety disorders

Behavioural inhibition = temperament style characterised by shyness, fear and avoidance of novel stimuli/situations. Longitudinally predicts anxiety disorders.

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Sandstrom et al. (2020)

Review. Odds ratio of developing any anxiety disorder from behavioural inhibition 2.8

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Psychosocial risk factors in early life

Prenatal stressors, childhood maltreatment, socioeconomic deprivation, stressful life events early childhood

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Zimmerman et al. (2020)

Review.

Identified risks:

  • Cig smoking frequency

  • Alcohol use

  • Cannabis use

  • Negative appraisals of life events

  • Avoidance

  • Occupational factors

Identified protective factors:

  • Social support

  • Adaptive coping skills

  • Physical activity

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HPA axis in anxiety

Increased sympathetic tone and decreased parasympathetic activity from anxiety disorders = increases inflammation.

Dysregulation of HPA axis leads to chronic, low-level inflammation, which creates neurotoxic effects on the brain.

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Brain circuits in anxiety

Mixed evidence - these are the most consistent:

  • Increased volume and hyperactivation of amygdala, anterior cingulate cortex, postcentral gyrus.

  • Decreased volume and hypoactivity of dorsolateral PFC.

  • Impaired communication between limbic areas and PFC.

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Cognitive processes

  1. Perceived lack of control

  2. Intolerance of uncertainty

  3. Positive and negative beliefs about worry

  4. Cognitive biases

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NICE recommendation for GAD and PD

Stepped-care approach, using low intensity treatment possible to match severity.

Recommends treatment switching if 1 doesn’t work

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Slee et al. (2019)

Review of meds vs placebo in GAD.

Small to moderate effects sizes for:

  • SNRIs and SSRIs e.g. escitalopram (first choice drug treatment for GAD, start at lower dose than depression then titrate above depression)

  • Anticonvulsants e.g. pregabalin (treat neuropathic pain)

  • Antipsychotics (for severe)

Side effects, risks and acceptability vary

Long term effectiveness rates we’re not so sure about

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Drugs in PD

Many meds appear effective for PD as GAD - remission less likely following treatment (Chawla et al., 2022).

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Psychological treatment for PD

‘Formulation’ = clinical psychologists do at beginning of treatment to create an individualised treatment course for an individual.

5 Ps:

1.      Presenting: What is problem itself e.g. functional impairment?

2.      Predisposing factors: What made patient vulnerable in first place?

3.      Precipitating factors: What triggered the current episode / escalation of symptoms?

4.      Perpetuating factors: What keeps the symptoms going?

5.      Protective factors: What protective factors are in place?

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Cognitive Model of Panic (Clark, 1986)

People that experience recurrent panic attacks do so because misinterpret benign bodily sensations as symptoms of an “immediately impending physical or mental catastrophe”.

Avoidance/safety behaviours - reduce anxiety, prevent person from discovering that their fears are groundless. Negatively reinforces them and catastrophic misinterpretation.

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Stages that CBT can work on (in Clark, 1986’s model)

Triggers - Identify anxiety triggers

Perceived threat - Reduce anxiety-driven biases that lead to ambiguous stimuli being interpreted as threatening

Avoidance and safety behaviours - Replace them

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Cuijpers et al. (2016)

Large positive effect for CBT for GAD

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Cuijpers et al. (2019)

Large positive effect for CBT for PD (better than GAD)

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Cuijpers et al. (2014)

Meta-analysis. Combined therapies (CBT and meds) sig reduce symptoms.