Lecture 5 - Anxiety Disorders Flashcards
anxiety and related pathologies
- involves anticipation of real or imagined future threat/danger
- state anxiety: transient experience with temp inc sympathetic NS response. ST response to stressor
- trait anxiety: more stable anxiety across time and situations. predisposition to stressors = behaviourally inhibited, wary in novel situations, cautious about risks, more likely to experience anxious states
- trait mapped onto superior frontal gyrus, state onto acc and precuneous cortex
clinically relevant anxiety
- disproportionate to size of stressor
- severe/enduring
- linked with impairments in functioning
GAD DSM criteria
A. excessive anxiety/worry on more days than not for >6m about several events and activities
B. difficult to control
C. linked to >3 symptoms below at least present for most days for 6m:
1. restless
2. fatigued
3. difficulty concentrating
4. irritable
5. muscle tension
6. sleep disturbance
D. clinically signif distress
E. not due to substance or another condition
- only 1 item from section C needed for diagnosis in children
GAD specifier - panic attack
- extension to diagnosis
- sudden episode of intense fear/discomfort
- physical symptoms: rapid heartbeat, shaking, sweating, nausea, chills, hot flush, breathlessness
- often occur w/o warning about 5-30mins
- 1 in 5 with GAD experience
panic disorder (DSM5)
A. recurrent panic attacks. 4 or more of:
1. palpitations
2. sweating
3. trembling/shaking
4. shortness of breath
5. feelings of choking
6. chest pain
7. nausea
8. dizzy/unsteady
9. chills/heats
10. numbness/tingling
11. derealisation
12. fear of losing control/going crazy
13. fear of dying
B. at least one attck followed by >1 month of: concern over more panic attacks AND/OR signif maladaptive behaviour change
C. disturbance not due to another condition
comorbidity
- patients with anxiety are at high risk for other mh conditions
- symptoms not specific to indiv anxiety disorders
- GAD highest cor with MD ep. panic disorder with dysthymia
lifetime prevalence
- Remes et al. (2016) prevalence of anxiety disorders 3.8-25%
- higher rates in women (5.2 - 8.7%)
- young adults (2.5 - 9.1%)
- chronic illness (1.4 - 7%)
- higher rates in lesbian, gay or bisexual people or recently pregnant
- prevalence in transgender people vary from 17% - 68% espec in transgender men
- highest prevalence in euro/anglo cultures
- non western cultures lower rates
- for every 1 man with PD or GAD, 1.7 women receive same diagnosis
gender differences in anxiety disorder profiles
- women more likely to be diagnosed with: MDD or BN. less for substance use disorder, ADHD or IED
- more women with lifetime incidence of anxiety disorder meet criteria for an additional anxiety disorder than men
- may be effect of hormones? difs in HPA axis?
age of onset
- mean age of onset 21
- more severe and comorbidities with earlier onset
time course of anxiety over 2 years
- people with anxiety had median duration of illness of 16m with 42% being chronic
- 7% switched to depression, 16% comorbid depression
- people with anxiety and depression at baseline had median duration of 24m and 57% chronic
- predictors of poorer trajectory: severity/duration of baseline episode, comorbid depression anxiety, earlier onset, older age
genetic risk factors for anxiety
- odds ratio 4 to 6 with first degree relative with anxiety. heritability approx 30-50%
- parents with anxiety = more likely to have anxiety and depressive disorders
- risk greater for offpsring anxiety than depressive disorders
- shared genetic risk between anxiety, sz and adhd and depressive disorders
behavioural inhibition
- temperament of shyness, fear, avoidance of novel stimuli
- appears to be genetic
- identified in childhood and longitudinally predicts anxiety disorders
- odds ratio of 2.8
- need to identify children who are highly behaviourally inhibited
early psychosocial risk factors
- prenatal stressors: maternal stress, depression & anxiety
- childhood maltreatment
- physical punishment
- socioeconomic deprivation
- stressful life events
- non specific
- affects stress response = overactivated HPA axis and unable to regulate = inflammation
inflammation in anxiety disorders
- dysregulation of HPA in face of inc sympathetic tone and dec parasympathetic activity characteristic of anxiety & affects brain regions critical to regulate fear & anxiety
- external stress provokes constant low level inflammatory response affecting function and structure of amygdala and hipp important in response to emotions and fear & managing HPA
- explains interactions between immune diseases and anxiety
psychosocial risk factors in adulthood
- zimmerman et al. (2020)
> risks: cigarette smoking, alcohol, cannabis, occupational factors, neg life appraisal, avoidance
> protective: social support, coping, physical activity
cognition in anxiety
- cog processes implicated in development and maintenance of anxiety:
> lack of control perceived
> intolerance of uncertainty
> pos and neg beliefs about worry
> cog biases e.g. attend more to threat related stimuli
pharmalogical treatment
- SNRIs and SSRIs (lower doses for GAD than MDD)
- anticonvulsants
- atypical antidepressants
- azapirones
- antipsychotics
- tricylics, MAOIs, SSRIs SNRIs have higher remission rates than placebo
cognitive behavioural case formulation for panic
- theoretically based explanation of the info obtained in clinical assessment
- case formulation tries to understand specific difficulties and treatment plan
- key qu (5ps)
1. predisposing
2. precipitating
3. presenting problem
4. perpetuating
5. protective factors in place
The cognitive model (Clark 1986)
- people exp recurrent panic attacks do so because they misinterpret benign bodily sensations as symptoms of immediately impending mental/physical catastrophe
- e.g. heart racing interpreted as heart attack which heightens anxiety related sensaitons
CBT: identifying triggers
- internal triggers: change to body sensations. thoughts
- external triggers: encountering a feared situation, talk about exp of panic,
CBT: replace avoidance and safety behaviours
- safety behaviours temporarily reduce anxiety but reinforce it in LT
> physical
> cognitive
> misinterpretations
= anxiety - CBT tries to break these links
- people believe safety behaviours are the reason the worst never happens
effectiveness of CBT
- large pos effect for GAD (g = 0.8)
- larger effects for PD than GAD or SA
- combined therapies more effective (0.47) for disorders in general 0.54 for PD in symptom reduction
