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2011-11-15 02:44:58

Anxiety disorders
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  1. What is anxiety?
    • Negative affect
    • Somatic symptoms of tension
    • Future oriented
    • Feelings that one cannot predict or control upcoming events.

    Anxiety usually doesn't go away.
  2. What is fear?
    • Negative affect
    • Strong sympathetic nervous system arousal
    • Immediate alarm reaction characterised by strong escapist tendencies in response to present danger or life-threatening emergencies.
  3. What is a panic attack?
    An abrupt experience of intense fear or acute discomfort.

    • Fear occurring at an inappropriate time.
    • ~ Situationally bound (specific and social phobia)
    • ~ Unexpected (panic disorder)
    • ~ Situationally predisposed (panic disorder)
  4. How does the body respond to anxiety?
    • Cognitive and emotional response.
    • Behavioural response.
    • Physiological response - autonomic nervous system:
    • ~ Sympathetic nervous system: "accelerator" - flight or fight
    • ~ Parasympathetic nervous system: "brake" - brings you back to normal.
  5. Can anxiety be useful?

    • Anxiety can be adaptive:
    • ~ Signals that threat is imminent
    • ~ Cues us to attend to important stimuli
    • ~ Signals for us to activate protective responses

    Social, physical and intellectual performances are often drive and enhanced by anxiety.

    The Yerkes-Dodson curve suggests there is an optimal level of anxiety.
  6. When does anxiety become a disorder?
    • Duration - lasts a really long time
    • Intensity of anxiety
    • Appropriateness of response - true vs. false alarms
    • Interference and distress
  7. What causes anxiety disorders?
    • Biological:
    • ~ Genetic vulnerability: inherit a tendency to be uptight and anxious, or to panic. High rates of comorbidity (55% have more than 1 anxiety disorder) among anxiety disorders (and depression) suggest shared vulnerabilities.
    • ~ Neurotransmitters: depletion of GABA (inhibitory hormone - makes you feel calm). Serotonin also involved.
    • ~ Corticotropin releasing factor (CRF) is a neurohormone that activates the HPA axis. CRF affects parts of the brain associated with anxiety e.g. limbic system, PFC, dopaminergic system, and GAPA.
    • ~ Limbic system (the "emotional brain"): mediator between the brain stem (monitors bodily function) and the cortex. Activates the Behavioural Inhibitory System (BIS) which produces anxiety (distinct from the circuit involved in panic).
    • ~ Flight-fight system (FFS - panic system): body reacts to danger by releasing adrenalin through the blood stream.

    Environmental factors (e.g. smoking) can change the sensitivity of brain circuits (BIS, FFS) making you more susceptible to developing anxiety and its comorbid disorders.

    In people with anxiety disorders the limbic system is over responsive to stimulation or new information AND the controlling functions of the cortex (that would down-regulate the hyperexcitable amygdala) are deficient.
  8. Explain the development of anxiety disorder (Barlow's triple vulnerability model).
    People inherit a biological vulnerability. This determines if you are likely to get an anxiety disorder.

    Specific psychological vulnerabilities tell us what specific anxiety disorder you will have, e.g. learning that situations are dangerous.

    Generalised psychological vulnerability puts you at high risk for a number of disorders, e.g. growing up believing the world is uncontrollable and dangerous.
  9. What are specific phobias?
    Irrational fear of a specific object or situation.

    • DSM criteria:
    • ~ Marked fear that is excessive or unreasonable, cued by the presence or anticipation of phobic object or situation.
    • ~ Exposure to the phobic stimulus invariably provokes an immediate anxiety response (may take the form of panic).
    • ~ Person recognises the fear is excessive.
    • ~ Phobic situation is avoided or endured with intense anxiety.
    • ~ Interference/impairment in life or marked distress.
    • ~ If under 18: must last for at least 6 months.

    • Subtypes:
    • ~ Animal
    • ~ Natural environment (e.g. storms, heights, water)
    • ~ Blood-injection injury (fainting common)
    • ~ Situational (e.g. flying, tunnels)
    • ~ Other (e.g. illness, vomiting, choking)
  10. What is separation anxiety?
    Children's unrealistic and persistent worry that something will happen to their parents or them while they are separated.
  11. How does blood-injury injection subtype differ from the others?
    Normally the fear response increases HR and BP but blood-injury injection will often faint (decreased BP).
  12. Why do specific phobias develop?
    • Behavioural view: acquired by classical conditioning and maintained by operant conditioning (negative reinforcement). But:
    • ~ Not all fears are related to an aversive experience prior to onset.
    • ~ Many trauma don't result in fear.
    • ~ Some stimuli can be conditioned more easily.
    • ~ Many people don't remember the initial trauma.
    • ~ Modelling.

    Cognitive view: main component of anxiety is appraisals - danger and harm, uncontrollability, unpredictability.
  13. Treatment for specific phobias?
    • Treatment for specific phobias is generally CBT. This involves:
    • ~ Education
    • ~ Graded education
    • ~ Cognitive therapy - challenging faulty appraisals.
  14. What is the difference between situational phobia and panic disorder with agoraphobia?
    Situational phobia will only have panic attack in that situation.

    PD might experience unexpected panic attack at any time.
  15. What is panic disorder?
    Have had a panic attack and develop substantial anxiety about developing another.

    • DSM criteria:
    • ~ Recurrent, unexpected panic attacks.
    • ~ At least 1 panic attack has been followed by 1 month or more of: persistent worry about having additional attacks, worry about the implications of the attack or its consequences, a significant change in behaviour.
    • ~ Rule out specific phobia/other conditions/substance effects.
  16. What is agoraphobia?
    Fear and avoidance of situations in which they would feel unsafe in the event of a panic attack.

    Panic disorder can occur with or without agoraphobia.

    More common for females to develop agoraphobia (more acceptable for women to report fear). Men more likely to abuse alcohol.
  17. What are the 3 anxiety systems for panic disorder?
    • Physical:
    • ~ Fight/flight response
    • ~ Physiological symptoms

    • Cognitions:
    • ~ Biased attentions
    • ~ Hyper-vigilence
    • ~ Biased interpretations

    • Behavioural:
    • ~ Avoidance
    • ~ Escape (negative reinforcement fuels PD)
  18. Why does panic disorder develop?
    • Biological model: false suffocation alarm hypothesis
    • ~ Threshold for setting of alarm is pathologically lowered.
    • ~ Controls given sodium lactate had similar physiological responses but experienced less fear
    • ~ The interpretation of the event is important.

    • Behavioural approach: Pavlovian conditioning
    • ~ Interoceptive stimuli is CS to aversive consequence (panic). Fear is the US.
    • ~ Mild symptoms become associated with full scale panic attack.

    • Cognitive approach:
    • ~ Key aspect is the interpretation of sensations
    • ~ Trigger -> perceived threat -> apprehension -> body sensations -> catastrophic interpretation -> perceived threat...

    • Barlows model of panic disorder:
    • Generalised psychological vulnerability -> stress -> false alarm -> associated with somatic sensations -> learned alarm -> specific psychological vulnerability -> anxious apprehension -> agoraphobia -> PD with agoraphobia.
    • ~ Specific psychological vulnerability: physical sensations are dangerous
    • ~ Anxious apprehension: hyper-vigilence
  19. Treatment for panic disorder?
    • CBT:
    • ~ Expose to CS and extinguish fear response.
    • ~ Finding out the symptoms won't lead to anything catastrophic.
    • ~ If they have a panic attack can talk them through it

    Panic disorder has an excellent success rate with CBT

    D-cycloserine enhances extinction training.

    (Benzodiazepines and SSRIs associated with addiction/dependence and relapse once stopped. May also interfere with psychological treatments.)
  20. What is social phobia?
    • DSM criteria:
    • ~ Marked, persistent fear of social situations
    • ~ Person recognises fear is unreasonable
    • ~ Feared situations are avoided
    • ~ Interference or distress

    Specify generalised if it includes most situations.
  21. What features are associated with social phobia?
    • Fear of negative evaluation
    • Belief others will see them as inept, stupid, foolish
    • Often cycle of: anxiety -> social deficits -> anxiety...
    • Hypersensitive to criticism
    • Non-assertive, low self-esteem
    • Often lack intimate relationships
    • Safety behaviours are common.

    Information processing biases: interpretation of social events, detection of positive response of others, anticipatory and post-event processing.

    Must have learned growing up that social evaluation can be dangerous.
  22. How is social phobia maintained?
    • Increased self focused attention
    • Use of misleading internal information
    • Use of safety behaviours
    • Pre- and post- event processing

    Processing self as social object -> extreme self focus, creates a lot of anxiety and leads to safety behaviours.
  23. What vulnerabilities might be involved in social phobia?
    Could inherit a generalised biological vulnerability to develop anxiety, a biological tendency to be socially inhibited, or both.
  24. Treatment for social phobia?
    • CBT:
    • ~ Role play phobic situation
    • ~ Cognitive therapy towards changing perception of danger.

    Medication: relapse once discontinued.
  25. What is generalised anxiety disorder?
    • Worry is the defining characteristic of GAD.
    • Pervasive, intrusive worries about day-to-day concerns.
    • Worry seen as helpful, then excessive but difficult to control.
    • Accompanied by motor tension and autonomic arousal.
  26. In terms of generalised anxiety disorder, what is the avoidance theory of worry?
    • Worry is a negative, verbal linguistic activity. It temporarily benefits the worrier by distancing them from anxiety provoking mental images.
    • Individuals with GAD show diminished responsiveness on physiological measures. GAD has a constant low level of arousal rather than a full autonomic arousal - autonomic restrictors.
    • Show elevations in EEG activity, reflecting intense cognitive processing particularly in language centres.
    • They may be so busy thinking about the upcoming problems they don't have the attentional capacity left to form images of the potential threat.
    • It is important to engage in negative affect and imagery in order to work through the problems and arrive at solutions.
  27. Treatment for generalised anxiety disorder?
    Generally quite resistant to treatment.

    • Benzodiazepines:
    • ~ Short term (< 2 weeks) relief
    • ~ Can impair cognitive and motor functioning
    • ~ Become dependent.

    • CBT:
    • ~ Help to process threatening information on an emotional level.
    • ~ Focus on accepting rather than avoiding distressing thoughts.
  28. What is obsessive compulsive disorder?
    A devastating culmination of anxiety disorders - may experience generalised anxiety, panic attacks, avoidance, depression and OCD symptoms.

    • DSM Criteria:
    • ~ Either obsessions or compulsions.
    • ~ Recognises them as excessive or unreasonable.
    • ~ Cause distress, are time consuming or significantly interfere with functioning.
    • ~ Content of obsessions is not restricted to another Axis I disorder.
    • ~ Not due to a substance or medical condition.
  29. What are obsessions?
    • Thoughts, images or impulses
    • Repetitive, intrusive, uncontrollable
    • Cause distress
    • Not just excessive worries about real life problems
    • Interpreted as strange/inappropriate
    • Compel the person to ignore/neutralise the obsession in some way - often feel responsible (thought-action fusion)
  30. What are compulsions?
    • Repetitive overt behaviours or covert mental acts
    • Goal is to "undo" the obsessions to prevent harm associated with obsession, or to alleviate anxiety.
    • Not connected in a realistic way to the obsession, or are clearly excessive.
    • Tics may sometimes actually be compulsions.
  31. What are the 4 main symptom dimensions of OCD?
    • Forbidden thoughts/actions - leads to checking rituals
    • Symmetry and ordering - leads counting/arranging
    • Cleanliness and washing - leads to washing rituals
    • Hoarding
  32. What is the cause of OCD?
    Precise cause is unknown.

    • Appears to be due to a combination of factors:
    • ~ Genetic factors influence a persons vulnerability to OCD - common for tic-disorder to be in the family.
    • ~ Neurochemical theory suggests serotonin is involved.
    • ~ Biological model: abnormal activity in brain areas responsible for filtering irrelevant information and perseveration (e.g. PFC)
    • ~ Psychological model: obsession give rise to anxiety, compulsions reduce anxiety -> negative reinforcement
    • ~ Cognitive model: OCD people attach personal significance to intrusive thoughts (which are normal). This promotes compulsions. Thought-action fusion, inflated responsibility.
  33. Treatment for OCD?
    Treatment reduces brain activity in the PFC, basal ganglia and thalamus.

    • Psychopharmacology:
    • ~ SSRIs found to be useful
    • ~ Half the patients experience average symptom reduction of 40%
    • ~ Majority relapse after discontinuation of drugs.

    • Exposure and response prevention:
    • ~ Anxiety must be aroused and experienced. New information about the basis of the fear must be provided and emotionally processed.
    • ~ Facilitates "reality testing"
    • ~ Effective and potentially curative treatment of OCD

    • Psychosurgery:
    • ~ Very radial treatment (last resort).
    • ~ With the increasing effectiveness of CBT soon expected to no longer occur.
  34. What is post-traumatic stress disorder (PTSD)?
    • DSM Criteria:
    • ~ Exposure to traumatic event
    • ~ Re-experiencing (intrusive recollections, nightmares, flashbacks, distress on reminders)
    • ~ Avoidance (cognitive avoidance, avoidance of physical reminders, amnesia, detachment, restricted range of affect, sense of foreshortened future)
    • ~ Arousal (difficulty falling asleep, irritability/outbursts, difficulty concentrating, hypervigilence, exaggerated started response).
    • ~ Symptoms present 1 month after trauma
    • ~ Clinically significant distress, functional impairment

    • Acute: 1 month after evenet
    • Chronic: continues >3 months
    • Delayed onset: > 6 months after trauma
  35. What affects the likelihood of developing PTSD?
    • Severity, duration and proximity of exposure to the trauma.
    • ~ High levels of trauma - most develop PTSD
    • ~ Low levels of trauma - vulnerability determines if PTSD develops.

    Concentration camps and sexual assault are more likely to develop PTSD (dehumanisation?).
  36. What causes PTSD?
    Proximal cause: exposure to traumatic event.

    Severity of trauma contributes to etiology, however doesn't account for all the variance. Even in cases of severe trauma not everyone develops PTSD (underlying vulnerability needed).

    • Distal cause: emerging evidence for pre-trauma psychological and biological vulnerability factors:
    • ~ Psychiatric dysfunction before trauma
    • ~ Pre-trauma psychosocial functioning (if low increases risk of developing PTSD)
    • ~ Family history of PTSD/anxiety

    Social factors: strong social support decreases likelihood of PTSD.
  37. What are the theoretical models of PTSD?
    • Behavioural: 2 factor learning
    • ~ Classical conditioning: stimuli associated with trauma elicit CR similar to initial trauma response.
    • ~ Operant conditioning: avoidance behaviours learnt, preventing extinction.
    • ~ Limitation: symptoms of irritability, exaggerated startle response and emotional numbing not readily accounted for.

    • Cognitive: information processing model
    • ~ Trauma creates complex "fear networks" in memory
    • ~ Many stimuli activate the network, result in symptoms of arousal, re-experiencing, and attempts to avoid/escape.

    • Cognitive: cognitive appraisal model
    • ~ PTSD persists when individuals process the trauma in a way that leads to a sense of current threat
    • ~ Perception of current threat is accompanied by re-experiencing symptoms, arousal, anxiety and other emotional responses.
    • ~ Perceived threat also motivates behavioural and cognitive responses designed to prevent perceived threat and distress.
  38. Treatment for PTSD?
    • CBT:
    • ~ Face the original trauma, process the intense emotions and develop effective coping procedures.
    • ~ Prolonged imaginal exposure (re-exposure needs to be therapeutic not traumatic)
    • ~ Cognitive therapy

    After trauma need to identify those at risk of developing PTSD and intervene early.

    Critical Stress Incident Debriefing is not effective and may actually make people worse.
  39. What is acute stress disorder?
    ASD relates to post-traumatic reactions in the first month after trauma.

    It was introduced to assist in the identification of individuals at risk of developing PTSD.

    Based on the theoretic position that ASD is a precurser to PTSD.

    CBT is an effective treatment.