anxiety Flashcards
clinical features of anxiety
Negative mood state, physical tension & apprehension about the future
→ ‘future oriented
- Symptoms interfere with important areas of functioning or cause marked distress.
- not caused by a drug or a medical condition.
- Symptoms persist for at least six months or at least one month for panic disorder.
- distinct from the symptoms of another anxiety disorder.
- some have specifiers
fear
- ‘immediate’ aspect of fear (a present threat)
- Strong escapist action tendencies – Present-oriented
anxiety and fear are adaptive
Both involve arousal or sympathetic nervous system activity.
Fear = ‘fight-or-flight’ reactions — it triggers rapid changes in the sympathetic nervous system to prepare the body for escape or fighting
Anxiety Good for us in moderate amounts
o plan for future threats — increase our preparedness
o a small degree of anxiety has been found to improve performance on laboratory tasks
* U-shaped curve with performance
No anxiety → unprepared
Little anxiety → adaptive
Too much anxiety → detrimental
specific phobias
- disproportionate fear caused by a specific object or situation (can elicit disgust)
- claustrophobia (fear of closed spaces) and acrophobia (fear of heights).
- tend to cluster around a small number of feared objects and situations but may be comorbid (a specific phobia for one type of object/situation can move to other objects/sitch)
Almost always provokes immediate fear/anxiety
Actively avoided or endured with intense fear/anxiety
4 major types of specific phobias
Blood, injection, injury (runs in family)
Situational (mid 20’s or childhood)
Animals & insects (during childhood)
Natural environments (childhood)
Physiology of anxiety, fear, panic
Primary response of HPA axis is to regulate the stress response
- Pituitary gland releases hormones into the blood stream to reach a variety of targets (travel down to the kidneys) and influences secretion of hormones from the endocrine glands (called adrenal glands)
- Hypothalamus releases corticotropin- releasing hormone (CRH) –> signals the pituitary gland –> which signals the release of adrenocorticotropic hormone (ACTH) –> cortisol
release of cortisol causes a number of changes to help the body deal with stress
Pituitary gland:
hormone secreting gland below the hypothalamus
Hypothalamus
(neuroendocrine structure) controls the release of hormones from the pituitary gland
neurobiological factors to anxiety
o GABA (small amounts of GABA leads to more anxiety)
o norepinephrine - more of this leads to increase in locus corrélées
o serotonin - decrease in serotonin and increase in anxiety
o Corticotropin-releasing factor system – Activates HPA axis
o Hypothalamus, pituitary gland, adrenal glands
o Limbic system most associated (stress anxiety and panic) overly responsive to stimulation = abnormal bottom-up processing (longer circuit= rumination occurs with GAD –> usually how we deal with our anxiety adaptively but only if we don’t get stuck in the longer circuit)
o Short circuit more likely to go wrong (quick short changes)
o Amygdala centrally involved
o Medial prefrontal cortex – Fails to down-regulate hyper-excitable amygdala = abnormal top-down processing
personality factors to anxiety
Personality:
Behavioural inhibition: a tendency to become agitated and cry when faced with novel toys, people or other stimuli. (in infants as young as four months old, may be inherited and may set the stage for the later development of anxiety disorders)
- strong predictor of social anxiety disorder:
– Strong predictor of social phobia
Neuroticism:
– Tendency to react with greater negative affect
– High levels = strong predictor of an anxiety disorder
cognitive factors to anxiety
Sustained negative beliefs about the future
- People with anxiety disorders often report believing that bad things are likely to happen.
- these beliefs are sustained because they engage in safety behaviours to protect themselves
Perceived lack of control
- traumatic events, punitive and restrictive parenting or abuse, after serious life events
- Other life experiences may shape the sense of control over the feared stimulus.
Attention to threat
- people with anxiety disorders pay more attention to negative cues in their environment than do people without anxiety disorders
- Once a threatening object captures their attention, anxious people have a difficult time pulling their attention away from that object;
- Anxiety related information can be created.
Behaviourist theories:
– Classical & operant conditioning
– Modeling
- people with anxiety disorders seem to acquire fears more readily through classical conditioning and to show a slower extinction of fears once they are acquired
Fear conditioning
Mowrer’s two-factor model of anxiety disorders
1) CC= person learns to fear a neutral stimulus (the conditioned stimulus or CS) that is paired with an intrinsically aversive stimulus (the unconditioned stimulus or UCS).
2) A person gains relief by avoiding the CS. (operant conditioning)
Modification to his theory
- modelling (e.g., seeing a dog bite a man or watching a video of a vicious dog attack)
- verbal instruction (e.g., hearing a parent warn that dogs are dangerous).
genetic factors of anxiety
- heritability of 20–40% for specific phobias, social anxiety disorder and GAD, and about 50% for panic disorder
- having a family member with a phobia is related to increased risk of developing not only a phobia but also other anxiety disorders
The medial prefrontal cortex
- helps to regulate amygdala activity and involved extinguishing fears
- engaged when people are regulating their emotions
o people with anxiety display less activity in the medial prefrontal cortex when threatening stimuli arises
o The pathway, or connectivity, linking the amygdala and the medial prefrontal cortex may be deficient which in turn may interfere with the effective regulation and extinction of anxiety
aetiology of specific phobia
two-factor model of behavioural conditioning
- phobias could be conditioned by direct trauma, modelling or verbal instruction.
risk factors; genetic vulnerability, neuroticism, negative cognition and affinity for fear conditioning –> operate as diatheses
prepared learning
evolutionary- learned to react strongly to stimuli hence preparing our fear circuit to certain stimuli (prepared learning –> exposure helps
social anxiety disorder
persistent fear or anxiety about social situations that might involve being scrutinised by, or even just exposed to, unfamiliar people (“social phobia”)
Exposure to the trigger leads to intense anxiety about being evaluated negatively
Almost always provoke fear/anxiety
Trigger situations are avoided or endured with intense fear/anxiety
Disproportionate to actual threat
In presence of another medical condition, fear/anxiety is unrelated or excessive
- work in occupations far below their talents because of their extreme social fears.
- ppl w/ social anxiety disorder, at least a third have avoidant personality disorder
- Social anxiety disorder generally begins during adolescence
- Chronic
Aetiology of social anxiety disorder
Behavioural factors: conditioning
- person has a negative social experience (directly, through modelling or through verbal instruction) and become classically conditioned to fear similar situations, which the person then avoids. (operant conditioning)
safety behaviour
o avoiding eye contact
o disengaging from conversation and standing apart from others.
o Other people tend to disapprove of these types of avoidant behaviours, which then intensifies the problem
Cognitive factors: focus on negative self-evaluations
1) Unrealistic and negative beliefs about the consequences of their social behaviours —believe that others will reject them if they blush or pause while speaking.
2) attend more to themselves in social situations and their own internal sensations than other people do.
3) attend more to internal cues than to external (social) cues Eg. spend more time monitoring for signs of their own anxiety.
Generalised biological vulnerability
– Stress increases anxiety & self-focused attention
Under stress → panic attack
– Social situation associated with panic
Real social trauma → true alarm
– Anxiety in similar situations
Belief that social evaluation can be dangerous
– Parental concern about opinion of others (Lieb eta l, 2000)
social anxiety prevalence
Prevalence: 3-13%
50:50 gender ratio
Generally begins in adolescence – Most prevalent in young, undereducated,low SES singles
Diagnosed as performance only or generalised
Comorbidities: – Other anxiety disorders, depression,
alcohol abuse
panic disorder
- recurrent panic attacks, unrelated to specific situations and worry about having more
- accompanied by at least four other panic symptoms.
shortness of breath, heart palpitations, nausea, upset stomach, chest pain, feelings of choking and smothering, dizziness, lightheadedness, faintness, sweating, chills, heat sensations, numbness or tingling sensations, and trembling.
flee situation
*tend to come on very rapidly and reach a peak of intensity within 10 minutes.
DSM-5 criteria for panic disorder
At least 1 of the attacks followed by ≥ 1 month of one or both:
- Persistent concern or worry about further attacks or their consequences
- Significant maladaptive behavioural changes because of the attacks.
Methods of avoiding panic attacks:
– Drug & alcohol use /abuse
– ‘Endure’ fear
Interoceptive avoidance: – Remove self from situations that might produce physiological arousal Exercise Saunas Watching sport
Misfire of the system panic attack
physiologically, the person experiences a level of sympathetic nervous system arousal matching what most people might experience when faced with an immediate threat to life.
- 40% + experience at least one panic attack (onset- adolescence)
- The symptoms of panic disorder tend to wax and wane over time
Panic Disorder
5% of people at some time - 2/3 female
Onset early adulthood (mid-teens to ~40)
60% experience nocturnal attacks:
– During delta wave (slow wave) sleep
– deepest sleep
Sleep terrors:
– Occurs in children – don’t wake, no memory
– At later stage of sleep
Isolated sleep paralysis:
– Transition between sleep & wake (REM)
– Unable to move, vivid hallucinations
– History of trauma
Aetiology of panic disorder
Neurobiological factors
- fear circuit
- locus coeruleus –> neurotransmitter norepinephrine in the brain which activates the HPA axis and triggers the sympathetic NS
- dramatic biological response to drugs that trigger norepinephrine
- Drugs that increase activity in the locus coeruleus can trigger panic attacks, and drugs that decrease activity in the locus coeruleus, including clonidine and some antidepressants, decrease the risk of panic attacks
Behavioural factors: classical conditioning
- panic attacks are classically conditioned responses to either the situations or…..
- interoceptive conditioning: classical conditioning of panic attacks in response to bodily sensations –> panic attacks then become a conditioned response to the somatic changes
Cognitive factors in panic disorder
- exposing people to air with high levels of carbon dioxide;
- People who develop panic attacks after being exposed to these agents differ to others— the extent to which they are frightened by the bodily changes
- when heart rate is monitored using psychophysiological equipment, people with panic disorder are more accurate than other people in knowing when an arrhythmia occurs and in detecting changes in their heart rate during periods of stress and arousal
treatment for panic disorder
Biological:
– SSRIs & SNRIs
– Benzodiapepines (GABA) Most widely used
– Addictive, affect motor /cognitive function
– 60% free of panic, but relapse high (50-90%)
once stopped
Cognitive behaviour treatment most successful
– Focus on exposure – combined with relaxation, breathing retraining
– Panic control therapy
– Exposure to interoceptive sensation e.g. by spinning in a chair
– Mimics panic attack
– Perceptions of danger identified & modified = symptoms less frightening
treatment for social anxiety disorder
Exposure therapy:
– Role-play /practice in small groups → public
Cognitive therapy:
– Challenges beliefs re: appraisal & worthlessness
– Effective where added to exposure therapy
Drug therapy:
– Antidepressants such as Tricyclic Antidepressants & MAO inhibitors are effective
Combined treatments:
– Adding D-cycloserine to CBT significantly enhances effect of treatment
agoraphobia
- Agoraphobia (agora= ‘marketplace’) = anxiety about situations in which it would be embarrassing or difficult to escape if anxiety symptoms occurred)
- DSM-5 now includes agoraphobia as a separate diagnosis.
- at least half of people with agoraphobia symptoms do not experience panic attacks (concerned about what will happen if other anxiety symptoms develop)
- related to significant impairment in daily functioning.
- The effects of agoraphobia on quality of life are as severe as those observed for the other anxiety disorders
DSM-5 criteria for agoraphobia
- experience a disproportionate and marked fear or anxiety about at least two situations where it would be difficult to escape or receive help
- These situations consistently provoke fear or anxiety.
- These situations are avoided, require the presence of a companion, or are endured with intense fear or anxiety.
Generalised anxiety disorder
- worry about minor things
- excessive, uncontrollable –> relationships, health, finances and daily hassles
- symptoms : difficulty concentrating, tiring easily, restlessness, irritability and muscle tension.
-GAD is not diagnosed if a person worries only about concerns driven by another psychological disorder; for example, a person with claustrophobia who only worries about being in closed spaces would not meet the criteria for GAD.
worry
cognitive tendency to chew on a problem and to be unable to let go of it (cannot settle on a solution)
DSM-5 criteria for generalised anxiety disorder
- experience excessive anxiety and worry at least 50 percent of days about a number of events or activities (e.g., family, health, finances, work and school).
- The person finds it hard to control the worry.
- the anxiety and worry are associated with at least three (or one in children) of the following:
restlessness or feeling keyed up or on edge
easily fatigued
difficulty concentrating or mind going blank
irritability
muscle tension
sleep disturbance. - GAD typically begins in adolescence, (many a tendency to worry all their lives)
- often chronic;
- GAD is more strongly related to marital dissatisfaction than any other anxiety disorder and people diagnosed with GAD report having few friendships compared to others
comorbidity w/ anxiety disorders
More than half meet the criteria for another anxiety disorder
- highly comorbid with other disorders.
- 3/4 of people have another psychological disorder
- 60% percent have major depression
- comorbid with substance abuse and personality disorders
- comorbidity is associated with greater severity and poorer outcomes of the anxiety disorders
DSM5 for agoraphobia
Marked fear or anxiety about ≥2 situations
Public transport, open spaces, enclosed spaces, in line or in crowd, outside of home alone
Fears because escape might be difficult or help not available
Almost always provokes fear or anxiety
These situations are avoided, require the presence of a companion, or endured with intense fear or anxiety
Out of proportion to actual danger
aetiology of agoraphobia
Genetic vulnerability (heritability 61%) ; life events
Fear-of-fear hypothesis:
– Driven by negative thoughts about the consequences of experiencing anxiety in public
Treatment:
Systematic exposure to feared situations:
– More effective with a partner – stop enabling!
aetiology of GAD
Genetic vulnerability
– Tends to run in families
Autonomic restrictors
– Less responsive on physiological measures
– Instead → chronically tense
Highly sensitive to threat → unconscious
– Restricted autonomic arousal but intense frontal lobe activity
– Frantic, thought processes proposed to reflect avoidance of unpleasant emotions that would be more powerful than worry
prevalence GAD
- 5.7% of the population meets criteria for GAD at some point in their lifetime
– One of the most common anxiety disorders
- 2/3 female
– May reflect a reporting bias
- Associated with an earlier & more gradual onset than most other disorders
– Many report feeling anxious & tense all their lives
Chronic course characterised by waxing & waning
Prevalent among older adults
– May be particularly susceptible to anxiety about failing health or other life situations that begin to diminish whatever control they have over their lives
function of worry in GAD
- worrying actually decreases psychophysiological signs of arousal
- use worrying to avoiding emotions that would be more unpleasant and more powerful than worry. But as a consequence of this avoidance, their underlying anxiety does not extinguish.
may be that worry distracts people with GAD from the distress of remembering these past traumas. - people who have a hard time accepting ambiguity are more likely to worry (that something bad might happen) and to develop GAD
Treatment of GAD
Benzodiazepines most commonly prescribed
– Short-term relief, temporary crisis
Psychological treatments more effective long term
– Challenging negative thoughts
– Confronting anxiety-provoking thoughts
– Acceptance rather than avoidance of distressing thought
– ‘Scheduling’ worry
Comorbidity of Anxiety Disorders
- > 50% of people with one anxiety disorder diagnosed with a second anxiety disorder
– Overlapping symptoms
– Shared vulnerabilities
– Different triggers & pattern of panic attacks
Around 75% of people diagnosed with an anxiety disorder also meet criteria for another disorder
– 60% meet criteria for major depression
– Less likely to recover, more likely to relapse
Other comorbidities:
– Substance abuse
– Personality disorders
Physical disorders:
– Anxiety disorder uniquely & significantly associated with:
– Thyroid disorder
– Respiratory disease
– Gastrointestinal disease
– Migraine & allergies
– Anxiety often precedes physical disorder – cause/contribute?
– Poorer quality of life than physical disorder alone
– Same relationship with cardiovascular disease
– Especially panic disorder
