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PIP - Anxiety disorders - Y2 - Coggle Diagram
PIP - Anxiety disorders - Y2
Extra information on specific anxiety disorders
Responsibility attitudes and interpretations are characteristic of OCD (Salkovskis et al, 2000):
Cognitive-behavioral theory of OCD suggests that a key factor in obsessional behaviour is the way in which intrusive thoughts are interpreted
Links between clinical symptoms and responsibility beliefs
-> Responsibility was categorised as both general responsibility attitudes, but also specific responsibility appraisals
-> Compared to those suffering anxiety and non-clinical controls
-> Good internal consistency and reliability
Results show specificity in the assumptions and appraisals in OCD, and good evidence of specificity of association between responsibility cognitions and obsessional symptoms across groups, which was not a consequence of links with anxiety or depressive symptoms
Although the two measures were correlated, they made different contributions
Overall, results were consistent with the hypothesis that responsibility beliefs are important in the experience of obsessional problems - they were elevated significantly, suggesting perceived responsibility increases the obsessions
This association could also be a consequence of OCD (Lopatka and Rachman, 1995)
The findings were specific to OCD compared to anxious controls
Cognitive behavioural therapy for adult anxiety disorders - meta-analysis of randomised placebo controlled trials (Hofmann and Smits, 2008);
Aimed to review the efficacy of CBT versus placebo for adult anxiety disorders
The advantage of CBT over placebo did not depend on placebo modality, number of sessions in a study year
It most effective for OCD and acute stress disorder, and this contradicts the idea that OCD is the most treatment resistant disorder
CBT outperformed the placebo specifically in reducing depression in PTSD and OCD
Biological contributions to anxiety -
Inheritable tendency to be tense, uptight and anxious (Barlow et al, 2014)
Tendency to panic also has a genetic component
Tends to come from a collection of genes in several chromosomes that make us vulnerable to anxiety when the right psychological and social factors are in place
Associated with depleted levels of GABA, noradrenergic systems and specific brain circuits
Serotonin has also being implicated
More recently, corticotropin-releasing factor (CRF) system has been noted to be central to anxiety and depression, and the groups of genes that increase the likelihood that this system will be turned on
CRF activates the HPA axis, impacting the limbic system, the prefrontal cortex, the locus coeruleus, amygdala and the dopaminergic neurotransmitter system
CRF is also linked to GABA, noradrenergic and serotonergic systems, and SNP coding was an important risk allele for anxiety (single-nucleotide polymorphism)
Limbic system is most commonly associated with anxiety - behavioural inhibition system (Gray and McNaughton, 2003) - danger signals then descend from the cortex to the sepal-hippocampal system, and the BIS is also boosted by the amygdala
-> BIS initiates the fight or flight system
However, activation of these systems can also help predict response to CBT - it is likely environmental factors change the sensitivity of circuits, making you more or less likely to develop anxiety disorders
Johnson et al, 2020 - teens who smoked were more likely to develop panic disorder and generalised anxiety disorder
-> Leventhal and Zvolenksy (2015) - complex interaction of the two - anxiety sensitivity, distress tolerance and anhedonia all contribute to smoking, and this makes quitting smoking difficult for those with anxiety
Limbic system is overly responsive to stimulation, and controlling that involves down regulation of the amygdala
Social contributions -
Stressful life events trigger biological and psychological vulnerabilities - most are social and interpersonal, and the same stressors can trigger physical and emotional reactions (Barlow, 2002)
The particular way we react to stress seems to run in families, and suggests at the very least a genetic contribution to panic attacks
Integrating the factors - Triple vulnerability theory (Barlow, 2000):
Diathesis is a generalised biological vulnerability, followed by a generalised psychological vulnerability (e.g. lack of healthy cognition)
This is then followed by a specific psychological vulnerability (life events), which is the stress
Once the cycle starts, it reinforces itself, and although anxiety can be general, it is normally evoked by one area of life
Psychological contributions to anxiety -
As children, we acquire an awareness events are not always under our control - this perception of control can create anxiety
-> A sense of lack of control can create anxiety, and this can also come from traumatic environments
-> Parental approaches (Barlow, et al 2014) appear to foster this - parents who are responsive, predictable and positive in regards to needs, particularly when the child is communicating, and these parents teach controllability in the environment
-> This adds to the secure home base and allows children to develop the skills they need to face new situations
-> In contrast, over intrusive, negative and overprotective parents create situations where children cannot deal with adversity (Barlow, 2002)
Anxiety sensitivity - personality trait that determines who will and will not experience anxiety in stressful situations (Reiss, 1991)
-> Conditioning and cognition have been linked to anxiety, and particularly conditioning has been linked to phobic disorders
-> Conditioning may occur due to cues or triggers travelling directly from the retina to the amygdala, without routing through the cortex and therefore bypassing conscious awareness
GAD - generalised anxiety disorder - causes:
High heritability of anxiety sensitivity and underlying biological vulnerability - inherent tendency to become anxious
Show less responsiveness on physiological measures - leading to autonomic inflexibility and autonomic restrictors
-> They are acutely aware of threat and allocate more attention to potential threat because of high sensitivity, and this appears to be automatic - Stroop task evidence for threat words (MacLeod and Matthews, 1991)
-> Frantic, intense thought processes and worry, causing autonomic restriction and the symptoms therefore seen
-> Thinking so hard about potential problems that they do not have the attentional capacity to visualise the threat, which would elicit more negative affect - avoid threat images
-> Therapy teaches visualisation of the threat and to process threats to cope
Learning early in life of lack of control and stressed parents also contributes to this - worry is a way to deal with this lack of control, as expecting a worse outcome prepares you for it but relieves you when it does not happen
-> Would rather be in a sustained state of distress to be prepared, meaning there is constant negative affect but no spike in negative emotion
-> Anxiety is future-oriented as a mood state, focused on potentials, rather than focused on actual present danger
Generalised psych vul. + generalised bio vul -> stress -> anxious apprehension -> worry process -
-> Intense cognitive processing, avoiding images, restricted autonomic response and inadequate problem solving skills = GAD
Treatment - SSRIs and therapy; benzodiazepines carry a number of risks
Agoraphobia and panic disorder - causes:
PD strongly related to biological and psychological causes - some people are more likely to have an emergency response to danger, and association of these cues with panic creates a cycle (Bouton et al, 2001)
-> Next time the symptoms occur, a panic attack is expected
-> This is enabled by a psychological vulnerability to perceive anything unusual in the body as a danger
-> Those who avoid developing anxiety attribute the panic to events at the time, whereas those who do not attribute it (Clark, 1986) to this explain it to be catastrophic and this triggers the sympathetic nervous system, creating a cycle where cues trigger the SNS
-> Psychodynamic theory states that early separation anxiety and object loss predisposes the individual to developing anxiety as an adult (Thyer, 1993)
Dependent personality characteristics can also contribute to agoraphobia (Barlow, 2002)
Treatment - medication and therapy:
Panic control treatment - exposing patients to the cluster of interoceptive sensations of panic attacks to teach relaxation, creating reciprocal inhibition of the panic around the symptoms
Booster sessions are often used to prevent relapse
Combined treatments - SSRIs or tricyclics and CBT; medication is however more short-term effective, especially when combined with therapy, but CBT only maintains the patient better
-> Some evidence that benzodiazepines interfere with effects of psychological treatments and as they cause cognitive impairment, they may interfere with the revision of cognition that is part of CBT
-> There is no benefit for panic disorder in combining treatments, and CBT is more effective in the long run
PD is common, at 4.7% prevalence over the life course and agoraphobia and panic disorder are disproportionately common in women:
Cultural influences - men tend to become alcoholics to cope with anxiety, creating a more severe problem, and treatment becomes more difficult as a result (McHugh, 2015)
There is cross-cultural validity for the diagnosis
For minority groups, panic disorder is often associated with fears of discrimination
The expression of the anxiety can also differ across cultures (Latin America - Susto, or fright disorder, with increased sweating and insomnia, but no anxiety despite severe fright being the cause)
Nocturnal panic - panic attacks that occur during slow wave sleep, which can lead to feelings of dying (Craske and Barlow, 2014)
-> The sensation of transition from light to deep sleep can feel like ‘letting go’, and this has been said to cause the attacks (Craske et al, 2002)
Specific phobia - there are four major categories of specific phobia:
Blood-injection-injury type - differ in their physiological reactions from people with other phobia types, and are more prone to fainting
-> Runs in families most strongly - inherit strong vasovagal response to blood, injury or possibility of injection creating a drop in blood pressure and fainting, rather than panic
-> Onset in childhood
Situational type - claustrophobia, onset in adolescence - 30% of first relations have similar phobia
-> Main difference to PD - panic attacks are not experienced outside of feared situation
Natural environment type - very young people developing fears of heights, storms or water
-> Tend to cluster together, as fearing deep water for example predisposes you to fearing heights
-> As they all have a common fear of danger, some fear is adaptive (Seligman - Biological predisposition)
Animal type - different from mild disgust response
Other - includes phobias that do not fit into these categories - vomiting, choking, illness, children, characters and sounds
Causes - Traumatic conditioning has been implicated in subsequent phobic behaviour
Example of phobias acquired through direct experience
However, there are three other ways - experiencing a false alarm in a specific situation, observing someone else experiencing severe fear and being told about danger (under the right conditions)
Experience of a false alarm - an unexpected panic attack in a specific situation may prime development of a phobia (Ehlers et al, 1994)
Learning vicariously - seeing someone else go through a traumatic experience or endure intense fear can predispose development of that phobia (Askew, Hagel and Morgan, 2015)
Information transfer is also a mode of developing a phobia - being warned repeatedly about something makes one more anxious about its occurrence
Terrifying experiences alone do not create phobias (DiNardo et al, 1988) -
Traumatic conditioning experience -> more likely to develop if already prepared to fear it -> susceptible to developing anxiety about the possibility of the event happening again
-> For example, having heritability for blood-injury-injection phobia only creates a phobia when psychological vulnerability to anxiety exists
-> Fyer (1990) - and replications - show that specific phobias were common amongst first relatives about 31% of the time, and Page and Martin (1998) found high estimates for heritability of specific phobias
-> This suggests there is both a genetic and psychological contribution to specific phobias (Smoller et al, 2005)
Social and cultural factors - specific phobias tend to occur in women as men do not report fear (Arrindell et al, 2003)
-> It is suggested that because of this, men expose themselves to their feared situation, and endurance eventually improves (Antony and Barlow, 2002)
-> More masculine girls were also less likely to report fear, suggesting the contribution of culture to specific phobias (Ginsburg and Silverman, 2000)
Mowrer’s two-factor model - acquisition and maintenance
Treatment - Exposure-based exercises - systematic desensitisation and flooding
Provides reciprocal inhibition of the fear and also counterconditioning of the stimulus (Antony, Craske and Barlow, 2006)
Separation anxiety over involves the parent to address causes from parental separation (Choate et al, 2005)
For blood-injury-injection phobias, the therapy involves muscle tensing exercises to prevent blood pressure falling (Ayala, Meuret and Ritz, 2009)
Separation anxiety disorder is characterised by children’s unrealistic and persistent worry that something will happen to their parents or other important people in their lives (Barlow et al, 2003) - this usually decreases with age
However, it also has to be separated from school phobia
In 35% of cases, if untreated, it can extend into adulthood
In some cases, the onset is in adulthood - as this can happen at any time, it became its own disorder in the DSM-5
Social anxiety disorder - causes:
Evolutionary fear of critical, rejecting and angry people (Ohman and Dimberg, 1978) - more quickly learn to fear angry expressions quicker than others
Eye region is specifically a scary area of the face (Fox and Damjanovic, 2006)
Those who avoid angry people may be surviving better, allowing passing of their genes
Individuals with excessive behavioural inhibition are also noted to be at an increased risk for developing phobic behaviour (Hirschfield et al, 1992), which can start as young as 4 months
Cognitive therapy to target what maintains the disorder - SAD is maintained by repeated exposure to the cues of anxiety, and the avoidance and safety behaviours that follow this:
Done as a group intervention to improve perception of social evaluation
Has shown changes in brain activity associated with emotional processing (Goldin et al, 2013)
Psychological treatments are superior to drug or mixed treatments (Mortberg, Clark and Bejerot, 2011)
However, the drug D-cycloserine (DCS) to CBT enhances exposure therapy, by making extinction work faster and last longer, but SSRIs can block DCS’ facilitating effect on exposure therapy (Andersson et al, 2015)
Trauma and stressor related disorders:
PTSD - experience of a trauma, developing PTSD
-> Generalised psychological vulnerability + generalised biological vulnerability -> experience of trauma
-> True alarm -> learned alarm -> anxious apprehension -> avoidance or numbing of emotional response -> moderated by social support and ability to cope -> PTSD
-> Treatments include exposure, either imagined or direct, and cognitive therapy for negative attributions
Three pathways - generalised psychological vulnerability + generalised biological vulnerability (heritable component of behavioural inhibition) -> stressors + direct experience (only for true alarm) -> true alarm, false alarm or no alarm (but perceived poor social skills)
--> No alarm -> anxious apprehension
--> False alarm + true alarm -> learned alarm -> anxious apprehension
--> This contributes to stressors
--> Anxious apprehension -> specific psychological vulnerability (social evaluation is dangerous) = social anxiety disorder
--> Resembles panic disorder and generalised anxiety, but with added element of identifying social evaluation as the specific source of anxiety
OCD - causes:
Intrusive and unacceptable thoughts of OCD are regulated by brain circuits of anxiety - tendency to develop anxiety over having compulsive thoughts, may have generalised psychological and biological triggers (Barlow et al, 2014)
Hypothesis -
-> Focus of anxiety on a thought comes from the idea that they were taught some thoughts are dangerous or unacceptable because those things may happen and they would be responsible
-> This would cause a psychological vulnerability which would transform the normal behaviour to OCD
-> This is known as thought-action fusion, which can also be caused by excessive responsibility and resulting guilt developed during childhood
-> Religious belief strength is associated with thought-action fusion and severity of OCD (Rassin and Koster, 2003)
-> As you cannot avoid thoughts, they have to be neutralised, leaving to strategies to neutralise them - these become compulsions
Can be comorbid with Body Dysmorphic Disorder, and OCD can be found in family members of BDD sufferers (Chosak et al, 2008)
-> BDD causes intrusive, persistent and horrible thoughts about their appearance, leading to compulsive behaviours such as looking mirrors to check their physical image
-> Have similar onset and run the same cause, and have some similar abnormal brain functioning (Rauch et al, 2003)
-> Most sufferers engage in plastic surgery
-> BDD - have more insight, and seek plastic surgery as an option - they are preoccupied with some imagined deficit in their appearance
Hoarding disorder is another type of Obsessive-Compulsive disorder, as is trichotillomania and excoriation (skin picking)
-> Hoarding - characterised by excessive acquisition of things, difficulty discarding anything and living with excessive clutter under conditions known as gross disorganisation
-> Similar to treatment for OCD but less effective
-> Trichotillomania and excoriation - excessive and compulsive picking
Treatments:
SSRIs are an effective treatment for OCD - relapse often occurs when the drug is removed (Dougherty et al, 2012)
Exposure and ritual prevention is also used, where rituals are prevented but individuals are exposed to feared thoughts or situations - however, this is not readily accessible
-> Intends to show the individual no harm comes when rituals do or do not happen
-> ERPs can be improved with combination of SSRIs
Cognitive treatments for overestimation of threat have been found to be as effective as ERPs
Deep brain stimulation - can be reversed (McLaughlin and Greenberg, 2012) but is considered a last resort
Main features of anxiety disorders
Anxiety disorders have a physiological basis - they are usually linked to overactivation of the HPA axis in the fight or flight system
Anxiety v anxiety disorders
-> Anxiety - normal, ubiquitous, and adaptive
-> Anxiety disorders - intense, longer lasting anxiety / fear that interferes with everyday functioning
Anticipation of and preparation for negative future events
Intense psychological and somatic features
Threat is unrealistic, disproportional or imagined
A heightened state of vigilance / threat bias
Avoidance / safety-seeking behaviours
Normal anxiety - motivation, helps to cope with stress, protection for survival (fight or flight), normal worry, some intrusive thoughts and images which are easily dismissed
Anxiety disorders -
Procrastination
Problems in functioning
Panic attacks
Excessive worry
Intrusive thoughts and images cause great distress
Anxiety disorders overview (DSM-5):
Disorder
Specific phobia -> specific object or situation
Social phobia -> Social or performance situations
Panic disorders -> experience of repeated and uncontrollable panic attack
Generalised anxiety disorder - continual apprehension about future events leading to pathological and chronic worry
The core emotion is anxiety but it manifests differently across these disorders
Moved from anxiety disorders section in DSM-5:
Obsessive compulsive disorder - recurrent obsessions or compulsions that are consuming and cause distress
Post-traumatic stress disorder - set of persistent anxiety related symptoms after witnessing an extremely traumatic event
Commonalities of the experience of anxiety - Wells, 1997:
Emotions - anxiety, fear and apprehension
Physiology - sweating, chest pain, dizziness, decreased sex drive, irritability, increased muscle tension, rapid breathing, breathlessness, heart palpitations, increased blood pressure, nausea and diarrhoea
Behavioural - avoidance, safety-seeking behaviours, sleep problems, over-eating, interpersonal problems
Cognitive - anxious thinking:
Catastophizing - believing something will have more of a consequence than it actually will
Fortune telling - believing you can predict the future and therefore discounting other possibilities
Selective attention - selectively attending to threatening information; scanning the internal and / or external environment for threat
Perservation - same worry thoughts go through your mind and you find it hard to switch off from them
Commonalities of aetiology (Barlow, 2002; Bievenue et al, 2004 & Kotov et al, 2010):
Biological - Gender, reactivity to stress / anxiety sensitivity, perservation / executive function
Psychological - cognition, beliefs, self-view and self-efficacy
Personality (psy+bio) - neuroticism, low extraversion and conscientiousness, perfectionism and attachment anxiety
Social - life experiences, traumas, modelling and peer group
A biospychosocial model is often adopted combining these - neuroticism is the most consistent personality trait included
Commonalities - maintenance:
Amygdala is in overdrive and thus easily triggered, which leads to cognitions about failure / anxiety
This results in escaping the stimuli that elicits these feelings, to create a sense of relief when returning to a safe space
This maintains the high alert of the amygdala, as running from the solutions outside the safe space reinforces the need to flee and the high threat sensitivity
Applying cognitive-behavioural theory to understanding and treating anxiety disorders
Common treatment principles -
Behavioural - desensitisation -
-> Exposure to feared stimulus without avoidance facilitates habituation and new learning
Cognitive - reattribution
-> Establishing core cognitions and cognitive processes and evaluating their accuracy and usefulness
Different disorders and the focus of exposure -
Specific phobia - focus of exposure is the target of phobia
Social anxiety - exposure to feared situations
Panic disorder - exposure to internal sensations of physiological arousal
Generalised anxiety disorder - exposure to worries, typically through imagination
Obsessive compulsive disorder - exposure to obsessive thoughts and triggers of compulsions with avoidance of compulsive behaviour (response prevention)
PTSD - exposure to traumatic memories first, followed by avoided places, peoples and activities
Panic disorder
Panic attacks -
Sudden, rapid increase in anxiety due to a single, very intense fear that something imminent is going to happen
Accompanied by at least 4 of 13 somatic or cognitive symptoms that escalate within 10 minutes
-> Physical - palpitations, breathlessness, dizziness, depersonalisation, sweating, choking and trembling
-> Cognitive - fear of dying, suffocating, going crazy etc
DSM-5 criteria - recurrent, unexpected panic attacks:
Followed by either relentless fear of facing another attack, changes in behaviour in an attempt to avoid a future attack, or a combination of both of these actions for a month or longer
Not otherwise explained by drug / alcohol use or an organic condition
Cognitive model of panic (Clark, 1986):
Trigger stimulus (external or internal)
-> Perceived threat -> anxiety / apprehension -> body sensations -> interpretations of sensations as catastrophic -> avoidance strategies -> hypervigilance to future perceived threats
This is the dominant model
There is some evidence for biological processes differing among PD sufferers such as HR responsivity but this is not causal - it appears to explain more how people interpret their physical experience
Hypervigilance and avoidance are the processes that contribute to the maintenance of the disorder
Obsessive compulsive disorder
Obsession - intrusive and recurring thought, impulse, image that one finds disturbing and uncontrollable
-> Contaminating / causing physical harm to others
-> Expressing immoral impulse
-> Doubt / uncertainty
Compulsion - repetitive, ritualised behaviour aimed at preventing the feared outcome (recognised as excessive) -> come as a way to prevent obsession; exaggeration of superstitious behaviour
-> Counting
-> Checking
-> Clearning / hand washing
-> Hoarding / arranging objects
OCD is highly debilitating and can be difficult to break - extent and disruptive nature of compulsion is high
Cognitive-behavioural model of OCD -
Most people experience intrusive thoughts
A minority develop OCD -
-> Biological - genes, heritable personality traits (neuroticism, anxiety sensitivity, perfectionism)
-> Psychological - general beliefs characterised by 'better safe than sorry', inflated responsibility
-> Social - critical incident - modelling, own ill-health and endemics
It is the appraisal, or interpretation, that makes the obsession (Salkovskis et al, 2000)
The model -
Intrusion e.g. I might catch an infection -
-> Dysfunctional appraisal or intrusion = over-estimation of harm, inflated responsibility and need for certainty
What contributes to this -
-> Attention and reasoning biases - thought-action fusion, jumping to conclusion bias and selective attention
-> Mood changes - anxiety, depression and distress
-> Safety behaviours - thought suppression and avoidance
-> Neutralising act / ritual - wash my hands
These all contribute to reinforcing the intrusion and maintaining the pattern of obsessions leading to compulsions - they lead to the dysfunctional appraisal, and this appraisal then causes these behaviours.
Cognitive techniques -
Responsibility pie charts
Risk analysis
Psychoeducation
Behavioural experiments -
Exposure and response prevention e.g. contaminating himself and testing whether fears come true
-> Touching dirty socks, spreading germs, touching door handles and not washing till arrives home
Evaluation of evidence-base for treatments
Effectiveness of CBT for anxiety -
Meta-analytic reviews of controlled trials (Hofman and Smits, 2008), have established small-large effect sizes
However, samples and procedures of control trials seldom resemble real life clients (Shean, 2012)
-> Comorbidities
-> Motivation to change
-> Professional training of therapists
-> Method of intervention - manualised v formulation
Current developments - 3rd wave:
Acceptance and Commitment Therapy (Hayes et al, 1998)
Mindfulness-based approaches (Segal, Teasdale & Williams, 2002)
-> Still under CBT umbrella
-> Based more on recovery as opposed to disease models
-> Aim to alter the way people relate to thoughts, rather than thoughts themselves
-> Enhance engagement in meaningful life areas
-> Reduce effects of psychopathology by increasing valued living
-> As effective but less researched
Summary
Anxiety disorders encompass a family of disorders that share maladaptive level/experience of normal anxiety, common aetiologies/patterns, and can be treated with some common principles (CBT)
Panic disorder involves recurrent experience and fear of panic attacks
Obsessive compulsive disorder involves intrusive thoughts and behaviours designed to reduce them
Both can be understood and treated in terms of cognitive-behavioural models, although evidence for their success is based on imperfect methods
They have environmental and biological contributions e.g. family history can mean a genetic and learned vulnerability through exposure to coping techniques with OCD etc