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Flashcards in Anxiety Disorders Deck (45):

Anxiety disorders are…

• Extremes of normal anxiety
• Evidence of autonomic nervous system dysregulation - excessive, inappropriate or deficient
• Common - Lifetime prevalence 15 -20%


Types of anxiety disorder

• Generalized Anxiety Disorder (GAD)
• Panic Disorder
• Agoraphobia
• Social Anxiety Disorder (previously social phobia)
• Specific Phobias
• Obsessive Compulsive Disorder (OCD)
• Body Dysmorphic Disorder (BDD)
• Post Traumatic Stress Disorder (PTSD)
• Selective Mutism
• Separation Anxiety Disorder


What is the DSM-5 criteria for anxiety disorder

The DSM-5 chapter on anxiety disorder no longer includes obsessive-compulsive disorder (which is included with the obsessive-compulsive and related disorders) or posttraumatic stress disorder and acute stress disorder (which is included with the trauma- and stressor-related disorders). However, the sequential order of these chapters in DSM-5 reflects the close relationships among them.


What are the shared features of anxiety disorders?

• Primarily stress linked
• Reality testing remains intact
• Symptoms are experienced as distressing
• Disorders tend to be enduring or recurrent


What is aetiology of anxiety disorders

• Genetic
– SLC6A4; short version transports serotonin less effectively (see Smoller et al., 2009)
• Lowered neurotransmitter levels
• Hypothalamic pituitary adrenal (HPA) axis dysregulation

• Social factors
– Early life adversity
– Stressful events especially those involving threat
– Lack of support network

• Personality factors
– Some personality traits predispose to certain anxiety disorders e.g. avoidant & perfectionistic


Parasympathetic Nervous System
Feed and Breed


Decreased: cardiac rate and output, BP,
respiration rate, glycogenolysis,
peripheral diversion of blood,
catecholamines and cortisol.

Increased: gut function, kidney function,
immune surveillance, fat stores,
sex steroids


Sympathetic Nervous System
Fight or Flight


Increased: cardiac rate and output, BP,
respiration rate, glycogenolysis,
peripheral diversion of blood,
catecholamines and cortisol.

Decreased: gut function, kidney function,
immune surveillance, fat stores,
sex steroids


“Fight or Flight”

• Physiological response to a stressor is mediated through the hypothalamus
• Initial activation of the sympathetic nervous system
• Subsequent activation of the pituitary adrenal axis
• Terminated by negative feedback and the parasympathetic system
NB ACTH is adrenocorticotropic hormone


Amygdala and Neurotransmitters

• Amygdala responds to emotional stimuli
• Produce changes in the HPA axis and sympathetic ns.
• GABA inhibits anxiety by modulating the amygdala and hypothalamus synapses e.g. benzodiazepines and alcohol act on same receptors.
• Serotonin and beta-blockers also have an effect on anxiety


Post traumatic stress disorder (PTSD)

• Delayed or protracted response to trauma (often involving threat to life)
• Onset usually within 6 months of event
• Core symptom is “reliving the event”
– Flashbacks, nightmares, waking dreams
• Emotional numbness and detachment
• Avoidance of activities, situations that remind person of trauma


Symptoms of PTSD

• Increased autonomic arousal (including exaggerated startle response, hypervigilance and sleep disturbance)
• Avoidance & emotional numbing
• Re-experiencing (flashbacks & nightmares)
• Lifetime prevalence of 3-8%


DSM-IV-TR Diagnostic Criteria for PTSD

• The person has been exposed to a traumatic event
• The traumatic event is persistently re-experienced
• Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness
• Persistent symptoms of increased arousal
• Duration of the disturbance is more than 1 month
• The disturbance causes clinically significant distress or impairment


Traumatic events that may precipitate PTSD

• Rape (90% develop PTSD symptoms)
• Torture (70-90%)
• Prisoners of war (>50%)
• Earthquake & flood (20-25%)
• Road traffic accidents (15%)
(Davey, 2014)


It’s not all bad news though…

• > 50% of people will
experience at least one trauma in
their lifetime – not all will develop

• Following trauma, women are
more likely to develop PTSD
than men (ratio of 2.4:1)

• Some will experience post-
traumatic growth (Joseph, 2012 )


The aetiology of PTSD

• Vulnerability factors
• Theory of shattered assumptions
• Conditioning theory
• Emotional processing theory
• Mental defeat
• Dual representation theory


Vulnerability factors

• What makes people vulnerable to developing PTSD?
– Tendency to take personal responsibility for the trauma
– Environmental factors such as unstable family life
– A family history of PTSD
– Existing high levels of anxiety or a pre-existing psychopathology


Theory of shattered assumptions

• Argues that trauma will shatter a person’s belief in the world as a safe place
• Individual is left in a state of shock and conflict
• However, paradoxically it is those who already view the world as an unsafe place that are most likely to develop PTSD (Resick, 2001)


Conditioning theory

• Trauma (UCS) becomes associated with situational cues associated with the place and time of the trauma (CS) (Keane et al., 1985)
• PTSD is therefore a conditioned fear reaction to cues associated with the trauma
• However, does not explain why some people who experience trauma do not develop PTSD


Emotional processing theory

• Trauma creates a representation of the trauma in memory that is associated with situational cues (Foa et al., 1989)
• Explains how fear memories are laid down and activated in fear networks in the brain
• Has given rise to influential exposure treatments for PTSD


Dual representation theory

• Views PTSD as a hybrid disorder involving two separate memory systems (Brewin, 2001; Dalgleish, 2004)
• The verbally accessible memory (VAM) system consciously processes memories of the event
• The situationally accessible memory (SAM) system records information that is too brief to take in consciously
• The SAM system is responsible for the vivid uncontrollable flashbacks experienced in PTSD


Mental defeat

• A frame of mind that makes individuals vulnerable to PTSD (Ehlers & Clark, 2000)
• Individuals who develop PTSD tend to:
– See themselves as a victim
– Process information about the trauma negatively
– View themselves as unable to act effectively
– Do not believe they have the coping skills to overcome the traumatic experience
– Believe the trauma has permanently changed their life


PTSD management includes

• Behavioural therapy
• Stress innoculation training
• Trauma focused CBT *
• Eye movement desensitisation and reprocessing (EMDR) *
• Debriefing after traumatic event *
– no clear evidence base for this
Narrative exposure therapy


Trauma focused CBT

• See Ehlers & Clark (2000)
• Psycho-education
• Exposure; imaginal and/or In vivo
• Reliving with cognitive restructuring
• Behavioural experiments
– Drop safety behaviours
– Stimulus discrimination
– Experience emotions
• Imagery work



• Developed by Francine Shapiro in the 1980s
• Involves bilateral stimulation of the brain whilst recalling the traumatic event (dual attention)
• Aims to desensitise the client to distress and reprocess ‘frozen’ traumatic memories so that the associated cognitions can become more adaptive - adaptive information processing Shapiro, 2007)
• Works towards the installation of a positive cognition



• A structured way of trying to intervene immediately after trauma to prevent the development of PTSD
• Also called Critical Incident Stress management (CISM) (Everly et al., 2000)
• A form of post-event counselling for victims
• Limited evidence that it is effective in preventing PTSD (McNally et al., 2003)


Narrative Exposure Therapy

• Development of testimony therapy (Cienfuegos & Monelli, 1983)
• A short term approach
• Developed for use with people who have experienced a series of traumatic events, resulting in PTSD (Schauer et al., 2005)
• Aims to enable a coherent and meaningful narrative of events to be developed, influencing fear networks
• Has been adapted for use with children – KIDNET (Onyut et al., 2005)


Anxiety Disorders in Children are...

 Anxiety disorders are one of the most prevalent emotional problems of childhood (e.g., Barrios & Hartmann, 1997)

 However, specific fears and anxieties are also one of the normal developmental challenges that face maturing individuals


The Features & Characteristics of Childhood Anxiety Problems

 Behavioural, cognitive and emotional aspects

 Primarily manifested as withdrawn behaviour (internalizing)

 Children avoid activities and are clinging and demanding of parents and carers

 Anxious children report significantly more somatic complaints (Hofflich et al., 2006)


The Aetiology of Childhood Anxiety Problems

 Genetic Factors

 Trauma & Stress Experiences

 Modelling & Exposure to Information

 Parenting Style & Parent-Child Interaction


Genetic Factors of anxiety problems in children

 Twin studies suggest a significant but modest inherited component

 Both heritable and environmental factors appear to be important (Lichtenstein & Annas, 2000)

 May be different for specific anxiety disorders

 State vs. trait anxiety (Lau et al., 2006)


Trauma & Stress Experiences

 There are clear links between extreme stressful experiences (e.g. childhood physical and sexual abuse) and childhood anxiety (Feerick & Snow, 2005)

 Events such as living with illness, the death of a pet, and minor road accidents can cause significant childhood anxiety


Modelling & Exposure to Information

 Exposure to information about threats can cause children to develop fears and phobias without direct experience (Field, 2006)

 For e.g., observation of parents reactions and behaviour patterns, or listening to parents explanations (Barrett et al., 1996)


Parenting Style and childhood anxiety

 Overprotective and overanxious parents may invoke anxiety in the child (Rapee, 1997)

 Overprotective parenting may increase the child’s perception of threat and reduce their sense of control (Van der Bruggen et al., 2008)

 Children who experience rejecting or detached parents also show increased levels of anxiety (Chartier, Walker & Stein, 2001)


Childhood Anxiety Disorders

 Generalized Anxiety Disorder (GAD)

 Obsessive-Compulsive Disorder (OCD)

 Specific Phobias (e.g., School Phobia)

 Separation Anxiety Disorder (SAD)
Selective Mutism (SM)


Separation Anxiety

 An intense and developmentally inappropriate fear of being separated from parents or carers

 May develop exaggerated fears that parents may become ill, die or be unable to look after them

 Consequences include reluctance to attend school or to require parents to stay with them until they fall sleep


Changes in the DSM 5 for childhood anxiety

 Acceptance of SAD in adulthood:

- Age of onset after 18 years
- Modification of criteria wording (e.g., attachment figures, workplace)
- Duration criteria: ‘typically lasting 6 months or more’


SAD and Parenting Style

Parental intrusiveness is linked to SAD in children predisposed to or currently experiencing anxiety (Wood, 2006)
Intrusiveness involves:

 Unnecessary assistance with daily self-help tasks

 Infantilising behaviour (e.g., excessive affection)

 Invasions of privacy
Developmentally inappropriate for the child’s age


Selective Mutism

A persistent failure to speak in certain social situations

- Excessive shyness, fear of social embarrassment, social isolation and withdrawal, clinging, compulsive traits, negativism

- May involve temper tantrums or oppositional behaviour, particularly at home


Diagnostic Criteria

 Lasts at least a month (but not the first month of school)

 Cannot be better accounted for by a communication disorder

 Interferes with educational or occupational achievement, or with social communication

 Does not occur exclusively within the course of a pervasive developmental or psychotic disorder


Key Issues

 A relatively rare and under-researched disorder

 Complicated co-morbidity issues

 Rather than an oppositional disorder, SM is increasingly considered as an anxiety disorder (a specific childhood manifestation of social phobia; Anstendig, 1999; Kristensen, 2000).

 Aphasia voluntaria > elective mutism (ICD-10) > selective mutism (DSM-IV-TR)> DSM 5 now classified as an anxiety disorder


General Treatment Issues

 Pharmacological: use of antidepressant or anti-anxiety medications? (e.g., Sertraline)

 Psychotherapeutic: wide use of and support for CBT (Hirshfeld et al., 2010)

 Combined approach? (See Ginsburg et al., 2011 CAMS study)


Childhood CBT: Key features

 Involves use of Psychoeducation

 Developmentally appropriate tools and materials

 Focus upon identification of symptoms

 Imaginal exercises and relaxation techniques

 Exposure is crucial (Barlow, 1988; Blagg & Yule, 1984)


Parental Involvement

 Parent as ‘coach’ who is directly involved with behavioural management.

 Identify problem, break it down, try a strategy, then evaluate strategy

 Parental involvement differs between programs,. Can be associated with improved outcomes (e.g., Barrett, Dadds, & Rapee, 1996; Mendelowitz et al., 2002) but results are not consistent (e.g., Nauta et al., 2001; 2003).


Treatment of Selective Mutism

 Traditionally considered to be difficult to treat (e.g., Kolvin & Fundudis, 1981)

 Treatment reconsidered in light of reappraisal as an anxiety disorder

 Successful use of behavioural approaches(e.g., contingency management, stimulus fading, systematic desensitisation and self modelling)

 Promising use of CBT approaches (Fung et al., 2002)

 Limited and methodologically weak research in this area

 Multi-modal, multi-agency approach seems most appropriate (Standart & Le Couteur, 2003)

 Treatment should continue after the achievement of speech


Alternative Methods: Computerised CBT (See Kendall et al., 2011)

 Computer-assisted or computer based

 Preliminary research to support use in the treatment of adult anxiety disorders (e.g., Anderson, Jacobs & Rothbaum, 2004)

 Camp-Cope-A-Lot (CCAL) for 7-12 year olds