PTSD Flashcards

1
Q

Janoff-Bulman (1992) and assumptions about the world

A

argued that all people hold three main assumptions about self and the world – that the world is benevolent and that we are meaningful and worthy. She suggested that traumatic events shatter these assumptions and recovery requires that the individual rebuilds a conceptual system incorporating the trauma experience.

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2
Q

Horowitz’s information-processing theory of PTSD

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Horowitz’s information-processing theory of PTSD argued that after initial distress or shock, some people are overwhelmed by massive amounts of new information, most of which is not matched by a pre-existing cognitive schema. As a result of this overload, defence mechanisms are mobilised that maintain the traumatic memory in the unconscious and produce the symptoms of denial and numbing. Information processing then usually takes place, with alternating phases of intrusion and denial, as traumatic memory is brought into consciousness through, for example, flashbacks and nightmares – a process Horowitz termed ‘the completion tendency’ (Horowitz, 1986).

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3
Q

Attachment theories

A

Attachment theory has also been influential in theories of PTSD. Insecure attachment has been associated with various difficulties, in particular with interpersonal relationships and affect regulation. Difficulties in these areas are characteristic of more complex forms of PTSD, for example, after exposure to repeated abuse as a child.

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4
Q

Behavioural theory

A

Early behavioural theories of PTSD drew on learning theory and classical conditioning.

In classical conditioning, pairing a neutral stimulus (e.g. a bell) with a stimulus (a so-called unconditioned stimulus, e.g. meat) that automatically produces a response (an unconditioned response, e.g. salivation) leads to the neutral stimulus also having the power to trigger salivation. The neutral stimulus has become a conditioned stimulus and the salivation it produces is called the conditioned response.

In PTSD, it was thought that the trauma was an unconditioned stimulus for fear and that other aspects of the experience, in themselves neutral, became conditioned stimuli. For example, a victim of an assault by a man wearing a black jacket may become acutely distressed every time they see a man wearing a black jacket.

Treatment involves prolonged exposure to traumatic memory itself and to triggers (such as the black jacket) leading to habituation of the conditioned response.

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5
Q

Information processing theory

A

Emotional processing theory has been one of the most influential theories of PTSD. It argues that complex fear structures exist in memory and produce cognitive, behavioural and physiological reactions when activated. They are important in triggering an appropriate response to danger, but can become pathological in certain situations (Foa & Kozak, 1986).

In PTSD, benign stimuli become associated with danger and representations of physiological arousal and behavioural reactions. Beliefs around aspects of the trauma, influenced by pre-existing schemas, become negative in two ways: firstly, a view of the world as a dangerous place; and secondly, a view of the self as incompetent.

Traumatic memory is stored in a fragmented manner and this interferes with information processing. In order to address the pathological fear structure, it has to be activated and then new and incompatible information needs to be made available and incorporated; for example, the lack of current danger experienced during in vivo exposure to triggers.

Resolution requires integration of new information with pre-existing structures usually following prolonged exposure treatment.

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6
Q

Cognitive theory

A

Cognitive theory has become more prominent in models of PTSD over time.

Cognitive models generally assume that what affects our current emotional state are the beliefs we hold about ourselves, and the world around us. Most people facing a man, holding a pistol pointed at them, will experience fear. This is an event that carries a significant danger.

Some people will also appraise the sight of a grass snake as dangerous and will have exactly the same sort of emotions. (Because a grass snake is not objectively dangerous, we tend to call this anxiety rather than fear but the reaction itself is identical.) What distinguishes those who feel anxious in this situation is not the grass snake but the belief that is held about it.

After a traumatic experience, it is argued that it is the persistently held acquired danger beliefs that are responsible for an over-estimation of threat and therefore anxiety. If there is persistent avoidance behaviour, it is argued that there is no natural opportunity to ‘disconfirm’ these danger beliefs and so the condition persists.

Treatment involves finding ways of challenging these beliefs. The cognitive model of Ehlers and Clark (2000) is discussed next as an example.

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7
Q

Ehlers and Clarke cognitive model

A

This cognitive model of PTSD has been extremely influential in the United Kingdom. It builds on classical cognitive theory to propose that negative appraisals of what happened underpin the development of PTSD.

People with PTSD develop excessively negative appraisals about external threat (viewing the world as a dangerous place) and internal threat (viewing the self as incapable). These misinterpretations continue to affect current beliefs and therefore emotions.

PTSD develops when the traumatic memory induces a sense of current threat promoted by excessively negative appraisals of what happened. Recall becomes biased by these appraisals and they need to be addressed for a successful outcome.

In addition, certain stimuli become strongly associated with particular responses and, unless these are addressed, the condition is maintained. Often individuals are not aware of the specific associated triggers and the therapy developed out of this model places great emphasis on detecting what these are and then developing experiments to overcome them.

This approach may involve some exposure treatment but with the primary aim of modifying these beliefs and alongside other cognitive strategies (Ehlers & Clark, 2000).

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8
Q

Dual representation theory: Brewin et al

A

Dual representation theory: Brewin et al

Dual representation theory is supported by memory research and proposes two classes of memory.

One of these is verbally accessible memory (VAM), corresponding to normal autobiographical and semantic memory.

The other is triggered situationally accessible memory (SAM); this seems to correspond to a simple pattern-recognition fear-memory. These pattern-recognition memories are probably subcortical (located in the amygdala) and serve to alert the organism very quickly to danger – even before the conscious mind has time to respond.

So, for example, if someone with PTSD is asked to describe a trauma, this will involve verbally accessible memory. It may well be distressing, although if someone is very practiced in giving this sort of account, the distress may be controllable. As they talk about the experience, especially if asked for detail, they may suddenly find that triggered situationally accessible memories intervene. These emotional ‘hotspots’ correspond to the experience of vivid reliving of an element of the trauma, as if in the present, with emotions which appear to be recreated with their original intensity. They may occur spontaneously as flashbacks, often intense reliving of an aspect of the trauma as if it is happening now.

Successful emotional processing involves incorporating the material held in SAM memory, especially the sensory and physiological material, into a detailed autobiographical account of what happened, integrated with pre-existing schemas about self and the world (Brewin et al, 1996). This means that the individual is able, automatically, to recognise these as past events and not to react emotionally in the same way.

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9
Q

summary theories PTSD

A

Emotional processing theory
Complex fear structures exist in the memory and produce cognitive, behavioural and physiological reactions when activated.
Resolution requires integration of new information with pre-existing structures.

Dual representation theory
Verbally accessible memories (VAMs) and situationally accessible memories (SAMs) can be processed simultaneously.
Resolution involves exposure to SAMs to aid cognitive readjustment and integration of the conflicting trauma-related information with pre-existing schemas about the world.

Cognitive model
Excessively negative appraisals about external threat (viewing the world as dangerous) and of internal threat (viewing self as incapable).
Resolution involves detecting the triggers and developing experiments to overcome them.

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10
Q

how to explain cognitive model for a case

A

According to the cognitive model, Alice has generalised her experience of the attack to formulate the negative appraisal that the world is an unsafe place.

As she was unable to defend herself, she now views herself as incompetent and unable to deal with threats. This has led to her constant nervous state and the development of PTSD.

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11
Q

Social models

A

Several authors have been highly critical of the concept of PTSD, arguing that culturally determined, understandable emotions to traumatic events are being pathologised.

Summerfield (2001) has argued that PTSD was constructed as much from sociopolitical ideas in America after the war in Vietnam as from psychiatric ones. This view does not take account of the much longer history in Europe, going back at least to the work of Charcot and Janet at the end of the 19th century, or the fact that the initial text description in DSM-III was based on work with civilian burn survivors (Andreasen, 2004).

Concern about overdiagnosis is realistic – with risks of promoting abnormal illness behaviour or of inappropriate treatment. (It is not uncommon in clinical practice to see someone with a posttraumatic depression, having had unsuccessful prolonged exposure treatment for a PTSD that they do not have).

Meta-analyses of factors predictive of PTSD (e.g. Brewin et al, 2000) highlight the importance of the traumatic event (essential) as well as other peri-traumatic factors among which lack of social support and the presence of other current stressors are especially important.

Although some have challenged the degree to which this condition can apply in non-Western societies, research has confirmed the presence of PTSD in diverse world settings and in diverse ethnic groups (de Jong et al, 2001).

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12
Q

Neurobiological models PTSD

A

The main brain areas of interest in PTSD research to date have been those associated with fear processing and memory.

The amygdala, which sits at the base of the temporal lobes, is known to be critical in the development of the fear response. The groups of nuclei located within it receive information about external stimuli and play a key role in determining their significance, sometimes triggering emotional responses including fight, flight and freezing. The amygdala sits two synapses away from sensory organs such as the retina and can respond very rapidly to perceived threat, probably using basic pattern recognition.

Other areas of the brain, especially the hippocampus and medial prefrontal cortex, can moderate these responses. For example, if a human sees a piece of rope that looks like a dangerous snake, a normal response might include a startle reaction. This will be relatively quickly followed by amelioration of the response as the true degree of threat is recognised. The hippocampus and medial prefrontal cortex are believed to attenuate the response triggered by the amygdala.

Neuroimaging studies support the involvement of these brain areas in PTSD. Although not proven beyond doubt, a replicated finding in PTSD sufferers has been increased amygdala activity that is correlated with decreased activity in the medial prefrontal cortex.

These findings have led to the hypothesis that PTSD represents a failure of the medial prefrontal networks to regulate amygdala activity, resulting in hyper-reactivity to threat (Shin et al, 2006).

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13
Q

Brain areas important

A

Hippocampus- attenuates response from amygdala as true threat appreciated. Moderates emotional response.

Amygdala- fear response, identifies external triggers and attaches significance to them. Increases response of stress hormones- cortisol, catecholamines

Prefrontal cortex- also attenuates response from amygdala

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14
Q

Hormones and neurotransmitters

A

(1.22) Hormones and neurotransmitters
There is some evidence that in PTSD levels of the stress hormone cortisol are relatively low and that there is an oversensitive negative feedback system whereby abnormally low levels of cortisol inhibit production of ACTH from the anterior pituitary gland.

There is also evidence of raised levels of CRF from the hypothalamus without increased production of ACTH, and therefore of cortisol, due to down-regulated sensitivity to CRF. As well as resulting in lower than optimal cortisol levels, this has a direct influence on increased noradrenaline release in the brain, through stimulating the locus coeruleus where it is primarily produced. This failure to limit the sympathetic response may lead to the consolidation of traumatic memories.

However, although low basal cortisol levels are widely reported as being characteristic of PTSD, there is considerable conflicting research evidence (reviewed by Meewisse et al, 2007).

Many other neurochemicals have been implicated in PTSD. These include:

serotonin

gamma-aminobutyric acid (GABA) – the inhibitory neurotransmitter

glutamate – the excitatory neurotransmitter

neuropeptide Y – a peptide neurotransmitter

brain-derived neurotrophic factor

oxytocin.

These analyses are probably made more complex because of gene by environment (G x E) interaction effects. There are two versions of the serotonin transporter gene, with evidence of an interaction between the short allele (S) and the processing of unpleasant stimuli (Kobiella et al, 2011). It is hypothesised that similar G x E effects are relevant to the generation of PTSD.

The true neurobiology of PTSD therefore is likely to be complex and involve a range of these and other chemicals acting in combination

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15
Q

Epidemiology

A

7~ % lifetime prev, 3.5% 12 mo
higher in high impact trauma (50% post rape)
80% co-morbid- depression, panic disorder, anxiety disorders, substance

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16
Q

Assisting response in immediate post mass trauma

A

he promotion of a sense of safety

calming

a sense of self and community efficacy

connectedness

hope.

NOT debriefing

17
Q

responding after mass trauma

A

There is no evidence that formal interventions directed at everyone involved in traumatic events prevent PTSD. Practical, pragmatic support provided in an empathic manner is required.

Systems that promote a sense of safety, calming, self and community efficacy, connectedness and hope should be encouraged.

Mental health professionals have a role in planning - ensuring that an appropriate psychosocial care plan is in place and delivered. Their main clinical input will be required later for those who develop continuing symptoms. This role will be facilitated if steps are taken early on to identify those most at risk.

18
Q

Psychological of chronic PTSD

A

Using a predetermined threshold, NICE found only TFCBT and EMDR to be clinically significant (NCCMH, 2005), with no major differences being found between the two in head-to-head comparison studies (Lee et al, 2002; Power et al, 2002). On the basis of further RCT evidence, NICE (2018) added narrative exposure therapy (NET) to this list of approved treatments (see page 3.8).

19
Q

TF therapies

A

Trauma-focused behaviour therapy (prolonged exposure treatment)
repeated confrontation of traumatic memories often through detailed recounting of the traumatic experience
repeated exposure to avoided and fear-evoking situations that are now safe but which are associated with the trauma.

Trauma-focused cognitive therapy
modification of misinterpretations that lead to overestimation of current threat
modification of other beliefs related to the traumatic experience, the individual’s behaviour during the trauma (e.g. guilt and shame) and currently (sense of personal incompetence).

Eye movement desensitisation and reprocessing
standardised procedure using bilateral physical stimulation (eye movements, taps or tones) while the individual focuses on memories and associations
thought to stimulate information processing to help produce an adaptive contextualised memory.

20
Q

Phased interventions in complex PTSD

A

A phased approach has been advocated, where phase one involves stabilisation, e.g. dealing with issues around accommodation, benefits, separation and emotional stabilisation. During phase two, trauma-focused psychological treatment is undertaken, and phase three involves integration into the community.

Cloitre et al (2002) have shown a two-phase treatment approach (STAIR-MPE) to be effective for adult survivors of childhood abuse.

The first phase of STAIR-MPE is Skills Training in Affective and Interpersonal Regulation (STAIR); the second phase is Modified Prolonged Exposure (MPE). STAIR was derived from generic cognitive behaviour and dialectical behaviour therapies. It includes the labelling and identification of feelings, emotion management, distress tolerance, acceptance of feelings, identification of trauma-based interpersonal schemas and role plays of power, control and flexibility.

21
Q

Narrative exposure therapy

A

NET is a modern, manualised intervention and the subject of a number of positive randomised controlled trials. In this approach, the client is helped to produce a chronological narrative of their life with a focus on traumatic events but also incorporating positive experiences.

This is another trauma-focused approach involving some elements from the other active treatments. The therapist asks the client to describe the traumas in detail, including the thoughts and sensations they experienced. Clients are encouraged to stay in the present as they do this (as in prolonged exposure).

However, NET allows the client to cultivate a stronger and more coherent sense of personal identity and to see this as continuing through both the good and bad times. Including positive experiences helps them to see their trauma experiences in context, to appreciate the political and social forces they experienced, and to rebuild their self-respect.

22
Q

why might there be a larger effect size in psychological treatments compares with pharm

A

It is noteworthy that there has been a large placebo effect in many pharmacological treatment trials. Despite participants taking the active medication reporting a marked reduction of symptoms, this is usually only just greater than the reduction for those taking a placebo, leading to a small effect size.

This is illustrated by the venlafaxine and sertraline trials detailed in Figure 1 on the next page.

It is therefore possible that the placebo effect in drug trials is more successfully removed from the randomised controlled trial design than in psychological treatment trials and this may explain why the psychological studies appear to demonstrate larger effect sizes.

23
Q

Co-morbid depression

A

Where there is a secondary depression, this often improves as the PTSD is treated (NICE, 2018) and so the PTSD should usually be treated first. More severe depressions may interfere with psychological treatment and should be managed in the usual way, with treatment of PTSD following when appropriate.