Trauma + Post Traumatic Stress Disorder Flashcards

1
Q

Define PTSD

A

A set of persistent anxiety-based symptoms that occurs after experiencing or witnessing an extremely fear-evoking or life-threatening traumatic event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the persistent issues in the definition of PTSD

A
  1. FREIDMAN et al. 2011: There is still debate as to whether PTSD should be considered an anxiety disorder, stress-induced fear response, a dissociative disorder or a trauma related disorder. Most can agree that the primary cause is a traumatic experience, so PTSD is placed in a broader category in the DSM.
  2. Broadening it too involve trauma involving viewing or learning about stressful events has been debated as some suggest it makes PTSD easier to fake in those who have to gian financially from a diagnosis ROSEN 2004 or because it confuses PTSD with merely experiencing stress MCNALLY 2003
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the diagnosis of PTSD

A

Special disorder where the cause of the condition is a defining factor: PTSD is only diagnosed if the individual has suffered from an extreme trauma prior to symptoms.
– Trauma can be (a) directly experienced or (b) witnessed (c) learnt that trauma has happened (4) subjected to repeated distressing details of trauma

Symptoms placed in 4 categories:

  1. INTRUSIVE (1): flashbacks, intrusive thoughts, physiological reactions
  2. AVOIDANCE RESPONDING (1): active avoidance of thoughts, memories or reminders of trauma
  3. NEG CHANGES IN COG+MOOD (2): persistent fear, horror, anger, guilt and other neg beliefs
  4. INCREASED AROUSAL+REACTIVITY (2): hyper vigilance and exaggerated startle responses

Duration of 1 month needed - below 1 month it is known as acute stress disorder.

Once these symptoms develop PTSD is often a chronic condition lasting for years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Prevalence of PTSD

A

– PTSD is estimated to affect about 1 in every 3 people who have a traumatic experience

  • -Men with PTSD identify combat and witnessing someone else’s injury or death most often as the cause. Women identify physical attack or threat most often as the cause for the disorder.
  • Gender differences also exist in the prevalence rates and vulnerability: women are more likely to develop PTSD than men after a traumatic event HOLBROOK et al 2002

– Cultural differences in prevalence rates: lower rates in Caucasian compared to latinos or african americans

– ROTHBAUM: 90% of rape victims develop condition, 70-90% torture victims, 50%+ war prisoners, 20% earthquake survivors - prevalence rates are much higher in groups such as these who are exposed to more severe trauma

– PTSD is more prevalent among war veterans than among any other group. The National Vietnam Veterans Readjustment Survey reports that approximately 25 percent of U.S. veterans, men and women, were suffering from PTSD in the early 1990s.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is key to know in understanding PTSD

A

50% of the population will experience at least one traumatic event however not everyone develops PTSD - it is understanding these individual differences in susceptibility that will give rise in understanding the mechanisms that underly PTSD

So theories of aetiology must answer this question

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the theories of PTSD

A
  1. Biological Factors (Genes/Brain)
  2. Behavioural - Conditioning
  3. Cognitive model - Appraisals/Memories
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Genetic theory of PTSD

A
  1. HEREDITARY
    TRUE+ RICE 1993: There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone, thus suggesting there is a gene x environment interaction whereby people who have genetic predispositions are more vulnerable to develop PTSD after a traumatic event that acts as a trigger
  2. TWIN STUDIES
    For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin’s having PTSD compared to twins that were dizygotic (non-identical twins)
  3. GENETIC PREDISPOSITION
    BREMNER 2003: There is evidence that those with a genetically smaller hippocampus are more likely to develop PTSD following a traumatic event. Hippocampus plays a role in memory and emotions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Brain theory of PTSD

A

Biological processes make people with PTSD hyper responsive to stressful stimuli, particularly those that bring about memories of the traumatic event
Some believe that this reduction in volume may lead to an enhanced reactivity to stress, and possibly memory deficits as well

Characteristic changes in brain structure and function have been identified in patients with PTSD using brainimaging methods. Brain regions that are altered in patients with PTSD include the hippocampus and amygdala as well as cortical regions including the anterior cingulate, insula, and orbitofrontal region. These areas interconnect to form a neural circuit that mediates, among other functions, adaptation to stress and fear conditioning

– NEUROCIURCTRY MODEL: Rauch, Shin & Phelps, 2006.

This model hypothesizes hyperresponsivity within the amygdala to threat-related stimuli, with inadequate top-down governance over the amygdala by medial frontal cortex and the hippocampus. Amygdala hyperresponsivity mediates symptoms of hyperarousal and explains the indelible quality of the emotional memory for the traumatic event.
Inadequate influence by medial frontal cortex underlies deficits of extinction as well as the capacity to suppress attention and response to trauma-related stimuli; and decreased hippocampal function underlies deficits in identifying safe contexts, as well as accompanying explicit memory difficulties (Bremner et al 1995).

– HIPPOCAMPUS
One part of the brain responsible for memory and emotions is known as the hippocampus. In people with PTSD, the hippocampus appears smaller in size. It’s thought that changes in this part of the brain may be related to fear and anxiety, memory problems and flashbacks.
The malfunctioning hippocampus may prevent flashbacks and nightmares from being properly processed, so the anxiety they generate doesn’t reduce over time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Issue with broadening the definiton of PTSD

A

The construct validity of posttraumatic stress disorder (PTSD) has been a source of scientific controversy ever since the diagnosis was introduced.

  1. No universel theory may be found due to the broadening the definition of traumatic stressor. With such diverse events deemed causally relevant to PTSD, it will be difficult to identify common psychobiologic mechanisms underlying symptomatic expression
  2. Noting that a traumatic stressor need not be life-threatening, Avina & O’Donohue (2002) have recently argued that repeatedly overhearing jokes in the workplace may qualify as a stressor that triggers PTSD. PTSD induced by repeated exposure to sexual jokes and, of course, other more serious forms of sexual harassment in the workplace provides the justification for lawsuits to secure “appropriate monetary compensations,” argued Avina & O’Donohue (2002, p. 74). Overhearing obnoxious sexual jokes in the workplace may provide a legal basis for litigation, but it seems unlikely to produce the same psychobiological state of PTSD as violent rape.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the behavioural theory of PTSD

A

CONDITIONING: MOWER TWO FACTOR LEARNING THEORY (KEANE etal 1986):
1. Classical conditioning: Certain stimuli that were present at the time of the trauma, for example sights or sounds, may become associated with the trauma. This leads to the avoidance of these stimuli and when these situational cues are encountered in the future, they elicit the arousal and fear that was experienced during the trauma.

  1. Instrumental learning: Conditioned fear responses do not extinguish because the sufferer develops both cognitive and physical avoidance responses to distract them from processing the cues and so the associations cannot become extinct. So, PTSD symptoms maintained

DOSE-RESPONSE MODEL

Suggests that PTSD symptoms worsen as the severity of the stressor increases (March 1993). Hence, traumatic stressors function like unconditioned stimuli that elicit the unconditioned response of terror, establishing neutral cues as conditioned stimuli that elicit the conditioned response of fear. Accordingly, they believe that a laboratory rat’s reaction to inescapable electric shock parallels at least some aspects of the human response to overwhelming trauma (Foa et al. 1992, van der Kolk et al. 1985). Just as increasing severity of shock exacerbates a rat’s conditioned fear, so should increasing severity of trauma exacerbate a victim’s PTSD symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Evaluation of the two-factor behavioural theory of PTSD

A

MOWRER THEORY
+ It does provide a powerful explanation of many prominent features of PTSD, particularly the wide range of potential trauma reminders, physiological and emotional arousal elicited by these reminders, and the central role of avoidance in the maintenance of PTSD. It is also compatible with observations of a general increase in conditionability.

  • INDIVIDUAL DIFFERENCES Behavioural models cannot provide a full explanation of PTSD as it does not explain why some individuals who experience trauma develop PTSD whilst others do not and it cannot easily explain the range of symptoms peculiar to PTSD but rarely found in other anxiety disorders.
    For this reason, the conditioning approach now tends to be supplemented by observation and theory drawn from a broader range of research on cognition and emotion (e.g., Pitman, Shalev, & Orr, 2000).
  • NOT JUST FEAR Conditioning theory provides a good account of how trauma cues acquire the ability to elicit fear and of the critical role played by avoidance, but is less useful when applied to questions concerning the influence of emotions other than fear, and the role of appraisals and coping strategies.
    The conditioning model implies that traumatic stressors cause PTSD by producing toxic levels of fear in victims, but stressors can also traumatize by inciting guilt and shame, not just fear. Among Vietnam veterans, commission of atrocities predicts risk for PTSD beyond that attributable to combat exposure alone (Breslau & Davis 1987). Even among those qualifying for a PTSD diagnosis, commission of atrocities (or at least passive exposure to them) predicts severity of PTSD symptoms beyond that predicted by extent of combat exposure (Beckham et al. 1998).
  • GOES BEYOND ASSOCIATED STIMULI whereby war veterans are shown to experience fear response and other PTSD symptoms to stimuli that wasn’t present during conditioning. Therefore they showcase far more complex symptomology beyond a simple startled fear response. To explain the broad range of stimuli that are shown to evoke anxiety in PTSD sufferers counter perspectives must be shown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Evaluation of brain theory

A

+ SUPPORT (Hippocampus):

  1. Initial magnetic resonance imaging (M.RI) studies demonstrated smaller hippocampal volumes in Vietnam Veterans with PTSD and patients with abuse-related PTSD compared with controls (BREMENER etal. 1995)
  2. Studies using proton magnetic resonance spectroscopy further observed reduced levels of N-acctyl aspartate (NAA), a marker of neuronal integrity, in the hippocampus of adult patients with PTSD. (RAUCH etal. 2006)
  3. Adult PTSD sufferers with histories of childhood physical or sexual abuse have significantly smaller left (by 12%) hippocampi than do nonabused control subjects (Bremner et al. 1997). Women with childhood sexual abuse histories, most qualifying for PTSD, had significantly smaller (4.9%) left hippocampi than nonabused control subjects (Stein et al. 1997).
  • CAUSALITY: the reduced size of the hippocampus in PTSD has remained an unresolved question for many years. There has been considerable debate as to whether this brain region shrinks as a result of trauma exposure, or whether the hippocampus of PTSD patients might be smaller prior to trauma exposure. Studies in twins discordant for trauma exposure have provided a means to address this question, though without complete resolution.

GILBERTSON etal. 40 pairs of identical twins, including Vietnam Veterans who were exposed to combat trauma and their twins who did not serve in Vietnam, and measured hippocampal volumes in all subjects. As expected, among Vietnam Veterans, the hippocampus was smaller in those diagnosed with PTSD as compared with those without a diagnosis.
However, this brain region was abnormally smaller in non-PTSD twins as well, despite the absence of trauma exposure and diagnosis. These findings suggest that a smaller hippocampus could be a pre-existing, potentially genetic, neurodevelopmental, and almost surely multifactorial vulnerability factor that predisposes to the development of PTSD.

  • HOWEVER, recent neuroimaging studies provide additional data against the hypothesis that stress shrinks the hippocampus of trauma survivors. BONNE etal. (2001) used MRI to scan 37 trauma survivors one week following their admission to a hospital emergency room. They rescanned them six months later. By this second assessment, 10 of the 37 subjects had developed PTSD. The PTSD and non-PTSD groups did not differ in hippocampal volume, and PTSD symptom severity was not correlated with hippocampal volume at either scan. Finally, hippocampal volume in the PTSD group remained stable over the course of the 6-month period.
  • LIBERZON 2012 The traditional neurocircuitry model might be constrained by its focus on threat. While some PTSD symptoms may stem from deficits in threat-related pro- cessing, other symptoms (e.g., emotional numbing, avoidance behaviors) are unexplained by this model. It is important to consider the complex roles of the medial prefrontal cortex afforded by its high connectivity with other areas, such as the anterior insula. Paulus and Stein (2006) propose that individuals who are likely to experience an interoceptive state as dangerous have an augmented signal between their observed and expected body state. This signal is thought to be mediated by heightened activity in the anterior insula.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the role of memory in PTSD

A

BUCKLEY etal. 2002
In PTSD, a number of changes in memory functioning have been identified that are comparable with studies of depressed patients: There tends to be a bias toward enhanced recall of trauma-related material and difficulties in retrieving autobiographical memories of specific incidents

The other notable feature of memory in PTSD is the reliving experiences or “flashbacks” to the trauma. Compared to normal autobiographical memory, flashbacks are dominated by sensory detail such as vivid visual images and may include sounds and other sensations. However, these images and sensations are typically disjointed and fragmentary. “Reliving” of these memories is reflected in a distortion in the sense of time such that the traumatic events seem to be happening in the present rather than (as in the case of ordinary memories) belonging to the past.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the cognitive theory of PTSD

A

EHLERS+CLARKS (2000) concept of ‘mental defeat’ (the perceived loss of all autonomy, a state of giving up in one’s own mind all efforts to retain one’s identity as a human being with a will of one’s own) which is responsible for making an individual more vulnerable to developing PTSD.

They proposed that pathological responses to trauma arise when individuals process the traumatic information in a way that produces a sense of current threat, either an external threat to safety or an internal threat to the self and the future. The two major mechanisms that produce this effect involve

  1. negative appraisals of the trauma (mental defeat) or its sequelae
  2. the nature of the trauma memory itself.

APPRAISAL: This model suggests the individual more susceptible to PTSD will see themselves as a victim and process all info about the trauma negatively - these maladaptive beliefs contribute to the way the sufferer recalls the trauma and might result in maladaptive cog and behavioural coping strategies that maintains the disorder

MEMORY: Another component of this model is that it is proposed that the individuals only partially processes their memory of the trauma because of their perceived lack of control over it. The memory of the event is poorly elaborated, not given a complete context in time and place, and inadequately integrated into the general database of autobiographical knowledge. Therefore, this leads to symptoms such as re-experincing the trauma in the present.

MAINTENANCE: Maladaptive behavioral strategies and cognitive processing styles important in maintaining the disorder. Among the behavioral strategies likely to cause PTSD to persist are active attempts at thought suppression, distraction, avoidance of trauma reminders, use of alcohol or medication to control anxiety, abandonment of normal activities, and adoption of safety behaviors to prevent or minimize trauma-related negative outcomes. Maladaptive cognitive styles include selective attention to threat cues and persistent use of rumination or dissociative responses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Evaluation fo cognitive theory of PTSD

A

+ Provides the most detailed account of the maintenance and treatment of PTSD. They have significantly expanded understanding of the wide range of relevant negative appraisals and have identified both appraisals and a variety of cognitive coping factors that influence the course of the disorder.
At present, Ehlers and Clark’s cognitive model places more emphasis on the way in which stimuli are processed during trauma (i.e., the data-driven versus conceptual distinction) rather than on the specific way in which the output of these processes is represented in memory. The model of autobiographical memory they employ (Conway & Pleydell-Pearce, 2000) distinguishes more general autobiographical knowledge from more specific sensory information, called event-specific knowledge

+ SUPPORT:

  1. EHLERS etal (2000) studied former political prisoners in East Germany and found that even allowing for the degree of torture experienced, those who still had PTSD years after their imprisonment were characterized by having reacted during the trauma with mental defeat whilst the rest had recovered
  2. JOESPH 1991 In shipping disasters, passengers who attributed the bad things that happened during the sinking to themselves and their actions had more symptoms of PTSD
  3. NICOLSON (2016), adolescents who had experienced the 2004 Sri Lankan tsunami were assessed for PTSD. They were then asked to complete the post-traumatic cognitions inventory (PTCI). This measures any negative cognitions that one has about their self or the world through making the individual rate how frequently different types of negative thoughts are experienced on a 7 point scale (Karl et al., 2009). From this it was revealed that those who had developed PTSD were more likely to have negative appraisals than those without PTSD; thereby suggesting that negative appraisals may be involved in maintaining one’s PTSD symptoms.

Relationships between early appraisals, control strategies, and processing styles and subsequent PTSD severity remained significant after statistically controlling for gender and perceived assault severity.

  • CAUSALITY:
    A limitation of studies that follow-up trauma survivors is that the nature of any association between predictor variables (even those assessed shortly after the trauma) and later PTSD symptoms is not unambiguous. Initial event or symptom factors could be causally influencing both these psychological variables and later severity of the disorder
  • MEASURES of trait or spontaneous trauma processing are consistently related to the experience of intrusive memories, whereas attempts to instruct participants to process material in a particular way tend to be ineffective. One implication is that deliberate attempts to dissociate or engage in data-driven processing are only weakly related to spontaneous reactions to trauma, in which there may be alterations in perceptual thresholds or other changes that are hard to model in the laboratory. As noted by Halligan et al., however, it is very difficult to infer causal effects without being able to bring variables under experimental control.
  • MURRAY etal 2000. The assessment of cognitive processing or memory disorganization is inherently complex, and measures are not always consistently related either to each other or to other variables.
    It is difficult to assess the extent of data-driven versus conceptual processing at the time the trauma is actually occurring on the basis of retrospective self-report items such as “Were you overwhelmed by different sensations and impressions?” and “Did you realize you were in a dangerous situation?” in part because responses may be influenced by the extent of subsequent processing or reexperiencing. Therefore the methodology used limits the validity of the findings demonstrated in supporting studies.
  • INCONCLUSIVE: Two areas which are agreed to be important and in which theoretical progress would be most valuable in increasing our understanding of PTSD involve the way in which trauma is encoded, and the connections between appraisals, emotions, and identity. One way of understanding encoding would be to specify in greater detail the processes that impede or facilitate it. This requires more theoretical elaboration of the different aspects of dissociation, data-driven processing, and conceptual processing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Overview of Ehlers and Clarks Model (2000)

A
    • Two processes lead to a sense of current threat
      1. Highly idiosyncratic meaning (appraisals) of the trauma and/or its sequelae
      2. Reexperiencing of disjointed moments from the trauma easily triggered due to poor inhibition (poor elaboration), strong priming and conditioning

– Maladaptive behaviours maintain appraisals and memories
Thought suppression/avoidance of reminders
Safety behaviours
Rumination
Hypervigilance
Alcohol and substance use

17
Q

General evaluation of explanations of PTSD

A
    1. Different theories focus upon different features of PTSD and so there is a lack of consensus. For example, conditioning theory attempts to describe why severe trauma causes the symptoms it does whilst the cognitive theories try to explain individual differences in PTSD. Therefore this reduces the usefulness of each model as it means that they fail to provide a full account of the disorder.
    1. Many studies rely on self-report measures however, several studies show that a survivor’s current clinical state affects how he or she remembers the traumatic experience. Longitudinal studies on staff present at a fatal shooting at an elementary school (Schwarz et al. 1993), researchers obtained self-reports of traumatic events on two occasions. The more PTSD symptoms a person had at time two, the more severe the person remembered the traumatic experience to have been. traumatic memories, like all autobiographical memories, are reconstructed from encoded elements distributed throughout the brain (Schacter 1996). The context of retrieval, including clinical state, affects how these recollections occur.
    1. Political issues surrounding PTSD research involve the incentive of faking PTSD which creates issues for researchers. As many as 94% of veterans with PTSD apply for financial compensation for their illness (McGrath & Frueh 2002), and the incentive to do so is strong, especially for those with limited occupational opportunities (Mossman 1994). A veteran who obtains a service-connected disability rating of 100% for PTSD can earn more than $36,000 per year, tax-free and indexed to inflation, for life (Burkett & Whitley 1998, p. 236).
18
Q

What are the aims of the treatment of PTSD

A
  1. To try and prevent the development of PTSD after an individual has experience a severe trauma. (Prevention)
  2. To treat the symptoms of PTSD once they have developed. (Management)
19
Q

General evaluation of treatments for PTSD

A
  1. More methods need to be explored for the prevention of PTSD occurring as PTSD may be more difficult to treat when it becomes chronic.
    Previous strategies have involved psychological debriefing - this is a structured way of trying to intervene immediately after trauma by debriefing victims 24-72 hours after the traumatic event such as using critical incident stress management where victims were reassured that they are normal people experiencing an abnormal event and given coping stratgies.
    However, several studies have shown that it is unhelpful and is potentially harmful (Friedman, 2007) and so further research is needed as this is key to improving many individuals quality of life.
20
Q

Describe exposure therapy

A

Based on conditioning theory: trauma-related stimuli and memories become associated with fear responses (S-S, S-R). PTSD characterised by very strong fear responses and a high number of interlinked conditioned triggers – “Fear networks”
Exposure therapy aims to de-condition fear responses by activating fear memories and allowing habituation.

Individuals are taught to confront and experience events and still related to their trauma and symptoms in order to help extinguish associations between trauma cues and fear responses and to help person to disconfirm and symtom-maintaing dysfunctional beliefs that have developed.

Individuals are exposed to their fear triggers in various ways; being asked to give a detailed written narrative of trauma or using imaginal flooding, a technique where the client is asked to visualise feared, trauma related cents for extended periods of time. overtime, they would be gradually exposed to real trauma related cues.

21
Q

Describe exposure therapy - extended

A

An extension of this therapy is the use of ‘Eye Movement Desensitisation and Reprocessing’ (Shapiro, 1995).

The client is required to focus their attention on a traumatic image or memory while simultaneously visually following the therapists finger that is moving backwards and forwards in front of their eyes. This continues until the client report a significant decrease in anxiety to the image or memory. The memory is then asked to be restructured to be more positive by thinking positive thoughts in relation to that image.

Rationale:
Adaptive Information Processing theory – This theory proposes that eye movement can be used to facilitate emotional processing of memories, changing the person’s memory to attend to more adaptive information
– Combining eye movements with attention to fearful images encourages rapid deconditioning and restructuring of the fears image

22
Q

Evaluation of the extended exposure treatment

A

+ SUPPORT

  1. JONAS etal. 2013: There have been multiple small controlled trials of four to eight weeks of EMDR in adults as well as children and adolescents. The strongest evidence of efficacy for improving PTSD symptoms is for exposure-based therapy. EMDR reduced PTSD symptoms enough in the short term that one in two adults no longer met the criteria for PTSD.
    - - but the number of people involved in these trials was small.

+ APPROPRIATNESS
1. JONAS etal. 2013: The benefits were greater for women with a history of sexual assault compared with people who had experienced other types of traumatizing events (such as accidents, physical assaults and war)

  • CONTROVERSY:
    Researchers have showcased that the eye movement component of the therapy may not be critical for benefit suggesting that the entire treatment method is not particularly special or useful.
    Herbert et al. (2000) argued that the eye movements did not play a central role, that the mechanisms of eye movements were speculative, and that the theory leading to the practice was not falsifiable and therefore not amenable to scientific inquiry. Also, Salkovskis (2002) reported that the eye movement is irrelevant, and that the effectiveness of EMDR was solely due to its having properties similar to CBT, such as desensitization and exposure
    — However, (Lee+Cuijpers, 2013) employed experimental designs that showed that the eye movements are essential for successful treatment and concludes that thinking of upsetting memories and simultaneously doing a task that facilitates eye movements reduces the vividness and distress associated with the upsetting memories.
    — BUT, these studies were limited as their meta-analysis’ quality of included studies was not optimal. This may have distorted the outcomes of the studies and our meta-analysis. Apart from ensuring adequate checks on treatment quality, there were other serious methodological problems with the studies in the therapy context
  • CUCKOR 2009 Despite the abundance of evidence pointing to the efficacy of exposure therapy, PTSD remains a difficult disorder to treat and identifying alternative treatment options is imperative. This is particularly true for Veterans and active duty personnel, given the likely return home of several hundred-thousand active duty soldiers over the course of the next 3 years combined with the probable need for re-deployment of U.S. soldiers to additional combat zones such as Afghanistan.
    Although there have been significant advances in the treatment of PTSD, treatment failures persist. A meta-analysis of 26 studies with 44 treatment conditions reported that overall, 56% of those enrolled in treatment and 67% of those who completed treatment no longer met criteria for PTSD after treatment and 44% of enrollees and 54% of completers had clinically meaningful improvement by standards defined by the authors
23
Q

What does cognitive theory suggest needs to be addressed in treatments

A

Ehlers+Clarks suggest that too treat PTSD, 2 areas need to be addressed and altered for individuals to recover:

  1. The trauma memory needs to be elaborated and integrated into the context of the individual’s preceding and subsequent experience in order to reduce intrusive reexperiencing.
  2. Problematic appraisals of the trauma and/or its sequelae that maintain the sense of current threat need to be modified.
  3. Dysfunctional behavioural and cognitive strategies that prevent memory elaboration, exacerbate symptoms or hinder reassessment of problematic appraisals need to be dropped.
24
Q

Describe cognitive treatments for PTSD

A

Cognitive Restructuring;
- involves teaching patients to identify and evaluate the evidence for negative automatic thoughts, as well as helping patients to evaluate and change their beliefs about the trauma, the self, the world, and the future

This restructuring is needed as it has been shown that those who experience severe trauma will develop negative thoughts about themselves, the world and the future but for most, these beliefs will be disconfirmed in everyday life. However, those who avoid trauma related cues will also avoid disconfirming these beliefs and will develop chronic PTSD - so cognitive therapy is needed as the main aim is to change maladaptive beliefs

25
Q

Evaluation of cognitive treatments for PTSD

A

+ COMPARISON: Compared to exposure therapy which alone encourages experiences that disconfirm these dysfunctional beliefs however, CT have proposed that procedures that directly attempt to alter PTSD related cognitions need to be included to effectively combat PTSD

  • However, LACK OF SUPPORT: Marks et al. (1998) randomly assigned 87 survivors of a variety of traumas to one of four treatment conditions: prolonged exposure alone, cognitive restructuring alone, combined cognitive restructuring and prolonged exposure, or relaxation without prolonged exposure or cognitive restructuring. The results indicated that prolonged exposure alone, cognitive restructuring alone, and the combined treatment produced similar outcomes.
26
Q

Future research for treatment methods

A

Although research on new treatments continues to emerge, interest has shifted to other questions: specically, how to make existing treatments more ef cient and how to maximize the delivery of treatment through telehealth strategies. This work includes the use of virtual reality for exposure therapy (Difede et al., 2007) and therapist-assisted Internet delivery (Litz at al., 2007).

27
Q

Evaluation of the dose-response model of PTSD

A

DOSE RESPONSE MODEL
+ SUPPORT: Some studies are consistent with this prediction.

  1. For example, a greater proportion of World War II combat veterans who had been tortured by the Japanese as prisoners of war (POWs) have current PTSD (70%) than do those who had never been captured and tortured (18%) (Sutker et al. 1993).
  2. Ex-servicemen wounded in Vietnam are two to three times more likely to have PTSD than are those who returned unharmed (Kulka et al. 1990, p. 54).
  3. Proximity to the epicenter of an earthquake predicted severity of PTSD symptoms (Pynoos et al. 1993)
  4. The higher the rate of wounds and fatalities within a combat unit, the higher the rate of psychiatric casualties (Jones & Wessely 2001).
  • The relationship between dosage of trauma and resultant psychopathology is far from straightforward. For example, objective measures of accident severity are unrelated to PTSD symptoms among victims of motor vehicle (and other) accidents (Schnyder et al. 2001), and the number of torture episodes is unrelated to PTSD symptom severity among imprisoned Turkish political activists (Başoğlu et al. 1994).
  • The relationship between dose and response might be nonlinear (Harvey & Yehuda 1999). That is, if PTSD symptoms reach near maximum severity after a certain dosage of exposure, further exposure might not add much to existing levels of psychiatric impairment. For example, a person who is tortured twice may have more symptoms than someone who had never been tortured. Yet a person who has been tortured a dozen times may be no more symptomatic than one who was only tortured twice. Unfortunately, by recasting the dose-response model in nonlinear terms, any pattern between dose and symptoms would be interpretable as confirming the model (except, of course, a linear one).
  • It is plagued by serious measurement difficulties as well. The animal conditioning laboratory provides the conceptual basis for the model, but calibrating stressor magnitude in trauma studies is vastly more complicated than in Pavlovian conditioning experiments. Laboratory stressors are measurable in purely physical terms entirely independent of the animal’s behavior (e.g., shock amperage, number of shocks). Yet in the trauma field, researchers usually rely on the retrospective self-reports of the survivors themselves as the sole basis for measuring stressor magnitude. This practice presupposes that psychiatrically distressed individuals can furnish reliable, objective accounts untarnished by clinical state