Some Basic Background • PTSD is an anxiety disorder that develops usually in response to an overwhelmingly terrifying, often life-threatening event • Its hallmark characteristic is the recurrent, involuntary recollection of the trauma in the form of intrusive thoughts, nightmares, and vivid sensory memories – i.e. they relive the trauma
Emotional Stroop Effect • Patients with PTSD take longer to name the word colour when the coloured word is related to their trauma • This task can be used to discriminate genuine PTSD sufferers from those malingering
Neural Mechanisms of ESE • Bremner et al used PET scans to show that women who had sexual abuse-related PTSD, as opposed to victims without PTSD, had less Anterior Cingulate Cortex activation during the ES task • This finding was replicated by Shin et al using Vietnam Veterans suffering PTSD -also found PTSD participants to exhibit heightened amygdala responses • Also found was that the smaller the anterior cingulate cortex, the worse the severity of the PTSD symptoms
Other Consequences of PTSD • More difficulty concentrating and remembering things in everyday life • Difficulty ignoring distracting information
IQ • It is thought that a lower IQ could result in more severe PTSD • Studies (including twin studies on veteran soldiers) show that a high IQ confers higher resilience or protection against developing PTSD following a severe trauma
Hippocampal Volume • Gilbertson et al performed a study to show that people with small hippocampi are more vulnerable to developing PTSD - Findings are supported with evidence from twin studies
Progress and Controversy in the Study of Posttraumatic Stress DisorderMcNally (2003)
Research into anxiety disorders has increased a lot since the 1980s • This article examines the most controversial issues in the area of PTSD
The emergence of PTSD • First began with studies of soldiers. Shepard (2001) found that after being subjected to events of war, normal individuals were suffering from acute stress. • Lifton found that these symptoms remained. • Introduced into the DSM-III in 1995 after it was suggested that other events e.g. natural disasters can cause these symptoms • Definition: ‘stressor that would evoke significant symptoms of distress in almost everyone’ • 3 aspects: re-experiencing (thoughts/flashbacks), numbing (attachment problems) and miscellaneous (sleep disturbance).
Conceptual bracket creep in the definition of trauma • PTSD is unique in that it requires an event (exposure to a traumatic event) as well as behavior • Event does not have to be directed at the individual, can develop PTSD by being shocked by others’ experiences • Traumatic event does not have to be life-threatening • Wakefield & Spitzer (2002) need to discriminate genuine symptoms from normal distress reactions e.g September 11th
Problems with the dose-response model of PTSD • This model states that the PTSD symptoms worsen as severity of stress increases • Proximity of individual to the epicentre of an earthquake predicted severity of PTSD symptoms (Pynoos et al 1993) • Although argued that the relationship is complicated • May not be linear e.g. if reach maximum severity, further exposure may not worsen the symptoms.
Distortion of Recollection of Trauma • In the trauma field experimenters rely on retrospective self report of survivors • Recent studies have shown that a survivors clinical state affects how they remember the traumatic event For example, Southwick et al. (1997) concluded that veterans with higher PTSD scores “tend to amplify their memory for traumatic events over time” • Traumatic memories, like autobiographical, appear to be subject to alteration over time
The Spectre of the “Phony Combat Vets” Two main problem areas in studying Vietnam veterans: • Deliberate exaggeration of symptoms in Vietnam veterans to obtain the PTSD diagnosis • “Phony combat vets” (Burkett & Whitley) Men who claim to be suffering from combat related PTSD but who either never saw combat, never served in Vietnam, or never served in the military at all.
Burkett and Whitley believe that many studies of combat-related PTSD are contaminated by the inadvertent inclusion of subjects who have lied about their combat trauma For example: Keane et al (1998) • examined psychophysiologic reactivity to personalised audiotaped scripts describing actual combat events • found those with past PTSD tended to fall midway between the other groups with regard to physiologic reactivity • but approx a third had no physiological reaction to combat stimuli • McNally argues that men who volunteer for research studies are from a different pool than those who have caught the attention of Burkett and Whitley
Guilt, shame, & Trauma • The conditioning model implies that stressors cause PTSD by producing toxic levels of fear, but it has been shown that stressors can also traumatize through causing guilt and shame. • This has been demonstrated among Vietnam veterans (Breslau & Davis 1987). • Unlike fear, which can be experienced by rats, guilt and shame are complex emotions which can only be experienced by animals possessing a sense of self. • As the animal conditioning model reduces trauma to its biological basis, it does not capture this uniquely human aspect of trauma.
Risk factors for PTSD: • A large number of people are exposed to stressors, yet very few develop PTSD. • There therefore must be risk factors that predict the emergence of the disorder among those exposed to trauma. • Some of these include low social support (although the causal relationship is debateable), low intelligence, neurological soft signs (non-specific behavioural indicators of central nervous system impairment), neuroticism, unstable family during childhood, pre-existing mood or anxiety disorder, a family history of anxiety or mood disorder and physical or sexual abuse in childhood.
Several studies (e.g. Macklim et al 1998 & Silva et al 2000) suggest that above average cognitive ability may enhance an individual’s ability to cope with stressors thereby buffering them against developing PTSD. • Researchers have also identified peritraumatic (i.e. during the trauma) variables that predict later PTSD. These include time distortion, feelings of unreality, sense of bodily distortion, emotional numbing, depersonalization, motor restlessness, a sense of reliving the trauma and elevated heart beat.
Can traumatic stress damage the brain? • Cortisol is are released as part of the flight or fight response in primates and although this stress hormones facilitates defence in the short term, prolonged cortisol exposure can cause hippocampal damage. • Studies looking at Vietnam veterans and physical and sexual abuse victims showed that their hippocampi were smaller; this is evidence for stress damaging the brain.
However, a study showed that urinary cortisol levels were the same in Vietnam veterans and controls and yet hippocampal damage can only occur in conditions of prolonged high levels of cortisol. • Recent neuroimaging studies have also provided additional data against the theory that stress can shrink the hippocampus. For example, Bonne et al (2001) showed that there was no difference in hippocampal volume between PTSD patients and people not suffering from PTSD. • In a recent landmark study, Gilberson et al may have decisively refuted the hippocampal damage hypothesis. They found no difference in size of hippocampus in monozygotic twins, one of which had PTSD and the other of which didn’t. Gibertson et al came to the conclusion that small hippocampi may constitute a pre-existing vulnerability factor for PTSD among trauma exposed.
RECOVERED MEMORIES OF SEXUAL ABUSE Brown et al. (1998) • He stated that: “Approximately a third of sexually abused victims report some period of their lives where they did not remember anything about the abuse and later recovered the memory of the abuse” i.e. they have repressed the event • However, some scholars argue that there is no convincing evidence that people can banish and then recover memories of horrific experiences
McNally’s Criticisms of Brown et al. (1998) • Inaccurate interpretation and presentation of the following studies: - DSM-III symptoms of non-specific memory impairment - Dollinger (1985) – lightning strike study - Wagenaar & Groeneweg (1990) – Nazi Holocaust Camp experiences - Williams (1994) & Femina et al (1990) – Sexual Abuse example
Repressed Memory or bad memory? McNally states that it is not repressed memory that is occurring in these cases but memories being recovered… Biased – Why? McNally performed a study on 4 participant groups and found: “repressed and recovered memory subjects do not exhibit a superior ability to forget trauma-related words on a directed forgetting task, contrary to hypothesis that they ought to be superior at blocking out memory for material related to abuse” Is this really proof against Brown et al’s recognition of repressed memories in sexual abuse cases?
THE POLITICS OF TRAUMA • Example is of a child abuse study by Rind et al (1998) • It was unanimously condemned on July 12th 1999 by members of the United States congress for its alleged moral and methodological flaws
Rind et al’s study… • Meta-analysis of 59 studies that had addressed the long-term psychological correlates of childhood sex abuse • Found that subjects who had been sexually abused were nearly as well adjusted and more resilient than their non-abused counterparts
Consequences of this negative publicity.. • The American Psychology Association was placed under extreme pressure and as a result refuted the article BUT… • Assessment by the AAAS found there to be “no clear evidence of improper application of methodology or other questionable practices on the part of the article’s authors” This example highlights the balance that must be maintained between science and politics..