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Presentation Outline
1.Definition of PTSD 2.Epidemiology 3.Neurobiology of PTSD 4.The motor vehicle accident and PTSD 5.Head injury and PTSD 6.Delayed PTSD
7. Malingering PTSD 8. Forensic evaluation of PTSD 9. The patient interview and PTSD 10. Clinical Implications of Neuroscience Research in PTSD 11. Conclusions
1.Definition of PTSD
DSM-IV-TR (2000)
Criterion A: STRESSOR
The person has been exposed to a traumatic event in which both of the following have been present: The person has experienced, witnessed, or been confronted with an event or events that involve actual or threatened death or serious injury, or a threat to the physical integrity of oneself or others. The person's response involved intense fear, helplessness, or horror. Note: in children, it may be expressed instead by disorganized or agitated behavior.
4
The traumatic event is persistently re-experienced in at least one of the following ways: Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: in young children, repetitive play may occur in which themes or aspects of the trauma are expressed. Recurrent distressing dreams of the event. Note: in children, there may be frightening dreams without recognizable content Acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes,including those that occur upon awakening or when intoxicated). Note: in children, trauma-specific reenactment may occur. Intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event. Physiologic reactivity upon exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
Criterion C: avoidant/numbing Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by at least three of the following: Efforts to avoid thoughts, feelings, or conversations associated with the trauma Efforts to avoid activities, places, or people that arouse recollections of the trauma Inability to recall an important aspect of the trauma Markedly diminished interest or participation in significant activities Feeling of detachment or estrangement from others Restricted range of affect (e.g., unable to have loving feelings) Sense of foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)
Criterion D: hyper-arousal Persistent symptoms of increasing arousal (not present before the trauma), indicated by at least two of the following: Difficulty falling or staying asleep Irritability or outbursts of anger Difficulty concentrating Hyper-vigilance Exaggerated startle response Criterion E: duration Duration of the disturbance (symptoms in B, C, and D) is more than one month. Criterion F: functional significance The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. Specify if: Acute: if duration of symptoms is less than three months Chronic: if duration of symptoms is three months or more Specify if: With or Without delay onset: Onset of symptoms at least six months after the stressor
2.Epidemiology
Approximately 30% of individuals who directly experienced events rarely seen by other people will develop PTSD through indirect experience approximately 10%
2.Epidemiology (cont.)
Brewin and colleagues (2000) identifying 14 risk factors:
Trauma severity, lack of social support and life stress - the largest effect for developing PTSD Followed by: adverse childhood events, low intelligence, low SES, childhood abuse, female gender, family and personal psychiatric history, previous trauma, lack of education, younger age, and minority status. Further analysis showed that peritraumatic dissociation and emotional responses, perceived support and perceived life threat were the strongest predictors. Prior trauma, prior adjustment, and family psychiatric history were weaker and equal predictors.
2.Epidemiology (cont.)
Similarly King, King and Foy (1996):
3.Neurobiology of PTSD
Does stress cause brain damage? Hippocampus: Research findings regarding whether PTSD causes reduction of hippocampal volume are contradictory Some research supports the idea that smaller hippocampi in PTSD is a preexisting condition
Veterans who recently returned from Iraq and Afghanistan underwent functional MR imaging while concurrently exposed to a symptom provocation task, involving alterations between emotional combatrelated and neutral civilian scenes, interleaved with an executive processing task. Activation for emotional compared to neutral stimuli was highly correlated with level symptoms in ventral frontolimbic (ventromedial prefrontal cortex, gyrus, and ventral anterior
3.Neurobiology of PTSD
Conversely, activation for the executive task was negatively correlated with PTSD symptoms in the dorsal executive network (middle frontal gyrus, dorsal anterior cingulate gyrus, and inferior parietal lobule) Strong link between the subjectively-assessed behavioral phenomenology of PTSD and objective neurobiological markers.
Misinterpretation: differentiate between the effects of MHI and PTSD is very difficult Reality: they are two separate clinical entities Evidence 1: in sports, cognitive capacities following a single concussion return to baseline within 1 week Evidence 2: research shows that concurrent occurrence of PTSD and MHI is uncommon Most-traumatic amnesia appears to be a protective factor against re-experiencing of symptoms Evidence 3: rate of malingering is about 40% MMPI-2 and TOMM test reveal that malingering in dual diagnosis group was 49.5% to 88%
6.Delayed PTSD
According to DSM-IV-TR delayed onset refers to PTSD symptom presentation more than 6 months after the traumatic event Strangely may occur closer to the hearing date! (Larrabees observation) Makes little neurological sense was initially introduced as a by-product of the Vietnam War. PTSD was not manifest itself before the veteran returns home. But, many make claims years after the event A lot of evidence that PTSD symptoms develop within hours or days after the event Most probably that delay is rather in the help-seeking than in the PTSD symptoms Delayed PTSD in the complete absense of previously unrecognized symptoms is rare
7.Malingering PTSD
It is rare to find a psychiatric diagnosis that anyone wants to have, but PTSD seems to be one of them. (Andersen, 1995, p.963) more has been written about combat than civil malingering compensable nature of PTSD makes it a desirable diagnosis Approximate reported prevalence among veterans ranges from 21.2% to 53.4% literature on malingering PTSD is limited PTSD is easy to fake 94% of naive subjects correctly identifies PTSD symptoms on selfreport measure. However, only one subject from 134 malingered enough symptoms for formal diagnosis
7.Malingering PTSD
Most common measures of malingering PTSD:
1.
Morel Emotional Numbing Test (MENT) is a forced-choice test where the subjects have to match facial expressions with the words that best describe the face reports an overall malingering rate of 95.6% in a veteran population. civilian study found that 40% failed the MENT, 51% the SIMS and WMT and 25% failed all three. No clear explanation as to why PTSD patients would fail to recognize emotional facial expressions. Plus, methodological difficulty: PTSD patients were given different set of instructions
Morel
One
Limitations:
2. The Detailed Assessment of Posttraumatic Stress (DAPS): is a 104-item self-report PTSD instrument. Advantage: Has a validity scale - the Negative Bias Scale (NBS) which captures feigned PTSD One study found that 25% of litigants seeking psychological assessment failed NBS Limitations: litigants group was very mixed in terms of etiology
3. The Trauma Symptom Inventory (TSI): self-report measure which includes the Atypical Response Scale (ATR). The most commonly used measure among selfdesignated traumatologists The research shows that is produces high rate of false positives Is better able to detect naive fakers Unclear degree of influence of secondary gain in genuine PTSD group
7.Malingering PTSD
PTSD as any other psychiatric disorder is often accompanied by The typical examination can be short (2.5 h) includes some neuropsychological tests gives an opportunity to administer SVTs The goal is not to detect a brain lesion persons who feign PTSD may also feign functional disability 37%-60% disability-seeking pain patients will fail TOMM even
though cognitive disfunction is not at the core of pain complaints
Self-report is problematic because of lack of falsifiability (= scientific evidence useful for diagnosis) Patient knowledge about symptoms of the disorder To be done after the completion of tests Volunteering of symptoms Structured symptom inquiry (the interviewer is asking about each symptom, its onset and progress of it mixing it with physical symptoms) Detailed description of the PTSD-causing event (narrative) Clinical Assessment of PTSD Scale (CAPS). The most widely used scale for assessment of PTSD and the suggested one from the author.
It is improbable for the nightmares be an exact replication of the traumatic event Although flashbacks are the only unique symptom of PTSD they are considered rare according to DSM-IV-TR
Any non-improvement after a period of time in symptoms should be viewed with skepticism Interview of a family member (serves the purpose of revealing information about the persons symptoms, failure to attend could be a sign of malingering)
10. Clinical Implications of Neuroscience Research in PTSD to Traumatized individuals are vulnerable
react to sensory information with subcortically initiated responses that are irrelevant, and often harmful, in the present. Reminders of traumatic experiences activate brain regions that support intense emotions, and decrease activation in the CNS regions involved in: a) the integration of sensory input with motor output, b) the modulation of physiological arousal, and c) the capacity to communicate experience in words.
Failures of attention and memory in PTSD) interfere with the capacity to engage in the present.
Effective treatment needs to involve (1) learning to tolerate feelings and sensations by increasing the capacity for interoception, (1) learning to modulate arousal, and (2) learning that after confrontation with physical helplessness it is essential to engage in taking effective action.
11. Conclusion