DSM-5: PTSD
PTSD first appeared as an official diagnosis in DSM III (1980) => Prior to this: DSM I: “Gross Stress Reaction”, DSM II: “Transient Situation Disturbances”
Emerged in DSM as a response from social movements in the 1970s => Women’s movement, War veterans, Holocaust survivors
Departure from other DSM categories:
Criteria:
Other DSM-5 Dx
Acute Stress Disorder
Course:
Adjustment Disorder
Controversies
1- No Longer An Anxiety Disorder => PTSD was relocated out of the Anxiety Disorders chapter and into a to a new diagnostic category
2- What constitutes a trauma?
Normal response to abnormal event? Abnormal response to normal, stressful event?
3- Normal vs Abnormal Event?
Recent studies have looked at rates of PTSD following: Traumas (meeting DSM Criterion A), Stressful life events (not necessarily traumatic)
4- PTSD and Depression
5- Political and Financial Interests
Epidemio
Prevalence rates following trauma
DSM-III: PTSD thought to be rare (3%) vs Now: Lifetime prevalence: 6.8% => But traumatic events are relatively common
*Traumatic event is necessary but not sufficient cause of PTSD
Gender diff => 2F: 1M
Are women more likely to experience traumatic event? => No men report more trauma (1st criterion) vs women
So, why are women less likely to have trauma but more likely to develop PTSD?
Difference in types of traumatic experiences
BUT
Cross-Cultural Studies
Variability in PTSD rates across cultures => Highest in Canada
Why? Violation of expectations of safety
But, symptoms vary across cultures => “Flashbacks” may be a Western phenomenon, More somatic presentation in other cultures
Risk Factors
Pre-Trauma Risk Factors => Who is more likely to experience trauma?
Post-Trauma Risk Factors => Who is more likely to develop PTSD after experiencing a trauma?
Individual Differences:
Nature of Trauma
Biological Factors
Vietnam twin registry
*Evidence for genetic factors as well as environmental events
Hippocampus: Involved in explicit memory processes and encoding of context during fear conditioning
Scar => Most of this research is cross-sectional (correlational)
=> Ample evidence from animal research that severe stress can damage the hippocampus
BUT correlation does not equal causation *Not everyone who experiences even severe acute stressors goes on to develop PTSD *In fact, majority do not (Also, evidence that hippocampal volume is heritable)
=> Possible alternative explanation: Brain abnormality might be vulnerability factor to developing PTSD?
*Prospective Designs: To tackle cause/effect questions, measure biological factor in individuals prior to traumatic event and again afterwards BUT, difficult to do this
Twins Discordant Study
Identify surrogates for what the trauma- exposed person would be like if they didn’t have the experience of the traumatic event
Non-trauma exposed, identical (MZ) twin => Shares all the genes of the trauma-exposed twin, shares a lot of twin’s early developmental environment (ex: same family, community, school) BUT Non-shared environment = trauma experience (unique to exposed twin)
Study: All male; in their early 50s
=> Examined hippocampal volumes in each of the four groups
If HC volume is a “scar” of trauma, we would expect differences between ExP+ and UxP+
If HC volume is a vulnerability factor for PTSD, we would expect NO difference between ExP+ and UxP+
Results brain volume correl with PTSD Sx:
Results brain volume diff in twin pair gr:
CONCLUSIONS:
Psychological Factors
Traumatic Memories
Differences in the way that memories may be stored and retrieved
=> Sensory impressions are experienced as if they are happening in the here-and- now, rather than memories from past (Can explain why talking about trauma in therapy is beneficial)
Cognitive Theory
PTSD becomes persistent when individuals process the trauma in a way that leads to a sense of serious, current threat
PTSD patients have difficulty intentionally retrieving memory BUT, have high frequency of involuntarily triggered intrusive memories
Treatment
Prevention-focused strategies
Crisis Intervention
Cognitive-Behavioral Therapies*