Welcome back to our current topic of post-traumatic stress disorder (PTSD). Today we are going to go one level deeper and overview some epidemiology, risk factors, and the typical course and prognosis of PTSD.
Today’s Content Level: Intermediate
•Prevalence = proportion of individuals who have a condition at a particular period of time
•Incidence = proportion or rate of individuals who newly develop a condition during a period of time
Prevalence: reported 12-month prevalence of PTSD varies depending on the source but is estimated to be ~1-4% globally (U.S. adults at the higher end of that range). Lifetime prevalence ~6-9%. Can occur at any age.
Gender: higher prevalence in women likely secondary to greater risk of exposure to traumatic events particularly sexual assault and other forms of interpersonal violence.
Race: in the U.S. higher rates of PTSD are reported among Latin Americans, African Americans, and American Indians compared to non-Latino whites. A lower rate has been reported among Asian Americans. Compared to the U.S. lower estimates are seen in Europe and most Asian, African, and Latin American countries.
Suicide risk: PTSD independently increases the risk for suicidal ideations and suicide attempts but it is debated if it increases death from suicide. Some studies have found a 5x increased risk of death by suicide whereas others have found no increased risk. 4, 5
•Biological, environmental, psychosocial, and genetic factors are all important in post-traumatic stress disorder.
"Pre-Traumatic" Risk Factors
Genetics: Estimated that 30-40% of variance in PTSD is caused from genetics alone (who develops PTSD after exposure to trauma and who does not). A number of common genetic variants have been associated with PTSD as well as the s/s genotype of the serotonin transporter gene which interacts with childhood adversity to increase PTSD risk.
Childhood: history of childhood adversity or trauma; history of childhood emotional problems such as anxiety or depression.
History: prior psychiatric history such as anxiety disorders, depressive disorders, or trauma and stressor related disorders; family history of mental illness.
Demographics: female; low socioeconomic status; minority racial/ethnic status; for adults a younger age at time of exposure.
Vocations that increase risk of traumatic exposure (military/veterans, police, firefighters, emergency medical personnel).
"Peri-Traumatic" Risk Factors
Type of trauma: highest risk with rape > other sexual assault > witnessing atrocities > being stalked > unexpected death of a loved one. Other types with increased relative risk includes interpersonal violence (particularly trauma perpetrated by a caregiver) and combat-related (particularly being a perpetrator, witnessing atrocities, killing the enemy, or accidental killing of non-combatants). Keep in mind that severe automobile accidents are the most common cause due to high overall incidence.
Features of trauma: Severity (dose); personal injury; perceived life threat, dissociation that occurs during the trauma that persists.
"Post-Traumatic" Risk Factors
Response to trauma: negative self-appraisals; inappropriate coping strategies; development of acute stress disorder (~80% will develop PTSD).
Environment/Social: repeated exposure to trauma or reminders or losses; subsequent adverse life events. Good social support is a protective factor.
The neuroscience of how trauma is processed is complex and important. I highly highly recommend the free curriculum created by the National Neuroscience Curriculum Initiative (NNCI). Day 3 is their PTSD curriculum and they do a fantastic job covering the neuroscience of fear and trauma, particularly their "Find it, Draw it, Know it: Fear Circuitry" lesson.
This blog post won't do this justice, but here are the highlights to wet your appetite:
1) Signal In-> Visual and auditory sensory processes take in the fear-invoking sensory information -> this information eventually reaches the amygdala which is a part of the limbic system and responsible for generating the fear response and emotional learning.
2) Context-> In order to process a fear response the amygdala obtains context from various brain regions in order to deem a situation as safe vs unsafe. These areas include the hippocampus (contextual memory), insula (somatosensory processing), and the prefrontal cortex which includes the anterior cingulate (interprets signals; resolves conflicting information) and the medial prefrontal cortex (inhibitory regulation of the amygdala).
3) Fear response-> The amygdala can now send a number of output signals to a number of regions that will be involved in generating the fear response. These include the hypothalamus (HPA axis-> neuroendocrine response-> adrenal gland will release the stress hormones cortisol, epinephrine, norepinephrine), basal ganglia (motor response), periaquaductal gray (freeze response), and certain brainstem nuclei that help mediate the response of the sympathetic nervous system (locus coeruleus releases norepinephrine and the ventral tegmental area releases dopamine).
In PTSD it is proposed that there is dysregulation in any of the above pathways. Some examples include -> poor attenuation of the HPA-axis by serotonin circuits; dysregulated attenuation of the amygdala by the anterior cingulate and ventromedial prefrontal cortex -> and other examples in the diagram below.
Image from FIGURE 17-1 in Kaplan and Sadock's Comprehensive Psychiatry. Neural regions implicated in PTSD. dmPFC = dorsomedial prefrontal cortex; rmPFC = rostral medial prefrontal cortex; vmPFC = ventromedial prefrontal cortex; ACC = anterior cingulate cortex.
Onset: PTSD usually begins within 3 months after the trauma, however a minority of patients have a "delayed expression" (>6 months) where full criteria for PTSD does not occur for months or years after the incident.
Course/Prognosis: Duration of symptoms vary with ~50% of patients experiencing a complete recovery within 3 months, while many individuals remain symptomatic for years and some for even decades. In general symptoms tend to diminish with older age, however that is not always true. Symptom recurrence may occur in response to reminders of the original trauma, new traumatic events, or ongoing life stressors.
Predictors of poor prognosis: type and dose of trauma (see pathogenesis section above); chronic course = "kindling" and "sensitization"; history of prior trauma; "complex PTSD"; moral injury; comorbid depressive disorder; comorbid substance use disorder; comorbid traumatic brain injury (TBI); veterans; poor social support.
The good news is that effective evidence-based treatments for PTSD have been developed in the past few decades and many therapists and psychiatrists are being trained in these modalities and will hopefully lead to a better prognosis. We will discuss these treatments in our post titled "Trauma-Focused Psychotherapy".
I hope today's lesson provided a nice overview about the "who" and the "why" of PTSD. In our next post we will discuss clinical pearls for PTSD.
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