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Symptoms and Diagnosis

The Merck Manual briefly describes Posttraumatic Stress Disorder (PTSD) as “recurring,
intrusive recollections of an overwhelming traumatic event” (Greist, 2014). Diagnosis is entirely
based on the history and symptoms. According to the Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition (DSM-5) (American Psychiatric Association [APA], 2013), to
receive the diagnosis one must meet the following criteria:
 Exposure to a real or threatened traumatic event, either directly or indirectly. Indirect
exposure includes witnessing the event, or learning that it happened to a close family
member or close friend. Traumatic events include war, physical or sexual violence,
restraint or kidnapping, sexual assault, severe motor vehicle accidents, witnessing
unnatural or violent death, sudden unexpected severe illness (examples include being
awake during surgery and anaphylaxis), or witnessing a “medical catastrophe” in a child.
 Recurring “intrusion symptoms” related to the event. Intrusion symptoms include
memories, dreams, awake flashbacks, and psychological distress or physiological
symptoms when exposed to related cues. These can be disturbingly vivid and range from
distressing, intrusive memories (voluntary recollection doesn’t count), to total
dissociative states that can last for seconds to days, where the individual essentially
relives the event.
 A pattern of intentionally avoiding reminders of the event. The individual may go to great
lengths to avoid these cues, because exposure causes psychological distress or
physiological symptoms.
 Negative changes in thoughts or mood that began after the event. This may include
amnesia, where the individual cannot remember certain details of the event. There may be
a persistent negative emotional state such as anger, depression, guilt, fear, or shame.
There may be a diminished interest in previously enjoyable activities and/or an inability
to experience positive emotions. There may be feelings of detachment from others and an
inability to experience closeness or intimacy.
 “Marked alterations in arousal and reactivity associated with the traumatic event” (p.
272). This includes outbursts of anger, recklessness, hypervigilance, exaggerated startle
response, concentration problems, or sleep disturbances. These symptoms must have
started (or gotten markedly worse) since the traumatic event.
 These symptoms last more than one month, and cause “distress or impairment in social,
occupational, or other important areas of functioning” (p. 272).
 The symptoms are not related to substance use. For example, angry outbursts when drunk
don’t count. (APA, 2013)
Children six and under have a modified set of categories, but the essentials are the same. The
presentation of these symptoms can vary wildly, but patients must have symptoms from all of
these categories to reach a diagnosis of PTSD (APA, 2013; Greist, 2014).
One particularly important feature to note is:
“Symptoms usually begin within the first 3 months after the trauma, although there may be a
delay of months, or even years, before criteria for the diagnosis are met. There is abundant
evidence for…’delayed expression,’ with the recognition that some symptoms typically appear
immediately and that the delay is in meeting full criteria.” (APA, 2013, p. 276).
In other words, while many of the symptoms may be present immediately after the traumatic
event, and may even be severe, a diagnosis of PTSD can only be made once all of the criteria are
met.
Aside from the psychological suffering, PTSD can impair many other areas of life.
“Impaired functioning is exhibited across social, interpersonal, developmental, educational,
physical health, and occupational domains. In community and veteran samples, PTSD is
associated with poor social and family relationships, absenteeism from work, lower income, and
lower educational and occupational success.” (APA, 2013, p. 278-279).
PTSD sufferers are 80% more likely to develop depression, bipolar, anxiety disorders, and
substance use disorders (APA, 2013; Greist, 2014).
In a recent study that included more than 86,000 people across 24 countries, Canada had the
highest rate of PTSD in the general population, at 9.2% (Dückers, Alisic, & Brewin, 2016).
Prevalence rates for PTSD in Canadian paramedics are difficult to accurately measure, as most of
the data is based on self-reporting symptoms and not necessarily psychiatric diagnosis. What is
clear is that the prevalence is many times higher than the general population, ranging from 26-
43% (Carleton, et al., 2017; Lefevre, 2017; Regehr, Goldberg, & Hughes, 2002; Wilson, Guliani,
& Boichev, 2016).
Pathophysiology
By definition, PTSD occurs as a result of direct or indirect exposure to a traumatic experience,
but the pathophysiological reason for why some people develop PTSD after exposure to such
events has not been established. Current theories are remarkably complex and involve genetics,
various brain regions (hippocampus, amygdala, prefrontal cortex, thalamus), and a variety of
neurotransmitters and receptors (norepinephrine, CNS adrenergic receptors, serotonin and
various 5-HT receptors, endocannabinoids, the hypothalamic-pituitary-adrenal axis, opioid
receptors,) (Bailey, Cordell, Sobin, & Neumeister, 2013; Liberzon & Sripada, 2007; Sareen,
2018).

Treatment
Treatment of PTSD can be complex and multi-faceted. First of all, because PTSD (by definition)
cannot be diagnosed until symptoms have been present for more than one month, some
treatments for PTSD may begin before it is officially diagnosed. Many people wait far longer
than one month to seek a diagnosis, so treatment in this population is delayed.
Treatment for PTSD should aim to be nonpharmacological at first. A 2013 Cochrane review
found that while there is very poor quality of evidence available for any particular therapy over
another, it is clear that treatment is only effective if it deals directly with the trauma, as opposed
to symptom management without confronting the trauma itself (Bisson, Roberts, Cooper, &
Lewis, 2013). It is generally agreed that the evidence best supports two treatment modalities:
cognitive behaviour therapy (CBT) and eye movement desensitization and reprocessing (EMDR)
(Bisson, et al., 2013; Greist, 2014; Katzman, et al., 2014; World Health Organization [WHO],
2013).
The first line of treatment is CBT (Greist, 2014; Katzman, et al., 2014). CBT is not a specific
therapy approach but a system of therapy approaches that includes:
 Exposure. Repeated exposure to reminders in a controlled and guided environment helps
patients learn to cope, dulls the fear response over time, and increases self-confidence.
 Safety response inhibition. Patients are exposed to anxiety-inducing stimuli and practice
coping without trying to escape or seeking external coping mechanisms. This again
develops appropriate coping skills and self-efficacy.
 Arousal management. Relaxation and breathing techniques to help patients learn to
manage the physiological response to anxiety.
 Surrender of safety signals. Patients learn to relinquish external “safety signals”, such as
a teddy bear, companion, knowing where the nearest exit is, etc. This helps them
strengthen their own internal coping strategies, increases self-confidence and self-
efficacy (Greist, 2014; Katzman, et al., 2014).
Essentially, CBT consists of controlled and gradual exposure to cues/stimuli while the patient is
guided by the therapist in developing the skills to control their negative responses without
external crutches.
Eye movement desensitization and reprocessing (EMDR) is a type of exposure therapy that
involves exposing the patient to cues/stimuli while they focus on tracking a moving object with
their eyes, which (in theory) gradually desensitizes the patient to the stimulus and develops new
neural pathways that can process the stimuli more appropriately (Figley, 2011; Greist, 2014;
Katzman, et al., 2014).
Although the evidence for nonpharmacological therapy vs pharmacological therapy shows
approximately equal efficacy, it is still considered best practice to start with nonpharmacological
therapies. The goal with drug treatment is to manage symptoms until the patient can get better
using nonpharmacological treatment. Drugs are sometimes necessary when patients are not
improving enough with CBT/EMDR, or where CBT/EMDR are not available (Katzman, et al.,
2014; WHO, 2013). They should not, however, be used to treat children or adolescents with
PTSD (WHO, 2013).
Drugs of choice are usually selective serotonin reuptake inhibitors (SSRIs), serotonin
norepinephrine reuptake inhibitors (SNRIs), or tricyclic antidepressants (TCAs), with
SSRI/SNRIs being the recommended first-line class of drugs due to a better safety profile
(Greist, 2014; Hoskins, et al., 2015; Katzman, et al., 2014). Benzodiazepines are sometimes used
to treat symptoms like anxiety attacks or sleep disturbances, but are not used as primary drug
therapy (Katzman, et al., 2014).
It is worth noting that while sometimes PTSD can last for many years, recovery is entirely
possible and approximately 50% of adults completely recover within three months (APA, 2013).

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental


disorders (5th ed.). Arlington, VA: American Psychiatric Publishing
Bailey, C. R., Cordell, E., Sobin, S. M., & Neumeister, A. (2013). Recent progress in
understanding the pathophysiology of post-traumatic stress disorder. CNS drugs, 27(3), 221-232.
Bisson, J. I., Roberts, N. P., Andrew, M., Cooper, R., & Lewis, C. (2013). Psychological
therapies for chronic post‐traumatic stress disorder (PTSD) in adults. The Cochrane Library.
Carleton, R. N., Afifi, T. O., Turner, S., Taillieu, T., Duranceau, S., Lebouthillier, D. M., ... &
Hozempa, K. (2017). Mental disorder symptoms among public safety personnel in Canada. The
Canadian Journal of Psychiatry.
Dückers, M. L., Alisic, E., & Brewin, C. R. (2016). A vulnerability paradox in the cross-national
prevalence of post-traumatic stress disorder. The British Journal of Psychiatry, bjp-bp.
Figley, C. (2011). Eye movement desensitization and reprocessing. Treating PTSD in Military
Personnel: A Clinical Handbook, 74.
Greist, J.H. (2014). Posttraumatic Stress Disorder. In R. S. Porter & J. L. Kaplan (Eds.), The
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database.
Hoskins, M., Pearce, J., Bethell, A., Dankova, L., Barbui, C., Tol, W. A., ... & Bisson, J. I.
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obsessive-compulsive disorders. BMC psychiatry, 14(1), S1.
Lefevre, N. L. (2017). Psychological Distress in Emergency Medical Services Practitioners:
Identifying and Measuring the Issues (Doctoral dissertation, University of Calgary).
Liberzon, I., & Sripada, C. S. (2007). The functional neuroanatomy of PTSD: a critical
review. Progress in brain research, 167, 151-169.
Regehr, C., Goldberg, G., & Hughes, J. (2002). Exposure to human tragedy, empathy, and trauma
in ambulance paramedics. American journal of orthopsychiatry, 72(4), 505.
Sareen, J. (2018). Posttraumatic stress disorder in adults: Epidemiology, pathophysiology,
clinical manifestations, course, assessment, and diagnosis. UpToDate. Retrieved Feb 8th, 2018
from https://www.uptodate.com/contents/posttraumatic-stress-disorder-in-adults-epidemiology-
pathophysiology-clinical-manifestations-course-assessment-and-diagnosis
Wilson, S., Guliani, H., & Boichev, G. (2016). On the economics of post-traumatic stress
disorder among first responders in Canada. Journal of Community Safety and Well-Being, 1(2),
26-31.
World Health Organization. (2013). WHO guidelines on conditions specifically related to
stress. Geneva: WHO.

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