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Posttraumatic Stress Disorder (PTSD)
Rachel Bramson, MD
Michael L. Brown, MD
Suzanne Shurtz, MLIS, AHIP
image BASICS
  • Posttraumatic stress disorder (PTSD) is an anxiety disorder defined as a reaction that can occur after exposure to an extreme traumatic event involving death, threat of death, serious physical injury, or a threat to physical integrity.
  • This reaction has three cardinal characteristics:
    • Reexperiencing the trauma
    • Avoidance of anything related to the traumatic event and/or numbing of general responsiveness
    • Increased arousal
  • Traumatic events that may trigger PTSD include natural/human disasters, serious accidents, war, sexual abuse, rape, torture, terrorism, hostage-taking, or being diagnosed with life-threatening disease.
  • PTSD can be:
    • Acute: symptoms lasting <3 months
    • Chronic: symptoms lasting ≥3 months
    • Delayed onset: 6 months (from event to symptom onset) in 25% of diagnosed cases
  • ˜30% of men and women who have spent time in a war zone experience PTSD.
  • Current estimates of PTSD in military personnel who served in Iraq range from 12-20%.
  • 16% children and adolescents exposed to trauma develop PTSD (high in girls with interpersonal trauma 33%; low in boys with noninterpersonal trauma 8%) (1).
˜7.7 million American adults aged ≥18 years (3.5% of this age group) are diagnosed with PTSD each year.
Lifetime prevalence for PTSD is 8-9%.
  • During trauma, the locus coeruleus mediates sympathetic outflows to the amygdala (rapid effect) and adrenal medulla (sustained effect). The adrenal medulla then releases catecholamines, which stimulate peripheral afferent vagal &bgr;-receptors. Vagal afferents innervate the nucleus tractus solitarius (NTS) in the brainstem medulla. NTS fibers innervate the amygdala with norepinephrine (NE).
  • With an increase in NE, the amygdala mediates coupling of emotional valence to declarative memories via long-term potentiation, forming deeply engraved trauma memories and leading to intrusive memories and emotions, potentially leading to PTSD.
  • The orbitoprefrontal cortex (which usually exerts an inhibiting effect on this activation) appears less capable of inhibiting this activation due to stressinduced atrophy of specific nuclei in this region.
  • Monozygotic twins exposed to combat in Vietnam were at increased risk of the cotwin having PTSD compared with twins who were dizygotic.
  • Some data suggest an association between dopamine transporter gene (DAT) SLC6A3 3′ (VNTR) polymorphism, and PTSD.
  • Pretrauma environment:
    • Female sex
    • Younger age
    • Psychiatric history
    • Sexual abuse
  • Peritrauma environment:
    • Severity of the trauma
    • Peritrauma emotionality
    • Perception of threat to life
    • Perpetration of the trauma
  • Posttrauma environment:
    • Perceived injury severity
    • Medical complications
    • Perceived social support
    • Persistent dissociation from traumatic event
  • Subsequent exposure to trauma-related stimuli
  • There is moderate evidence for hydrocortisone (2) and some evidence for propranolol (3) reducing development of full posttraumatic syndrome.
  • Compulsory psychological debriefing immediately after a trauma (critical incident stress management) does not prevent PTSD and may be harmful (4).
  • Major depressive disorder
  • Alcohol/substance abuse
  • Panic disorder
  • Obsessive-compulsive disorder
  • Agoraphobia and/or social phobia
  • Traumatic brain injury
  • Smoking (especially with assaultive trauma)
  • Major neurocognitive disorders, dementia, or amnesia
Pediatric Considerations
Oppositional defiant disorder and separation anxiety are common comorbid conditions.
  • Patients may present with physical injuries from the traumatic event.
  • Mental status examination:
    • Thoughts and perceptions (e.g., hallucinations, delusions, suicidal ideation, phobias)
    • General appearance: disheveled, poor hygiene
    • Behavior: agitation; startle reaction extreme
    • Psychological numbness
    • Orientation may be affected.
    • Memory: forgetfulness, especially concerning the details of the traumatic event
    • Poor concentration
    • Poor impulse control
    • Altered speech rate and flow
    • Mood and affect may be changed: depression, anxiety, guilt, and/or fear
Pediatric Considerations
Elevated heart rate immediately following trauma is associated with development of PTSD (5)[A].
  • Acute stress disorder (symptoms <4 weeks)
  • Generalized anxiety disorder
  • Adjustment disorder
  • Obsessive-compulsive disorder
  • Schizophrenia
  • Major depressive disorder
  • Mood disorder with psychotic features
  • Substance abuse
  • Personality disorders
  • Dissociative disorders
  • Conversion disorder

Better prognosis if treated with a combination of psychotherapy and pharmacotherapy, initiated soon after the trauma.
First Line
  • SSRIs: depression, panic attacks, startle response, sleep disruption (6)[A]. All commonly used SSRIs have been shown to be effective in the treatment of PTSD and are the first-line treatment:
    • Sertraline: 50 to 200 mg every day (FDA approved)
    • Paroxetine: starting dose: 10 mg every day; may be increased in 10 mg increments at intervals ≥1 week (FDA approved)
    • Fluoxetine: 20 mg every day/BID not to exceed 80 mg/day (demonstrates some efficacy for all three symptom clusters)
  • Sleep disruption: Sleep disruption due to hyperarousal is ubiquitous in PTSD. Standard sedatives, such as trazodone 50 to 300 mg at bedtime, mirtazapine 7.5 to 30 mg qhs, or amitriptyline 25 to 100 mg qhs
  • Nightmares/nighttime hyperarousal: prazosin 2 to 15 mg qhs (7)[A], clonidine 0.1 to 0.2 mg qhs, amitriptyline 25 to 100 mg qhs
Second Line
Refractory/residual symptoms: Consider augmentation with:
  • Depression: mirtazapine 15 to 45 mg/day; consider switch to a serotonin-norepinephrine reuptake inhibitor (SNRI), such as venlafaxine XR 37.5 to 300 mg/day, duloxetine 60 to 120 mg/day, or desvenlafaxine 50 to 100 mg/day. Nefazodone 300 to 600 mg/day in divided doses can be very effective, but requires quarterly LFTs.
  • Reexperiencing/intrusive thoughts: first-/second-generation antipsychotic medications: aripiprazole 5 to 15 mg/day, risperidone 0.5 to 2 mg/day, olanzapine 2.5 to 10 mg/day, quetiapine 50 to 400 mg/day (8)[A]. Second-generation Rx less prone to extrapyramidal symptoms (EPS): cognitive dulling
  • Hyperarousal: clonidine, start 0.05 mg BID/TID; slowly titrate to as much as 0.45 mg/day divided doses; guanfacine 1 to 3 mg/day in divided doses (long-acting forms of both clonidine and guanfacine now available). Also consider second-generation antipsychotics quetiapine, risperidone, and olanzapine as above. Divided doses often more helpful.
  • Impulsivity/explosiveness: anticonvulsants: valproic acid 500 to 2,000 mg/day, carbamazepine 200 to 600 mg/day, topiramate 50 to 200 mg/day
  • Anxiety: benzodiazepines (see “ALERT”), including clonazepam, 1 to 4 mg/day in divided doses for a limited duration. Consider also hydroxyzine 25 to 50 mg TID/QID PRN or risperidone 0.25 to 0.5 mg TID PRN
  • Psychotherapeutic interventions:
    • Exposure therapies have shown the highest effectiveness for treatment of PTSD (10)[A]:
      • Behavioral and cognitive-behavioral therapy (CBT): Early CBT has been shown to speed recovery. CBT is currently considered the standard of care for PTSD by the U.S. Department of Defense.
      • 1-week intensive CBT was as effective as 3-month weekly CBT in one study (11)[A].
      • Internet-based CBT has shown benefit in reduction of PTSD symptoms.
      • Prolonged exposure therapy: Reexperience distressing trauma-related memories and reminders to facilitate habituation and successful emotional processing of memory.
      • EMDR (eye movement desensitization and reprocessing) has been shown to benefit patients with PTSD (12)[A].
    • Stress-reduction techniques:
      • Immediate symptom reduction (e.g., rebreathing in a bag for hyperventilation)
      • Early recognition and removal from a stress
      • Relaxation, meditation, and exercise techniques are also helpful in reducing the reaction to stressful events.
    • Telemedicine-based collaborative care (with nurse case manager, pharmacy, psychology, and psychiatry) is more effective than usual care (13)[A].
  • Interpersonal psychotherapy:
    • Supportive psychotherapy with an emphasis on the here and now
  • Social:
    • Establish the social framework of the problem. Clarifying this allows the patient to begin viewing it within the proper context (e.g., change of job/relocation of adult-dependent offspring)
Inpatient care is necessary only if the patient becomes suicidal/homicidal or for treatment of comorbid conditions (e.g., depression, substance abuse).
National Center for PTSD: www.ptsd.va.gov
  • Varies significantly from patient to patient
  • In 50% of cases, the symptoms spontaneously remit after 3 months; however, in other cases, symptoms may persist, often for many years, and cause longterm impairment in life functioning.
  • Factors associated with a good prognosis include:
    • Rapid engagement of treatment
    • Early and ongoing social support
    • Avoidance of retraumatization
    • Positive premorbid function
    • Absence of other psychiatric disorders/substance abuse
1. Alisic E, Zalta AK, van Wesel F, et al. Rates of post-traumatic stress disorder in trauma-exposed children and adolescents: meta-analysis. Br J Psychiatry. 2014;204:335-340.
2. Amos T, Stein DJ, Ipser JC. Pharmacological interventions for preventing post-traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2014;(7):CD006239.
3. Searcy CP, Bobadilla L, Gordon WA, et al. Pharmacological prevention of combatrelated PTSD: a literature review. Mil Med. 2012;177(6):649-654.
4. Rose S, Bisson J, Churchill R, et al. Psychological debriefing for preventing post traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2002;(2):CD000560.
5. Brosbe MS, Hoefling K, Faust J. Predicting posttraumatic stress following pediatric injury: a systematic review. J Pediatr Psychol. 2011;36(6):718-729.
6. Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2006;(1):CD002795.
7. Writer BW, Meyer EG, Schillerstrom JE. Prazosin for military combat-related PTSD nightmares: a critical review. J Neuropsychiatry Clin Neurosci. 2014;26(1):24-33.
8. Han C, Pae CU, Wang SM, et al. The potential role of atypical antipsychotics for the treatment of posttraumatic stress disorder. J Psychiatr Res. 2014;56:72-81.
9. Jeffreys M, Capehart B, Friedman MJ. Pharmacotherapy for posttraumatic stress disorder: review with clinical applications. J Rehabil Res Dev. 2012;49(5):703-715.
10. Kornør H, Winje D, Ekeberg Ø, et al. Early traumafocused cognitive-behavioural therapy to prevent chronic post-traumatic stress disorder and related symptoms: a systematic review and metaanalysis. BMC Psychiatry. 2008;8:81.
11. Ehlers A, Hackmann A, Grey N, et al. A randomized controlled trial of 7-day intensive and standard weekly cognitive therapy for PTSD and emotion-focused supportive therapy. Am J Psychiatry. 2014;171(3):294-304.
12. Goodson J, Helstrom A, Halpern JM, et al. Treatment of posttraumatic stress disorder in U.S. combat veterans: a meta-analytic review. Psychol Rep. 2011;109(2):573-599.
13. Fortney JC, Pyne JM, Kimbrell TA, et al. Telemedicine-based collaborative care for posttraumatic stress disorder: a randomized clinical trial. JAMA Psychiatry. 2015;72(1):58-67.
Additional Reading
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-V). 5th ed. Washington, DC: American Psychiatric Publishing; 2013.
  • F43.10 Post-traumatic stress disorder, unspecified
  • F43.11 Post-traumatic stress disorder, acute
  • F43.12 Post-traumatic stress disorder, chronic
Clinical Pearls
  • Treatment is often best accomplished with a combination of psychotherapy and pharmacotherapy.
  • The sooner therapy is initiated after the trauma, the better the prognosis.