June is post-traumatic stress disorder (PTSD) awareness month.

PTSD is a severe, potentially chronic and disabling disorder that develops in some persons following exposure to a traumatic event involving actual or threatened death, serious injury, or sexual assault. Some common symptoms include intrusive thoughts, nightmares and flashbacks of traumatic events, avoidance of trauma reminders, hypervigilance, and sleep disturbance. These symptoms can be highly distressing and substantially impair social, occupational, and interpersonal functioning. The intensely distressing and impairing symptoms of traumatic stress are highly prevalent immediately following traumatic exposure and dissipate over the following days and weeks in most people. Persistence beyond one-month post-trauma suggests PTSD [1].

The Diagnostic and Statistical Manual of Mental Disorders, 4th Edition stipulates that for an individual to be diagnosed with posttraumatic stress disorder, he or she must have experienced or witnessed a life-threatening event and reacted with intense fear, helplessness, or horror. The traumatic event is persistently reexperienced (e.g., distressing recollections), there is persistent avoidance of stimuli associated with the trauma, and the victim experiences some form of hyperarousal (e.g., exaggerated startle response). These symptoms persist for more than one month and cause clinically significant impairment in daily functioning. When the disturbance lasts a minimum of two days and as long as four weeks from the traumatic event, Acute Stress Disorder may be a more accurate diagnosis.

The prevalence of PTSD in the U.S. population is approximately 8%, with incidence as high as 17% in primary care patients. PTSD can become chronic in as many as 40% of cases [2]. 50% of women in the United States have experienced a traumatic event, with the majority reporting trauma exposure also reporting two or more traumatic events. The National Comorbidity Survey Replication estimated the lifetime prevalence of PTSD among adult Americans to be 6.8%. Current past year PTSD prevalence was estimated at 3.5%. The lifetime prevalence of PTSD among men was 3.6% and among women was 9.7%. The twelve-month prevalence was 1.8% among men and 5.2% among women. However, PTSD only develops in 10% of those exposed to trauma, a finding that has prompted intense research efforts in identifying risk factors and early intervention to prevent or reduce the development of PTSD [2]. Populations at risk for PTSD include refugee victims of torture, combat veterans, persons released from incarceration, victims of sexual assault, and adults who endured repeated sexual or physical abuse as children http://phoenixaustralia.org/wp-content/uploads/2015/03/Phoenix-ASD-PTSD”>[4].

Explanatory models of PTSD have been proposed to better understand psychotraumatization processes and PTSD. [5] These perspective models include:

1. Disease/Illness Perspective [6-11]-

2. Dimensional Perspective

3. Cognitive-Axiologic Perspective [12,13][6]

4. Behavioral Perspective [6]

5. Spiritual/Transcendental Perspective [14]

6. The Narrative Perspective [15]

PTSD is viewed as a maladaptive response to a traumatic stressor, characterized by altered fear-related learning (fear conditioning) and extinction, behavioral sensitization and kindling, and alterations in brain regions and neurotransmitter systems closely linked to these processes. The hypothalamic-pituitary-adrenal (HPA) axis is the primary system activated as a stress response and a potential source of vulnerability to trauma-related psychopathology such as PTSD. Normal response to stress exposure initiates a neuroendocrine cascade in the HPA axis, leading to adrenal gland hypersecretion of the glucocorticoid cortisol. HPA axis activity is tightly controlled through complex regulatory mechanisms of glucocorticoid negative feedback. Glucocorticoids regulate the secretion of hypothalamic corticotropin-releasing factor (CRF) and pituitary adrenocorticotropic hormone. HPA axis activity is also regulated by glucocorticoid receptors (GRs) in the hippocampus and prefrontal cortex [[16,17] HPA stress response pathways are intimately linked with neurotransmitter systems and key brain regions in PTSD. The neural circuitry that mediates fear memory involves complex interactions among three brain centers: the hippocampus, involved in short-term memory and contextual fear; the amygdala, involved in conditioned fear response; and the medial prefrontal cortex, which mediates suppression of subcortical (e.g., amygdala, hippocampus) responses. Several neurotransmitter systems serve as chemical messengers in this neurocircuit. Alterations in these transmitter systems reflect a dysregulated stress response and substantially impact conditioned fear response and the consolidation and retrieval of traumatic memories [18,19].

Treatment of PTSD is aimed at interfering with this persistence of traumatic memories. The treatments of PTSD are varied and diverse including:

1 Psychosocial

2 Rehabilitation

3 Somatic and Alternative Therapy

4 Pharmacotherapy

In 2002 Marsicano found that the CB1 receptors in the amygdala are required for the extinction of fear memories [20]. A further study by Hillard in 2015 showed that following chronic stress signaling in the endocannabinoid system (ECS) is downregulated [21]. This downregulation impaired reversal learning (the ability to be trained differently to two stimuli based on reward or punishment response) in mice and as anticipated induced perservatory behaviors. The study also found that the effects of chronic stress were reversed when an exogenous CB1 agonist was applied. Hill found Reductions in circulating endocannabinoid levels in individuals with post-traumatic stress disorder following exposure to the World Trade Center attacks [22]. These studies showed that there may be a scientific rational behind the use of marijuana by veterans to reduce PTSD. Medical marijuana has been shown to be an effective adjuvant in the treatment of PTSD. It may even be possible to treat PTSD without the side effects caused by THC.

If you think that you might have PTSD or would like to discuss the possibility of Cannabinoid therapy, please speak with me or your primary care physician.

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association Press; 2013.Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey.Arch Gen Psychiatry. 1995;52(12):1048-1060.

2. National Center for PTSD. How Common is PTSD? Available at https://www.ptsd.va.gov/public/PTSD-overview/basics/how-common-is-ptsd.asp. Last accessed February 16, 2018.

3. Phoenix Australian Centre for Posttraumatic Mental Health. Australian Guidelines for the Treatment of Adults with Acute Stress Disorder and Posttraumatic Stress Disorder. Available at http://phoenixaustralia.org/wp-content/uploads/2015/03/Phoenix-ASD-PTSD-Guidelines.pdf. Last accessed February 16, 2018.

4. Jakovljević M, Brajković L, Jakšić N, Lončar M, Aukst-Margetić B, Lasić D. Posttraumatic stress disorders (PTSD) from different perspectives: a transdisciplinary integrative approach. Psychiatria Danub. 2012;24(3):246-255.21. McHugh PR, Slavney PR. The Perspectives of Psychiatry. 2nd ed. Baltimore, MD: John Hopkins University Press; 1998.

5. 22. Tyrer P, Steinberg D. Models for Mental Disorders: Conceptual Models in Psychiatry. 3rd ed. Chichester: John Wiley & Sons; 1998.

6. 23. Summerfield D. Cross-cultural perspective on the medicalization of human suffering. In: Rosen GM (ed). Posttraumatic Stress Disorder: Issues and Controversies. Chichester: John Wiley & Sons; 2005: 233-245.

7. 24. Frueh BC, Elhai JD, Kaloupek DG. Unresolved issues in the assessment of trauma exposure and posttraumatic reactions. In: Rosen GM (ed). Posttraumatic Stress Disorder: Issues and Controversies. Chichester: John Wiley & Sons; 2005: 63-84.

8. 25. Herbert JD, Sageman M. First do no harm: emerging guidelines for the treatment of posttraumatic reactions. In: Rosen GM (ed). Posttraumatic Stress Disorder: Issues and Controversies. Chichester: John Wiley & Sons; 2005: 213-232.

9. 26. Friedman MJ. PTSD and related disorders. In: Stein D, Friedman M, Blanco C (eds). Post-Traumatic Stress Disorder. 1st ed. Chichester: John Wiley & Sons; 2011.

10. 27. McNally RJ, Frueh BC. Why we should worry about malingering in the VA system: comment on Jackson et al. (2011). J Trauma Stress. 2012;25(4):454-456.

11. 28. McNally RJ. Conceptual problems with the DSM-IV criteria for posttraumatic stress disorder. In: Rosen GM (ed). Posttraumatic Stress Disorder: Issues and Controversies. Chichester: John Wiley & Sons; 2005.

12. 29. Reivich KJ, Seligman MEP, McBride S. Master resilience training in the U.S. Army. Am Psychol. 2011;66(1):25-34.

13. 30. Maguen S, Litz B. Moral injury in veterans of war. PTSD Res Q. 2012;23(1):1-6.

14. 31. Amendolia RA. A Narrative Constructivist Perspective of Treatment of PTSD with Ericksonian Hypnosis and EMDR. Available at http://www.aaets.org/article32.htm. Last accessed February 16, 2018.

15. Morris MC, Compas BE, Garber J. Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: a systematic review and meta-analysis. Clin Psychol Rev. 2012;32(4):301-315.

16. George SA, Stout SA, Tan M, Knox D, Liberzon I. Early handling attenuates enhancement of glucocorticoid receptors in the prefrontal cortex in an animal model of post-traumatic stress disorder. Biol Mood Anxiety Disord. 2013;3(1):22.

17. Ressler KJ, Mayberg HS. Targeting abnormal neural circuits in mood and anxiety disorders: from the laboratory to the clinic.Nat Neurosci. 2007;10(9):1116-1124.

18. Rauch SL, Shin LM, Phelps EA. Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research—past, present, and future. Biol Psychiatry. 2006;60:376-382.

19. Neumeister A, Corsi-Travali S, Green CR. The role of BDNF-TrkB signaling in the pathogenesis of PTSD. J Depress Anxiety. 2013;S4:006

20. G Marsicano, CT Wotjak, SC Azad, T Bisogno. The endogenous cannabinoid system controls extinction of aversive memories. -Nature volume 418, pages 530–534

21. Maria Morena, Sachin Patel, Jaideep S Bains & Matthew N Hill. Neurobiological Interactions Between Stress and the Endocannabinoid System. Neuropsychopharmacology volume41, pages80–102 (2016)

22. Hill MN1, Bierer LM, Makotkine I, Golier JA, Galea S, McEwen BS, Hillard CJ, Yehuda R. Reductions in circulating endocannabinoid levels in individuals with post-traumatic stress disorder following exposure to the World Trade Center attacks. Psychoneuroendocrinology. 2013 Dec;38(12):2952-61

23. George Fraser, M.D., F.R.C.P.C., The Use of a Synthetic Cannabinoid in the Management of Treatment‐Resistant Nightmares in Posttraumatic Stress Disorder (PTSD). CNS Neuroscience and Therapeutics. 2009 February 13; Volume15, Issue1 Pages 84-88