Advertisement

Neurophysiology

, Volume 47, Issue 6, pp 482–489 | Cite as

Posttraumatic Stress Disorder (PTSD): Mechanisms and Possible Treatments

  • S. Asalgoo
  • G. P. JahromiEmail author
  • G. H. Meftahi
  • H. Sahraei
REVIEWS

Posttraumatic stress disorder (PTSD) is a debilitating mental condition occurring after a tragedy or a traumatic experience, such as rape, assault, natural disasters, war, car or plane accidents, etc. PSTD can cause a number of symptoms, such as fear, high anxiety, hyperarousal, bad dreams, nightmares, etc., existing for a long time after the traumatic event. In recent years, the spread of PTSD has increased in the world, especially in Asia (Middle East), particularly among soldiers who have taken part in military conflicts. This situation confirms the importance of understanding how PTSD develops and of improving its treatment. This paper is a review of the literature related to the respective topics. Like other anxiety disorders, PTSD is related to disruption of the endocrine system, particularly disintegration of the hypothalamus-pituitary-adrenal axis (HPAA). People suffering from PTSD are characterized by elevated levels of corticotropin-releasing hormone, low basal cortisol levels, and enhanced negative feedback suppression of the HPAA. At the present time, certain plant-derived compounds are considered to be a new important source to treat PTSD. For example, remedies obtained from saffron are such possible means. According to our findings, saffron components may considerably affect some parts of the HPAA for reduction of stress-induced corticosterone release.

Keywords

posttraumatic stress disorder (PTSD) hypothalamo-pituitary (hypophyseal)-adrenal axis (HPAA) corticosteroids corticotropin-releasing hormone 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    D. G. Kilpatrick, C. Edmunds, and A. Seymour, Rape in America: A Report to the Nation. National Victim Center and the Crime Victims Research and Treatment Center, Medical University of South Carolina, Charleston (1992).Google Scholar
  2. 2.
    P. B. John, S. Russell, and P. S. Russell, “The prevalence of posttraumatic stress disorder among children and adolescents affected by tsunami disaster in Tamil Nadu,” Disaster Manag. Response., 5, No. 1, 3–7 (2007).CrossRefPubMedGoogle Scholar
  3. 3.
    M. H. Swartz, Textbook of Physical Diagnosis: History and Examination, Saunders Elsevier (2006).Google Scholar
  4. 4.
    4. G. C. Gray, K. S. Kaiser, A. W. Hawksworth, et al., “Increased postwar symptoms and psychological morbidity among U.S. Navy Gulf War veterans,”Am. J. Trop. Med. Hyg., 60, No. 5, 758-766 (1999).Google Scholar
  5. 5.
    T. M. Keane, A. D. Marshall, and C. T. Taft, “Posttraumatic stress disorder: Etiology, epidemiology, and treatment outcome,” Annu. Rev. Clin. Psychol., 2, 161-197 (2006).CrossRefPubMedGoogle Scholar
  6. 6.
    R. C. Kessler, A. Sonnega, E. Bromet, et al., “Posttraumatic stress disorder in the National Comorbidity Survey,” Arch. Gen. Psychiatr., 52, No. 12, 1048-1060 (1995).CrossRefPubMedGoogle Scholar
  7. 7.
    A. Bahreinian and H. Borhani, “Mental health in group of war veterans and their spouses in Qom,” Quart. J. School Med., 27, No. 4, 305–312 (2003).Google Scholar
  8. 8.
    M. Mendenhall, Chaplains in Mental Health: Healing the Spiritual Wounds of War (Cover Story), Am. Psychotherapy Assoc., Springfield (2010).Google Scholar
  9. 9.
    9. K. C. Koenen, S. D Stellman, J. F Sommer, Jr., and J. M. Stellman, “Persisting posttraumatic stress disorder symptoms and their relationship to functioning in Vietnam veterans: A 14 year follow-up,” J. Trauma Stress, 21, No. 1, 49–57 (2008).Google Scholar
  10. 10.
    G. Meftahi, Z. Ghotbedin, M. J. Eslamizade, et al., “Suppressive effects of resveratrol treatment on the intrinsic evoked excitability of CA1 pyramidal neurons,” Cell J. (Yakhteh), 17, No. 3, (2015).Google Scholar
  11. 11.
    M. Olff, Y. Güzelcan, G. J. de Vries, et al., “HPA- and HPT-axis alterations in chronic posttraumatic stress disorder,” Psychoneuroendocrinology, 31, No. 10, 1220–1230 (2006).Google Scholar
  12. 12.
    R. Yehuda, “Advances in understanding neuroendocrine alterations in PTSD and their therapeutic implications,” Ann. N.Y. Acad. Sci, 1071, 137–156 (2006).Google Scholar
  13. 13.
    D. Simeon, M. Knutelska, R. Yehuda, et al., “Hypothalamic-pituitary-adrenal axis function in dissociative disorders, post-traumatic stress disorder, and healthy volunteers,” Biol. Psychiatry, 61, No. 8, 966–973 (2007).CrossRefPubMedPubMedCentralGoogle Scholar
  14. 14.
    M. A. Oquendo, G. Echavarria, H. C. Galfalvy, et al., “Lower cortisol levels in depressed patients with comorbid posttraumatic stress disorder,” Neuropsychopharmacology, 28, No. 3, 591–598 (2003).Google Scholar
  15. 15.
    C. S. de Kloet, E. Vermetten, E. Geuze, et al., “Elevated plasma corticotrophin-releasing hormone levels in veterans with posttraumatic stress disorder,” Prog. Brain Res., 167, 281–291 (2007).CrossRefGoogle Scholar
  16. 16.
    V. M. Voloshin, PTSD, Phenomenology, Clinical Aspects Systematics, Dynamics, and Contemporary Approaches to Psychopharmacotherapy [in Russian], Anakharsis, Moscow (2005).Google Scholar
  17. 17.
    C. S. de Kloet, E. Vermetten, C. J. Heijnen, et al., “Enhanced cortisol suppression in response to dexamethasone administration in traumatized veterans with and without posttraumatic stress disorder,” Psychoneuroendocrinology, 32, No. 3, 215–226 (2007).Google Scholar
  18. 18.
    A. J. Douglas, N. H. Steckler, and N. H. Kalin, Vasopressin and Oxytocin, Handbook of Stress and the Brain, The Neurobiology of Stress, Elsevier, Amsterdam, 205–230 (2005).Google Scholar
  19. 19.
    M. V. Ugryumov, Mechanisms of Neuroendocrine Regulation [in Russian], Nauka, Moscow (1999).Google Scholar
  20. 20.
    P. Ouimette, D. Coolhart, D. Sugarman, et al., “A pilot study of posttraumatic stress and associated functioning of Army National Guard following exposure to Iraq warzone trauma,” Traumatology, 14, No. 3, 51–56 (2008).Google Scholar
  21. 21.
    I. M. Engelhard, M. A. van den Hout, J. Weerts, et al., “Deployment-related stress and trauma in Dutch soldiers returning from Iraq. Prospective study,” Br. J. Psychiatr., 191, 140–145 (2007).CrossRefGoogle Scholar
  22. 22.
    D. J. Newport and C. B. Nemeroff, “Neurobiology of posttraumatic stress disorder,” Curr. Opin. Neurobiol., 10, No. 2, 211–218 (2000).CrossRefPubMedGoogle Scholar
  23. 23.
    D. L. Schacter, D. T. Gilbert, D. M. Wegner, et al., Introducing Psychology, Worth Publishers, New York (2011).Google Scholar
  24. 24.
    M. J. Eslamizadeh, F. Saffarzadeh, S. M. Mousavi, et al., “Alterations in CA1 pyramidal neuronal intrinsic excitability mediated by Ih channel currents in a rat model of amyloid beta pathology,” Neuroscience, 305, 279–292 (2015).CrossRefGoogle Scholar
  25. 25.
    K. Skelton, K. J. Ressler, S. D. Norrholm, et al., “PTSD and gene variants: New pathways and new thinking,” Neuropharmacology, 62, No. 2, 628–637 (2012).Google Scholar
  26. 26.
    J. Zohar, A. Juven-Wetzler, V. Myers, and L. Fostick, “Post-traumatic stress disorder: Facts and fiction,” Curr. Opin. Psychiatr., 21, No. 1, 74–77 (2008).CrossRefGoogle Scholar
  27. 27.
    R. Yehuda, S. L. Halligan, J. A. Golier, et al., “Effects of trauma exposure on the cortisol response to dexamethasone administration in PTSD and major depressive disorder,” Psychoneuroendocrinology, 29 (3), 389–404 (2004).CrossRefPubMedGoogle Scholar
  28. 28.
    E. B. De Souza, D. E. Grigoriadis, “Corticotropinreleasing factor: physiology, pharmacology, and role in central nervous system and immune disorders”, Amer. Coll. Neuropsychopharmacol., Chap. 7, 91–107 (2002).Google Scholar
  29. 29.
    V. G. Shalyapina, “Corticoliberin in the regulation of adaptive behavior in the pathogenesis of post-stress depression,” in: Basic Neuroendocrinology [in Russian], ÉLBI, St. Petersburg, 84–146 (2005).Google Scholar
  30. 30.
    C. S. de Kloet, E. Vermetten, E. Geuze, et al., “Assessment of HPA-axis function in posttraumatic stress disorder: Pharmacological and non-pharmacological challenge tests, a review,” J. Psychiatr. Res., 40, No. 6, 550–567 (2006).CrossRefPubMedGoogle Scholar
  31. 31.
    F. M. Dautzenberg, S. Braun, and R. L. Hauger, “GRK3 mediates desensitization of CRF1 receptors: a potential mechanism regulating stress adaptation,” Am. J. Physiol. Regul. Integr. Comp. Physiol., 280, No. 4, 935–946 (2001).Google Scholar
  32. 32.
    M. Salehi, H. Eimani, H. Sahraei, and G. H. Meftahi, “Stress can change reward system function in secondgeneration (F2): a review,” Adv. Biores., 6, No. 5, 4–14 (2015).Google Scholar
  33. 33.
    J. C. Shipherd, A. E. Street, P. A. Resick, “Cognitive therapy for posttraumatic stress disorder,” in: Cognitive-Behavioral Therapies for Trauma (2nd ed.), Guilford Press, New York, 96–116 (2006).Google Scholar
  34. 34.
    J. Bisson and M. Andrew, “Psychological treatment of post-traumatic stress disorder (PTSD),” Cochrane Database Syst. Rev., 18, No. 3 (2007).Google Scholar
  35. 35.
    M. Ghodrat, H. Sahraei, J. Razjouyan, and G. H. Meftahi, “Effects of a saffron alcoholic extract on visual short-term memory in humans: a psychophysical study,” Neurophysiology, 46, No. 3, 247–253 (2014).Google Scholar
  36. 36.
    S. K. Verma and A. Bordia, “Antioxidant property of Saffron in man,” Indian J. Med. Sci., 52, No. 5, 205–207 (1998).PubMedGoogle Scholar
  37. 37.
    H. Yaribeygi, H. Sahraei, A. R. Mohammadi, and G. H. Meftahi, “Saffron (Crocus sativus L.) and morphine dependence: A systematic review article,” Am. J. Biol. Life Sci., 2, No. 2, 41–45 (2014).Google Scholar
  38. 38.
    H. Sahraei, J. Shams, S. Marjani, et al., “Effects of the Crocus sativus L. Extract on the acquisition and expression of morphine-induced behavioral sensitization in female mice,” J. Med. Plants, 6, No. 21, 26-35 (2007).Google Scholar
  39. 39.
    S. Soeda, T. Ochiai, L. Paopong, et al., “Crocin suppresses tumor necrosis factor-α-induced cell death of neuronally differentiated PC-12 cells,” Life Sci., 69, No. 24, 2887–2898 (2001).CrossRefPubMedGoogle Scholar
  40. 40.
    H. Sahraei, Z. Fatahi, A. H. Rohani, et al., “Ethanolic extract of saffron and its constituent crocin diminish stress-induced metabolic signs and alterations of dopamine-related behaviours in rats,” Int. Res. J. Pharm. Pharmacol., 2, No. 7, 165–173 (2012).Google Scholar
  41. 41.
    H. Sahraei, Z. Fatahi, A. Eidi, et al., “Inhibiting post traumatic stress disorder (PTSD) induced by electric shock using ethanol extract of saffron in rats,” J. Biol. Res. Thessalon, 18, 320–327 (2012).Google Scholar
  42. 42.
    K. Abe and H. Saito, “Effects of saffron extract and its constituent crocin on learning behavior and longterm potentiation,” Phytother. Res., 14, No. 3, 149–152 (2000).CrossRefPubMedGoogle Scholar
  43. 43.
    G. H. Meftahi, M. Janahmadi, and M. J. Eslamizade, “Effects of resveratrol on intrinsic neuronal properties of CA1 pyramidal neurons in rat hippocampal slices,” Physiol. Pharmacol., 18, No. 2, 144–155 (2014).Google Scholar
  44. 44.
    B. A. Halataei, M. Khosravi, S. Arbabian , et al., “Saffron (Crocus sativus) aqueous extract and its constituent crocin reduces stress-induced anorexia in mice.” Phytother. Res., 25, No. 12, 1833–1838 (2011).CrossRefPubMedGoogle Scholar
  45. 45.
    D. B. Miller and J. P. O’Callaghan, “Neuroendocrine aspects of the response to stress,” Metabolism, 51, 6 Suppl., 5–10 (2002).Google Scholar
  46. 46.
    T. C. Adam and E. S. Epel, “Stress, eating and the reward system,” Physiol. Behav., 91, No. 4, 449–458 (2007).CrossRefPubMedGoogle Scholar
  47. 47.
    M. Erfani, H. Sahraei, and G. H. Meftahi, “Study of the effects of maternal psychological and physical stress on morphine-induced tolerance in F2 NMRI generation mice,” Adv. Biores., 6, No. 6, 134-140 (2015).Google Scholar
  48. 48.
    D. Chalabi-Yani, H. Sahraei, G. H. Meftahi, et al, “Effect of transient inactivation of ventral tegmental area on the expression and acquisition of nicotine-induced conditioned place preference in rats,” Iran. Biomed. J., 19, No. 4, 214–219 (2015).PubMedPubMedCentralGoogle Scholar
  49. 49.
    S. B. Hosseini, H. Sahraei, A. Mohammadi, et al., “Inactivation of the nucl. accumbens core exerts no effect on nicotine-induced conditioned place preference,” Neurophysiology, 47, No. 4, 295–301 (2015).CrossRefGoogle Scholar
  50. 50.
    M. C. Moffett, J. Harley, D. Francis, et al., “Maternal separation and handling affects cocaine selfadministration in both the treated pups as adults and the dams,” J. Pharmacol. Exp. Ther., 317, No. 3, 1210–1218 (2003).CrossRefGoogle Scholar
  51. 51.
    A. McFarlane, C. R. Clark, R. A. Bryant, et al., “The impact of early life stress on psychophysiological, personality and behavior measures in 740 non-clinic subjects,” J. Integr. Neurosci., 4, No. 1, 27–40 (2005).CrossRefPubMedGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  • S. Asalgoo
    • 1
  • G. P. Jahromi
    • 2
    Email author
  • G. H. Meftahi
    • 2
  • H. Sahraei
    • 2
  1. 1.Behavioral Sciences Research CenterBaqiyatallah University of Medical SciencesTehranIran
  2. 2.Neuroscience Research CenterBaqiyatallah University of Medical SciencesTehranIran

Personalised recommendations