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.
This is a preview of subscription content, access via your institution.
Buy single article
Instant access to the full article PDF.
Tax calculation will be finalised during checkout.
Subscribe to journal
Immediate online access to all issues from 2019. Subscription will auto renew annually.
Tax calculation will be finalised during checkout.
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).
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).
M. H. Swartz, Textbook of Physical Diagnosis: History and Examination, Saunders Elsevier (2006).
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).
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).
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).
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).
M. Mendenhall, Chaplains in Mental Health: Healing the Spiritual Wounds of War (Cover Story), Am. Psychotherapy Assoc., Springfield (2010).
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).
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).
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).
R. Yehuda, “Advances in understanding neuroendocrine alterations in PTSD and their therapeutic implications,” Ann. N.Y. Acad. Sci, 1071, 137–156 (2006).
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).
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).
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).
V. M. Voloshin, PTSD, Phenomenology, Clinical Aspects Systematics, Dynamics, and Contemporary Approaches to Psychopharmacotherapy [in Russian], Anakharsis, Moscow (2005).
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).
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).
M. V. Ugryumov, Mechanisms of Neuroendocrine Regulation [in Russian], Nauka, Moscow (1999).
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).
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).
D. J. Newport and C. B. Nemeroff, “Neurobiology of posttraumatic stress disorder,” Curr. Opin. Neurobiol., 10, No. 2, 211–218 (2000).
D. L. Schacter, D. T. Gilbert, D. M. Wegner, et al., Introducing Psychology, Worth Publishers, New York (2011).
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).
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).
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).
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).
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).
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).
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).
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).
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).
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).
J. Bisson and M. Andrew, “Psychological treatment of post-traumatic stress disorder (PTSD),” Cochrane Database Syst. Rev., 18, No. 3 (2007).
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).
S. K. Verma and A. Bordia, “Antioxidant property of Saffron in man,” Indian J. Med. Sci., 52, No. 5, 205–207 (1998).
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).
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).
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).
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).
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).
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).
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).
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).
D. B. Miller and J. P. O’Callaghan, “Neuroendocrine aspects of the response to stress,” Metabolism, 51, 6 Suppl., 5–10 (2002).
T. C. Adam and E. S. Epel, “Stress, eating and the reward system,” Physiol. Behav., 91, No. 4, 449–458 (2007).
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).
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).
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).
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).
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).
About this article
Cite this article
Asalgoo, S., Jahromi, G.P., Meftahi, G.H. et al. Posttraumatic Stress Disorder (PTSD): Mechanisms and Possible Treatments. Neurophysiology 47, 482–489 (2015). https://doi.org/10.1007/s11062-016-9559-9
- posttraumatic stress disorder (PTSD)
- hypothalamo-pituitary (hypophyseal)-adrenal axis (HPAA)
- corticotropin-releasing hormone