Posttraumatic Stress Disorder
Author / Source: Wikipedia
It is a severe and ongoing emotional reaction to an extreme psychological trauma.3 This stressor may involve someone’s actual death, a threat to the patient’s or someone else’s life, serious physical injury, an unwanted sexual act, or a threat to physical or psychological integrity, overwhelming psychological defenses.
In some cases it can also be from profound psychological and emotional trauma, apart from any actual physical harm. Often, however, incidents involving both things are found to be the cause.
PTSD is a condition distinct from traumatic stress, which has less intensity and duration, and combat stress reaction, which is transitory. PTSD has also been recognized in the past as railway spine, stress syndrome, shell shock, battle fatigue, traumatic war neurosis, or post-traumatic stress syndrome (PTSS).
Diagnostic symptoms include reexperience such as flashbacks and nightmares, avoidance of stimuli associated with the trauma, increased arousal such as difficulty falling or staying asleep, anger and hypervigilance. Per definition, the symptoms last more than six months and cause significant impairment in social, occupational, or other important areas of functioning (e.g. problems with work and relationships.)1
PTSD is believed to be caused by psychological trauma.1 Possible sources of trauma includes encountering or witnessing childhood or adult physical, emotional or sexual abuse.1 In addition, encountering or witnessing an event perceived as life-threatening such as physical assault, adult experiences of sexual assault, accidents, drug addiction, illnesses, medical complications, or employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers).
Traumatic events that may cause PTSD symptoms to develop include violent assault, kidnapping, sexual assault, torture, being a hostage, prisoner of war or concentration camp victim, experiencing a disaster, violent automobile accidents or getting a diagnosis of a life-threatening illness.1 Children may develop PTSD symptoms by experiencing sexually traumatic events like age-inappropriate sexual experiences.1
Witnessing traumatic experiences or learning about these experiences may also cause the development of PTSD symptoms.1 The amount of dissociation that follows directly after a trauma predicts PTSD: individuals who are more likely to dissociate during a traumatic event are considerably more likely to develop chronic PTSD.4
Members of the Marines and Army are much more likely to develop PTSD than Air Force and Navy personnel, because of greater exposure to combat.1 A preliminary study found that mutations in a stress-related gene interact with child abuse to increase the risk of PTSD in adults.567
PTSD sufferers re-experience the traumatic event or events in some way. As a result, they tend to avoid places, people, or other things that remind them of the event, and are exquisitely sensitive to normal life experiences. Untreated Post Traumatic Stress Disorder can have devastating, far-reaching consequences for sufferers’ functioning in relationships, their families, and in society.
PTSD displays biochemical changes in the brain and body that differ from other psychiatric disorders such as major depression. Individuals diagnosed with PTSD respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression.89
In addition, most PTSD also show a low secretion of cortisol and high secretion of catecholamines in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals.10 This is in contrast to the normative fight-or-flight response, in which both catecholamine and cortisol levels are elevated after exposure to a stressor.
Brain catecholamine levels are low,11 and corticotropin-releasing factor (CRF) concentrations are high.1213 Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis.
Given the strong cortisol suppression to dexamethasone in PTSD, HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors.14 Some researchers have associated the response to stress in PTSD with long-term exposure to high levels of norepinephrine and low levels of cortisol, a pattern associated with improved learning in animals.
Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive and hyperresponsive HPA axis.15
Low cortisol levels may predispose individuals to PTSD; following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels.16 Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for PTSD.
However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. Only a slight majority have found a decrease in cortisol levels while others have found no effect or even an increase.17
In addition to biochemical changes, PTSD also involves changes in brain morphology. In a study by Gurvits et al., Combat veterans of the Vietnam war with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans who suffered no such symptoms.18
In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD.
The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition.
PTSD potential can be hereditary: For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin having PTSD compared to twins that were dizygotic (non-identical twins).19 Because of the difficulty in performing genetic studies on a condition with a major environmental factor (e.g., trauma), genetic studies of PTSD are in their infancy.
Recently, it has been found that several single nucleotide polymorphisms (SNPs) in FK506 binding protein 5 (FKBP5) interact with childhood trauma to predict severity of adult PTSD.20 These findings suggest that individuals with these SNPs who are abused as children are more susceptible to PTSD as adults.
This is particularly interesting given that FKBP5 SNPs have previously been associated with peritraumatic dissociation (that is, dissociation at the time of the trauma),21 which has itself been shown to be predictive of PTSD.2223
Risk and Protective Factors for PTSD Development
Although most people (50-90%) encounter trauma over a lifetime,2425 only about 8% develop full PTSD.24 Vulnerability to PTSD presumably stems from an interaction of biological diathesis, early childhood developmental experiences, and trauma severity.
Predictor models have consistently found that childhood trauma, chronic adversity, and familial stressors increase risk for PTSD as well as risk for biological markers of risk for PTSD after a traumatic event in adulthood.26272829 This effect of childhood trauma, which is not well understood, may be a marker for both traumatic experiences and attachment problems.3031
Proximity to, duration of, and severity of the trauma also make an impact; and interpersonal traumas cause more problems than impersonal ones.32
Schnurr, Lunney, and Sengupta identified risk factors for the development of PTSD in Vietnam veterans. Among those are:
• Hispanic ethnicity, coming from an unstable family, being punished severely during childhood, childhood asocial behavior and depression as pre-military factors
• war-zone exposure, peritraumatic dissociation, depression as military factors
• recent stressful life events, post-Vietnam trauma and depression as post-military factors
They also identified certain protective factors, such as:
• Japanese-American ethnicity, high school degree or college education, older age at entry to war, higher socioeconomic status and a more positive paternal relationship as pre-military protective factors
• Social support at homecoming and current social support as post-military factors.33 Other research also indicates the protective effects of social support in averting and recovery from PTSD.3435
There may also be an attitudinal component; for example, a soldier who believes that they will not sustain injuries may be more likely to develop symptoms of PTSD than one who anticipates the possibility, should either be wounded. Likewise, the later incidence of suicide among those injured in home fires above those injured in fires in the workplace suggests this possibility.
The diagnostic criteria for PTSD, per the Diagnostic and Statistical Manual of Mental Disorders IV (Text Revision) (DSM-IV-TR), may be summarized as:1
A. Exposure to a traumatic event
B. Persistent reexperience (e.g. flashbacks, nightmares)
C. Persistent avoidance of stimuli associated with the trauma (e.g. inability to talk about things even related to the experience, avoidance of things and discussions that trigger flashbacks and reexperiencing symptoms fear of losing control)
D. Persistent symptoms of increased arousal (e.g. difficulty falling or staying asleep, anger and hypervigilance)
E. Duration of symptoms more than 1 month
F. Significant impairment in social, occupational, or other important areas of functioning (e.g. problems with work and relationships.)
Notably, criterion A (the “stressor”) consists of two parts, both of which must apply for a diagnosis of PTSD. The first (A1) requires that “the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others.”
The second (A2) requires that “the person’s response involved intense fear, helplessness, or horror.” The DSM-IV-TR criterion differs substantially from the previous DSM-III-R stressor criterion, which specified the traumatic event should be of a type that would cause “significant symptoms of distress in almost anyone,” and that the event was “outside the range of usual human experience.”
Since the introduction of DSM-IV, the number of possible PTSD traumas has increased and one study suggests that the increase is around 50%.36 Various scales exist to measure the severity and frequency of PTSD symptoms.3738
Many forms of psychotherapy have been advocated for trauma-related problems such as PTSD. Basic counseling for PTSD includes education about the condition and provision of safety and support.39
Cognitive therapy shows good results,40 and group therapy may be helpful in reducing isolation and social stigma.41 The psychotherapy programs with the strongest demonstrated efficacy include cognitive behavioral programs, variants of exposure therapy, stress inoculation training (SIT), variants of cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR), and many combinations of these procedures.4243 Psychodynamic psychotherapy, while widely employed, has not been well tested as a treatment for PTSD.
Exposure involves assisting trauma survivors to therapeutically confront distressing trauma-related memories and reminders in order to facilitate habituation and successful emotional processing of the trauma memory. Most exposure therapy programs include both imaginal confrontation with the traumatic memories and real-life exposure to trauma reminders.
Indeed, the success of exposure-based therapies has raised the question of whether exposure is a necessary ingredient in the treatment of PTSD. Some organizations have endorsed the need for exposure.4445 Yet other approaches, particularly involving social supports,3435 may also be important.
Critical Incident Stress Management
Early intervention after a traumatic incident,48 known as Critical Incident Stress Management (CISM) is used to attempt to reduce traumatic effects of an incident, and potentially prevent a full-blown occurrence of PTSD. However, recent studies regarding CISM seem to indicate iatrogenic effects.4950
Six studies have formally looked at the effect of CISM, four finding no benefit for preventing PTSD, and the other two studies indicating that CISM actually made things worse. Hence this is not a recommended treatment.
Some benefit was found from being connected early to cognitive behavioral therapy, or for some medications such as propranolol. Effects of all these prevention strategies was modest.51
Eye Movement Desensitization and Reprocessing
Eye Movement Desensitization and Reprocessing (EMDR) is specifically targeted as a treatment for PTSD.52 Research on EMDR is largely supported by those with the copyright for EMDR and third-party studies of its effectiveness are lacking, but a meta-analytic comparison of EMDR and cognitive behavioral therapy found both protocols indistinguishable in terms of effectiveness in treating PTSD.53
Comorbid Substance Dependence
Recovery from post traumatic stress disorder or other anxiety disorders may be hindered or even worsened by alcohol or benzodiazepine dependence. Treating comorbid substance dependences particularly alcohol or benzodiazepine dependence can bring about a marked improvement in the patients mental health status and anxiety levels. Recovery from benzodiazepines tends to take a lot longer than recovery from alcohol but people can regain their previous good health. Symptoms may temporarily worsen however, during alcohol withdrawal or benzodiazepine withdrawal.54
See also: Self-medication When considering any treatment it is important to consider validity ratings and testing protocols used. For example rapid eye movement has a low validity rating and genuine attmepts to falsify CBT have shown it to have results not more effective than drugs or placibo.
Medications have shown benefit in reducing PTSD symptoms, but rarely achieve complete remission. Standard medication therapy useful in treating PTSD includes SSRIs (selective serotonin reuptake inhibitors) and TCAs (tricyclic antidepressants).
Tricyclics tend to be associated with greater side effects and lesser improvement of the three PTSD symptom clusters than SSRIs. SSRIs for which there are data to support use include: citalopram, escitalopram, fluvoxamine, paroxetine and sertraline.55565758
There are data to support the use of “autonomic medicines” such as Propranolol (beta blocker) and Clonidine (alpha-adrenergic agonist) if there are significant symptoms of “over-arousal”. These may inhibit the formation of traumatic memories by blocking adrenaline’s effects on the amygdala, has been used in an attempt to reduce the impact of traumatic events.59 or they may simply demonstrate to the patient that the symptoms can be controlled thereby assisting with “self efficacy” and helping the patient remain calmer.
There are also data to support the use of mood-stabilizers such lithium carbonate, divalproex sodium and carbamazepine if there is significant uncontrolled mood or aggression. Risperidone is used to help with dissociation, mood and aggression, and benzodiazepines are used for short-term anxiety relief.60
There is some evidence suggesting that administering glucocorticoids immediately after a traumatic experience may help prevent PTSD. Several studies have shown that patients who receive high doses of hydrocortisone for treatment of septic shock or following surgery have a lower incidence and fewer symptoms of PTSD.616263 Additionally, post-stress high dose corticosterone administration was recently found to reduce ‘PTSD-like’ behaviors in a rat model of PTSD. In this study, corticosterone impaired memory performance, suggesting that it may reduce risk for PTSD by interfering with consolidation of traumatic memories.64
While MDMA (methylenedioxymethamphetamine, commonly known as Ecstasy) had its first exposure to the psychiatric community in the 1960s, gaining a reputation for its communication enhancing qualities, it hasn’t been until recent years that formal studies have been carried out. The US Food and Drug Administration (FDA) recently approved a clinical protocol that combines the drug MDMA with talk therapy sessions.65
Funded by the non-profit Multidisciplinary Association for Psychedelic Studies (MAPS),66 the studies are taking place in South Carolina under the supervision and direction of Dr. Michael Mithoefer. Other PTSD/MDMA research include a pilot study in Switzerland, co-sponsored by MAPS and the Swiss Medical Association for Psycholytic Therapy (SAePT),67 and another study approved in Israel to investigate MDMA as a tool in the psychotherapeutic treatment of crime and terrorism-related PTSD.68
There are several features of MDMA that make it an excellent candidate for treating PTSD in psychotherapy. The effects of MDMA are such that activity in the left amygdala,69 responsible for fear and anxiety, decreases in rats.
This makes it a promising candidate as a tool in psychotherapy, allowing the patient to explore and examine their trauma (and accompanying emotions) without the fear and retraumatization encountered without drug. Ordinarily incapacitated by the resurgence of emotions (fear, shame, anger) attached to the trauma, subjects are rendered capable of approaching their trauma in a new and constructive way.
Further helpful in treating PTSD, is the new capacity to experience empathy and compassion for both others and the self.70
MDMA still holds controversy as being listed for anxiolytic purposes in many forums and sites such as wikipedia. See Anxiolytic
PTSD is commonly treated using a combination of psychotherapy (cognitive-behavioral therapy, group therapy, and exposure therapy are popular) and medications such as antidepressants (e.g. SSRIs such as fluoxetine and sertraline, SNRI’s such as venlafaxine, NaSSA’s such as mirtazapine and tricyclic antidepressant such as amitriptyline71) or atypical antipsychotic drugs (such as quetiapine and olanzapine).72
Recently the anticonvulsant lamotrigine has been reported to be useful in treating some people with PTSD.737475 Geodon (ziprasidone) is one of the most effective treatments shown to work 89% of the time in PTSD patients.76 Geodon works by blocking two of the fight-or-flight chemicals (catecholamines): norepinephrine (noradrenaline) and dopamine.77
Carrot of Hope has been promoting the benefits of combining Geodon with the beta-adrenergic blocker propranolol to create a PTSD cocktail. Since propranolol works by blocking the third catecholamine, epinephrine (adrenaline),78 the combination of the two medicines work to block all three fight-or-flight chemicals. Propranolol (40 mg) has been commonly prescribed off-label for stage fright in the late 1970s.7980
The television show 60 Minutes featured propranolol where low doses (10-20 mg) used in research have been shown to stop panic attacks and reduce the impact of traumatic memories. As propranolol lasts in the system for 4 hours, the study dosages are typically given 4 times a day to cover a 16 hour span.81
Alpha-adrenergic blocker prazosin has also shown impressive effects in PTSD patients, curbing brain damage and reducing nightmares.8283 Unlike propranolol, prazosin acts on norepinephrine and, therefore, is contraindicated for use with Geodon.
Attachment- and relationship-based treatments are also often used.8485 In these cases, the treatment of complex trauma often requires a multi-modal approach. Yoga Nidra has been used to help soldiers cope with the symptoms of PTSD.86 Vipassanā Meditation has also generated positive results, having been known to end symptoms such as the exaggerated startle response characteristic of PTSD. Continuing practice of Vipassana meditation has also been shown to reverse the kinds of physical changes in the brain that are found in PTSD sufferers. 87
PTSD may be experienced following any traumatic experience, or series of experiences that satisfy the criteria and that do not allow the victim to readily recuperate from the detrimental effects of stress. The National Comorbidity Survey Report provided the following information about PTSD in the general adult population: The estimated lifetime prevalence of PTSD among adult Americans is 7.8%, with women (10.4%) twice as likely as men (5%) to have PTSD at some point in their lives.24
The National Vietnam Veterans’ Readjustment Study (NVVRS) found 15.2% of male and 8.5% of female Vietnam Vets to suffer from current PTSD at the time of the study. Life-Time prevalence of PTSD was 30.9 for males and 26.9 for females. In a reanalysis of the NVVRS data, along with analysis of the data from the Matsunaga Vietnam Veterans Project, Schnurr, Lunney, Sengupta, and Waelde found that, contrary to the initial analysis of the NVVRS data, a large majority of Vietnam veterans suffered from PTSD-symptoms. Four out of five reported recent symptoms when interviewed 20-25 years after Vietnam.33
In recent history, catastrophes (by human means or not) such as the Indian Ocean Tsunami Disaster may have caused PTSD in many survivors and rescue workers. Today relief workers from organizations such as the Red Cross and the Salvation Army provide counseling after major disasters as part of their standard procedures to curb severe cases of post-traumatic stress disorder.
There is debate over the rates of PTSD found in populations, but despite changes in diagnosis and the criteria used to define PTSD between 1997 and 2007, epidemiological rates have not changed significantly.2
Reports of battle-associated stress appear as early as the 6th century BC.88 Although PTSD-like symptoms have also been recognized in combat veterans of many military conflicts since, the modern understanding of PTSD dates from the 1970s, largely as a result of the problems that were still being experienced by Vietnam veterans.88
One of the first descriptions of PTSD was made by the Greek historian Herodotus. In 490 BCE he described, during the Battle of Marathon, an Athenian soldier who suffered no injury from war but became permanently blind after witnessing the death of a fellow soldier.89
The term post-traumatic stress disorder or PTSD was coined in the mid 1970s.88 Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.90 The term was formally recognized in 1980.88
(In the DSM-IV, which is considered authoritative, the spelling “posttraumatic stress disorder” is used. Elsewhere, “posttraumatic” is often rendered as two words — “post-traumatic stress disorder” or “post traumatic stress disorder” — especially in less formal writing on the subject.)
Veterans and Politics
The diagnosis was removed from the DSM-II, which resulted in the inability of Vietnam veterans to receive benefits for this condition. In part through the efforts of anti Vietnam war activists and the anti war group Vietnam Veterans Against the War and Chaim F. Shatan, who worked with them and coined the term Post-Vietnam Syndrome, the condition was added to the DSM-III as posttraumatic stress disorder.90
In the United States, the provision of compensation to veterans for PTSD is under review by the Department of Veterans Affairs (VA). The review was begun in 2005 after the VA had noted a 30% increase in PTSD claims in recent years. The VA undertook the review because of budget concerns and apparent inconsistencies in the awarding of compensation by different rating offices.
This led to a backlash from veterans’-rights groups, and to some highly-publicized suicides by veterans who feared losing their benefits, which in some cases constituted their only income. In response, on November 10, 2005, the Secretary of Veterans Affairs announced that “the Department of Veterans Affairs (VA) will not review the files of 72,000 veterans currently receiving disability compensation for post-traumatic stress disorder…”91
The diagnosis of PTSD has been a subject of some controversy due to uncertainties in objectively diagnosing PTSD in those who may have been exposed to trauma, and due to this diagnosis’ association with some incidence of compensation-seeking behavior.92
The social stigma of PTSD may result in under-representation of the disorder in military personnel, emergency service workers and in societies where the specific trauma-causing event is stigmatized (e.g. sexual assault).2
Many US veterans of the wars in Iraq and Afghanistan returning home have faced significant physical, emotional and relational disruptions. In response the United States Marine Corps has instituted programs to assist them in re-adjusting to civilian life – especially in their relationships with spouses and loved ones – to help them communicate better and understand what the other has gone through.85 Similarly, Walter Reed Army Institute of Research (WRAIR) developed the Battlemind program to assist service members avoid or ameliorate PTSD and related problems. In the UK there has been some controversy that National Health Service is dumping veterans on service charities like Combat Stress939495.
Veterans Affairs Canada is a new program including rehabilitation, financial benefits, job placement, health benefits program, disability awards and family support.96
In recent decades, with the concept of trauma and PTSD in particular becoming just as much a cultural phenomenon as a medical or legal one, artists have engaged the issue in their work. Many movies, such as First Blood, Birdy, Brothers, Coming Home, The Deer Hunter, Born on the Fourth of July, Heaven & Earth, and In the Valley of Elah deal with PTSD. It is an especially popular subject amongst “war veteran” films, often portraying Vietnam war veterans suffering from extreme PTSD and having difficulties adjusting to civilian life.
In more recent work, an example is that of Krzysztof Wodiczko who teaches at MIT and who is known for interviewing people and then projecting these interviews onto large public buildings.97 Wodiczko aims to bring trauma not merely into public discourse but to have it contest the presumed stability of cherished urban monuments. His work has brought to life issues such as homelessness, rape, and violence. Other artists who engage the issue of trauma are Everlyn Nicodemus of Tanzania and Milica Tomic of Serbia.98
George Carlin comments on the various incarnations of PTSD terminology on his 1990 album Parental Advisory: Explicit Lyrics. He traces the progression of what he views as euphemisms, which followed “shell shock” in World War I, “battle fatigue” in World War II, “operational exhaustion” in the Korean War, and finally PTSD, a clinical, hyphenated term, in the Vietnam War. “The pain is completely buried under jargon. Post-traumatic stress disorder. I’ll bet you if we’d have still been calling it shell shock, some of those Viet Nam veterans might have gotten the attention they needed at the time.” 99
1. ^ a b c d e f g h i American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. ISBN 0890420610.; on-line
2. ^ a b c Brunet A, Akerib V, Birmes P (2007). “Don’t throw out the baby with the bathwater (PTSD is not overdiagnosed)” (pdf). Can J Psychiatry 52 (8): 501–2; discussion 503. PMID 17955912. http://publications.cpa-apc.org/media.php?mid=490. Retrieved on 2008-03-12.
3. ^ David Satcher et al. (1999). “Chapter 4.2”. Mental Health: A Report of the Surgeon General. http://www.surgeongeneral.gov/library/mentalhea….
4. ^ Brown, Scheflin and Hammond (1998). Memory, Trauma Treatment, And the Law. New York, NY: W. W. Norton. ISBN 0-393-70254-5.
5. ^ Binder, MD. PhD, E. B.; Bradley, PhD, R. G.; Liu, PhD, W.; Epstein, PhD, M.; Deveau, BS, T.; Mercer, MPH, K.; Tang, MD, PhD, Y; Gillespie, MD, PhD, C.; Heim, PhD, C; Nemeroff, MD, C. ; Schwartz, MD, A.; Cubells, MD, PhD, J.; Ressler, MD, PhD, K. (March 19 2008). “Association of FKBP5 Polymorphisms and Childhood Abuse With Risk of Posttraumatic Stress Disorder Symptoms in Adults”. JAMA 299 (11): 1291–1305. doi:10.1001/jama.299.11.1291. PMID 18349090. http://jama.ama-assn.org/cgi/content/short/299/…. Retrieved on 2008-03-31.
6. ^ Peggy Peck, Executive Editor (2008-03-09). “Genes May Affect Lifelong Impact of Child Abuse”. MedPage Today. http://www.medpagetoday.com/Genetics/GeneticTes….
7. ^ Constance Holden (2008-03-18). “Seeds of PTSD Planted in Childhood”. ScienceNOW Daily News. http://sciencenow.sciencemag.org/cgi/content/fu…
8. ^ Yehuda R, Halligan SL, Golier JA, Grossman R, Bierer LM (2004). “Effects of trauma exposure on the cortisol response to dexamethasone administration in PTSD and major depressive disorder”. Psychoneuroendocrinology 29 (3): 389-404. PMID 14644068.
9. ^ Yehuda R, Halligan SL, Grossman R, Golier JA, Wong C (2002). “The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust aurvivors with and without posttraumatic stress disorder”. Biol Psychiatry 52 (5): 393-403. PMID 12242055.
10. ^ Mason JW, Giller EL, Kosten TR, Harkness L (1988). “Elevation of urinary norepinephrine/cortisol ratio in posttraumatic stress disorder”. J Nerv Ment Dis 176 (8): 498–502. doi:10.1097/00005053-198808000-00008. PMID 3404142.
11. ^ Geracioti TD Jr, Baker DG, Ekhator NN, West SA, Hill KK, Bruce AB, Schmidt D, Rounds-Kugler B, Yehuda R, Keck PE Jr, Kasckow JW (2001). “CSF norepinephrine concentrations in posttraumatic stress disorder”. Am J Psychiatry 158 (8): 1227-1230. PMID 11481155.
12. ^ Sautter FJ, Bisette G, Wiley J, Manguno-Mire G, Schoenbachler B, Myers L, Johnson JE, Cerbone A, Malaspina D (2003). “Corticotropin-releasing factor in posttraumatic stress disorder with secondary psychotic symptoms, nonpsychotic PTSD, and healthy control subjects”. Biol Psychiatry 54 (12): 1382–8. doi:10.1016/S0006-3223(03)00571-7. PMID 14675802.
13. ^ de Kloet CS, Vermetten E, Geuze E, Lentjes EG, Heijnen CJ, Stalla GK, Westenberg HG (2008). “Elevated plasma corticotrophin-releasing hormone levels in veterans with posttraumatic stress disorder”. Prog Brain Res 167: 287–91. PMID 18037027.
14. ^ Yehuda R (2001). “Biology of posttraumatic stress disorder”. J Clin Psychiatry 62 Suppl 17: 41–6. PMID 11495096.
15. ^ Yehuda R (2002). “Clinical relevance of biologic findings in PTSD”. Psychiatr Q 73 (2): 123–33. doi:10.1023/A:1015055711424. PMID 12025720.
16. ^ Aardal-Eriksson E, Eriksson TE, Thorell LH (2001). “Salivary cortisol, posttraumatic stress symptoms, and general health in the acute phase and during 9-month follow-up”. Biol. Psychiatry 50 (12): 986–93. doi:10.1016/S0006-3223(01)01253-7. PMID 11750895.
17. ^ Lindley SE, Carlson EB, Benoit M (2004). “Basal and dexamethasone suppressed salivary cortisol concentrations in a community sample of patients with posttraumatic stress disorder”. Biol. Psychiatry 55 (9): 940–5. doi:10.1016/j.biopsych.2003.12.021. PMID 15110738.
18. ^ Carlson, Neil R. (2007). Physiology of Behavior (9 ed.). Pearson Education, Inc.
19. ^ True WR, Rice J, Eisen SA, et al (1993). “A twin study of genetic and environmental contributions to liability for posttraumatic stress symptoms”. Arch. Gen. Psychiatry 50 (4): 257–64. PMID 8466386.
20. ^ Binder EB, Bradley RG, Liu W, et al (2008). “Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults”. JAMA 299 (11): 1291–305. doi:10.1001/jama.299.11.1291. PMID 18349090.
21. ^ Koenen KC, Saxe G, Purcell S, et al (2005). “Polymorphisms in FKBP5 are associated with peritraumatic dissociation in medically injured children”. Mol Psychiatry 10 (12): 1058–9. doi:10.1038/sj.mp.4001727. PMID 16088328.
22. ^ Birmes P, Brunet A, Carreras D, et al (2003). “The predictive power of peritraumatic dissociation and acute stress symptoms for posttraumatic stress symptoms: a three-month prospective study”. Am J Psychiatry 160 (7): 1337–9. doi:10.1176/appi.ajp.160.7.1337. PMID 12832251.
23. ^ Schnurr PP, Lunney CA, Sengupta A (2004). “Risk factors for the development versus maintenance of posttraumatic stress disorder”. J Trauma Stress 17 (2): 85–95. doi:10.1023/B:JOTS.0000022614.21794.f4. PMID 15141781.
24. ^ a b c Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB (December 1995). “Posttraumatic stress disorder in the National Comorbidity Survey”. Arch Gen Psychiatry 52 (12): 1048–60. PMID 7492257.
25. ^ Breslau N, Kessler RC, Chilcoat HD, Schultz LR, Davis GC, Andreski P (July 1998). “Trauma and posttraumatic stress disorder in the community: the 1996 Detroit Area Survey of Trauma”. Arch Gen Psychiatry 55 (7): 626–32. doi:10.1001/archpsyc.55.7.626. PMID 9672053. http://archpsyc.ama-assn.org/cgi/pmidlookup?vie…
26. ^ Koenen KC, Moffitt TE, Poulton R, Martin J, Caspi A (February 2007). “Early childhood factors associated with the development of post-traumatic stress disorder: results from a longitudinal birth cohort”. Psychol Med 37 (2): 181–92. doi:10.1017/S0033291706009019. PMID 17052377.
27. ^ Lapp KG, Bosworth HB, Strauss JL, et al (September 2005). “Lifetime sexual and physical victimization among male veterans with combat-related post-traumatic stress disorder”. Mil Med 170 (9): 787–90. PMID 16261985.
28. ^ Otte C, Neylan TC, Pole N, et al (January 2005). “Association between childhood trauma and catecholamine response to psychological stress in police academy recruits”. Biol. Psychiatry 57 (1): 27–32. doi:10.1016/j.biopsych.2004.10.009. PMID 15607297.
29. ^ Resnick HS, Yehuda R, Pitman RK, Foy DW (November 1995). “Effect of previous trauma on acute plasma cortisol level following rape”. Am J Psychiatry 152 (11): 1675–7. PMID 7485635. http://ajp.psychiatryonline.org/cgi/pmidlookup?…
30. ^ Laor N, Wolmer L, Mayes LC, et al (May 1996). “Israeli preschoolers under Scud missile attacks. A developmental perspective on risk-modifying factors”. Arch Gen Psychiatry 53 (5): 416–23. PMID 8624185.
31. ^ Laor N, Wolmer L, Mayes LC, Gershon A, Weizman R, Cohen DJ (March 1997). “Israeli preschool children under Scuds: a 30-month follow-up”. J Am Acad Child Adolesc Psychiatry 36 (3): 349–56. doi:10.1097/00004583-199703000-00013. PMID 9055515. http://meta.wkhealth.com/pt/pt-core/template-jo…
32. ^ Janoff-Bulman R: Shattered Assumptions: Toward a New Psychology of Trauma. New York: Free Press, 1992
33. ^ a b Jennifer L. Price, Ph.D.: Findings from the National Vietnam Veterans’ Readjustment Study – Factsheet. National Center for PTSD. United States Department of Veterans Affairs 1
34. ^ a b Brewin CR, Andrews B, Valentine JD (October 2000). “Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults”. J Consult Clin Psychol 68 (5): 748–66. doi:10.1037/0022-006X.68.5.748. PMID 11068961. http://content.apa.org/journals/ccp/68/5/748.
35. ^ a b Ozer EJ, Best SR, Lipsey TL, Weiss DS (January 2003). “Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis”. Psychol Bull 129 (1): 52–73. doi:10.1037/0033-2909.129.1.52. PMID 12555794. http://content.apa.org/journals/bul/129/1/52.
36. ^ Breslau N, Kessler RC (2001). “The stressor criterion in DSM-IV posttraumatic stress disorder: an empirical investigation”. Biol. Psychiatry 50 (9): 699–704. doi:10.1016/S0006-3223(01)01167-2. PMID 11704077.
37. ^ Blake DD, Weathers FW, Nagy LM, et al (January 1995). “The development of a Clinician-Administered PTSD Scale”. J Trauma Stress 8 (1): 75–90. PMID 7712061.
38. ^ Foa E: The Post Traumatic Diagnostic Scale Manual. Minneapolis, NCS, 1995
39. ^ Foa 1997
40. ^ Resick 2002
41. ^ Foy 2002
42. ^ Cahill, S. P., & Foa, E. B. (2004). A glass half empty or half full? Where we are and directions for future research in the treatment of PTSD. In S. Taylor (ed.), Advances in the Treatment of Posttraumatic Stress Disorder: Cognitive-behavioral perspectives (pp. 267-313) New York: Springer.
43. ^ Brom D, Kleber RJ, Defares PB (October 1989). “Brief psychotherapy for posttraumatic stress disorders”. J Consult Clin Psychol 57 (5): 607–12. doi:10.1037/0022-006X.57.5.607. PMID 2571625. http://content.apa.org/journals/ccp/57/5/607.
44. ^ Ursano RJ, Bell C, Eth S, et al (November 2004). “Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress disorder”. Am J Psychiatry 161 (11 Suppl): 3–31. doi:10.1176/appi.ajp.161.1.3. PMID 15617511.
45. ^ Committee on Treatment of Posttraumatic Stress Disorder, Institute of Medicine: Treatment of Posttraumatic Stress Disorder: An Assessment of the Evidence. Washington, D.C.: National Academies Press, 2008 ISBN -10: 0-309-10926-4
46. ^ Weissman MM, Markowitz JC, Klerman GL: Clinician’s Quick Guide to Interpersonal Psychotherapy. New York: Oxford University Press, 2007
47. ^ Bleiberg KL, Markowitz JC (January 2005). “A pilot study of interpersonal psychotherapy for posttraumatic stress disorder”. Am J Psychiatry 162 (1): 181–3. doi:10.1176/appi.ajp.162.1.181. PMID 15625219.
48. ^ Brown, Asa Don Ph.D., “The effects of childhood trauma on adult perception and worldview”, Capella University, 2008, 152 pages; AAT 3297512
49. ^ Carlier, IVE; Lamberts RD; van Uchelen AJ; Gersons BPR (1998). “Disaster-related post-traumatic stress in police officers: A field study of the impact of debriefing”. Stress Medicine 14 (3): 143–8. doi:10.1002/(SICI)1099-1700(199807)14:3<143::AID-SMI770>3.0.CO;2-S. http://doi.apa.org/?uid=1998-10258-001.
50. ^ Mayou RA, Ehlers A, Hobbs M (2000). “Psychological debriefing for road traffic accident victims. Three-year follow-up of a randomised controlled trial”. Br J Psychiatry 176: 589–93. doi:10.1192/bjp.176.6.589. PMID 10974967.
51. ^ Feldner MT, Monson CM, Friedman MJ (2007). “A critical analysis of approaches to targeted PTSD prevention: current status and theoretically derived future directions”. Behav Modif 31 (1): 80–116. doi:10.1177/0145445506295057. PMID 17179532.
52. ^ Devilly GJ, Spence SH (1999). “The relative efficacy and treatment distress of EMDR and a cognitive-behavior trauma treatment protocol in the amelioration of posttraumatic stress disorder”. J Anxiety Disord 13 (1-2): 131–57. doi:10.1016/S0887-6185(98)00044-9. PMID 10225505.
53. ^ Seidler GH, Wagner FE (2006). “Comparing the efficacy of EMDR and trauma-focused cognitive-behavioral therapy in the treatment of PTSD: a meta-analytic study”. Psychol Med 36 (11): 1515–22. doi:10.1017/S0033291706007963. PMID 16740177.
54. ^ Cohen SI (February 1995). “Alcohol and benzodiazepines generate anxiety, panic and phobias”. J R Soc Med 88 (2): 73–7. PMID 7769598.
55. ^ Yehuda R (2000). “Biology of posttraumatic stress disorder”. J Clin Psychiatry 61 (Suppl 7): 14–21. PMID 10795605.
56. ^ Marshall RD, Beebe KL, Oldham M, Zaninelli R (December 2001). “Efficacy and safety of paroxetine treatment for chronic PTSD: a fixed-dose, placebo-controlled study”. Am J Psychiatry 158 (12): 1982–8. doi:10.1176/appi.ajp.158.12.1982. PMID 11729013. http://ajp.psychiatryonline.org/cgi/pmidlookup?…
57. ^ Brady K, Pearlstein T, Asnis GM, et al (April 2000). “Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial”. JAMA 283 (14): 1837–44. doi:10.1001/jama.283.14.1837. PMID 10770145. http://jama.ama-assn.org/cgi/pmidlookup?view=lo…
58. ^ Davidson JR, Rothbaum BO, van der Kolk BA, Sikes CR, Farfel GM (May 2001). “Multicenter, double-blind comparison of sertraline and placebo in the treatment of posttraumatic stress disorder”. Arch Gen Psychiatry 58 (5): 485–92. doi:10.1001/archpsyc.58.5.485. PMID 11343529. http://archpsyc.ama-assn.org/cgi/pmidlookup?vie…
59. ^ Pitman RK, Sanders KM, Zusman RM, et al (2002). “Pilot study of secondary prevention of posttraumatic stress disorder with propranolol”. Biol. Psychiatry 51 (2): 189–92. doi:10.1016/S0006-3223(01)01279-3. PMID 11822998.
60. ^ Reist C (2005) Post-traumatic Stress Disorder. Compendia, Build ID: F000005, published by Epocrates.com
61. ^ Schelling G, Roozendaal B, Krauseneck T, Schmoelz M, DE Quervain D, Briegel J. (2006). “Efficacy of hydrocortisone in preventing posttraumatic stress disorder following critical illness and major surgery.”. Ann N Y Acad Sci 1071: 46-53. PMID 16891561.
62. ^ Weis F, Kilger E, Roozendaal B, de Quervain DJ, Lamm P, Schmidt M, Schmölz M, Briegel J, Schelling G. (2006). “Stress doses of hydrocortisone reduce chronic stress symptoms and improve health-related quality of life in high-risk patients after cardiac surgery: a randomized study.”. J Thorac Cardiovasc Surg 131 (2): 277-282. PMID 16434254.
63. ^ Schelling G, Kilger E, Roozendaal B, de Quervain DJ, Briegel J, Dagge A, Rothenhäusler HB, Krauseneck T, Nollert G, Kapfhammer HP. (2004). “Stress doses of hydrocortisone, traumatic memories, and symptoms of posttraumatic stress disorder in patients after cardiac surgery: a randomized study.”. Biol Psychiatry 55 (6): 627-633. PMID 15013832.
64. ^ Cohen H, Matar MA, Buskila D, Kaplan Z, Zohar J. (2008). “Early post-stressor intervention with high-dose corticosterone attenuates posttraumatic stress response in an animal model of posttraumatic stress disorder.”. Biol Psychiatry 64 (8): 708-717. PMID 18635156.
65. ^ MAPS FDA and IRB approved MDMA/PTSD protocol
66. ^ [www.maps.org]
67. ^ http://www.maps.org/mdma/swissmdmaptsd/protocol…
68. ^ MDMA-assisted Psychotherapy in Twelve People with War and Terrorism-related PTSD
69. ^ http://www.maps.org/research/mdma/ptsd_study/tr…
70. ^ “Ecstasy is the Key to Treating PTSD”. Times Online. 2008-05-04. http://www.timesonline.co.uk/tol/life_and_style…. Retrieved on 2009-03-08.
71. ^ National Institute for Clinical Excellence: The Treatment of PTSD in Adults and Children
72. ^ Schatzberg, Alan F.; Jonathan O. Cole, Charles DeBattista (2007). Manual of Clinical Psychopharmacology. American Psychiatric Pub, Inc.. ISBN 1585623172.
73. ^ “Lamotrigine FAQ”. http://www.psycom.net/depression.central.lamotr…. Retrieved on 2007-05-01.
74. ^ SSRIs versus Non-SSRIs in Post-traumatic Stress Disorder, Department of Psychiatry and Behavioral Sciences, Montefiore Medical Center, Albert Einstein College of Medicine
75. ^ Hertzberg MA, Butterfield MI, Feldman ME, et al (May 1999). “A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder”. Biol. Psychiatry 45 (9): 1226–9. doi:10.1016/S0006-3223(99)00011-6. PMID 10331117. http://linkinghub.elsevier.com/retrieve/pii/S00….
76. ^ Annitto W (September 2005). “Ziprasidone treatment for posttraumatic stress disorder: 128 cases”. Psychiatry 2 (9): 19. ISSN 1045-7860. http://www.psychiatrymmc.com/displayArticle.cfm…
77. ^ “Geodon pharmacology FAQ”. https://www.pfizerpro.com/product_info/geodon_p…. Retrieved on 2008-07-24.
78. ^ “Propranolol pharmacology FAQ”. http://dailymed.nlm.nih.gov/dailymed/drugInfo.c… Retrieved on 2008-07-24.
79. ^ Brantigan CO, Brantigan TA, Joseph N (January 1982). “Effect of beta blockade and beta stimulation on stage fright”. Am J Med. 72 (1): 88–94. doi:10.1016/0002-9343(82)90592-7. PMID 6120650. http://linkinghub.elsevier.com/retrieve/pii/000….
80. ^ Gates GA, Saegert J, Wilson N, Johnson L, Shepherd A, Hearne EM (1985). “Effect of beta blockade on singing performance”. Ann Otol Rhinol Laryngol. 94 (6 Pt 1): 570–4. PMID 2866749.
81. ^ “A Pill to Calm Traumatic Memories FAQ”. http://www.hno.harvard.edu/gazette/2004/03.18/0…. Retrieved on 2008-07-24.
82. ^ “Prazosin curbs brain damage from PTSD FAQ”. http://www.news-medical.net/?id=32288. Retrieved on 2008-07-24.
83. ^ “Prazosin drug helps post-traumatic stress nightmares FAQ”. http://www.news-medical.net/?id=23491. Retrieved on 2008-07-24.
84. ^ Johnson, Susan (2005). Emotionally Focused Couple Therapy with Trauma Survivors: Strengthening Attachment Bonds (Guilford Family Therapy Series). New York: The Guilford Press. ISBN 1-59385-165-0.
85. ^ a b ""Marine Corps Offers Yoga, Massages to Marriages Strained by War"". Associated Press. 2008-04-02. http://www.foxnews.com/story/0,2933,344991,00.html. Retrieved on 2008-04-03.
86. ^ Eileen Rivers, Washington Post, Tuesday, May 6, 2008; Page HE01
87. ^ http://www.psychosomaticmedicine.org/cgi/conten…
88. ^ a b c d When trauma tips you over: PTSD Part 1 All in the Mind, Australian Broadcasting Commission, 9 October 2004
89. ^ Swartz’ Textbook of Physical Diagnosis: History and Examination
90. ^ a b Shalev, Arieh Y.; Yehuda, Rachel; Alexander C. McFarlane (2000). International handbook of human response to trauma. New York: Kluwer Academic/Plenum Press. ISBN 0-306-46095-5.; on-line
91. ^ United States Department of Veteran Affairs
92. ^ Vedantam, Shankar (2005-12-27). “A Political Debate On Stress Disorder: As Claims Rise, VA Takes Stock”. The Washington Post. http://www.washingtonpost.com/wp-dyn/content/ar…. Retrieved on 2008-03-12.
93. ^ http://www.dailymail.co.uk/news/article-1158350…
94. ^ http://www.timesonline.co.uk/tol/news/politics/…
95. ^ http://news.bbc.co.uk/1/hi/uk/7916852.stm
96. ^ VAC-ACC.GC.CA
97. ^ Mark Jarzombek (2006). “The Post-traumatic Turn and the Art of Walid Ra’ad and Krzysztof Wodiczko: from Theory to Trope and Beyond”. in Rosenberg E, Saltzman L. Trauma and Visuality in Modernity (Interfaces: Studies in Visual Culture). Dartmouth College Press. ISBN 1-58465-516-X.
98. ^ Elizabeth Cowie, “Perceiving Memory and Tales of the Other: the work of Milica Tomic,” Camera Austria, no. [?], pp. 14-16.
99. ^ George Carlin – Parental Advisory Explicit Lyrics
Article Reference: http://en.wikipedia.org/wiki/Posttraumatic_stress_disorder