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Post-Traumatic Stress Disorder (PTSD) is an anxiety disorder that can develop after exposure to a terrifying event or ordeal in which grave physical harm occurred or was threatened.[1] It is a severe and ongoing emotional reaction to an extreme psychological trauma.[2] This stressor may involve someone's actual death or a threat to the patient's or someone else's life, serious physical injury, or threat to physical and/or psychological integrity, to a degree that usual psychological defenses are incapable of coping. PTSD is a condition distinct from Traumatic stress, which is of less intensity and duration, and combat stress reaction, which is transitory. The condition has also been recognized in the past as shell shock, traumatic war neurosis, or post-traumatic stress syndrome (PTSS).

Causes

Main article: Psychological trauma

PTSD is believed to be caused by psychological trauma. Possible sources of trauma includes experiencing or witnessing childhood or adult physical, emotional, or sexual abuse, or prolonged or extreme childhood neglect.[citation needed] In addition, experiencing or witnessing an event perceived as life-threatening such as physical assault, adult experiences of sexual assault, accidents, illnesses, medical complications, or the experience of, or employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers).

Mechanism

Neurochemistry

PTSD displays biochemical changes in the brain and body, which are different from other psychiatric disorders such as major depression; the discipline of biological psychiatry attempts to understand the relationship between mental disorders and biological functioning of the nervous system.

In PTSD patients, the dexamethasone cortisol suppression is strong, while it is weak in patients with major depression. In most PTSD patients the urine secretion of cortisol is low, at the same time as the catecholamine secretion is high, and the norepinephrine/cortisol ratio is increased. Brain catecholamine levels are low, and corticotropin-releasing factor (CRF) concentrations are high. There is also an increased sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis, with a strong negative feedback of cortisol, due to a generally increased sensitivity of cortisol receptors.[3]

In addition to biochemical changes, PTSD also involves changes in the brain itself. Combat veterans of the Vietnam war with PTSD showed an 8% reduction in the volume of their hippocampus in comparison with veterans who suffered no such symptoms.[citation needed]

Cortisol

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 facilitated learning in animals. Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response.[4] With this deduction follows that the clinical picture of hyperreactivity and hyperresponsiveness in PTSD is consistent with the sensitive HPA-axis.

Low cortisol levels are also discussed as a possible pre-existing condition that neurochemically predisposes a person to PTSD. Swedish United Nation 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.[5]

There is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relation between cortisol levels and PTSD. For example, only a slight majority of studies have found a decrease in cortisol levels; many others have found no effect or even an increase.[6]

Neuroanatomy

In animal research as well as 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.

Genetics

PTSD runs in families: 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).[7] Because of the difficulty in performing genetic studies on a condition with a major environmental factor (ie., trauma), genetic studies of PTSD are in their infancy.

Diagnosis

The diagnostic criteria for PTSD, per the Diagnostic and Statistical Manual of Mental Disorders IV (Text Revision) (DSM-IV-TR), may be summarized as:[8]

A. Exposure to a traumatic event
B. Persistent reexperience
C. Persistent avoidance of stimuli associated with the trauma
D. Persistent symptoms of increased arousal (e.g. difficulty falling or staying asleep or hypervigilance)
E. Duration of symptoms more than 1 month
F. Significant impairment in social, occupational, or other important areas of functioning

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%.[9]

Treatment

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.[10] Cognitive therapy shows good results,[11] and group therapy may be helpful in reducing isolation and social stigma.[12] The psychotherapy programs with the strongest demonstrated efficacy are all cognitive behavioral programs and include variants of exposure therapy, stress inoculation training (SIT), variants of cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR), and combinations of these procedures.[13] 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.

Critical incident stress management

Early intervention after a traumatic incident, known as Critical Incident Stress Management (CISM) is often used 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.[14][15] Six studies have formally looked at the effect of CISM, four finding that although patients and providers thought it was helpful, there was no benefit for preventing PTSD. Two other studies have indicated that CISM actually made things worse. 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.[16]

Eye movement desensitization and reprocessing

Eye Movement Desensitization and Reprocessing (EMDR) is specifically targetted as a treatment for PTSD.[17] 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.[18]

Medication

Propranolol, a beta blocker which appears to 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.[19]

Combination therapies

PTSD is commonly treated using a combination of psychotherapy (cognitive-behavioral therapy, group therapy, and exposure therapy are popular) and medications such as antidepressants (i.e. SSRI's such as fluoxetine and sertraline, SNRI's such as venlafaxine, and NaSSA's such as mirtazapine) or atypical antipsychotic drugs (such as quetiapine and olanzapine).[20] Recently the anticonvulsant lamotrigine has been reported to be useful in treating some people with PTSD.[21][22][23] The US Food and Drug Administration (FDA) recently approved a clinical protocol that combines the drug MDMA with talk therapy sessions.[24]

Other techniques

Relationship based treatments are also often used.[25] These, and other approaches, use attachment theory and an attachment model of treatment. In these cases, the treatment of complex trauma often requires a multi-modal approach.

Epidemiology

PTSD may be experienced following any traumatic experience, or series of experiences which 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.[citation needed]

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.[26]

History

Earliest reports

Reports of battle-associated stress appear as early as the 6th century BC.[27]

While PTSD-like symptoms have also been recognized in combat veterans of many military conflicts since then, the modern understanding of PTSD dates from the 1970s, largely as a result of the problems that were was still being experienced by Vietnam veterans.[27]

The term post-traumatic stress disorder or PTSD was created in the mid 1970s.[27] Early in 1978, the term was used in a working group finding presented to the Committee of Reactive Disorders.[28]

The term was formally recognised in 1980.[27]

Veterans and politics

Early cases of the disorder were recognized after World War I, including individuals treated by Sigmund Freud. 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 Chaim F. Shatan, who coined the term post-Vietnam Syndrome, the condition was added to the DSM-III as posttraumatic stress disorder.[28]

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..."[29]

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.[30]

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 (i.e. sexual assault).[26]

Canadian veterans

Veterans Affairs Canada is a new program including rehabilitation, financial benefits, job placement, health benefits program, disability awards and family support.[31]

Cultural references

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 begun to engage the issue in their work. Many movies 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.[32] 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.[33]

See also

Notes

  1. ^ National Institute of Mental Health, US National Institutes of Health
  2. ^ David Satcher; et al. (1999). "Chapter 4.2". Mental Health: A Report of the Surgeon General. {{cite book}}: Explicit use of et al. in: |author= (help)
  3. ^ Yehuda R (2001). "Biology of posttraumatic stress disorder". J Clin Psychiatry. 62 Suppl 17: 41–6. PMID 11495096.
  4. ^ Yehuda R (2002). "Clinical relevance of biologic findings in PTSD". Psychiatr Q. 73 (2): 123–33. PMID 12025720.
  5. ^ 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. PMID 11750895.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  8. ^ Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. 1994. ISBN 0890420610.; on-line
  9. ^ Breslau N, Kessler RC (2001). "The stressor criterion in DSM-IV posttraumatic stress disorder: an empirical investigation". Biol. Psychiatry. 50 (9): 699–704. PMID 11704077.
  10. ^ Foa 1997
  11. ^ Resick 2002
  12. ^ Foy 2002
  13. ^ 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.
  14. ^ Carlier, IVE (1998). "Disaster-related post-traumatic stress in police officers: A field study of the impact of debriefing". Stress Medicine. 14 (3): 143–8. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  15. ^ 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. PMID 10974967.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ 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. PMID 10225505.
  18. ^ 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.
  19. ^ 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. PMID 11822998. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  20. ^ Schatzberg, Alan F. (2007). Manual of Clinical Psychopharmacology. American Psychiatric Pub, Inc. ISBN 1585623172. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  21. ^ "Lamotrigine FAQ". Retrieved 2007-05-01.
  22. ^ SSRIs versus Non-SSRIs in Post-traumatic Stress Disorder, Department of Psychiatry and Behavioral Sciences, Montefiore Medical Center, Albert Einstein College of Medicine
  23. ^ A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder, Biol Psychiatry 1999 May 1;45(9):1226-9
  24. ^ MAPS FDA and IRB approved MDMA/PTSD protocol
  25. ^ Johnson, Susan. Emotionally Focused Couple Therapy with Trauma Survivors : Strengthening Attachment Bonds (Guilford Family Therapy Series). New York: The Guilford Press. ISBN 1-59385-165-0.
  26. ^ a b 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. Retrieved 2008-03-12.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ a b c d When trauma tips you over: PTSD Part 1 All in the Mind, Australian Broadcasting Commission, 9 October 2004
  28. ^ 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.{{cite book}}: CS1 maint: multiple names: authors list (link); on-line
  29. ^ United States Department of Veteran Affairs
  30. ^ Vedantam, Shankar (2005-12-27). "A Political Debate On Stress Disorder: As Claims Rise, VA Takes Stock". The Washington Post. Retrieved 2008-03-12.
  31. ^ VAC-ACC.GC.CA
  32. ^ Mark Jarzombek, "The Post-traumatic Turn and the Art of Walid Ra'ad and Krzysztof Wodiczko: from Theory to Trope and Beyond," in Trauma and Visuality, Saltzman, Lisa and Eric Rosenberg, editors (University Press of New England, 2006)
  33. ^ Elizabeth Cowie, "Perceiving Memory and Tales of the Other: the work of Milica Tomic," Camera Austria, no. [?], pp. 14-16.

References

  • Timothy Kendrick. PTSD: Pathways Through the Secret Door. Lulu.com. ISBN 1430313196.

Further reading

  • Shephard, Ben (2002). A war of nerves: soldiers and psychiatrists, 1914-1994. London: Pimlico. ISBN 0-7126-6783-0.
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