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Recognition and Treatment of Posttraumatic Stress Disorder

Recognition and Treatment of Posttraumatic Stress Disorder The reports on posttraumatic stress disorder (PTSD) in this issue of THE JOURNAL1-3 draw attention to 3 important facts: PTSD is a worldwide problem, reaching alarming proportions in countries torn by violent conflict; it is associated with persistent disability and comorbidity for many people; and treatments can produce a meaningful reduction in distress. These studies, which tell clinicians not to forget about PTSD, provide the opportunity to focus on what is known about PTSD as a medical problem, and its presentation, recognition, and management. Perhaps the 3 main lessons to be learned are that PTSD often presents in medical disguise, it is largely unrecognized, and it can be treated successfully. A Widespread Health Problem Posttraumatic stress disorder was first introduced as a diagnosis in 1980,4 but it has been slow to gain general acceptance. It has undergone some diagnostic modifications5,6 but remains in its essential features a disorder in which 1 or more traumatic events give rise to 4 symptom clusters: recurrent and painful reexperiencing of the event, phobic avoidance of trauma-related situations and memories, emotional numbing and withdrawal, and hyperarousal. In the US population, lifetime prevalence rates are in the range of 8%,7 with women affected twice as often as men. However, studies from other countries and studies of high-risk populations have reported widely ranging prevalence rates from a low of 1.3% in Germany8 to 37.4% in Algeria.3 It has been estimated that, on average, a person with PTSD will endure 20 years of active symptoms and will experience almost 1 day a week of work impairment, perhaps resulting in a $3 billion annual productivity loss in the United States.9 Rates of attempted suicide are as high as 19%.10 Besides being associated with increased risk for depression, anxiety, and alcohol or substance use disorders,7 PTSD is associated with higher rates of hypertension, bronchial asthma, and peptic ulcer10 and with other diseases of the cardiovascular, digestive, musculoskeletal, endocrine, respiratory, and nervous systems, as well as increased rates of infectious disease for up to 20 years following exposure to major trauma and after controlling for other variables.11 Adult survivors of childhood abuse, many of whom are likely to have experienced PTSD, have higher rates of smoking, sexually transmitted disease, severe obesity, ischemic heart disease, cancer, chronic obstructive pulmonary disease, fractures, and liver disease than the general population.12 The cost of PTSD exceeds that of all other anxiety disorders, and much of this expenditure is accounted for by direct costs of treatment seeking and medical evaluation.13 Recognition and Presentation People with PTSD might be expected to seek mental health treatment. However, evidence suggests that this is relatively uncommon14 and that, even in academic and community mental health settings,15,16 rates of recognition may be low with clinical diagnosis of PTSD occurring in as few as 4% of individuals with the disorder. In a national cohort of Israeli primary care patients, 9% met criteria for current PTSD, but only 2% of actual cases were recognized by their treating physicians. Although 49% of physicians recognized the existence of psychological distress, this rate was still far less than the 88% frequency of self-rated distress in the sample.17 In a US primary care survey,18 11.8% of patients met diagnostic criteria for full or partial PTSD. These findings are important since more than 70% of respondents with PTSD symptoms in the general population have used general medical services in the past 6 months.14 The question then arises as to how PTSD might be recognized and what are the likely disguises behind which it might be found. An unusually high rate of somatization disorder10 suggests that individuals with PTSD may be marked and persistent somatizers, a finding subsequently borne out in a study of women with a history of physical or sexual abuse who were seen in a gastrointestinal disorders clinic.17 Musculoskeletal, genitourinary, dermatologic, respiratory, panic, sleep-related, and appetite disturbances were commonly seen. The number of symptoms, as well as severity of abuse, explained much of the variance, accounting for subsequent physician visits during the next year. Such patients made 3 to 8 more health care visits per year than did women without abuse. High rates of PTSD also have been reported in association with irritable bowel syndrome.20 The notion that PTSD at times may be associated with "hypervigilance to symptoms" has been advanced and receives some support from a study of abuse survivors with gastroesophageal reflux who showed lower cutaneous sensitivity thresholds and hypervigilance in labeling stimuli as being painful. Their pain-coping mechanisms were considered to be poor.21 Another study22 has shown that heavy smoking is much more likely in trauma survivors with PTSD compared with those who had experienced similar trauma but did not have PTSD. Thus, in the health care system, PTSD or the role of trauma should be considered in patients experiencing prominent chronic pain or persistent somatization, especially when these symptoms are not otherwise fully accounted for. Posttraumatic stress syndrome can only be diagnosed if the existence of a traumatic event has been established. However, clinical suspicion may be warranted based on symptoms or behaviors even if no such event has yet been established. To elicit this information may in some cases be relatively straightforward. But in other cases, it will be more difficult, requiring the establishment of trust and confidence between patient and physician and requiring the physician's unwillingness to accept initial denial as being the final answer in some cases. Suggested approaches to uncovering a trauma have been described.23,24 For example, in the case of suspected domestic violence, the physician, when alone with the patient, should raise the concern that the patient's medical problems might be related to injury inflicted by another person. The patient may be asked if he or she feels safe at home. Routine questioning about trauma has been suggested along the lines of inquiring about whether a traumatic event has ever been experienced and whether the experience is still upsetting to the patient. The use of brief screening instruments may also be helpful, including clinician administered scales such as the Primary Care Evaluation of Mental Disorders (PRIME-MD),25 the MINI-International Neuropsychiatric Interview,26 the PTSD Checklist,27 and the self-rated startle, physiological arousal, anger, and numbness (SPAN) scale.28 Treatment Approaches Accurate diagnosis is essential for effective treatment.29 Of all disorders, PTSD requires that physicians give patients adequate time for disclosing their stories. Brief treatment does not mean rushed treatment. Education involves explaining to survivors and their families about the nature of PTSD and responses to stress and it involves encouraging them to speak about their traumatic experience with family or friends to the extent that they wish to do so yet not in a pressured way. Advice about health behaviors and avoidance of use of alcohol, other drugs, and tobacco is often needed. Primary care physicians are ideally placed to provide front-line support to patients in the first weeks after exposure to a trauma and to offer symptomatic treatment as indicated. Pharmacotherapy What effect can treatment with medication make? After a series of studies in the 1980s, mostly in combat veterans, the effect of medications appeared modest at best. Although imipramine hydrochloride, amitriptyline hydrochloride, and phenelzine sulfate were all more effective than placebo in treating severe forms of PTSD, residual morbidity was considerable.30,31 An early trial of fluoxetine hydrochloride also showed modest benefits of the drug in a population that included many combat veterans.32 A later study with fluoxetine33 showed that a selective serotonin reuptake inhibitor (SSRI) could have a very substantial impact on the symptoms of PTSD. In a population of civilian women, mostly traumatized through interpersonal violence, more than 40% reached a state of clinical remission (ie, absence of PTSD symptoms) at the end of 12 weeks. The drug was also found to improve resilience, a potentially important finding for a disorder that is often characterized by low levels of resilience in the face of stress. More recently, 2 larger multicenter trials of sertraline hydrochloride have demonstrated good benefit across the full range of PTSD symptoms, as well as quality of life and disability.34,35 Selective serotonin reuptake inhibitors modulate affects, memories, and impulses in PTSD, conferring protection against their overwhelming intensity on one hand and loosening excessive inhibitions on the other, and they often act rapidly. Beyond the short term, what can be said for maintenance pharmacotherapy in PTSD? Here the data are scant, but such a chronic disorder is likely to require maintenance pharmacotherapy for at least 12 months. One report36 has shown that continued use of sertraline for 9 months can progress to symptom remission in a substantial number of patients. Twenty-five percent of the PTSD symptom improvement obtained and 31% of the improvement attained in quality of life occurred after 12 weeks of treatment. Also, 54% of those who had failed to respond at 12 weeks became responders with the continuation of treatment. Therefore, 12 weeks of treatment with an SSRI may not be an adequate trial. On the other hand, if there has been no improvement within 4 weeks at an adequate dose, continued treatment with an SSRI is unlikely to be beneficial.37 Little work exists about predicting who will do well in the long term following short-term pharmacotherapy. In one trial,38 the strongest predictor of 1-year outcome after fluoxetine treatment was the degree of response at week 12, suggesting that the practitioner should make every effort in the acute phase to retain patients by engaging them in treatment and to use drugs to their maximal advantage. Effect sizes of SSRI vs placebo in PTSD are moderate to strong,37 and this class of drugs now receives consensus opinion as first-line medication in PTSD.39 Evidence for the benefit of other drug classes is extremely sparse, and their study remains critical. Reports, which so far have been mostly uncontrolled and based on small samples, have suggested benefit for paroxetine (however, several unpublished placebo-controlled studies that have shown paroxetine to be beneficial in treating PTSD may result in FDA approval within the next 2 to 3 months),40 citalopram hydrochloride,41 fluvoxamine maleate,42 nefazodone hydrochloride,43 trazodone hydrochloride,44 bupropion hydrochloride,45 mirtazapine,46 clonidine,47 and propranolol.47 Non-SSRI drugs are now considered second-line or augmenting treatments, and trazodone has been suggested for managing insomnia in PTSD.39 Disappointing results have been reported for buspirone hydrochloride48 and inositol niacinate.49 Mood stabilizers have some utility.50-52 The only placebo-controlled trial evaluating an antipsychotic agent showed no benefit.53 Benzodiazepines are probably not helpful and can be harmful when given as monotherapy for any length of time,54-56 but they may be useful in the acute phase as short-term treatment or as adjuncts in chronic PTSD. Given that symptoms which peak within 2 weeks of trauma, may carry a better prognosis than the slow buildup of symptoms of more than 3 months,57 vigorous attempts should be made to treat PTSD early and effectively. Initial use of a hypnotic agent, followed up after 3 weeks by an SSRI, has been recommended for persistent acute PTSD symptoms in primary care.29 Early facilitation of normal 24-hour arousal regulation prior to consolidation of changes associated with chronic PTSD may be an important form of secondary prevention immediately following exposure to trauma.58 This critical, yet demanding, area of therapeutics demands much more attention than it has so far received. Few data exist about whether extended pharmacotherapy protects patients against relapse in PTSD, but one report suggests a substantially lower rate of relapse when sertraline is continued for 15 months vs a placebo switch after successful open-label treatment.59 Psychosocial Treatment Psychosocial treatments are well established and effective in many different PTSD populations. Three factors are considered essential in the successful processing of traumatic events: emotional engagement with the trauma memory, organization of the trauma story, and correction of dysfunctional thoughts that are commonly found following trauma.57 Most psychosocial (cognitive-behavioral) approaches make use of exposure and/or anxiety management training. Exposure to details, memories, and feelings of the trauma can be accomplished by imaginal or in vivo (real life) exposure with therapeutic guidance. Anxiety management training includes relaxation and breathing techniques, social skills training, cognitive restructuring, role-play, and positive self-dialogue.57 Although both techniques are effective, it may be that exposure is critical for the most efficient use of psychosocial treatment. For example, one study showed that following exposure, 57% of the sample attained a 70% symptom reduction after 9 sessions vs 23% who had received cognitive restructuring and exposure.57 Psychosocial treatments benefit PTSD following rape, nonsexual assault, unintentional injury, combat, and other forms of traumatic stress.57,60-63 Eye movement desensitization and reprocessing can also be effective but appears to be less so than prolonged exposure with stress inoculation training.63 An appealing aspect of psychosocial treatments is the low relapse rate found for up to a year after termination of acute treatment.60,61 On the other hand, limitations of psychosocial treatments include that they are not for everyone, many communities do not have access to skilled practitioners, and no more than 50%, as with medication, achieve full remission in the short term.57 To improve the chance of remission, a case could be made for combining medication and psychosocial treatments but no comparative studies have yet been reported using this approach. For the primary care practitioner, it is important to realize the benefits of psychosocial treatment and to make use of accessible referrals. Psychosocial treatments are unlikely to be adopted in primary care unless treatment is considerably modified and simplified. Precedents exist for adapting psychosocial treatments to primary care settings for depression64 and social phobia.65 One technique that might deserve further study in this context is encouraging patients to write about their traumatic experiences. For example, writing about personal stress or trauma with expression of affect on 3 occasions during 1 week was associated with substantial improvement in bronchial asthma and rheumatoid arthritis,66 showing, at the very least, that simple trauma processing techniques can facilitate recovery from chronic medical disorder, even when no ostensible relationship has been demonstrated between the trauma and the disorder. Whether a similar treatment approach for PTSD might be helpful in the medical setting or whether other adaptations of exposure-based treatment are feasible remains to be seen. Debriefing after trauma may be helpful in coping with acute stress, but it has not convincingly been shown to prevent PTSD29 and is not advocated alone to prevent the disorder.67 In the treatment of children, cognitive-behavioral treatment, SSRI, and clonidine are recommended although evidence for the latter 2 is weak.68 Conclusions Despite major advances in the field, there are still many gaps in current knowledge of effective treatment for PTSD,69 and the cross-cultural application of treatments deserves more extensive study. It is clear that the importance of PTSD as a worldwide health problem must be recognized and that it is important for clinicians to be alert to the presence and presentation of PTSD in medical and psychiatric settings. There is no reason PTSD cannot be treated effectively in primary care. The Global Burden of Disease Project70 predicted that the following causes of disease burden in the United States would increase in their current ranks by the year 2020: depression, the second highest; road traffic accidents, the third highest; war, the eighth highest; and violence, the 12th highest. Although PTSD was not specifically included as a disease, each one of these conditions is known to carry with it a high risk for or association with the disorder. It is time to heed the wake-up call provided by recent research into PTSD. The disorder should be treated early. It should be treated effectively. References 1. Krakow B, Hollifield M, Johnston L. et al. Imagery rehearsal therapy for chronic nightmares in sexual assault survivors with posttraumatic stress disorder: a randomized controlled trial. JAMA.2001;286:537-545.Google Scholar 2. Mollica RF, Sarajlić N, Chernoff M, Lavelle J, Sarajlić Vuković I, Massagli MP. Longitudinal study of psychiatric symptoms, disability, mortality, and emigration among Bosnian refugees. JAMA.2001;286:546-555.Google Scholar 3. deJong JTVM, Komproe IH, van Ommeren M. et al. Lifetime events and posttraumatic stress disorder in 4 postconflict settings. JAMA.2001;286:555-562.Google Scholar 4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Third Edition. Washington, DC: American Psychiatric Association; 1980. 5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition. Washington, DC: American Psychiatric Association; 1987. 6. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric Association; 1994. 7. Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry.1995;52:1048-1060.Google Scholar 8. Perkonigg A, Kessler RC, Stortz S, Wittchen HU. Traumatic events and post-traumatic stress disorder in the community: prevalence, risk factors and comorbidity. Acta Psychiatr Scand.2000;101:46-59.Google Scholar 9. Kessler RC. Posttraumatic stress disorder: the burden to the individual and to society. J Clin Psychiatry.2000;61(suppl 5):4-14.Google Scholar 10. Davidson JRT, Hughes DC, Blazer DG, George LK. Post-traumatic stress disorder in the community: an epidemiological study. Psychol Med.1991;21:713-721.Google Scholar 11. Boscarino JA. Diseases among men 20 years after exposure to severe stress: implications for clinical research and medical care. Psychosom Med.1997;59:605-614.Google Scholar 12. Felitti VJ, Anda RF, Nordenberg D. et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. Am J Prev Med.1998;14:245-258.Google Scholar 13. Greenberg PE, Sisitsky T, Kessler RC. et al. The economic burden of anxiety disorders in the 1990s. J Clin Psychiatry.1999;60:427-435.Google Scholar 14. Amaya-Jackson L, Davidson JRT, Hughes DC. et al. Functional impairment and utilization of services associated with posttraumatic stress in the community. J Trauma Stress.1999;12:709-724.Google Scholar 15. Davidson JRT, Smith RD. Traumatic experiences in psychiatric outpatients. J Trauma Stress.1990;3:459-474.Google Scholar 16. Switzer GE, Dew MA, Thompson K, Goycootea JM, Derricott T, Mullins SD. Posttraumatic stress disorder and service utilization among urban mental center clients. J Trauma Stress.1999;12:25-39.Google Scholar 17. Taubman-Ben-Ari O, Rabinowitz J, Feldman D, Vaturi R. Post-traumatic stress disorder in primary care settings: prevalence and physicians' detection. Psychol Med.2001;31:555-560.Google Scholar 18. Stein MB, McQuaid JR, Pedrelli P, Lenox R, McCahill ME. Posttraumatic stress disorder in the primary care medical setting. Gen Hosp Psychiatry.2000;22:261-269.Google Scholar 19. Leserman J, Li Z, Drossman DA, Hu YJB. Selected symptoms associated with sexual and physical abuse history among female patients with gastrointestinal disorders: the impact on subsequent healthcare visits. Psychol Med.1998;28:417-425.Google Scholar 20. Irwin C, Falsetti SA, Lydiard RB, Ballenger JC, Brock CD, Brener W. Comorbidity of posttraumatic stress disorder and irritable bowel syndrome. J Clin Psychiatry.1996;57:576-578.Google Scholar 21. Scarinci IC, Halle JM, Bradley LT, Richter JE. Altered pain perception and psychosocial features among women with gastrointestinal disorders and history of abuse: a preliminary model. Am J Med.1994;97:108-118.Google Scholar 22. Beckham JC, Kirby AC, Feldman ME. et al. Prevalence and correlates of heavy smoking in Vietnam veterans with chronic posttraumatic stress disorder. Addict Behav.1997;22:637-647.Google Scholar 23. Culpepper L. Recognizing and treating post-traumatic stress disorder. Hippocrates.2000;14:45-52.Google Scholar 24. Lamberg L. Domestic violence: what to ask, what to do. JAMA.2000;284:554-556.Google Scholar 25. Spitzer RL, Kroenke K, Linzer M. et al. Health-related quality of life in primary care patients with mental disorders: results from the PRIME-MD 1000 study. JAMA.1995;274:1511-1517.Google Scholar 26. Ballenger JC, Davidson JRT, Lecrubier Y, Nutt DJ.for the International Consensus Group on Depression and Anxiety. A proposed algorithm for improved recognition and treatment of the depression/anxiety spectrum in primary care. J Clin Psychiatry.In press.Google Scholar 27. Breslau N, Peterson EL, Kessler RC, Schultz LR. Short screening scale for DSM-IV posttraumatic stress disorder. Am J Psychiatry.1999;156:908-911.Google Scholar 28. Meltzer-Brody S, Churchill LE, Davidson JRT. Derivation of the SPAN: a brief diagnostic screening test for PTSD. Psychiatry Res.1999;88:63-70.Google Scholar 29. Ballenger JC, Davidson JRT, Lecrubier Y. et al. Consensus statement on posttraumatic stress disorder from the International Consensus Group on Depression and Anxiety. J Clin Psychiatry.2000;61(suppl 5):60-66.Google Scholar 30. Davidson JRT, Kudler HS, Smith RD. et al. Treatment of posttraumatic stress disorder with amitriptyline and placebo. Arch Gen Psychiatry.1990;47:259-266.Google Scholar 31. Kosten TR, Frank JB, Dan E, McDougle CJ, Giller Jr EL. Pharmacotherapy for posttraumatic stress disorder using phenelzine or imipramine. J Nerv Ment Dis.1991;179:366-370.Google Scholar 32. van der Kolk BA, Dreyfuss D, Michaels M. Fluoxetine in posttraumatic stress disorder. J Clin Psychiatry.1994;55:517-522.Google Scholar 33. Connor KM, Sutherland SM, Tupler LA. et al. Fluoxetine in post-traumatic stress disorder: randomized double-blind study. Br J Psychiatry.1999;175:17-22.Google Scholar 34. Brady KT, Pearlstein T, Asnis GM. et al. Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial. JAMA.2000;283:1837-1844.Google Scholar 35. Davidson JRT, Rothbaum BO, van der Kolk BA, Sikes CR, Farfel GM. Multicenter, double-blind comparisons of sertraline and placebo in the treatment of posttraumatic stress disorder. Arch Gen Psychiatry.2001;58:485-492.Google Scholar 36. Londborg PD, Hegel MT, Goldstein S. et al. Sertraline treatment of posttraumatic disorder: results of 24 weeks of open-label continuation treatment. J Clin Psychiatry.2001;62:325-331.Google Scholar 37. Davidson JRT, Malik MI, Sutherland SM. Response characteristics to antidepressants and placebo in post-traumatic stress disorder. Int Clin Psychopharmacol.1997;12:291-296.Google Scholar 38. Davidson JRT. Pharmacotherapy of posttraumatic stress disorder: treatment options, long-term follow-up and predictors of outcome. J Clin Psychiatry.2000;61 Suppl 5:52-56.Google Scholar 39. Foa EB, Davidson JRT, Frances A. Expert Consensus Guideline Series: treatment of posttraumatic stress disorder. J Clin Psychiatry.1999;60:1-76.Google Scholar 40. Marshall RD, Schneier FR, Fallon BA. et al. An open trial of paroxetine in patients with non-combat-related, chronic posttraumatic stress disorder. J Clin Psychopharmacol.1998;18:10-18.Google Scholar 41. Seedat S, Stein DJ, Emsley RA. Open trial of citalopram in adults with post-traumatic stress disorder. Int J Neuropsychopharmacol.2000;3:135-140.Google Scholar 42. Davidson JRT, Weisler RH, Malik ML, Tupler LA. Fluvoxamine in civilians with posttraumatic stress disorder. J Clin Psychopharmacol.1998;18:93-95.Google Scholar 43. Hidalgo RB, Hertzberg MA, Mellman TA. et al. Nefazodone in post-traumatic stress disorder: results from six open-label trials. Int Clin Psychopharmacol.1999;14:61-68.Google Scholar 44. Hertzberg MA, Feldman ME, Beckham JC, Davidson JRT. Trial of trazodone for posttraumatic stress disorder using a multiple baseline group design. J Clin Psychopharmacol.1996;16:294-298.Google Scholar 45. Canive JM, Clark RD, Calaris LA, Quails C, Tuason VB. Bupropion treatment in veterans with posttraumatic stress disorder: an open study. J Clin Psychopharmacol.1998;18:379-383.Google Scholar 46. Connor KM, Davidson JRT, Weisler AH, Ahearn EP. A pilot study of mirtazapine in post-traumatic stress disorder. Int Clin Psychopharmacol.1999;14:29-31.Google Scholar 47. Kolb LC, Burris BC, Griffiths S. Propranolol and clonidine in the treatment of post-traumatic stress disorders of war. In van der Kolk BA, ed. Post-Traumatic Stress Disorder: Psychological and Biological Sequelae. Washington, DC: American Psychiatric Press; 1984:98-105. 48. Fichtner CG, Crayton JW. Buspirone in combat-related posttraumatic stress disorder. J Clin Psychopharmacol.1994;14:79-80.Google Scholar 49. Kaplan Z, Amir M, Swartz M, Levine J. Inositol treatment of post-traumatic stress disorder. Anxiety.1994;2:51-52.Google Scholar 50. Lipper S, Davidson JRT, Grady TA. et al. Carbamazepine in posttraumatic stress disorder: a preliminary evaluation. Psychosomatics.1986;27:849-854.Google Scholar 51. Fesler FA. Valproate in combat-related posttraumatic stress disorder. J Clin Psychiatry.1991;52:361-364.Google Scholar 52. Hertzberg MA, Butterfield MI, Feldman ME. et al. Lamotrigine vs placebo for the treatment of posttraumatic stress disorder. Biol Psychiatry.1999;45:1226-1229.Google Scholar 53. Butterfield MI, Becker ME, Connor KM. et al. A preliminary study of olanzapine in the treatment of post-traumatic stress disorder. Int Clin Psychopharmacol.In press.Google Scholar 54. Braun P, Greenberg D, Dasberg H, Lerer B. Core symptoms of posttraumatic stress disorder unimproved by alprazolam treatment. J Clin Psychiatry.1990;51:226-238.Google Scholar 55. Gelpin E, Bonne O, Peri T, Brandes D, Shalev AY. Treatment of recent trauma survivors with benzodiazepines: a prospective study. J Clin Psychiatry.1996;57:390-394.Google Scholar 56. Risse SC, Whitters A, Burke J, Chen S, Scurfield RM, Raskind MA. Severe withdrawal symptoms after discontinuation of alprazolam in eight patients with combat induced posttraumatic stress disorder. J Clin Psychiatry.1990;51:206-209.Google Scholar 57. Hembree EA, Foa EB. Posttraumatic stress disorder: psychological factors and psychosocial intervention. J Clin Psychiatry.2000;61(suppl 7):33-39.Google Scholar 58. Mellman TA, Byers PM, Augenstein JS. Pilot evaluation of hypnotic medication during acute traumatic stress response. J Trauma Stress.1998;11:563-570.Google Scholar 59. Davidson JRT, Londborg PD, Pearlstein T, Rothbaum BO, Brady KT, Farfel GM. Sertaline and posttraumatic stress disorder: results of 24 weeks of open-label sertraline followed by a 28-week discontinuation study [abstract]. Eur Neuropsychopharmacol.2000:S349.Google Scholar 60. Marks I, Lovell K, Noshirvani H. et al. Treatment of posttraumatic stress disorder by exposure and/or cognitive restructuring. Arch Gen Psychiatry.1998;55:317-322.Google Scholar 61. Foa EB, Dancu CV, Hembree E. et al. The efficacy of exposure therapy, stress inoculation training and their combination in ameliorating PTSD for female victims of assault. J Consult Clin Psychol.1999;67:194-200.Google Scholar 62. Tarrier N, Pilgrim H, Sommerfield C. et al. A randomized trial of cognitive therapy and imaginal exposure in the treatment of chronic posttraumatic stress disorder. J Consult Clin Psychol.1999;67:13-18.Google Scholar 63. Devilly GJ, Spence SH. 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.1999;13:131-157.Google Scholar 64. Mynors-Wallis LM, Gath DH, Lloyd-Thomas AR, Tomlinson D. Randomized controlled trial comparing problem-solving treatment with amitriptyline and placebo in primary care. BMJ.1995;310:441-445.Google Scholar 65. Haug TT, Hellstrøm K, Blomhoff S, Humble M, Madsbu HP. The treatment of social phobia in general practice: is exposure therapy feasible? Fam Pract.2000;17:114-118.Google Scholar 66. Smyth JM, Stone AA, Hurewitz A, Kaell A. Effects of writing about stressful experiences on symptom reduction in patients with asthma or rheumatoid arthritis. JAMA.1999;281:1304-1309.Google Scholar 67. Bisson JI, McFarlane AC, Rose S. Psychological debriefing. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for PTSD. New York, NY: The Guilford Press; 2000:317-319. 68. Cohen JA, Berliner L, March JS. Treatment of children and adolescents. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for PTSD. New York, NY: The Guilford Press; 2000;330-332. 69. Foa EB, Keane TM, Friedman MJ. Effective Treatments for PTSD. New York, NY: The Guilford Press; 2000:1-17. 70. Murray CJL, Lopez AD. Introduction. In: Murray CJL, Lopez AD, eds. The Global Burden of Disease. Boston, Mass: Harvard University School of Public Health; 1996;5. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA American Medical Association

Recognition and Treatment of Posttraumatic Stress Disorder

JAMA , Volume 286 (5) – Aug 1, 2001

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References (83)

Publisher
American Medical Association
Copyright
Copyright © 2001 American Medical Association. All Rights Reserved.
ISSN
0098-7484
eISSN
1538-3598
DOI
10.1001/jama.286.5.584
Publisher site
See Article on Publisher Site

Abstract

The reports on posttraumatic stress disorder (PTSD) in this issue of THE JOURNAL1-3 draw attention to 3 important facts: PTSD is a worldwide problem, reaching alarming proportions in countries torn by violent conflict; it is associated with persistent disability and comorbidity for many people; and treatments can produce a meaningful reduction in distress. These studies, which tell clinicians not to forget about PTSD, provide the opportunity to focus on what is known about PTSD as a medical problem, and its presentation, recognition, and management. Perhaps the 3 main lessons to be learned are that PTSD often presents in medical disguise, it is largely unrecognized, and it can be treated successfully. A Widespread Health Problem Posttraumatic stress disorder was first introduced as a diagnosis in 1980,4 but it has been slow to gain general acceptance. It has undergone some diagnostic modifications5,6 but remains in its essential features a disorder in which 1 or more traumatic events give rise to 4 symptom clusters: recurrent and painful reexperiencing of the event, phobic avoidance of trauma-related situations and memories, emotional numbing and withdrawal, and hyperarousal. In the US population, lifetime prevalence rates are in the range of 8%,7 with women affected twice as often as men. However, studies from other countries and studies of high-risk populations have reported widely ranging prevalence rates from a low of 1.3% in Germany8 to 37.4% in Algeria.3 It has been estimated that, on average, a person with PTSD will endure 20 years of active symptoms and will experience almost 1 day a week of work impairment, perhaps resulting in a $3 billion annual productivity loss in the United States.9 Rates of attempted suicide are as high as 19%.10 Besides being associated with increased risk for depression, anxiety, and alcohol or substance use disorders,7 PTSD is associated with higher rates of hypertension, bronchial asthma, and peptic ulcer10 and with other diseases of the cardiovascular, digestive, musculoskeletal, endocrine, respiratory, and nervous systems, as well as increased rates of infectious disease for up to 20 years following exposure to major trauma and after controlling for other variables.11 Adult survivors of childhood abuse, many of whom are likely to have experienced PTSD, have higher rates of smoking, sexually transmitted disease, severe obesity, ischemic heart disease, cancer, chronic obstructive pulmonary disease, fractures, and liver disease than the general population.12 The cost of PTSD exceeds that of all other anxiety disorders, and much of this expenditure is accounted for by direct costs of treatment seeking and medical evaluation.13 Recognition and Presentation People with PTSD might be expected to seek mental health treatment. However, evidence suggests that this is relatively uncommon14 and that, even in academic and community mental health settings,15,16 rates of recognition may be low with clinical diagnosis of PTSD occurring in as few as 4% of individuals with the disorder. In a national cohort of Israeli primary care patients, 9% met criteria for current PTSD, but only 2% of actual cases were recognized by their treating physicians. Although 49% of physicians recognized the existence of psychological distress, this rate was still far less than the 88% frequency of self-rated distress in the sample.17 In a US primary care survey,18 11.8% of patients met diagnostic criteria for full or partial PTSD. These findings are important since more than 70% of respondents with PTSD symptoms in the general population have used general medical services in the past 6 months.14 The question then arises as to how PTSD might be recognized and what are the likely disguises behind which it might be found. An unusually high rate of somatization disorder10 suggests that individuals with PTSD may be marked and persistent somatizers, a finding subsequently borne out in a study of women with a history of physical or sexual abuse who were seen in a gastrointestinal disorders clinic.17 Musculoskeletal, genitourinary, dermatologic, respiratory, panic, sleep-related, and appetite disturbances were commonly seen. The number of symptoms, as well as severity of abuse, explained much of the variance, accounting for subsequent physician visits during the next year. Such patients made 3 to 8 more health care visits per year than did women without abuse. High rates of PTSD also have been reported in association with irritable bowel syndrome.20 The notion that PTSD at times may be associated with "hypervigilance to symptoms" has been advanced and receives some support from a study of abuse survivors with gastroesophageal reflux who showed lower cutaneous sensitivity thresholds and hypervigilance in labeling stimuli as being painful. Their pain-coping mechanisms were considered to be poor.21 Another study22 has shown that heavy smoking is much more likely in trauma survivors with PTSD compared with those who had experienced similar trauma but did not have PTSD. Thus, in the health care system, PTSD or the role of trauma should be considered in patients experiencing prominent chronic pain or persistent somatization, especially when these symptoms are not otherwise fully accounted for. Posttraumatic stress syndrome can only be diagnosed if the existence of a traumatic event has been established. However, clinical suspicion may be warranted based on symptoms or behaviors even if no such event has yet been established. To elicit this information may in some cases be relatively straightforward. But in other cases, it will be more difficult, requiring the establishment of trust and confidence between patient and physician and requiring the physician's unwillingness to accept initial denial as being the final answer in some cases. Suggested approaches to uncovering a trauma have been described.23,24 For example, in the case of suspected domestic violence, the physician, when alone with the patient, should raise the concern that the patient's medical problems might be related to injury inflicted by another person. The patient may be asked if he or she feels safe at home. Routine questioning about trauma has been suggested along the lines of inquiring about whether a traumatic event has ever been experienced and whether the experience is still upsetting to the patient. The use of brief screening instruments may also be helpful, including clinician administered scales such as the Primary Care Evaluation of Mental Disorders (PRIME-MD),25 the MINI-International Neuropsychiatric Interview,26 the PTSD Checklist,27 and the self-rated startle, physiological arousal, anger, and numbness (SPAN) scale.28 Treatment Approaches Accurate diagnosis is essential for effective treatment.29 Of all disorders, PTSD requires that physicians give patients adequate time for disclosing their stories. Brief treatment does not mean rushed treatment. Education involves explaining to survivors and their families about the nature of PTSD and responses to stress and it involves encouraging them to speak about their traumatic experience with family or friends to the extent that they wish to do so yet not in a pressured way. Advice about health behaviors and avoidance of use of alcohol, other drugs, and tobacco is often needed. Primary care physicians are ideally placed to provide front-line support to patients in the first weeks after exposure to a trauma and to offer symptomatic treatment as indicated. Pharmacotherapy What effect can treatment with medication make? After a series of studies in the 1980s, mostly in combat veterans, the effect of medications appeared modest at best. Although imipramine hydrochloride, amitriptyline hydrochloride, and phenelzine sulfate were all more effective than placebo in treating severe forms of PTSD, residual morbidity was considerable.30,31 An early trial of fluoxetine hydrochloride also showed modest benefits of the drug in a population that included many combat veterans.32 A later study with fluoxetine33 showed that a selective serotonin reuptake inhibitor (SSRI) could have a very substantial impact on the symptoms of PTSD. In a population of civilian women, mostly traumatized through interpersonal violence, more than 40% reached a state of clinical remission (ie, absence of PTSD symptoms) at the end of 12 weeks. The drug was also found to improve resilience, a potentially important finding for a disorder that is often characterized by low levels of resilience in the face of stress. More recently, 2 larger multicenter trials of sertraline hydrochloride have demonstrated good benefit across the full range of PTSD symptoms, as well as quality of life and disability.34,35 Selective serotonin reuptake inhibitors modulate affects, memories, and impulses in PTSD, conferring protection against their overwhelming intensity on one hand and loosening excessive inhibitions on the other, and they often act rapidly. Beyond the short term, what can be said for maintenance pharmacotherapy in PTSD? Here the data are scant, but such a chronic disorder is likely to require maintenance pharmacotherapy for at least 12 months. One report36 has shown that continued use of sertraline for 9 months can progress to symptom remission in a substantial number of patients. Twenty-five percent of the PTSD symptom improvement obtained and 31% of the improvement attained in quality of life occurred after 12 weeks of treatment. Also, 54% of those who had failed to respond at 12 weeks became responders with the continuation of treatment. Therefore, 12 weeks of treatment with an SSRI may not be an adequate trial. On the other hand, if there has been no improvement within 4 weeks at an adequate dose, continued treatment with an SSRI is unlikely to be beneficial.37 Little work exists about predicting who will do well in the long term following short-term pharmacotherapy. In one trial,38 the strongest predictor of 1-year outcome after fluoxetine treatment was the degree of response at week 12, suggesting that the practitioner should make every effort in the acute phase to retain patients by engaging them in treatment and to use drugs to their maximal advantage. Effect sizes of SSRI vs placebo in PTSD are moderate to strong,37 and this class of drugs now receives consensus opinion as first-line medication in PTSD.39 Evidence for the benefit of other drug classes is extremely sparse, and their study remains critical. Reports, which so far have been mostly uncontrolled and based on small samples, have suggested benefit for paroxetine (however, several unpublished placebo-controlled studies that have shown paroxetine to be beneficial in treating PTSD may result in FDA approval within the next 2 to 3 months),40 citalopram hydrochloride,41 fluvoxamine maleate,42 nefazodone hydrochloride,43 trazodone hydrochloride,44 bupropion hydrochloride,45 mirtazapine,46 clonidine,47 and propranolol.47 Non-SSRI drugs are now considered second-line or augmenting treatments, and trazodone has been suggested for managing insomnia in PTSD.39 Disappointing results have been reported for buspirone hydrochloride48 and inositol niacinate.49 Mood stabilizers have some utility.50-52 The only placebo-controlled trial evaluating an antipsychotic agent showed no benefit.53 Benzodiazepines are probably not helpful and can be harmful when given as monotherapy for any length of time,54-56 but they may be useful in the acute phase as short-term treatment or as adjuncts in chronic PTSD. Given that symptoms which peak within 2 weeks of trauma, may carry a better prognosis than the slow buildup of symptoms of more than 3 months,57 vigorous attempts should be made to treat PTSD early and effectively. Initial use of a hypnotic agent, followed up after 3 weeks by an SSRI, has been recommended for persistent acute PTSD symptoms in primary care.29 Early facilitation of normal 24-hour arousal regulation prior to consolidation of changes associated with chronic PTSD may be an important form of secondary prevention immediately following exposure to trauma.58 This critical, yet demanding, area of therapeutics demands much more attention than it has so far received. Few data exist about whether extended pharmacotherapy protects patients against relapse in PTSD, but one report suggests a substantially lower rate of relapse when sertraline is continued for 15 months vs a placebo switch after successful open-label treatment.59 Psychosocial Treatment Psychosocial treatments are well established and effective in many different PTSD populations. Three factors are considered essential in the successful processing of traumatic events: emotional engagement with the trauma memory, organization of the trauma story, and correction of dysfunctional thoughts that are commonly found following trauma.57 Most psychosocial (cognitive-behavioral) approaches make use of exposure and/or anxiety management training. Exposure to details, memories, and feelings of the trauma can be accomplished by imaginal or in vivo (real life) exposure with therapeutic guidance. Anxiety management training includes relaxation and breathing techniques, social skills training, cognitive restructuring, role-play, and positive self-dialogue.57 Although both techniques are effective, it may be that exposure is critical for the most efficient use of psychosocial treatment. For example, one study showed that following exposure, 57% of the sample attained a 70% symptom reduction after 9 sessions vs 23% who had received cognitive restructuring and exposure.57 Psychosocial treatments benefit PTSD following rape, nonsexual assault, unintentional injury, combat, and other forms of traumatic stress.57,60-63 Eye movement desensitization and reprocessing can also be effective but appears to be less so than prolonged exposure with stress inoculation training.63 An appealing aspect of psychosocial treatments is the low relapse rate found for up to a year after termination of acute treatment.60,61 On the other hand, limitations of psychosocial treatments include that they are not for everyone, many communities do not have access to skilled practitioners, and no more than 50%, as with medication, achieve full remission in the short term.57 To improve the chance of remission, a case could be made for combining medication and psychosocial treatments but no comparative studies have yet been reported using this approach. For the primary care practitioner, it is important to realize the benefits of psychosocial treatment and to make use of accessible referrals. Psychosocial treatments are unlikely to be adopted in primary care unless treatment is considerably modified and simplified. Precedents exist for adapting psychosocial treatments to primary care settings for depression64 and social phobia.65 One technique that might deserve further study in this context is encouraging patients to write about their traumatic experiences. For example, writing about personal stress or trauma with expression of affect on 3 occasions during 1 week was associated with substantial improvement in bronchial asthma and rheumatoid arthritis,66 showing, at the very least, that simple trauma processing techniques can facilitate recovery from chronic medical disorder, even when no ostensible relationship has been demonstrated between the trauma and the disorder. Whether a similar treatment approach for PTSD might be helpful in the medical setting or whether other adaptations of exposure-based treatment are feasible remains to be seen. Debriefing after trauma may be helpful in coping with acute stress, but it has not convincingly been shown to prevent PTSD29 and is not advocated alone to prevent the disorder.67 In the treatment of children, cognitive-behavioral treatment, SSRI, and clonidine are recommended although evidence for the latter 2 is weak.68 Conclusions Despite major advances in the field, there are still many gaps in current knowledge of effective treatment for PTSD,69 and the cross-cultural application of treatments deserves more extensive study. It is clear that the importance of PTSD as a worldwide health problem must be recognized and that it is important for clinicians to be alert to the presence and presentation of PTSD in medical and psychiatric settings. There is no reason PTSD cannot be treated effectively in primary care. The Global Burden of Disease Project70 predicted that the following causes of disease burden in the United States would increase in their current ranks by the year 2020: depression, the second highest; road traffic accidents, the third highest; war, the eighth highest; and violence, the 12th highest. Although PTSD was not specifically included as a disease, each one of these conditions is known to carry with it a high risk for or association with the disorder. It is time to heed the wake-up call provided by recent research into PTSD. The disorder should be treated early. It should be treated effectively. References 1. Krakow B, Hollifield M, Johnston L. et al. Imagery rehearsal therapy for chronic nightmares in sexual assault survivors with posttraumatic stress disorder: a randomized controlled trial. JAMA.2001;286:537-545.Google Scholar 2. Mollica RF, Sarajlić N, Chernoff M, Lavelle J, Sarajlić Vuković I, Massagli MP. Longitudinal study of psychiatric symptoms, disability, mortality, and emigration among Bosnian refugees. JAMA.2001;286:546-555.Google Scholar 3. deJong JTVM, Komproe IH, van Ommeren M. et al. Lifetime events and posttraumatic stress disorder in 4 postconflict settings. JAMA.2001;286:555-562.Google Scholar 4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Third Edition. Washington, DC: American Psychiatric Association; 1980. 5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition. Washington, DC: American Psychiatric Association; 1987. 6. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric Association; 1994. 7. Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry.1995;52:1048-1060.Google Scholar 8. Perkonigg A, Kessler RC, Stortz S, Wittchen HU. Traumatic events and post-traumatic stress disorder in the community: prevalence, risk factors and comorbidity. Acta Psychiatr Scand.2000;101:46-59.Google Scholar 9. Kessler RC. Posttraumatic stress disorder: the burden to the individual and to society. J Clin Psychiatry.2000;61(suppl 5):4-14.Google Scholar 10. Davidson JRT, Hughes DC, Blazer DG, George LK. Post-traumatic stress disorder in the community: an epidemiological study. Psychol Med.1991;21:713-721.Google Scholar 11. Boscarino JA. Diseases among men 20 years after exposure to severe stress: implications for clinical research and medical care. Psychosom Med.1997;59:605-614.Google Scholar 12. Felitti VJ, Anda RF, Nordenberg D. et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. Am J Prev Med.1998;14:245-258.Google Scholar 13. Greenberg PE, Sisitsky T, Kessler RC. et al. The economic burden of anxiety disorders in the 1990s. J Clin Psychiatry.1999;60:427-435.Google Scholar 14. Amaya-Jackson L, Davidson JRT, Hughes DC. et al. Functional impairment and utilization of services associated with posttraumatic stress in the community. J Trauma Stress.1999;12:709-724.Google Scholar 15. Davidson JRT, Smith RD. Traumatic experiences in psychiatric outpatients. J Trauma Stress.1990;3:459-474.Google Scholar 16. Switzer GE, Dew MA, Thompson K, Goycootea JM, Derricott T, Mullins SD. Posttraumatic stress disorder and service utilization among urban mental center clients. J Trauma Stress.1999;12:25-39.Google Scholar 17. Taubman-Ben-Ari O, Rabinowitz J, Feldman D, Vaturi R. Post-traumatic stress disorder in primary care settings: prevalence and physicians' detection. Psychol Med.2001;31:555-560.Google Scholar 18. Stein MB, McQuaid JR, Pedrelli P, Lenox R, McCahill ME. Posttraumatic stress disorder in the primary care medical setting. Gen Hosp Psychiatry.2000;22:261-269.Google Scholar 19. Leserman J, Li Z, Drossman DA, Hu YJB. Selected symptoms associated with sexual and physical abuse history among female patients with gastrointestinal disorders: the impact on subsequent healthcare visits. Psychol Med.1998;28:417-425.Google Scholar 20. Irwin C, Falsetti SA, Lydiard RB, Ballenger JC, Brock CD, Brener W. Comorbidity of posttraumatic stress disorder and irritable bowel syndrome. J Clin Psychiatry.1996;57:576-578.Google Scholar 21. Scarinci IC, Halle JM, Bradley LT, Richter JE. Altered pain perception and psychosocial features among women with gastrointestinal disorders and history of abuse: a preliminary model. Am J Med.1994;97:108-118.Google Scholar 22. Beckham JC, Kirby AC, Feldman ME. et al. Prevalence and correlates of heavy smoking in Vietnam veterans with chronic posttraumatic stress disorder. Addict Behav.1997;22:637-647.Google Scholar 23. Culpepper L. Recognizing and treating post-traumatic stress disorder. Hippocrates.2000;14:45-52.Google Scholar 24. Lamberg L. Domestic violence: what to ask, what to do. JAMA.2000;284:554-556.Google Scholar 25. Spitzer RL, Kroenke K, Linzer M. et al. Health-related quality of life in primary care patients with mental disorders: results from the PRIME-MD 1000 study. JAMA.1995;274:1511-1517.Google Scholar 26. Ballenger JC, Davidson JRT, Lecrubier Y, Nutt DJ.for the International Consensus Group on Depression and Anxiety. A proposed algorithm for improved recognition and treatment of the depression/anxiety spectrum in primary care. J Clin Psychiatry.In press.Google Scholar 27. Breslau N, Peterson EL, Kessler RC, Schultz LR. Short screening scale for DSM-IV posttraumatic stress disorder. Am J Psychiatry.1999;156:908-911.Google Scholar 28. Meltzer-Brody S, Churchill LE, Davidson JRT. Derivation of the SPAN: a brief diagnostic screening test for PTSD. Psychiatry Res.1999;88:63-70.Google Scholar 29. Ballenger JC, Davidson JRT, Lecrubier Y. et al. Consensus statement on posttraumatic stress disorder from the International Consensus Group on Depression and Anxiety. J Clin Psychiatry.2000;61(suppl 5):60-66.Google Scholar 30. Davidson JRT, Kudler HS, Smith RD. et al. Treatment of posttraumatic stress disorder with amitriptyline and placebo. Arch Gen Psychiatry.1990;47:259-266.Google Scholar 31. Kosten TR, Frank JB, Dan E, McDougle CJ, Giller Jr EL. Pharmacotherapy for posttraumatic stress disorder using phenelzine or imipramine. J Nerv Ment Dis.1991;179:366-370.Google Scholar 32. van der Kolk BA, Dreyfuss D, Michaels M. Fluoxetine in posttraumatic stress disorder. J Clin Psychiatry.1994;55:517-522.Google Scholar 33. Connor KM, Sutherland SM, Tupler LA. et al. Fluoxetine in post-traumatic stress disorder: randomized double-blind study. Br J Psychiatry.1999;175:17-22.Google Scholar 34. Brady KT, Pearlstein T, Asnis GM. et al. Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial. JAMA.2000;283:1837-1844.Google Scholar 35. Davidson JRT, Rothbaum BO, van der Kolk BA, Sikes CR, Farfel GM. Multicenter, double-blind comparisons of sertraline and placebo in the treatment of posttraumatic stress disorder. Arch Gen Psychiatry.2001;58:485-492.Google Scholar 36. Londborg PD, Hegel MT, Goldstein S. et al. Sertraline treatment of posttraumatic disorder: results of 24 weeks of open-label continuation treatment. J Clin Psychiatry.2001;62:325-331.Google Scholar 37. Davidson JRT, Malik MI, Sutherland SM. Response characteristics to antidepressants and placebo in post-traumatic stress disorder. Int Clin Psychopharmacol.1997;12:291-296.Google Scholar 38. Davidson JRT. Pharmacotherapy of posttraumatic stress disorder: treatment options, long-term follow-up and predictors of outcome. J Clin Psychiatry.2000;61 Suppl 5:52-56.Google Scholar 39. Foa EB, Davidson JRT, Frances A. Expert Consensus Guideline Series: treatment of posttraumatic stress disorder. J Clin Psychiatry.1999;60:1-76.Google Scholar 40. Marshall RD, Schneier FR, Fallon BA. et al. An open trial of paroxetine in patients with non-combat-related, chronic posttraumatic stress disorder. J Clin Psychopharmacol.1998;18:10-18.Google Scholar 41. Seedat S, Stein DJ, Emsley RA. Open trial of citalopram in adults with post-traumatic stress disorder. Int J Neuropsychopharmacol.2000;3:135-140.Google Scholar 42. Davidson JRT, Weisler RH, Malik ML, Tupler LA. Fluvoxamine in civilians with posttraumatic stress disorder. J Clin Psychopharmacol.1998;18:93-95.Google Scholar 43. Hidalgo RB, Hertzberg MA, Mellman TA. et al. Nefazodone in post-traumatic stress disorder: results from six open-label trials. Int Clin Psychopharmacol.1999;14:61-68.Google Scholar 44. Hertzberg MA, Feldman ME, Beckham JC, Davidson JRT. Trial of trazodone for posttraumatic stress disorder using a multiple baseline group design. J Clin Psychopharmacol.1996;16:294-298.Google Scholar 45. Canive JM, Clark RD, Calaris LA, Quails C, Tuason VB. Bupropion treatment in veterans with posttraumatic stress disorder: an open study. J Clin Psychopharmacol.1998;18:379-383.Google Scholar 46. Connor KM, Davidson JRT, Weisler AH, Ahearn EP. A pilot study of mirtazapine in post-traumatic stress disorder. Int Clin Psychopharmacol.1999;14:29-31.Google Scholar 47. Kolb LC, Burris BC, Griffiths S. Propranolol and clonidine in the treatment of post-traumatic stress disorders of war. In van der Kolk BA, ed. Post-Traumatic Stress Disorder: Psychological and Biological Sequelae. Washington, DC: American Psychiatric Press; 1984:98-105. 48. Fichtner CG, Crayton JW. Buspirone in combat-related posttraumatic stress disorder. J Clin Psychopharmacol.1994;14:79-80.Google Scholar 49. Kaplan Z, Amir M, Swartz M, Levine J. Inositol treatment of post-traumatic stress disorder. Anxiety.1994;2:51-52.Google Scholar 50. Lipper S, Davidson JRT, Grady TA. et al. Carbamazepine in posttraumatic stress disorder: a preliminary evaluation. Psychosomatics.1986;27:849-854.Google Scholar 51. Fesler FA. Valproate in combat-related posttraumatic stress disorder. J Clin Psychiatry.1991;52:361-364.Google Scholar 52. Hertzberg MA, Butterfield MI, Feldman ME. et al. Lamotrigine vs placebo for the treatment of posttraumatic stress disorder. Biol Psychiatry.1999;45:1226-1229.Google Scholar 53. Butterfield MI, Becker ME, Connor KM. et al. A preliminary study of olanzapine in the treatment of post-traumatic stress disorder. Int Clin Psychopharmacol.In press.Google Scholar 54. Braun P, Greenberg D, Dasberg H, Lerer B. Core symptoms of posttraumatic stress disorder unimproved by alprazolam treatment. J Clin Psychiatry.1990;51:226-238.Google Scholar 55. Gelpin E, Bonne O, Peri T, Brandes D, Shalev AY. Treatment of recent trauma survivors with benzodiazepines: a prospective study. J Clin Psychiatry.1996;57:390-394.Google Scholar 56. Risse SC, Whitters A, Burke J, Chen S, Scurfield RM, Raskind MA. Severe withdrawal symptoms after discontinuation of alprazolam in eight patients with combat induced posttraumatic stress disorder. J Clin Psychiatry.1990;51:206-209.Google Scholar 57. Hembree EA, Foa EB. Posttraumatic stress disorder: psychological factors and psychosocial intervention. J Clin Psychiatry.2000;61(suppl 7):33-39.Google Scholar 58. Mellman TA, Byers PM, Augenstein JS. Pilot evaluation of hypnotic medication during acute traumatic stress response. J Trauma Stress.1998;11:563-570.Google Scholar 59. Davidson JRT, Londborg PD, Pearlstein T, Rothbaum BO, Brady KT, Farfel GM. Sertaline and posttraumatic stress disorder: results of 24 weeks of open-label sertraline followed by a 28-week discontinuation study [abstract]. Eur Neuropsychopharmacol.2000:S349.Google Scholar 60. Marks I, Lovell K, Noshirvani H. et al. Treatment of posttraumatic stress disorder by exposure and/or cognitive restructuring. Arch Gen Psychiatry.1998;55:317-322.Google Scholar 61. Foa EB, Dancu CV, Hembree E. et al. The efficacy of exposure therapy, stress inoculation training and their combination in ameliorating PTSD for female victims of assault. J Consult Clin Psychol.1999;67:194-200.Google Scholar 62. Tarrier N, Pilgrim H, Sommerfield C. et al. A randomized trial of cognitive therapy and imaginal exposure in the treatment of chronic posttraumatic stress disorder. J Consult Clin Psychol.1999;67:13-18.Google Scholar 63. Devilly GJ, Spence SH. 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.1999;13:131-157.Google Scholar 64. Mynors-Wallis LM, Gath DH, Lloyd-Thomas AR, Tomlinson D. Randomized controlled trial comparing problem-solving treatment with amitriptyline and placebo in primary care. BMJ.1995;310:441-445.Google Scholar 65. Haug TT, Hellstrøm K, Blomhoff S, Humble M, Madsbu HP. The treatment of social phobia in general practice: is exposure therapy feasible? Fam Pract.2000;17:114-118.Google Scholar 66. Smyth JM, Stone AA, Hurewitz A, Kaell A. Effects of writing about stressful experiences on symptom reduction in patients with asthma or rheumatoid arthritis. JAMA.1999;281:1304-1309.Google Scholar 67. Bisson JI, McFarlane AC, Rose S. Psychological debriefing. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for PTSD. New York, NY: The Guilford Press; 2000:317-319. 68. Cohen JA, Berliner L, March JS. Treatment of children and adolescents. In: Foa EB, Keane TM, Friedman MJ, eds. Effective Treatments for PTSD. New York, NY: The Guilford Press; 2000;330-332. 69. Foa EB, Keane TM, Friedman MJ. Effective Treatments for PTSD. New York, NY: The Guilford Press; 2000:1-17. 70. Murray CJL, Lopez AD. Introduction. In: Murray CJL, Lopez AD, eds. The Global Burden of Disease. Boston, Mass: Harvard University School of Public Health; 1996;5.

Journal

JAMAAmerican Medical Association

Published: Aug 1, 2001

Keywords: post-traumatic stress disorder

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