Correspondence
Post-Traumatic Stress Disorder
N Engl J Med 2002; 346:1495-1498May 9, 2002
- Article
To the Editor:
After the September 11 terrorist attacks, many people in the United States had substantial symptoms of stress.1-3 However, little information is available from other countries.
Between October 6 and October 13, 2001, we conducted a survey measuring subjective health status by means of a standardized instrument — the 12-item Short-Form Health Survey — in a sample of 1928 persons who were representative of the population of Italy. This instrument had been calibrated to provide an expected mean value of 50.4,5 Trained interviewers collected data in the context of a personal telephone interview.
The main results — the scores on the summary scales for physical and mental health — are shown in Table 1Table 1
Subjective Health Status in a Representative Sample of the Italian Population, October 2001.. The mean overall score on the scale measuring physical health was 50.1 — that is, very close to the expected value. In contrast, the mean overall score on the scale measuring mental health was 48.2 — that is, about 20 percent of 1 SD below the expected value, with lower numbers indicating lower perceived mental health.4,5 Mean scores on both scales were higher among younger and more educated persons.These results, indicating a slight depression in the mental health score, can be compared with historical data. In 2000, as part of a nationwide survey conducted by the Italian National Institute of Statistics, these surveys were administered to a sample of 140,000 citizens; the mean scores were 50.3 on the physical health summary scale and 50.0 on the mental health summary scale. We conclude that the September terrorist attacks negatively influenced mental health summary scores outside the United States.
5 ReferencesGiovanni Apolone, M.D.
Paola Mosconi, Biol.Sc.D.
Istituto di Ricerche Farmacologiche Mario Negri, 20157 Milan, ItalyCarlo La Vecchia, M.D.
Università degli Studi di Milano, 20133 Milan, Italy
lavecchia@marionegri.it 1
Schuster MA ,Stein BD ,Jaycox LH , et al. A national survey of stress reactions after the September 11, 2001, terrorist attacks. N Engl J Med 2001;345:1507-1512
Full Text | Web of Science | Medline2
Lavie P . Sleep disturbance in the wake of traumatic events. N Engl J Med 2001;345:1825-1832
Full Text | Web of Science | Medline3
Yehuda R . Post-traumatic stress disorder. N Engl J Med 2002;346:108-114
Full Text | Web of Science | Medline4
Gandek B ,Ware JE ,Aaronson NK , et al. Cross-validation of item selection and scoring for the SF-12 Health Survey in nine countries: results from the IQOLA Project. J Clin Epidemiol 1998;51:1171-1178
CrossRef | Web of Science | Medline5
Kodraliu G ,Mosconi P ,Groth N , et al. Subjective health status assessment: evaluation of the Italian version of the SF-12 Health Survey: results from the MiOS Project. J Epidemiol Biostat 2001;6:305-316
CrossRef | Medline
To the Editor:
In his editorial, in discussing the relation between the traumatic events of September 11 and post-traumatic stress disorder (PTSD) in patients, Ursano (Jan. 10 issue)1 remarks that “cases of bioterrorism-related anthrax that have occurred since September 11 have highlighted the need for changes in the health care system. Substantial funds and effort are needed to render the system capable of handling a serious attack . . . whether it involves biologic, chemical, or radiologic weapons.” Although there is much truth in this advice, it should not completely distract us from the more effective approaches of primary prevention.
Recent history provides a good example. During the early 1980s, hospitals in the United States were asked to prepare for an influx of casualties from a “limited nuclear war” that might occur in Europe. Members of the International Physicians for the Prevention of Nuclear War and Physicians for Social Responsibility, among others, thoughtfully responded that the health care system cannot save large numbers of casualties of nuclear disaster and emphasized instead international cooperation for the reduction of nuclear arsenals. This proved to be a successful approach.
1 ReferencesWilliam S. Beckett, M.D.
University of Rochester School of Medicine and Dentistry, Rochester, NY 14642
bill_beckett@urmc.rochester. edu 1
Ursano RJ . Post-traumatic stress disorder. N Engl J Med 2002;346:130-132
Full Text | Web of Science | Medline
To the Editor:
In her review of PTSD (Jan. 10 issue),1 Yehuda confounds the vulnerability to traumatic events with the vulnerability to PTSD after such events and draws a mistaken conclusion — namely, that the data argue against an increased vulnerability to PTSD among women. One of the most consistent findings in epidemiologic research involving samples of civilians is the higher vulnerability of women than men to PTSD.2-5 Although women are less likely to have the type of traumatic experiences that lead to PTSD, they are more likely to succumb to PTSD after such experiences. This is the case even when the type of traumatic event is controlled for3,5 and when traumatic sexual experiences, which are more prevalent among women, are excluded and the rates of PTSD resulting from other traumatic events are compared.4,5
In addition, Yehuda's statement that the finding in one study5 that 50 percent of cases of PTSD in women (as compared with 15 percent of those in men) appear to result from sexual or physical assault is attributable to “the extremely high frequency of sexual and physical assault among women” is false. The cited article reports that the prevalence of exposure to assaultive violence was lower among women (traumatic sexual experiences occurred more frequently among women, but physical assaults in general occurred less frequently), and that the difference between the sexes in the proportions of cases of PTSD that were attributable to assaultive violence resulted primarily from the greater vulnerability of women to PTSD after such events.
5 ReferencesNaomi Breslau, Ph.D.
Henry Ford Health System, Detroit, MI 48202
nbresla1@hfhs.org 1
Yehuda R . Post-traumatic stress disorder. N Engl J Med 2002;346:108-114
Full Text | Web of Science | Medline2
Brewin CR ,Andrews B ,Valentine JD . Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychol 2000;68:748-766
CrossRef | Web of Science | Medline3
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
Web of Science | Medline4
Stein MB ,Walker JR ,Forde DR . Gender differences in susceptibility to posttraumatic stress disorder. Behav Res Ther 2000;38:619-628
CrossRef | Web of Science | Medline5
Breslau N ,Chilcoat HD ,Kessler RC ,Peterson EL ,Lucia VC . Vulnerability to assaultive violence: further specification of the sex difference in post-traumatic stress disorder. Psychol Med 1999;29:813-821
CrossRef | Web of Science | Medline
To the Editor:
In the section on epidemiologic aspects of PTSD, Yehuda does not mention coexisting conditions such as major depression. The rate of coexisting major depression among patients with PTSD is high — 47.9 percent among women and 48.5 percent among men.1 In Figure 1 in the section on the biologic aspects of PTSD, Yehuda concludes that in patients with PTSD, there is an increased sensitivity of the negative-feedback system of the hypothalamic–pituitary–adrenal axis, whereas the opposite is found in patients with major depression. How can we understand the high rate of major depression coexisting with PTSD in the light of these contrasting hormone profiles?
I think traumatic stress influences not only the norepinephrine system and the hypothalamic–pituitary–adrenal axis, but also systems such as the dopaminergic, serotonergic, endogenous opiate, and γ-aminobutyric acid–benzodiazepine systems.2 Moreover, since there are two types of steroid receptors (type I [mineralocorticoid] and type II [glucocorticoid]), the balance between the two types has an important role in developing psychopathology.3
Yehuda also describes brain areas involved in fear responses, such as the amygdala, the anterior paralimbic region, and the anterior cingulate and orbitofrontal areas, but she does not discuss in detail the interaction between the limbic system (amygdala and hippocampus) and the prefrontal cortex. One of the important functions of the prefrontal cortex, however, is extinction — the inhibition of fear responses caused by the amygdala.4
4 ReferencesR.J.L. Lindauer, M.D.
Academic Medical Center, 1105 BC Amsterdam, the Netherlands
r.j. lindauer@amc. uva. nl 1
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
Web of Science | Medline2
Charney DS ,Deutch AY ,Krystal JH ,Southwick SM ,Davis M . Psychobiologic mechanisms of posttraumatic stress disorder. Arch Gen Psychiatry 1993;50:294-305
Web of Science3
De Kloet ER ,Vreugdenhil E ,Oitzl MS ,Joels M . Brain corticosteroid receptor balance in health and disease. Endocr Rev 1998;19:269-301
CrossRef | Web of Science | Medline4
Morgan MA ,Romanski LM ,LeDoux JE . Extinction of emotional learning: contribution of medial prefrontal cortex. Neurosci Lett 1993;163:109-113
CrossRef | Web of Science | Medline
To the Editor:
I was disappointed that the review by Yehuda did not address the question of the legitimacy of the diagnosis of PTSD as it has been elucidated by others.1 It appears that some authorities think that this diagnosis is overused.
1 ReferencesT. Mark Meyer, M.D.
Aiken Internal Medicine, Aiken, SC 298011
Summerfield D . The invention of post-traumatic stress disorder and the social usefulness of a psychiatric category. BMJ 2001;322:95-98
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Author/Editor Response
Dr. Yehuda replies:
To the Editor: The greater probability that PTSD will occur after rape than after an accident is best attributed to differences in the ability of these events to engender fear or feelings of helplessness, not to preexisting vulnerabilities of those who have the two types of experiences. Similarly, it is arguable that being assaulted by a man who weighs 200 lb is a different experience for a woman who weighs 110 lb than for a man who weighs 190 lb. Accordingly, the increased likelihood of PTSD in women may reflect more severe traumatic experiences, rather than an inherent vulnerability to illness. This explanation is bolstered by the fact that the prevalence of PTSD after events such as an accident, a natural disaster, or the death of a loved one is not significantly higher among women than among men.1 It cannot be assumed that controlling for the type of traumatic event sufficiently accounts for the manner in which differences between the sexes alter the character of an event within a broadly conceived category.
The coexistence of depression with PTSD may simply reflect an overlap of symptoms (e.g., insomnia, impaired concentration, irritability, loss of interest, and restricted emotion).2 Most studies have found little or no contribution of depression to the neuroendocrine alterations associated with PTSD.3 Conversely, women with depression who have been abused early in life have reduced cortisol levels and increased responsiveness of the hypothalamic–pituitary–adrenal axis, as do patients with PTSD,4 raising the possibility that biologic subtypes of PTSD and depression may be categorized according to whether traumatization occurred early or later in life, rather than according to the nature, severity, and coexistence of symptoms.
The objective of the review was to report findings associated specifically with PTSD, not fear or stress in general, and to highlight the fact that such findings are in some ways distinct from those related to the physiology of fear or stress. PTSD is worthy of study precisely because its understanding will require more than the repackaging of current ideas about “stress” as explanations for its occurrence and pathophysiology. Increased recognition of the unique and circumscribed biologic profile associated with PTSD warrants the development of new pharmacologic approaches that might take into account the specific biologic underpinnings of this disorder.
It has historically been convenient to question the legitimacy of the diagnosis of PTSD for a number of social and political reasons, including the potential culpability of those who inflict traumatic stress on others.5 That the diagnosis may sometimes be overused does not speak to its legitimacy but to the lack of widespread understanding about what PTSD is, who is at risk, and how the disorder can best be diagnosed. As our understanding of these matters increases, the confusion, debate, and misuse that surround the diagnosis will abate.
5 ReferencesRachel Yehuda, Ph.D.
Mount Sinai School of Medicine, New York, NY 10029
rachel.yehuda@med. va. gov 1
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
Web of Science | Medline2
Friedman MJ, Yehuda R. Post-traumatic stress disorder and comorbidity: psychobiological approaches to differential diagnosis. In: Friedman JM, Charney DS, Deutch AY, eds. Neurobiological and clinical consequences of stress: from normal adaptation to post-traumatic stress disorder. Philadelphia: Lippincott-Raven, 1995:429-45.
3
Yehuda R . Psychoneuroendocrinology of post-traumatic stress disorder. Psychiatr Clin North Am 1998;21:359-379
CrossRef | Web of Science | Medline4
Heim C ,Newport DJ ,Heit S , et al. Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood. JAMA 2000;284:592-597
CrossRef | Web of Science | Medline5
Yehuda R ,McFarlane AC . Conflict between current knowledge about posttraumatic stress disorder and its original conceptual basis. Am J Psychiatry 1995;152:1705-1713
Web of Science | Medline
Author/Editor Response
The editorialist replies:
To the Editor: In discussing the prevention of terrorist attacks, Dr. Beckett highlights the value of the primary prevention of PTSD and other trauma-related psychiatric disorders such as depression. Primary prevention of post-traumatic psychiatric disorders1 is particularly important, since 34 to 44 percent of those in whom PTSD or depression develops after a traumatic event have no previous predisposing psychiatric illness.2 In our complex sociopolitical world, of which terrorism and war are a part, the prevention of these human-made disasters is important work for all, including physicians and health care providers. As in the case with seat belts and car accidents or smoking and lung cancer, event-related psychiatric disorders offer the opportunity for primary prevention by changing the types of behavior that trigger the disease process.
One of the most successful prevention programs was initiated in Australia to prevent malignant melanoma, a disease that is expected to affect more than 53,000 new patients and cause 7400 deaths in the United States this year.3 The campaign was built on a community-wide effort to “slip, slap, slop” — that is, slip on a T-shirt, slap on a hat, and slop on sunscreen lotion. Community action was the mechanism of primary disease prevention — a “vaccination” that resulted in a change in behavior.
Primary prevention often leads to collaboration with communities, educators, journalists, the media, and most important, community leaders. Prevention of the human-made disaster of war and terrorism will require similar but more complex psychosocial interventions. It is a worthy goal.
3 ReferencesRobert J. Ursano, M.D.
Uniformed Services University School of Medicine, Bethesda, MD 20814-4799
rursano@usuhs.mil 1
Ursano RJ, Grieger TA, McCarroll JE. Prevention of post-traumatic stress: consultation, training and early treatment. In: van der Kolk BA, McFarlane AC, Weisaeth L, eds. Traumatic stress: the effects of overwhelming experience on mind, body, and society. New York: Guilford Press, 1996:441-62.
2
North CS ,Nixon SJ ,Shariat S , et al. Psychiatric disorders among survivors of the Oklahoma City bombing. JAMA 1999;282:755-762
CrossRef | Web of Science | Medline3
Jemal A ,Thomas A ,Murray T ,Thun M . Cancer statistics, 2002. CA Cancer J Clin 2002;52:23-47
CrossRef | Web of Science | Medline
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