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Abstract

This study investigated whether impairment persists after posttraumatic stress disorder (PTSD) has resolved. Traumatically injured patients (N = 1,035) were assessed during hospital admission and at 3 (85%) and 12 months (73%). Quality of life prior to traumatic injury was measured with the World Health Organization Quality of Life–BREF during hospitalization and at each subsequent assessment. PTSD was assessed using the Clinician-Administered PTSD Scale at 3 and 12 months. After controlling for preinjury functioning, current pain, and comorbid depression, patients whose PTSD symptoms had resolved by 12 months were more likely to have poorer quality of life in psychological (OR = 3.51), physical (OR = 10.17), social (OR = 4.54), and environmental (OR = 8.83) domains than those who never developed PTSD. These data provide initial evidence that PTSD can result in lingering effects on functional capacity even after remission of symptoms.

Reprinted from Clin Psychol Sci 2016; 4:493–498, with permission from Sage. Copyright © 2016

Posttraumatic stress disorder (PTSD) affects up to 8% of the population (Breslau, 1998), and among mental disorders is one of the major causes of burden of disease (Gadermann, Alonso, Vilagut, Zaslavsky, & Kessler, 2012). A major reason for the marked economic and social cost of PTSD is the negative impact it has on people’s capacity to function optimally. It has been widely documented that PTSD can be a debilitating condition that results in a range of impairments to functioning and quality of life (Lunney & Schnurr, 2007). Quality of life has been conceptualized as consisting of a range of dimensions, including interpersonal, marital, occupational, and personal satisfaction domains (Gladis, Gosch, Dishuk, & Crits-Christoph, 1999). Across these core areas of functioning, it has been shown that people with PTSD experience significant impairments in occupational (Bolton et al., 2004; Hoge et al., 2008), family and marital (Rona et al., 2009; Sayers, Farrow, Ross, & Oslin, 2009), and socialization (O’Connell, Kasprow, & Rosenheck, 2008; Schnurr, Hayes, Lunney, McFall, & Uddo, 2006) domains. It is interesting that trauma survivors who do not experience the requisite symptoms to meet PTSD diagnostic criterion also display marked levels of impairment. There is evidence that elevated levels of impairment are seen in people with subsyndromal levels of PTSD (Stein, Walker, Hazen, & Forde, 1997), even when lifetime PTSD and comorbid depression are controlled (Zlotnick, Franklin, & Zimmerman, 2002). Indeed, one study found that people with subsyndromal PTSD had a higher prevalence rate of impairment than those who met PTSD criteria (Stein et al., 1997).

Although the impact of current PTSD on functioning has been repeatedly demonstrated, there is little study on the long-term effects of PTSD once the condition has resolved. There are hints from available evidence that having PTSD may lead to lingering adverse effects on functioning. For example, veterans from the Gulf War assessed years after the deployment still reported marked impairment relative to nondeployed counterparts (Li, Mahan, Kang, Eisen, & Engel, 2011). Specifically, no studies have addressed the possibility that having PTSD for a period of time impacts on people in ways that persist after resolution of PTSD symptoms. Considering that approximately one third of people with PTSD remit in the initial 5 months (Morina, Wicherts, Lobbrecht, & Priebe, 2014), it is critical to understand the extent to which the condition leaves residual ongoing functional impairment.

Method

Participants

Randomized weekday admissions to four major hospitals across three states in Australia were recruited into the study between April 2004 and February 2006. The study was approved by the Human Research Ethics Committee at each hospital. Inclusion criteria included hospital admission of greater than 24 hours following traumatic injury, aged between 16 and 70 years, and could understand and speak English proficiently. Individuals were excluded if they had moderate or severe brain injury, were currently psychotic or suicidal, were non-Australian visitors, or were under police guard.

There were 1,590 trauma patients who met inclusion criteria, and 1,035 completed the full initial assessment (65%). A total of 414 patients (40%) experienced a mild traumatic brain injury (MTBI), which was defined by the ICD-9 requirement of documented injury to the head, loss of consciousness for less than 30 minutes, no focal neurological deficit or intracranial complications, Glasgow Coma Scale score of least 13, and normal computerized tomography findings (Carroll et al., 2004). Individuals who refused to participate in the current study did not differ from participants in terms of gender (χ2 = 0.80, df = 1, p = .23), length of hospital admission, t(df = 1082) = 0.03, p = .88, injury severity score (ISS; American Association for Automotive Medicine, 1990), t(df = 1419) = 1.1, p = .16, or age, t(df = 1475) = 1.6, p = .14.

At the 3-month assessment, 883 completed the protocol (85%), and 755 (73%) completed the 12-month assessment. Participants and nonparticipants at the 12-month assessment did not differ in terms of gender (χ2 = 1.20, df = 1, p = .27), or length of hospital admission, t(1033) = 0.02, p = .98. Dropouts at 12 months were more likely to have a lower ISS (10.00 ± 7.06 vs. 11.36 ± 8.21), t(1022) = 2.38, p = .02, and be younger (35.59 ± 12.45 vs. 39.86 ± 13.89), t(1023) = 4.35, p = .000, than those who did participate. Table 1 presents the sample characteristics. The mean ISS was 10.87 ± 7.94. Participants spent an average of 12.38 (SD = 12.93) days in hospital.

Table 1. Participant Characteristics of Those Completing 12-Month Assessment

CharacteristicSubsyndromal/Full PTSD (n = 137), % (n)No PTSD (n = 618), % (n)
Gender
 Male68.6 (94)73.9 (457)
 Female31.4 (43)26.1 (161)
Age (M, SD)37.38 (11.31)39.33 (14.21)
Previous disorder
 Prior disorder30.7 (42)56.6 (350)
 No prior disorder69.3 (95)43.4 (268)
Type of injury
 Transport73.7 (101)64.9 (401)
 Assault8.8 (12)5.8 (36)
 Fall11.0 (16)16.8 (104)
 Work injury1.4 (1)5.8 (36)
 Other injury5.1 (7)6.7 (41)
Length of hospital stay (days) (M, SD)15.42 (15.91)11.89 (11.44)
Injury severity score (M, SD)12.27 (9.17)11.26 (8.21)
Mild traumatic brain injury (MTBI)
 MTBI57.7 (79)40.9 (253)
 No MTBI42.3 (58)59.1 (365)
Ethnic status
 Caucasian86.9 (119)86.6 (535)
 Other13.1 (18)13.4 (83)
Marital status
 Married/de facto40.1 (55)52.3 (323)
 Single59.9 (82)47.7 (295)
Employment status
 Employed83.2 (114)92.6 (572)
 Unemployed16.8 (23)7.4 (46)
Education
 Trade/higher degree62.0 (85)61.5 (380)
 High school38.0 (52)38.5 (238)

Table 1. Participant Characteristics of Those Completing 12-Month Assessment

Enlarge table

Measures

PTSD was assessed at 3 and 12 months using the Clinician-Administered PTSD Scale–IV (CAPS; Blake et al., 1995). The CAPS is a structured clinical interview that possesses good sensitivity (.84) and specificity (.95) relative to the Structured Clinical Interview for DSM Disorders (SCID) PTSD diagnosis, and also possesses sound test-retest reliability (.90; Blake et al., 1995).

The Mini-International Neuropsychiatric Interview (Version 5.5; MINI; Sheehan et al., 1998) was used to assess for major depressive disorder at each assessment. The MINI is a short, structured diagnostic interview based on the DSM-IV and the ICD-10 classification of mental illness.

World Health Organization Quality of Life–BREF (WHOQOL) was used to assesses quality of life across four domains of functioning: physical health (daily living, pain, work capacity), psychological (mood, self-esteem, concentration), social relationships (personal relationships, social support, sexual activity), and environment (financial resources, health care, home environment; WHOQOL Group, 1996). Poor functional impairment was defined by Australian norms for each scale of the WHOQOL (Hawthorne, Herrman, & Murphy, 2006). The WHOQOL was administered during hospitalization in relation to 2 weeks prior to the traumatic injury, and again at 3 and 12 months. General pain level was rated for the prior two weeks (1 = no pain at all, 10 = worst pain possible).

Procedure

After obtaining written informed consent, participants were assessed prior to hospital discharge, an average of 7.2 days (±9.6) after injury. Information regarding demographic, hospital admission, and injury-related factors was obtained from medical records. At 3 and 12 months after injury, participants were contacted by telephone and completed the CAPS and MINI, and the WHOQOL was returned by post. All assessments were audio-recorded to ensure adherence, and 5% were rescored blind to the original scoring to test interrater reliability. The interrater reliability was strong for both PTSD diagnostic consistency and symptom severity at 3 (1.00 and .84, respectively) and 12 months (.98 and .85, respectively).

Data Analysis

We calculated the proportion of participants who met full, subsyndromal, or no PTSD at baseline, 3 months, and 12 months according to participants’ diagnostic or subsyndromal (defined as meeting at least two of the three symptom clusters of DSM-IV criteria) status. We focused on a minimal cut-off of subsyndromal PTSD because of evidence that this level of symptoms is associated with impairment (Stein et al., 2002). To determine the influence of resolved PTSD on subsequent WHOQOL indices at 12 months, we identified participants who met at least subsyndromal PTSD at 3 months but did not meet subsyndromal level of PTSD at 12 months. In recognition that functioning following traumatic injury can be influenced by severe pain, we excluded patients who reported pain levels at 12 months greater than 5 (on the 10-point scale). Furthermore, to ensure that the lingering effects on impairment were not attributed to functioning levels prior to the trauma, current levels of pain, or comorbid depression, we calculated odds ratios that adjusted for WHOQOL scores in the 2 weeks prior to traumatic injury, rated pain, and presence of major depression at 12 months.

Results

Incidence of Posttraumatic Stress Disorder

In terms of PTSD at 3 months, 77 (8.7%) patients met all the criteria for PTSD and 168 (19.0%) patients displayed at least subsyndromal PTSD. At 12 months, 69 (9.2%) patients met all the criteria for PTSD and 137 (18.1%) patients displayed subsyndromal PTSD. To ensure that we focused only on patients who had remitted PTSD symptoms at 12 months, we removed the 137 patients with at least subsyndromal PTSD at 12 months; this resulted in 618 in the final sample. We defined remitted PTSD as patients who met at least subsyndromal PTSD at 3 months but did not meet all or subsyndromal criteria for PTSD at 12 months; on this basis, 62 (10.0%) patients reported PTSD remission at 12 months.

Incidence of Impairment

At 12 months, levels of impairment varied across domains (psychological: 20%; physical: 11%; social: 30%; environmental: 27%). Table 2 presents the proportion of participants who reported functional impairment at 12 months according to whether they had previously experienced at least subsyndromal PTSD since the traumatic injury but did not suffer at least subsyndromal PTSD at the time of assessment. Relative to participants who have no PTSD, those who had previously suffered at least subsyndromal PTSD at 3 months were significantly more likely to suffer persistent problems with psychological (OR = 2.73), physical (OR = 9.76), social (OR = 2.52), and environmental (OR = 2.65) domains of quality of life after controlling for preinjury quality of life, concurrent pain, and concurrent depression. By way of comparison, Table 2 also presents comparable rates for participants with at least subsyndromal PTSD at 12 months; those with current PTSD were more likely to suffer impaired quality of life in psychological (OR = 2.33), physical (OR = 9.70), and social (OR = 2.82) domains.

Table 2. Frequency and Adjusted Odds Ratio for Suffering Impaired Quality of Life or Functioning Controlling for Preinjury Functioning Level, Current Pain, and Comorbid Depression

ImpairmentNo PTSD (n = 556), % (n)Resolved PTSD (n = 62), % (n)OR (95% CI) pCurrent PTSD (n = 42), % (n)OR (95% CI) p
1-year psychological QoL17.5 (97)46.8 (29)2.73 (1.39-5.36) .00442.9 (18)2.33 (0.98-5.49) .05
1-year physical QoL7.7 (43)40.3 (25)9.76 (3.87-24.60) .00019.0 (8)9.70 (2.38-39.51) .002
1-year social QoL27.5 (153)51.6 (32)2.52 (1.34-4.74) .00452.4 (22)2.82 (1.24-6.40) .01
1-year environmental QoL24.1 (134)54.8 (62)2.65 (1.40-5.00) .00338.1 (16)2.18 (0.93-5.10) .07

Note: Adjusted odds ratios calculated on impairment in participants who (a) had at least subsyndromal PTSD at 3 months but experienced no subsyndromal PTSD at 12 months relative to participants who never experienced PTSD and (b) had at least subsyndromal PTSD at 12 months. Adjusted odds ratios controlled for functioning prior to injury and depression and pain at 12 months. CI = confidence interval; OR = odds ratio; QoL = quality of life.

Table 2. Frequency and Adjusted Odds Ratio for Suffering Impaired Quality of Life or Functioning Controlling for Preinjury Functioning Level, Current Pain, and Comorbid Depression

Enlarge table

Discussion

Traumatic injury survivors who had recovered from their PTSD continued to experience markedly poorer quality of life than those who had not previously had PTSD. This effect was noted even after controlling for pretrauma levels of functioning, pain, and comorbid depression. This is the first demonstration that PTSD may leave residual functional effects on people despite remission of their PTSD symptoms.

Although many cases of PTSD remit (Morina et al., 2014), it appears that there are functional scars from having the disorder. There are several possible explanations for this. First, PTSD has been linked to impaired hypothalamic-pituitary-adrenal axis functioning (Yehuda, 2003), altered gene expression (Yehuda & Bierer, 2007), and impairment to neural networks implicated in emotion regulation (Lanius, Bluhm, Lanius, & Pain, 2006). It is well documented that these changes can have a broad array of ripple effects on stress responses, physical health, and capacity to manage ongoing stressors in the environment. It is unknown to what extent these dysfunctions persist after PTSD symptoms abate; however, there is evidence from animal studies that the neurobiological effects of severe stress can be long-lasting (Cotella, Mestres Lascano, Franchioni, Levin, & Suarez, 2013). Patients who experience PTSD for an extended period may experience persisting alteration of fundamental physiological process that underpin stress response and this can extend beyond remission of symptoms, which can then affect one’s capacity to function.

Second, PTSD can result in altered appraisals of oneself and environment that can undermine one’s capacity to function. Many studies attest to the tendency for people with PTSD to develop cognitive patterns in which they ruminate on the trauma or exaggerate the extent to which they are likely to be threatened again (Ehlers & Clark, 2000). This form of thinking may become habitual and contribute to social, occupational, and psychological impairments.

Third, PTSD can result in withdrawal from established social networks (Mikulincer, Solomon, & Shaver, in press), which results in social isolation that can perpetuate negative emotional states. Related to this, detachment and emotional numbing have been specifically linked with reduced psychosocial functioning, especially in more chronic stages of posttrauma adjustment (Riggs, Byrne, Weathers, & Litz, 1998; Samper, Taft, King, & King, 2004). It is possible that patients withdraw from social connections as a result of the active PTSD avoidance symptoms, and consequently develop socially avoidant habits that persist beyond the remission of their PTSD symptoms. This behavior may also distance others from the patient, and so when PTSD symptoms resolve, their prior social networks are no longer accessible.

Fourth, even though we controlled for pretrauma levels of functioning, it is possible that other preexisting risk factors could have contributed to functional levels beyond remission of PTSD symptoms. Impaired functioning prior to deployment has been shown to increase risk for PTSD in troops deployed to the Middle East, suggesting that difficulties with functional capacity may compromise one’s ability to manage the stresses of trauma (LeardMann et al., 2009). Prospective studies are required to comprehensively assess the role of pretrauma functioning and other variables (including genetic, personality, and environmental) on subsequent long-term functioning.

We note several limitations of the study. First, we conducted our follow-up clinical assessments via telephone rather than face-to-face; although these two formats have been shown to perform comparably (Aziz & Kenford, 2004). Second, those who dropped out during the course of the study were younger and less severely injured patients than those who participated at the follow-up, and this may have influenced the conclusions regarding residual impairment. Third, we did not assess treatment throughout the study. Fourth, as our sample was drawn from injured patients, it remains to be seen if the lingering effects of PTSD on functional impairment extends to other trauma populations.

This study raises a number of intriguing questions rather than representing a definitive demonstration of the long-term impact of ever having suffered PTSD. A key question to arise from these findings is the extent to which the lingering impact of remitted PTSD on functioning is unique to PTSD. Many studies have highlighted the range of psychiatric conditions that can arise from exposure to a traumatic event (e.g., Shalev et al., 1998), and it is possible that these also contribute to ongoing difficulties after the condition has resolved. A related issue is whether this impact is limited to posttraumatic psychological conditions or whether it equally applies to remitted conditions generally, regardless of trauma exposure. It is possible that exposure to a traumatic event carries with it certain longer-term effects that contribute to functional problems that are not observed in other psychiatric populations following remission. To test these issues, studies need to be conducted that include large numbers of people with a range of psychiatric conditions (both comorbid and singular conditions) that developed both in and out of trauma contexts, and in which thorough testing of functional outcomes are conducted over the course of recovery.

A related question pertains to the extent to which people who develop PTSD have an underlying vulnerability toward functional problems. Only the minority of trauma-exposed people develop PTSD, and these individuals are characterized by a range of preexisting risk candidates that include genetic (Cornelis, Nugent, Amstadter, & Koenen, 2010), psychophysiological (Guthrie & Bryant, 2006), cognitive (Bryant, Sutherland, & Guthrie, 2007), and social-demographic (Brewin, Andrews, & Valentine, 2000) factors. Our design assessed people only after trauma exposure and development of PTSD, which precludes disentangling the effects of PTSD on functional outcomes from preexisting vulnerability factors that may contribute to functioning. A better design would be to assess people on a range of known risk factors prior to trauma exposure, and determine the relative contributions of these factors and remitted PTSD on longer-term functioning.

Finally, it is premature to draw firm inferences from this study regarding treatment implications. Nonetheless, these findings raise the possibility that evidence-based treatment for PTSD may be optimized by integrating interventions that also focus on functional outcomes. Although a patient may enjoy remission of their symptoms, they may still experience problems in occupational, social, or other forms of functioning. Controlled trials that compared long-term outcomes for those who received evidence-based interventions, such as trauma-focused psychotherapy (Foa, Keane, Friedman, & Cohen, 2009), with interventions augmented with functional rehabilitation would shed important light on whether clinicians could be achieving better outcomes for patients by directly treating functional deficits.

School of Psychology, University of New South Wales (Bryant); Brain Dynamics Centre, Westmead Millennium Institute (Bryant); Centre for Military and Veteran Health, University of Adelaide (McFarlane); School of Psychiatry, University of New South Wales (Silove); and Phoenix Australia, Centre for Posttraumatic Mental Health, Department of Psychiatry, University of Melbourne (O'Donnell, Forbes, Creamer).
Corresponding Author: Richard A. Bryant, School of Psychology, University of New South Wales, Sydney NSW 2052, Australia. E-mail:

Funding: This research was supported by National Health and Medical Research Council Program Grant 568970, Victorian Trauma Foundation Grant #V-11, and National Health and Medical Research Council Australian Clinical Research Fellowship 359284. The study sponsors had no role in the design or conduct of the study, or in the collection, analysis, or interpretation of the data. R.A.B. had full access to all the data and had final responsibility for the decision to submit for publication.

Declaration of Conflicting Interests: The authors declared that they had no conflicts of interest with respect to their authorship or the publication of this article.

Author Contributions: R. A. Bryant, M. Creamer, D. Silove, and A. C. McFarlane obtained study funding. All authors contributed to study design and preparation of the manuscript. R. A. Bryant conducted data analysis.

References

American Association for Automotive Medicine. (1990). The Abbreviated Injury Scale 1990–Revision. Des Plaines, IL: Author. Google Scholar

Aziz, M., & Kenford, S. (2004). Comparability of telephone and face-to-face interviews in assessing patients with posttraumatic stress disorder. Journal of Psychiatric Practice, 10, 307–313. CrossrefGoogle Scholar

Blake, D. D., Weathers, F., Nagy, L. M., Kaloupek, D. G., Gusman, F. D., Charney, D. S., & Keane, T. M. (1995). The development of a Clinician-Administered PTSD Scale. Journal of Traumatic Stress, 8, 75–90. CrossrefGoogle Scholar

Bolton, D., Hill, J., O’Ryan, D., Udwin, O., Boyle, S., & Yule, W. (2004). Long-term effects of psychological trauma on psychosocial functioning. Journal of Child Psychology Psychiatry, 45, 1007–1014. CrossrefGoogle Scholar

Breslau, N. (1998). Epidemiology of trauma and posttraumatic stress disorder. In R. Yehuda (Ed.), Psychological trauma (pp. 1–29). Washington, DC: American Psychiatric Press. Google Scholar

Brewin, C. R., Andrews, B., & Valentine, J. D. (2000). Metaanalysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. Journal of Consulting and Clinical Psychology, 68, 748–766. CrossrefGoogle Scholar

Bryant, R. A., Sutherland, K., & Guthrie, R. M. (2007). Impaired specific autobiographical memory as a risk factor for posttraumatic stress after trauma. Journal of Abnormal Psychology, 116, 837–841. CrossrefGoogle Scholar

Carroll, L. J., Cassidy, J. D., Peloso, P. M., Borg, J., von Holst, H., Holm, L., et al. WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. (2004). Prognosis for mild traumatic brain injury: Results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. Journal of Rehabilitation Medicine, 36, 84–105. CrossrefGoogle Scholar

Cornelis, M. C., Nugent, N. R., Amstadter, A. B., & Koenen, K. C. (2010). Genetics of post-traumatic stress disorder: Review and recommendations for genome-wide association studies. Current Psychiatry Reports, 12, 313–326. CrossrefGoogle Scholar

Cotella, E. M., Mestres Lascano, I., Franchioni, L., Levin, G. M., & Suarez, M. M. (2013). Long-term effects of maternal separation on chronic stress response suppressed by amitriptyline treatment. Stress, 16, 477–481. CrossrefGoogle Scholar

Ehlers, A., & Clark, D. M. (2000). A cognitive model of post-traumatic stress disorder. Behaviour Research & Therapy, 38, 319–345. CrossrefGoogle Scholar

Foa, E. B., Keane, T. M., Friedman, M. J., & Cohen, J. A. (Eds.). (2009). Effective treatments for PTSD: Practice guidelines from the International Society of Traumatic Stress Studies (2nd ed.). New York, NY: Guilford. Google Scholar

Gadermann, A. M., Alonso, J., Vilagut, G., Zaslavsky, A. M., & Kessler, R. C. (2012). Comorbidity and disease burden in the National Comorbidity Survey Replication (NCS-R). Depression and Anxiety, 29, 797–806. CrossrefGoogle Scholar

Gladis, M. M., Gosch, E. A., Dishuk, N. M., & Crits-Christoph, P. (1999). Quality of life: Expanding the scope of clinical significance. Journal of Consulting and Clinical Psychology, 67, 320–331. CrossrefGoogle Scholar

Guthrie, R. M., & Bryant, R. A. (2006). Extinction learning before trauma and subsequent posttraumatic stress. Psychosomatic Medicine, 68, 307–311. CrossrefGoogle Scholar

Hawthorne, G., Herrman, H., & Murphy, B. (2006). Interpreting the WHOQOL-Brèf: Preliminary population norms and effect sizes. Social Indicators Research, 77, 37–59. CrossrefGoogle Scholar

Hoge, C. W., McGurk, D., Thomas, J. L., Cox, A. L., Engel, C. C., & Castro, C. A. (2008). Mild traumatic brain injury in US Soldiers returning from Iraq. New England Journal of Medicine, 358, 453–463. CrossrefGoogle Scholar

Lanius, R. A., Bluhm, R., Lanius, U., & Pain, C. (2006). A review of neuroimaging studies in PTSD: Heterogeneity of response to symptom provocation. Journal of Psychiatric Research, 40, 709–729. CrossrefGoogle Scholar

LeardMann, C. A., Smith, T. C., Smith, B., Wells, T. S., Ryan, M. A., & Millennium Cohort Study. (2009). Baseline self reported functional health and vulnerability to post-traumatic stress disorder after combat deployment: Prospective US military cohort study. British Medical Journal, 338, b1273. CrossrefGoogle Scholar

Li, B., Mahan, C. M., Kang, H. K., Eisen, S. A., & Engel, C. C. (2011). Longitudinal health study of US 1991 Gulf War veterans: Changes in health status at 10-year follow-up. American Journal of Epidemiology, 174, 761–768. doi:10.1093/aje/kwr154 CrossrefGoogle Scholar

Lunney, C. A., & Schnurr, P. P. (2007). Domains of quality of life and symptoms in male veterans treated for posttraumatic stress disorder. Journal of Traumatic Stress, 20, 955–964. CrossrefGoogle Scholar

Mikulincer, M., Solomon, Z., & Shaver, P. R. (in press). Attachment-related consequences of war captivity and trajectories of posttraumatic stress disorder: A 17-year longitudinal study. Journal of Social and Clinical Psychology. Google Scholar

Morina, N., Wicherts, J. M., Lobbrecht, J., & Priebe, S. (2014). Remission from post-traumatic stress disorder in adults: A systematic review and meta-analysis of long term outcome studies. Clinical Psychology Review, 34, 249–255. CrossrefGoogle Scholar

O’Connell, M. J., Kasprow, W., & Rosenheck, R. A. (2008). Rates and risk factors for homelessness after successful housing in a sample of formerly homeless veterans. Psychiatric Services, 59, 268–275. CrossrefGoogle Scholar

Riggs, D. S., Byrne, C. A., Weathers, F. W., & Litz, B. T. (1998). The quality of the intimate relationships of male Vietnam veterans: Problems associated with posttraumatic stress disorder. Journal of Traumatic Stress, 11, 87–101. CrossrefGoogle Scholar

Rona, R. J., Jones, M., Iversen, A., Hull, L., Greenberg, N., Fear, N. T., et al. Wessely, S. (2009). The impact of post-traumatic stress disorder on impairment in the UK military at the time of the Iraq war. Journal of Psychiatric Research, 43, 649–655. CrossrefGoogle Scholar

Samper, R. E., Taft, C. T., King, D. W., & King, L. A. (2004). Posttraumatic stress disorder symptoms and parenting satisfaction among a national sample of male Vietnam veterans. Journal of Traumatic Stress, 17, 311–315. CrossrefGoogle Scholar

Sayers, S. L., Farrow, V. A., Ross, J., & Oslin, D. W. (2009). Family problems among recently returned military veterans referred for a mental health evaluation. Journal of Clinical Psychiatry, 70, 163–170. CrossrefGoogle Scholar

Schnurr, P. P., Hayes, A. F., Lunney, C. A., McFall, M., & Uddo, M. (2006). Longitudinal analysis of the relationship between symptoms and quality of life in veterans treated for posttraumatic stress disorder. Journal of Consulting and Clinical Psychology, 74, 707–713. CrossrefGoogle Scholar

Shalev, A. Y., Freedman, A., Peri, T., Brandes, D., Sahara, T., Orr, S., & Pitman, R. K. (1998). Prospective study of post-traumatic stress disorder and depression following trauma. American Journal of Psychiatry, 155, 630–637. CrossrefGoogle Scholar

Sheehan, D. V., Lecrubier, Y., Harnett-Sheehan, K., Amorim, P., Janavs, J., Weiller, E., et al. Dunbar, G. (1998). The Mini International Neuropsychiatric Interview (M.I.N.I.): The development and validation of a structured diagnostic psychiatric interview. Journal of Clinical Psychiatry, 59(Suppl. 20), 22–33. Google Scholar

Stein, M. B., Höfler, M., Perkonigg, A., Lieb, R., Pfister, H., Maercker, A., & Wittchen, H.-U. (2002). Patterns of incidence and psychiatric risk factors for traumatic events. International Journal of Methods in Psychiatric Research, 11, 143–153. CrossrefGoogle Scholar

Stein, M. B., Walker, J. R., Hazen, A. L., & Forde, D. R. (1997). Full and partial posttraumatic stress disorder: Findings from a community survey. American Journal of Psychiatry, 154, 1114–1119. CrossrefGoogle Scholar

WHOQOL Group. (1996). WHOQOL-BREF: Introduction, administration, scoring and generic version of the assessment. Geneva, Switzerland: World Health Organization. Google Scholar

Yehuda, R. (2003). Adult neuroendocrine aspects of PTSD. Psychiatric Annals, 33, 30–36. CrossrefGoogle Scholar

Yehuda, R., & Bierer, L. M. (2007). Transgenerational transmission of cortisol and PTSD risk. Progress in Brain Research, 167, 121–135. CrossrefGoogle Scholar

Zlotnick, C., Franklin, C. L., & Zimmerman, M. (2002). Does “subthreshold” posttraumatic stress disorder have any clinical relevance? Comprehensive Psychiatry, 43, 413–419. CrossrefGoogle Scholar