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Sleep in Lifetime Posttraumatic Stress Disorder
A Community-Based Polysomnographic Study
Naomi Breslau, PhD;
Thomas Roth, PhD;
Eleni Burduvali, MA;
Alissa Kapke, MS;
Lonni Schultz, PhD;
Timothy Roehrs, PhD
Arch Gen Psychiatry. 2004;61:508-516.
ABSTRACT
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Background Sleep complaints are common in posttraumatic stress disorder (PTSD) and are included in the DSM criteria. Polysomnographic studies conducted on small samples of subjects with specific traumas have yielded conflicting results. We therefore evaluated polysomnographic sleep disturbances in PTSD.
Methods A representative cohort of young-adult community residents followed-up for 10 years for exposure to trauma and PTSD was used to select a subset for sleep studies for 2 consecutive nights and the intermediate day. Subjects were selected from a large health maintenance organization and are representative of the geographic area except for the extremes of the socioeconomic status range. The subset for the sleep study was selected from the 10-year follow-up of the cohort (n = 913 [91% of the initial sample]). Eligibility criteria included (1) subjects exposed to trauma during the preceding 5 years; (2) others who met PTSD criteria; and (3) a randomly preselected subsample. Of 439 eligible subjects, 292 (66.5%) participated, including 71 with lifetime PTSD. Main outcomes included standard polysomnographic measures of sleep induction, maintenance, staging, and fragmentation; standard measures of apnea/hypopnea and periodic leg movement; and results of the multiple sleep latency test.
Results On standard measures of sleep disturbance, no differences were detected between subjects with PTSD and control subjects, regardless of history of trauma or major depression in the controls. Persons with PTSD had higher rates of brief arousals from rapid eye movement (REM) sleep. Shifts to lighter sleep and wake were specific to REM and were significantly different between REM and non-REM sleep (F1,278 = 5.92; P = .02).
Conclusions We found no objective evidence for clinically relevant sleep disturbances in PTSD. An increased number of brief arousals from REM sleep was detected in subjects with PTSD. Sleep complaints in PTSD might represent amplified perceptions of brief arousals from REM sleep.
INTRODUCTION
The official definition of posttraumatic stress disorder (PTSD) in the DSM-III and subsequent DSM editions includes sleep problems as criterion symptoms of reexperiencing (ie, "recurrent distressing dreams of the event") and increased arousal (ie, "difficulty falling or staying asleep"). The presence of sleep disturbance (as that of other defining symptoms) is determined on the basis of subjects' reports and does not require any objective, independent verification. Although sleep complaints are not necessary for the diagnosis of PTSD (as diagnostic criteria can be fulfilled in their absence), disturbing dreams and insomnia are reported by most persons with the disorder.1-3 The centrality of traumatic memories in PTSD and their intrusion in sleep have led to the application of sleep research methods to this disorder, extending previous research on affective disorders and other anxiety disorders.
To date, sleep studies on PTSD have focused primarily on combat veterans and, to a lesser extent, on victims of specific traumas who are recruited in clinical settings. In stark contrast to the consistent findings of high rates of sleep complaints in PTSD, sleep-laboratory studies have yielded conflicting results. Some studies reported difficulties in initiating and maintaining sleep, reduced sleep efficiency, and increased rates of brief arousals during sleep.4-10 Reports that sleep difficulties in patients with PTSD were observed only on the first night in the laboratory have suggested an increased sensitivity to novel sleep environments in PTSD.8 Attenuated first-night effects in Vietnam veterans with PTSD were reported as well.11 Other studies failed to find objective evidence of sleep disturbances in patients with PTSD.12-16
Rapid eye movement (REM) abnormalities are characteristic findings in affective disorders, which are frequently comorbid with PTSD.17-18 However, indicators of abnormalities in REM sleep (eg, latency to REM and total REM sleep) have not been detected in studies of anxiety disorders such as obsessive compulsive disorder,19 panic disorder,20 and social phobia.21 In contrast to other anxiety disorders, the observation that nightmares and recurrent dreams associated with traumatic memories are prototypic symptoms in PTSD1-2,22-23 has suggested the possibility that REM abnormalities might be observed in PTSD. Studies of REM functions have yielded conflicting results. Some studies reported shortened latency to REM sleep, increased REM density, and increased percentage of REM sleep.15, 24-26 Other studies reported contrasting patterns, characterized by increased REM latency and reduced REM sleep.4-5 Still other studies failed to detect differences in REM parameters between persons with PTSD and control subjects.27-28
Recent reports from small clinical samples have called attention to the possibility of an increased rate of breathing disturbances during sleep in patients with PTSD.29-31 The generalizability of these results to PTSD in the community has not been examined.
Previous sleep studies in PTSD have been limited by their small sample sizes and unrepresentativeness. Some lacked standardized diagnostic approaches or systematic assessment of all salient variables, including measures of more nuanced sleep fragmentation, adaptation to a novel sleep environment, and daytime sleepiness. The present study attempts to address some of these limitations. The study was conducted in the context of a large-scale, longitudinal community study. We present data from polysomnographic studies of 2 successive nights and from a measure of daytime sleepiness in the intervening day, collected on a subset of this epidemiological sample, including 71 persons with lifetime PTSD (12 with current and 59 with past PTSD).
Our analysis proceeds as follows. First, we compare subjects with lifetime PTSD vs those with no history of PTSD. Second, we compare sleep measures across the following 3 subgroups: PTSD, exposed to trauma/no PTSD, and never exposed to trauma. Third, we compare sleep measures of subjects with PTSD, major depression (MDD), and neither disorder. Our analytic models are designed to detect first-night effects overall (main effects) and across subgroups (interactions) and test other interactions of interest. As a preliminary step, we compared subjects with current vs past PTSD but found no evidence that the groups differed or that those with past cases display lower sleep quality than those with current cases. Consequently, we combined current and past cases in the analysis.
METHODS
SAMPLE AND PROCEDURES
The sleep investigation of PTSD was nested in a large-scale longitudinal community study of young adults. The study was described in detail previously.32-33 In brief, a sample of 1200 subjects was randomly selected in 1989 from all 21- to 30-year-old members of a large health maintenance organization in southeast Michigan. The membership of the health maintenance organization is representative of the population of the geographic area as depicted in the 1990 US census data, with the exception of the extremes of the socioeconomic range.22 Personal interviews were conducted in 1989 with 83.9% of the sample (n = 1007). Follow-up interviews were conducted in 1992, 1994, and 1999-2001. In each wave, more than 90% follow-up completion was achieved. In the 10-year 1999-2001 follow-up, 913 of the initial sample (91.0%) completed interviews. Sleep measures were collected on a subset of these respondents, whose ages ranged from 31 to 40 years at that time.
The following subjects from among those who completed the 10-year follow-up were eligible: (1) those who were exposed to traumatic events in the interval from 1994 to the last assessment, approximately 5 years later; (2) those not included under the first criterion who met PTSD criteria in previous assessments; and (3) those not included under the first or the second criterion from a randomly preselected subsample of the total sample. Subjects who moved away from the metropolitan area were not eligible. As a rule, those with recent (in the past month) substance abuse and use of psychotropic medications are not eligible for sleep studies. In this general population sample, no such exclusions were necessary. Respondents were invited to spend 2 consecutive nights and the intervening day at the Sleep Center of Henry Ford Hospital, Detroit, Mich. Of a total of 439 eligible subjects, 292 (66.5%) participated. Complete polysomnographic data are available on 283 respondents.
SLEEP-WAKE POLYSOMNOGRAPHIC ASSESSMENT
Each eligible participant was contacted by telephone and recruited for participation. Those agreeing to participate were further interviewed to determine their usual sleep schedule and use of prescribed, over-the-counter, and recreational drugs. On arrival at the sleep laboratory, the study procedures and requirements were again outlined verbally, and the participant read and signed a written informed consent approved by the Henry Ford Hospital institutional review board.
The sleep study consisted of 2 consecutive 8-hour nights of polysomnography and a multiple sleep latency test (MSLT) conducted during the day between the consecutive nights. Bedtime was established on the basis of the respondent's sleep schedule, as reported in the telephone interview. Determining the midpoint of a participant's usual sleep schedule and adding 4 hours to each side of the midpoint set the 8-hour sleep time. Caffeine and nicotine use was excluded in light to moderate users, whereas consumption was reduced and scheduled for heavy users (ie, daily use of >12 cigarettes and/or >400 mg of caffeine) so as not to interfere with the polysomnographic and MSLT assessments.
The polysomnography included the standard central (C3-A2) and occipital (Oz-A2) electroencephalograms, bilateral horizontal electro-oculograms, a submental electromyogram, and an electrocardiogram recorded with a V5 lead.34 In addition, airflow was monitored with oral and nasal thermistors, and leg movements were monitored with electrodes placed over the left tibialis muscles.35-36 The recordings, collected at a speed of 10 mm/s, were traced onto paper with polygraphs (Model 7D; Grass-Telefactor, West Warwick, RI) or digitized and stored (Heritage; Grass-Telefactor) electronically on equipment located in a separate monitoring room. Respiration and tibialis electromyogram recordings were evaluated and tabulated as to frequency of respiratory and leg movement events using the standard scoring criteria.35-36 Briefly, apneas, defined as 10-second or longer cessations of airflow, and hypopneas, defined as 10-second or longer 50% reductions of airflow, were summed and expressed as number of events per hour. In scoring periodic leg movements, only those tibialis electromyogram flexions of 0.5 second and greater associated with electroencephalographic arousals were tabulated. All sleep recordings were scored in 30-second epochs, according to the standards of Rechtschaffen and Kales34 for sleep stages. Scorers maintained a 90% scoring reliability and were unaware of study night or respondent's group membership.
The primary polysomnographic measures used to compare groups were latency to persistent sleep (latency from lights out to the first 10 minutes of continuous sleep); minutes of wake during sleep (epochs scored wake after sleep onset and before the final awakening divided by 2); sleep efficiency ([Total Sleep Time/Time in Bed] x 100); number of awakenings (2 consecutive epochs scored wake); percentages of stages 1, 2, 3 and 4 (combined), and REM sleep; latency to REM sleep (nonwake minutes from lights out to first epoch scored REM; and number of entries to stage 1 sleep and wake (1 epoch or more) from non-REM and REM sleep.
Measurement of daytime sleepiness by means of the MSLT was performed according to the standard protocol37 on the day between the 2 nocturnal recordings, at 2-hour intervals after arising, typically at 10 AM, 12 PM, 2 PM, and 4 PM. Participants laid down in a bed in quiet and dark rooms with the instruction to go to sleep. They remained in bed for 20 minutes after 3 consecutive epochs of stage 1 sleep, an epoch of another sleep stage, or 20 minutes of continuous wake. Sleep latency was scored as the minutes to the first epoch of sleep. The mean latency of the 4 tests was used as the measure of daytime sleepiness.
ASCERTAINING PTSD
The National Institute of Mental Health–Diagnostic Interview Schedule (NIMH-DIS)38 for DSM-III-R was used to diagnose psychiatric disorders. The baseline interview in 1989 inquired about lifetime history of disorders, and each follow-up assessment inquired about disorders occurring during the interval period since the previous assessment. The diagnosis of PTSD in DSM-III-R requires exposure to a qualifying traumatic event and the presence of PTSD criterion symptoms that are linked to the traumatic event. Two earlier studies reported high concordance between the diagnosis of lifetime PTSD by lay interviewers using structured interviews based on the DIS and independent clinical reinterviews.38-39 The latter used the Clinician-Administered PTSD Scale (CAPS)40-41 and reported sensitivity of 76% and specificity of 97%.42
STATISTICAL ANALYSIS
Statistical analyses were performed on log-transformed data. In the few instances when the log transformation did not correct for the distribution's skewness, nonparametric tests were used (eg, Wilcoxon rank sum test). To facilitate comparisons with previous work, the tables display raw means and standard deviations (SDs). Three series of analyses were conducted. The first series compared the PTSD group with no-PTSD controls. The second series consisted of comparisons across 3 groups, in which the no-PTSD group was divided into subjects exposed to trauma with no PTSD (exposed/no-PTSD group) and those who had never been exposed to trauma (nonexposed group). This series provided 2 control groups with which the PTSD group was compared. The third series consisted of comparisons across the following 3 groups, defined by history of PTSD and MDD: (1) neither disorder; (2) MDD only; and (3) PTSD with and without history of MDD. A separate analysis revealed no differences between PTSD alone vs PTSD comorbid with MDD.
We used multiple regression analysis applying generalized estimating equations (GEE),43-45 to test and estimate associations between group membership (eg, PTSD vs no-PTSD) and each of the sleep laboratory measures across the 2 nights. The GEE approach permits simultaneous modeling of the relationship between group classification and sleep measures from each of the 2 nights. The GEE takes into account correlations within subjects across the 2 nights. The addition of interaction terms allowed us to examine, in addition to main effects, whether differences across groups varied between the 2 nights and by covariates of interest (eg, sex). The model for testing interactions (using sex as an example) is illustrated in the following equation:
Y =  +  1(Group) + 2(Sex) + 3(Group x Sex) + 4(Time),
where sleep measures at 2 times (nights 1 and 2) are the outcomes (Y).
Although there were main effects of first vs second night, no significant interactions between night (first vs second) and group membership were detected in any model. Therefore, post hoc tests of differences by group membership across nights were not performed. No significant group x sex interaction was detected. The raw means and standard deviations appearing in the tables are averages of the 2 nights.
The statistical power available to test differences in this analysis is as follows. At = .05 and power of 80%, a comparison between the PTSD and no-PTSD groups could detect an effect size as small as 0.386, an effect size falling between small (0.2) and medium (0.5) for a t test, as defined by Cohen.46 The effect size in the 3 group models that can be detected between any 2 groups (eg, PTSD vs no exposure) was slightly larger but less than medium.
RESULTS
Characteristics of the subsample on which sleep-laboratory measures are available and the total sample of respondents who participated in the 10-year follow-up are depicted in Table 1. The subsample reflects closely the total sample composition with respect to sex, race, education, age, and history of alcohol or other drug abuse or dependence. No significant differences were observed on these variables when groups were defined by history of exposure and diagnostic categories. The prevalence of sleep complaints in persons with PTSD, measured by items in the NIMH-DIS PTSD module, was 87% (n = 62). Of all PTSD cases, 42% (n = 30) were attributable to assaultive violence (physical assault in 19 and rape in 11), 17% (n = 12) were attributable to sudden unexpected death of a loved one, 14% (n = 10) to accidents, 13% (n = 9) to witnessing violence, and 14% (n = 10) to miscellaneous traumatic events.
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Table 1. Sample Characteristics*
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SLEEP MEASURES IN PTSD VS NO-PTSD GROUPS
The GEE analysis of sleep-laboratory measures across the 2 nights revealed no significant differences in measures of sleep induction and sleep maintenance between the PTSD vs no-PTSD groups (Table 2). Significant differences were observed in the rate per hour of shifts to lighter sleep and wake (ie, stage 1 and stage 1 plus entry to wake) from REM. The specificity of these findings to REM sleep was evaluated by testing interactions between group membership (PTSD vs no-PTSD) and sleep type (REM vs non-REM), using analysis of variance with repeated measures. For entry to stage 1, F1,278 = 7.16 (P = .008), and for entry to stage 1 plus entry to wake, F1,278 = 5.92 (P = .02). These results indicate that the findings on these arousal variables were significantly different for REM vs non-REM sleep. The mean rate per hour of entry from REM to wake also was higher in the PTSD than in the no-PTSD group, but the difference did not reach statistical significance (P = .07). A related finding was the significantly lower percentage of REM sleep in the PTSD vs the no-PTSD group (P = .046).
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Table 2. Comparisons of PTSD vs No PTSD Groups
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Other findings of interest are the differences between first and second night in percentage of REM sleep, latency to REM, percentage of stage 2 sleep, and entry to stage 1 from non-REM sleep (Table 2). (The statistics for group comparisons on these variables are adjusted for first-night effects.) No interactions between group membership (PTSD vs no-PTSD) and assessment night were detected on any variable, indicating that subjects with PTSD were not different from controls in their adaptation to the first night in the laboratory.
CURRENT VS PAST PTSD
Subjects with current PTSD were compared with those with past PTSD on the array of sleep variables covered in the study (Table 3). No significant differences were detected on any variable. Furthermore, the means of the 2 groups are close and, to the extent that they differ, past PTSD was generally associated with worse sleep.
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Table 3. Comparisons of Past PTSD vs Current PTSD Groups
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PTSD AND EXPOSURE TO TRAUMA
We next evaluated sleep disturbance in PTSD by dividing the no-PTSD group into the following 2 subsets: exposed subjects with no PTSD and subjects with no history of exposure (Table 4). The GEE analysis on the 2 nights of data revealed main effects of group membership (ie, PTSD, exposed only, and nonexposed) on the number of shifts per hour to lighter sleep (ie, stage 1, wake, and stage 1 plus wake) from REM sleep. Subjects with a history of exposure to traumatic events who did not have PTSD had significantly lower rates of arousals from REM sleep than those with PTSD, whereas the nonexposed group was similar to the PTSD group. No differences were detected on any of the variables that signify sleep disturbance.
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Table 4. Comparisons of PTSD, Exposed Only (No PTSD), and Not Exposed Groups
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As in the 2-group analysis, presented in Table 2, we found evidence of significant main effects of first vs second night but no significant interactions between night and group membership.
PTSD, MDD, AND NEITHER DISORDER
In Table 5 we display results in which the no-PTSD control group was classified according to the presence or absence of history of MDD. The PTSD group includes persons with and without lifetime MDD. A separate series of analyses showed that PTSD comorbid with MDD (n = 49) did not differ from PTSD with no history of MDD (n = 22) on any of the sleep variables. The purpose in this set of analyses was to compare the PTSD group with a healthy control group that had neither PTSD nor MDD. Results for rates per hour of entry to stage 1 sleep and the combined rates of entry to stage 1 plus entry to wake from REM sleep are significant, indicating more arousals to lighter sleep and wake specific to REM sleep in PTSD, compared with controls with neither disorder. No differences were detected on variables that signify clinical sleep disturbance.
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Table 5. Comparisons of PTSD, MDD, and Neither Disorder Groups
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SLEEP BREATHING AND PERIODIC LEG MOVEMENT
We used a cutoff of 10 events/h to measure sleep breathing disturbances (apnea-hypopnea). Findings were 14% in the first night and 7% in the second night (P = .20). The difference between the PTSD and no-PTSD groups was not significant (P = .20). The only significant finding was the higher rate in men than women (odds ratio, 6.8; 95% confidence interval, 2.2-20.7). Using a cutoff of 10 events/h, analysis of periodic leg movement revealed no significant differences between the PTSD vs no-PTSD groups (P = .43). There were no significant night or sex effects.
DAYTIME SLEEPINESS
The GEE analyses of MSLT scores used the same models applied to the polysomnographic data. Differences across groups were not significant in any of the analyses. The 2-group comparison (PTSD vs no-PTSD) showed a higher average MSLT score for the PTSD (mean, 10.4; SD, 5.0) than for the no-PTSD (mean, 9.7; SD, 4.7) (P = .30) group. There were no significant differences between the PTSD, exposed/no-PTSD, and not-exposed groups. The 3-group comparison by psychiatric history (PTSD, MDD, and neither disorder) showed a lower MSLT average in persons with MDD (mean, 8.9; SD, 4.8) than in persons in the other 2 groups (P = .24). No difference was found between the PTSD and no-PTSD groups on sleep-onset–REM periods; 15.5% and 16.1%, respectively, registered 1 or more sleep-onset–REM period ( 2 = 0.02; P = .90).
COMMENT
This study failed to find objective evidence of sleep disturbance in persons with lifetime PTSD. On measures of sleep induction and sleep maintenance, no differences were detected between PTSD subjects and controls, regardless of history of exposure to trauma or history of MDD in the controls. No evidence was found of a first-night effect specific to PTSD, although the prototypic indicators of a first-night effect47-49 were observed in the sample as a whole. Ross et al50 also reported a first-night effect that was not specific to PTSD. Furthermore, there was no evidence to support a deficit in daytime alertness in PTSD. In contrast, we found significant associations of PTSD with shifts from REM sleep to lighter stages and to wake. The specificity of these findings to REM sleep was tested and confirmed.
Exposed subjects with no PTSD displayed a lower number of arousals from REM sleep than did PTSD and nonexposed subjects. Two potential explanations should be considered. First, a lower rate of arousal from REM might reflect a coping mechanism in trauma victims who did not have PTSD. Previous studies reported elevated awaking thresholds in REM30 and non-REM29 sleep in chronic PTSD and interpreted the findings as active coping. Our findings do not replicate that pattern, in that the lower arousal rates were specific to REM sleep and were observed only in trauma victims who did not have PTSD.
A second potential explanation is that history of exposure to trauma segregated the respondents into a susceptible group (ie, those with PTSD) vs a nonsusceptible group (ie, those who were exposed to trauma but did not have PTSD). The nonexposed group (which showed more arousals from REM sleep than the exposed/no-PTSD group) might have included respondents with a preexisting susceptibility to PTSD correlated with REM arousals, who would have PTSD if exposed. The presence of susceptible persons with elevated REM-related arousals would push upward the average of the nonexposed group as a whole. A similar pattern has been observed for level of catecholamines.51 Consideration should be given to the use of subjects who were exposed to traumatic events but did not have PTSD as a control group for evaluating sleep correlates of PTSD.
The findings from this study are consistent with recent reports from clinical samples that have concluded that objective measurements of sleep by standard polysomnographic methods do not demonstrate clinically relevant sleep disturbances in PTSD.52 The interpretation of the discrepancy between subjective complaints of disturbed sleep, including insomnia, nightmares, and recurrent distressing dreams about the trauma, and objective evidence of normal or adequate sleep is unclear.
The brief arousals from REM sleep associated with lifetime PTSD suggest the possibility that complaints of disturbed sleep in PTSD might have some basis in objectively measured facts. Although the subtle excess of arousals from REM sleep does not constitute evidence of clinical sleep disturbance, these arousals may signify phenomena that are misperceived as marked disturbances. Whether or not the REM phenomena are an aspect of the syndrome of PTSD or instead represent preexisting characteristics associated with vulnerability for PTSD cannot be answered in this study. Our finding that trauma-exposed subjects who did not have PTSD had a lower rate of arousals from REM sleep is consistent with the second interpretation.
The results of this study should be interpreted in light of the following considerations. First, the 66.5% participation in this community-based study, which required a 32-hour stay in the sleep laboratory, is high, considering the respondents' burden, but it limits the generalizability of the findings. However, the exceptionally high 10-year follow-up rate across multiple assessments allows us to evaluate the representativeness of the subset that participated in the sleep study by comparing it with the total sample from which it was drawn. As depicted in Table 1, no differences between the subset in the sleep study and the total sample were detected on sociodemographic characteristics and history of substance use disorders. Second, although previous sleep studies have used patients with current PTSD, we studied lifetime cases. The typically low current prevalence of PTSD in the community is reflected in our sample, in which less than one fifth of lifetime cases were current. A comprehensive comparison of current vs past cases across the entire array of sleep variables used in the study failed to detect any significant differences. Furthermore, an examination of the means reveals a pattern that is inconsistent with poorer sleep in current vs past cases. Thus, the failure to find sleep disturbances in PTSD cannot be attributed to the large proportion of past cases. The number of current PTSD cases is similar to that of previous studies of clinical samples of active PTSD, in which small sizes of samples (n<20) were typical.
Third, the model in which we separated the no-PTSD controls into those with history of MDD and those with no PTSD or MDD combined in a single category PTSD cases with and without history of MDD. Separate analyses failed to find significant differences between PTSD cases with MDD vs PTSD cases without comorbid MDD. Similar findings were reported by Hurwitz et al.14 Fourth, we used the NIMH-DIS across all assessments. The DIS has been found to be highly specific and more conservative than a clinically administered instrument. The possibility of misclassification of PTSD cases as noncases (false-negative classification) cannot be ruled out. However, its implications in this study were thoroughly evaluated in the comparison of the PTSD, exposed/no-PTSD, and nonexposed groups presented in Table 4. Because PTSD, by definition, depends on exposure to DSM-qualifying traumatic events, there can be no false-negative cases among the nonexposed group. With respect to the failure to find evidence of sleep disturbances associated with PTSD, diagnostic uncertainty is an unlikely explanation.
Finally, we tested more than 20 individual comparisons in several series, leaving ample opportunity for chance findings. In giving weight to the observed significant differences, we rely on the pattern of the results, specifically, the clustering of the significant results in 1 specific domain, ie, brief arousals from REM sleep, which were observed in each series of analyses.
Important strengths of the study deserve mention. To our knowldege, this is the first study to evaluate objective indicators of sleep in PTSD in a large community sample. Previous studies, by and large, have used small clinical samples or samples of volunteers, which are biased in terms of severity of psychopathology, other clinical features, and social factors that influence self-selection to treatment and clinical research. The use of 2 nights in the sleep laboratory and standard measurement of daytime sleepiness in this large sample are noteworthy. Our statistical analysis that used data on the 2 nights and tested interactions among variables maximized statistical power to detect group differences. An important strength is the longitudinal nature of the epidemiological study, with multiple assessments of the occurrence of traumatic events. As a result, the classification of the subset with no history of exposure to trauma in lifetime is exceptionally strict, especially in view of the common occurrence of exposure to traumatic events in recent population studies and the high proportions of persons with history of multiple traumas.53
AUTHOR INFORMATION
Corresponding author and reprints: Naomi Breslau, PhD, Department of Epidemiology, College of Human Medicine, Michigan State University, B645 West Fee Hall, East Lansing, MI 48824 (e-mail: breslau{at}epi.msu.edu).
Submitted for publication September 4, 2003; final revision received October 29, 2003; accepted November 18, 2003.
This study was supported by grant NIH-48802 from the National Institute of Mental Health, Rockville, Md.
From the Department of Epidemiology, College of Human Medicine, Michigan State University, East Lansing (Dr Breslau); and the Departments of Biostatistics (Ms Kapke and Dr Schultz) and Behavioral Health (Dr Breslau), Henry Ford Health System, and the Sleep Research Center, Henry Ford Hospital (Drs Roth and Roehrs and Ms Burduvali), Detroit, Mich.
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