Nightly Sleep Disruption Predicts Next-Day PTSD Symptoms: A Pilot Ecological Momentary Assessment Study in Sexual Assault Survivors With and Without PTSD.

Nightly sleep disruption predicts next-day PTSD symptoms: A pilot ecological momentary assessment study in sexual assault survivors with and without PTSD - PMC Skip to main content An official website of the United States government Here's how you know Here's how you know Search Log in Primary site navigation Search Log in Search PMC Full-Text Archive Search in PMC Journal List User Guide As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more: PMC Disclaimer | PMC Copyright Notice J Sleep Res . Author manuscript; available in PMC: 2026 Jun 4. Published in final edited form as: J Sleep Res. 2026 May 26;35(5):e70361. doi: 10.1111/jsr.70361 Nightly sleep disruption predicts next-day PTSD symptoms: A pilot ecological momentary assessment study in sexual assault survivors with and without PTSD Rebecca C Cox 1, * , Bunmi O Olatunji 2 Author information Article notes Copyright and License information 1 Sleep, Circadian Rhythms, and Psychopathology Laboratory, Department of Psychological and Brain Sciences, Washington University in St. Louis, St. Louis, MO, USA 2 Emotion and Anxiety Research Laboratory, Department of Psychology, Vanderbilt University, Nashville, TN, USA * Corresponding author: Rebecca C. Cox, Washington University in St. Louis, St. Louis, MO, USA. cox.r@wustl.edu Issue date 2026 Oct. PMC Copyright notice PMCID: PMC13232708  NIHMSID: NIHMS2178700  PMID: 42186679 The publisher's version of this article is available at J Sleep Res Abstract Sleep disruption is a hallmark feature of posttraumatic stress disorder (PTSD). Studies using ecological momentary assessment suggest sleep disruption predicts next-day PTSD symptoms, though evidence for the reverse effect is inconsistent. We examined bidirectional associations between subjective sleep and PTSD symptom severity in a pilot sample of sexual assault survivors with and without PTSD ( N =35). Participants completed a sleep diary each morning and self-report measures of PTSD symptom severity and negative affect 3 times/day for 1 week. Multilevel models revealed that shorter sleep duration and longer sleep onset latency significantly predicted higher PTSD symptoms the following day, controlling for prior PTSD symptoms and negative affect ( p ’s < .05). In contrast, tests of reverse models revealed no significant associations between daytime PTSD symptoms and subsequent sleep disruption on any sleep outcome ( p ’s > .05). These findings suggest night-to-night disruptions in sleep may signal risk for increased PTSD symptoms. Implications for targeting sleep to treat PTSD symptoms are discussed. Keywords: sleep, PTSD, trauma, sexual assault, daily, ecological momentary assessment Introduction Sleep disruption has been called a hallmark feature of posttraumatic stress disorder (PTSD) 1 . Indeed, a vast body of research has demonstrated both subjective and objective sleep disruption in PTSD, including lower sleep efficiency, less time spent in slow wave sleep, and difficulties with sleep initiation and maintenance 2 – 4 . Further, sleep disruption is not meaningfully improved by standard PTSD treatment 5 and is a common residual symptom 6 . Conversely, treatment research also suggests that improvements in sleep disruption during PTSD treatment are associated with better treatment outcomes 5 , and directly intervening on sleep disruption significantly reduces PTSD symptoms 7 . These findings highlight the importance of sleep for both the etiology and treatment of PTSD. However, much of the extant research on sleep disruption and PTSD has focused on male combat veterans 2 , and relatively less work has examined the role of sleep disruption in PTSD among sexual assault survivors. The extant literature in this area offers mixed results. Though some studies found sexual assault survivors with PTSD report worse insomnia symptoms 8 , 9 , longer sleep onset latency 9 , more nighttime awakenings 9 , and lower sleep quality compared to healthy controls 8 , 9 , other studies have not found sleep continuity or architecture effects in sexual assault survivors with PTSD 8 , 10 . These discrepant findings suggest additional work is needed to clarify the role of sleep disruption in PTSD symptoms among sexual assault survivors. Importantly, both sleep and PTSD symptoms are dynamic processes that vary from day to day. Ecological momentary assessment, or repeated, naturalistic sampling of processes in real-world environments 11 , has particular value for understanding daily variability in PTSD symptoms. Studies using ecological momentary assessment have revealed within-day associations between PTSD symptom severity and alcohol use 12 and suicide ideation 13 . Among sexual assault survivors, ecological momentary assessment studies have identified time-of-day effects on PTSD symptoms and affect 14 , 15 and a bidirectional relation between PTSD symptoms and mental contamination 16 . Understanding risk factors for daily increases in PTSD symptom severity may inform the development of just-in-time interventions 17 . Given the robust association between sleep disruption and PTSD observed between persons, sleep disruption is a candidate predictor for daily variation in PTSD symptoms. Examining the daily associations between sleep and PTSD symptoms can reveal their temporal sequencing and identify specific components of sleep that predict next-day PTSD symptoms. For example, prior research has shown that shorter sleep duration 18 – 21 , longer sleep onset latency 18 , 21 , higher number of awakenings 18 , and lower sleep quality 13 , 18 , 22 predict higher next-day PTSD symptoms. Conversely, evidence for a prospective link between PTSD symptoms and subsequent sleep disruption is mixed. Though one study found that days with higher PTSD symptoms are followed by nights with shorter sleep duration 20 , other studies have found no such effect 19 , 21 , 22 . Similar inconsistencies have been observed for the effect of PTSD symptoms on subsequent sleep quality 20 – 22 . Further, only two studies examining daily associations between sleep disruption and PTSD symptoms controlled for prior PTSD symptom severity 19 , 22 , and no study to date has controlled for prior negative affect. Thus, a unique predictive relationship between nightly sleep and PTSD symptom severity over and above lagged symptoms and mood has not been established. It is unclear, therefore, whether there is a bidirectional relation between nightly sleep and daily PTSD symptoms or a unique relation over and above prior symptoms. Further, no study to date has examined the associations between nightly sleep and daily PTSD symptoms in sexual assault survivors. The present pilot study addressed these issues by using an ecological momentary assessment design to examine bidirectional associations between nightly sleep and daily PTSD symptoms in sexual assault survivors with and without PTSD. We hypothesized that sleep disruption, including shorter sleep duration, longer sleep onset latency, higher number of awakenings, lower sleep quality, lower sleep efficiency, and later sleep timing, would predict higher next-day PTSD symptoms, controlling for prior PTSD symptoms and negative affect. Given the inconsistent evidence for a prospective relation between PTSD symptom severity and subsequent sleep, we tested reverse effects as an exploratory analysis. Methods Participants This study included adults who experienced a sexual assault after age 14 ( N = 35) who participated prior to and during the COVID-19 pandemic. 1 17 met criteria for PTSD (PTSD+; 49%), and 18 did not meet criteria for PTSD (PTSD-; 51%). The mean age of the sample was 36.61 years (SD = 15.06) ranging from 20 to 69. Most participants were female ( n = 30; 91%), and the racial composition was as follows: White ( n = 22; 67%), African American ( n = 8; 24%), Hispanic/Latino ( n = 1; 3%), or other ( n = 2; 6%). See Table 1 for demographics by diagnostic group. Table 1. Descriptive statistics by diagnostic group. PTSD+ ( n =17) PTSD- ( n =18) All ( n =35) Age 38.13 (14.78) 35.18 (15.63) 36.61 (15.06) Sex Male 2 (11.8%) 1 (5.6%) 3 (8.6%) Female 14 (82.4%) 16 (88.9%) 30 (85.7%) Did not respond 1 (5.9%) 1 (5.6%) 2 (5.7%) Race White 10 (58.5%) 12 (66.7%) 22 (62.9%) African American/Black 5 (29.4%) 3 (16.7%) 8 (22.9%) Hispanic/Latino 1 (5.9%) 0 (0%) 1 (2.9%) Other 0 (0%) 2 (11.1%) 2 (5.7%) Did not respond 1 (5.9%) 1 (5.6%) 2 (5.7%) Current major depressive disorder 7 (41.2%) 2 (11.1%) 9 (25.7%) Current anxiety-related disorder 12 (70.6%) 4 (22.2%) 16 (45.7%) PCL-5 40.06 (18.12) 11.62 (10.37%) 27.31 (20.72) d-PCL 23.71 (8.50) 12.01 (2.52) 17.69 (8.51) Sleep onset latency 27.99 (17.85) 19.64 (15.50) 23.81 (17.00) Number of awakenings 2.57 (1.65) 1.83 (0.90) 2.20 (1.36) Wake after sleep onset 21.63 (18.38) 17.23 (14.52) 19.43 (16.46) Sleep quality 2.97 (0.82) 3.51 (0.64) 3.25 (0.77) Sleep duration 404.17 (71.43) 439.96 (67.00) 422.57 (70.53) Sleep efficiency 76.90 (13.14) 81.28 (9.76) 79.09 (11.61) Mid-sleep 04:11 (01:28) 03:37 (01:47) 03:54 (01:38) Daily PANAS NA 8.38 (2.87) 5.88 (1.48) 7.09 (2.56) Open in a new tab Note. PCL-5 = Posttraumatic Stress Disorder Checklist. Measures The MINI International Neuropsychiatric Interview (MINI) 23 is a well-validated and widely used semi-structured diagnostic interview that assesses common DSM-5 (American Psychiatric Association, 2013) disorders. The MINI was used to determine diagnostic status, including PTSD status. The MINI was administered by lab personnel who received extensive training and supervision from the last author, who is a licensed clinical psychologist. The PTSD module of the MINI has acceptable test-retest reliability (kappa = .73), excellent interrater reliability (kappa = .95), and strong concordant validity with the Structured Clinical Interview, Patient Version (SCID-P; Sheehan et al., 1998). The Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5) 24 is a 20-item measure of DSM-5 (American Psychiatric Association, 2013) PTSD symptoms in the past month. The PCL consists of four subscales that assess the DSM-5 symptom clusters. Items are rated on a Likert scale from 1 ( not at all ) to 5 ( extremely ), and higher scores indicate more severe PTSD symptoms. A score of 31–33 or higher is suggestive of probable PTSD 25 . The PCL-5 has demonstrated good internal consistency and convergent and discriminant validity 26 . The daily Posttraumatic Stress Disorder Checklist (d-PCL) 22 is a 10-item adaptation of the PCL for ecological momentary assessment with demonstrated psychometric validity 15 . Participants were asked to report symptom severity experienced since the last assessment. Items are rated on a Likert scale from 1 ( not at all ) to 5 ( extremely ), and higher scores indicate more severe daily PTSD symptoms. The d-PCL has demonstrated acceptable internal consistency and test-retest reliability, as well as good convergent validity 15 . Importantly, the d-PCL does not include items related to sleep disruption. The Positive and Negative Affect Schedule Short Form (PANAS) 27 is a 10-item version of the PANAS 28 and includes 5 positive affect and 5 negative affect items. Items on the PANAS are rated on a Likert scale from 1 ( very slightly or not at all ) to 5 ( extremely ). Participants were asked to report their momentary affect based on how they felt at the moment they were completing the items. The PANAS has demonstrated acceptable internal consistency 27 . The Consensus Sleep Diary (CSD; 29 is a 9-item sleep diary that asks participants about the prior night’s sleep. Sleep variables examined included sleep onset latency, wake after sleep onset, number of awakenings, sleep duration, sleep quality, sleep efficiency (sleep duration/time in bed multiplied by 100), and mid-sleep (calculated as the midpoint between sleep onset and sleep offset; converted to decimal format [i.e., minutes divided by 60 to reflect a proportion of an hour]). Procedure Participants were recruited through advertisements for individuals who had “previously experienced a sexual assault” placed on campus and in local mental health clinics and through a university research listserv. Potential participants were screened via phone prior to enrollment in the study. All participants endorsed a sexual assault after age 14 and denied current or previous psychotic disorder or pervasive developmental disorder. Participants included in the PTSD+ group identified the sexual assault as their most traumatic experience if they endorsed multiple criterion A traumas and met criteria for PTSD. Participants included in the PTSD- group did not meet criteria for PTSD. Participants were excluded from the study following enrollment if they endorsed moderate to high suicidality on the MINI. On day 1, participants attended a laboratory session that included informed consent and administration of the MINI and PCL-5 (following the onset of the COVID-19 pandemic, visit 1 was completed via Zoom). On days 2 through 8, participants completed the CSD upon awakening each morning and received an email prompt to complete the d-PCL and PANAS via RedCAP 30 at 8:00am, 2:00pm, and 8:00pm. All procedures were approved by the university Institutional Review Board. All potential participants provided verbal informed consent for screening and written informed consent prior to enrollment in the study. Data analysis Outlier values (i.e., values 1.5*interquartile range above the 3 rd quartile) were identified for sleep onset latency (values > 100 minutes), number of awakenings (values > 10 awakenings), wake after sleep onset (values > 110 minutes), and sleep efficiency (values < 20%) and removed from analyses using each variable. We conducted statistical analyses in Mplus version 8 (Muthén & Muthén, 2017). We tested a series of 2-level multilevel linear regression models. We first conducted uncontrolled models without covariates, followed by models adjusted for covariates (lagged PTSD symptoms, lagged negative affect, and diagnostic group). Level 1 predictors were the sleep predictor, lagged negative affect, and lagged PTSD symptoms. Level 1 variables were person-mean centered, such that deviations from 0 represented a deviation from the participants own mean during the study. Thus, the model effects at level 1 tested whether nights with more sleep disruption than typical for the individual were followed by days with higher PTSD symptoms (i.e., a within-subject effect). Level 2 predictors were the sleep predictor and diagnostic group. Level 2 variables were grand-mean centered, such that deviations from 0 represented a deviation from the sample mean. Thus, the model effects at level 2 tested whether participants with higher sleep disruption reported higher PTSD symptoms on average (i.e., a between-subject effect). All models included a random intercept at level 2 because the intraclass correlations (ICC) were meaningfully large (ICC = .82−.84). Full information maximum likelihood (FIML) estimation was used. Finally, to probe the directionality of associations between sleep disruption and PTSD symptoms, we also tested reverse models to examine whether higher symptom severity would predict subsequent sleep disruption. Results Descriptive statistics and associations between study variables Sample demographic characteristics and means and descriptive statistics are shown in Table 1 . Bivariate correlations for study variables are shown in Table 2 . Table 2. Within- and between-subject Pearson correlations. Lower left triangle shows between-subject correlations, and upper right triangle shows within-subject correlations ( N = 35). Measure 1. 2. 3. 4. 5. 6. 7. 8. 9. 1. d-PCL -- .48 ** −.10 * .07 −.06 .04 −.10 * −.04 −.01 2. Daily PANAS NA .81 ** -- −.07 .07 −.02 .03 −.09 * −.03 −.12 * 3. Sleep duration −.26 −.15 -- −.18 ** −.03 −.12 ** .49 ** .40 ** .15 ** 4. Sleep onset latency .54 ** .46 ** −.46 ** -- .14 ** .63 ** −.24 ** −.41 ** .16 ** 5. Wake after sleep onset .36 * .47 ** −.38 * .25 -- .09 * −.21 ** −.62 ** −.07 6. Number of awakenings .37 * .43 ** −.20 .10 .49 * -- −.16 ** −.26 ** .10 * 7. Sleep quality −.46 * −.25 .48 * −.32 −.38 * −.41 * -- .38 ** .07 8. Sleep efficiency −.36 * −.33 * .57 ** −.68 −.58 ** −.27 .55 ** -- .07 9. Mid-sleep .20 .11 −.01 −.01 −.13 .02 −.13 .03 -- Open in a new tab Note . d-PCL=daily PTSD Checklist; PANAS NA = Positive and Negative Affect Schedule, negative affect * p < .05 ** p < .01 Associations between last night’s sleep and next-day PTSD symptoms. Nights with shorter sleep duration, longer sleep onset latency, and lower sleep quality were followed by days with higher momentary PTSD symptoms ( p’s < .05). Effects of last night’s sleep on next day PTSD symptoms were not observed for wake after sleep onset, number of awakenings, sleep efficiency, or mid-sleep timing. Between subjects, those with longer sleep onset latency, more awakenings, lower sleep quality, and lower sleep efficiency on average reported higher momentary PTSD symptoms on average ( p’s < .05). No between-subjects effects were observed for sleep duration, wake after sleep onset, or midsleep timing. See Table 3 . Table 3. Standardized coefficients for models examining associations between sleep disruption and daily PTSD symptoms without covariates ( N = 34). Sleep duration Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Sleep duration −.09 .04 <.05 −.17, −.02 Level 2 Sleep duration −.24 .16 .13 −.56, .07 Variance components Level 1 Residual variance .99 .01 <.001 .98, 1.01 Level 2 Intercept variance .94 .08 <.001 .79, 1.09 Sleep onset latency Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Sleep onset latency .13 .04 <.01 .05, .22 Level 2 Sleep onset latency .35 .15 <.05 .05, .65 Variance components Level 1 Residual variance .98 .01 <.001 .96, 1.00 Level 2 Intercept variance .88 .11 <.001 .67, 1.09 Wake after sleep onset Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Wake after sleep onset .05 .04 .22 −.03, .14 Level 2 Wake after sleep onset .26 .16 .11 −.06, .58 Variance components Level 1 Residual variance 1.00 .004 <.001 1.00, 1.01 Level 2 Intercept variance .93 .08 <.001 .77, 1.10 Number of awakenings Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Number of awakenings .07 .04 .10 −.01, .15 Level 2 Number of awakenings .32 .16 <.05 .01, .62 Variance components Level 1 Residual variance 1.00 .06 <.001 .99, 1.01 Level 2 Intercept variance .90 .10 <.001 .71, 1.09 Sleep quality Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Sleep quality −.09 .04 <.05 −.17, −.02 Level 2 Sleep quality −.45 .14 <.01 −.72, −.19 Variance components Level 1 Residual variance .99 .01 <.001 .98, 1.01 Level 2 Intercept variance .80 .12 <.001 .56, 1.04 Sleep efficiency Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Sleep efficiency −.03 .04 .54 −.11, .06 Level 2 Sleep efficiency −.32 .16 <.05 −.62, −.01 Variance components Level 1 Residual variance 1.00 .002 <.001 1.00, 1.004 Level 2 Intercept variance .90 .10 <.001 .71, 1.09 Midsleep timing Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Midsleep timing −.01 .04 .82 −.09, .07 Level 2 Midsleep timing .20 .17 .23 −.13, .53 Variance components Level 1 Residual variance 1.00 .001 <.001 1.0, 1.001 Level 2 Intercept variance 0.96 .07 <.001 .83, 1.09 Open in a new tab Note . PTSD = Posttraumatic stress disorder. Level 1 (within-subject) variables were person-mean centered, such that deviations from 0 represent deviations at a given timepoint from one’s own average. Level 2 (between-subject) variables were grand-mean centered, such that deviations from 0 represent deviations from the sample average. Associations between last night’s sleep and next-day PTSD symptoms adjusted for covariates. Nights with shorter sleep duration and longer sleep onset latency were followed by days with higher momentary PTSD symptoms, controlling for lagged PTSD symptoms and negative affect ( p’s < .05). Effects of last night’s sleep on next day PTSD symptoms were not observed for wake after sleep onset, number of awakenings, sleep quality, sleep efficiency, or mid-sleep timing. Further, no between-subjects effects were observed for any sleep variable; that is, sleep disruption on average was not associated with daily PTSD symptom severity on average. See Table 4 . Table 4. Standardized coefficients for models examining associations between sleep disruption and daily PTSD symptoms, controlling for lagged daily PTSD symptoms, lagged daily negative affect, and diagnostic group ( N = 35). Sleep duration Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged PTSD symptoms .12 .05 <.01 .03, .22 Lagged negative affect .01 .05 .88 −.09, .10 Sleep duration −.09 .04 <.05 −.17, −.01 Level 2 Group .70 .09 <.001 .51, .88 Sleep duration −.07 .13 .60 −.31, .18 Variance components Level 1 Residual variance .98 .01 <.001 .95, 1.00 Level 2 Intercept variance .49 .12 <.001 .25, .72 Sleep onset latency Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged PTSD symptoms .16 .05 <.01 .07, .26 Lagged negative affect .01 .05 .77 −.08, .11 Sleep onset latency .10 .04 <.05 .01, .18 Level 2 Group .65 .10 <.001 .46, .85 Sleep onset latency .19 .13 .14 −.06, .43 Variance components Level 1 Residual variance .96 .02 <.001 .93, .99 Level 2 Intercept variance .48 .12 <.001 .24, .72 Wake after sleep onset Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged PTSD symptoms .11 .05 <.05 .02, .21 Lagged negative affect .01 .05 .84 −.09, .11 Wake after sleep onset .04 .05 .42 −.05, .12 Level 2 Group .68 .09 <.001 .51, .86 Wake after sleep onset .16 .12 .19 −.08, .40 Variance components Level 1 Residual variance .98 .01 <.001 .96, 1.01 Level 2 Intercept variance .48 .12 <.001 .24, .71 Number of awakenings Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged PTSD symptoms .12 .05 <.05 .03, .22 Lagged negative affect .01 .05 .91 −.09, .10 Number of awakenings .03 .04 .49 −.05, .11 Level 2 Group .67 .10 <.001 .48, .86 Number of awakenings .13 .13 .29 −.12, .38 Variance components Level 1 Residual variance .98 .01 <.001 .96, 1.01 Level 2 Intercept variance .49 .12 <.001 .25, .73 Sleep quality Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged PTSD symptoms .12 .05 <.05 .03, .21 Lagged negative affect .01 .05 .81 −.08, .10 Sleep quality −.07 .04 .12 −.15, .02 Level 2 Group .64 .10 <.001 .44, .84 Sleep quality −.22 .12 .07 −.46, .02 Variance components Level 1 Residual variance .98 .01 <.001 .96, 1.00 Level 2 Intercept variance .45 .115 <.001 .23, .68 Sleep efficiency Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged PTSD symptoms .11 .05 <.05 .01, .20 Lagged negative affect .02 .05 .76 −.08, .11 Sleep efficiency −.02 .04 .59 −.11, .06 Level 2 Group .67 .09 <.001 .48, .85 Sleep efficiency −.19 .12 .12 −.43, .05 Variance components Level 1 Residual variance .99 .01 <.001 .97, 1.01 Level 2 Intercept variance .47 .12 <.001 .24, .70 Midsleep timing Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged PTSD symptoms .12 .05 <.05 .03, .21 Lagged negative affect .01 .05 .81 −.08, .11 Midsleep timing .03 .04 .54 −.06, .11 Level 2 Group .69 .09 <.001 .51, .87 Midsleep timing .07 .13 .56 −.17, .32 Variance components Level 1 Residual variance .98 .01 <.001 .96, 1.01 Level 2 Intercept variance .50 .12 <.001 .26, .74 Open in a new tab Note . PTSD = Posttraumatic stress disorder. Level 1 (within-subject) variables were person-mean centered, such that deviations from 0 represent deviations at a given timepoint from one’s own average. Level 2 (between-subject) variables were grand-mean centered, such that deviations from 0 represent deviations from the sample average. Reverse effects: Associations between PTSD symptoms and subsequent night sleep. Tests of reverse effects revealed that there were no significant effects of daily PTSD symptoms on the subsequent night’s sleep for any sleep metric ( p ’s > .05). See Table 5 . Table 5. Standardized coefficients for reverse models examining associations between daily PTSD symptoms and sleep disruption, controlling for lagged daily sleep, lagged daily negative affect, and diagnostic group ( N = 35). Sleep duration Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged sleep duration −.28 .04 <.001 −.36, −.20 Lagged negative affect −.07 .05 .13 −.17, .02 PTSD symptoms .06 .05 .24 −.04, .15 Level 2 Group −.32 .22 .16 −.76, .12 PTSD symptoms −.11 .23 .63 −.56, .34 Variance components Level 1 Residual variance .92 .02 <.001 .87, .96 Level 2 Intercept variance .84 .12 <.001 .60, 1.08 Sleep onset latency Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged sleep onset latency −.03 .05 .51 −.12, .06 Lagged negative affect .09 .05 .08 −.01, .19 PTSD symptoms .05 .05 .37 −.06, .15 Level 2 Group −.06 .23 .79 −.50, .38 PTSD symptoms .42 .21 .05 −.01, .84 Variance components Level 1 Residual variance .99 .01 <.001 .96, 1.01 Level 2 Intercept variance .86 .12 <.001 .63, 1.08 Wake after sleep onset Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged wake after sleep onset −.02 .05 .74 −.11, .08 Lagged negative affect .01 .05 .81 −.09, .12 PTSD symptoms .04 .05 .45 −.06, .14 Level 2 Group −.03 .24 .92 −.49, .44 PTSD symptoms .36 .23 .12 −.09, .81 Variance components Level 1 Residual variance 1.00 .01 <.001 .99, 1.01 Level 2 Intercept variance .88 .11 <.001 .66, 1.10 Number of awakenings Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged number of awakenings .06 .05 .22 −.03, .14 Lagged negative affect −.01 .05 .83 −.11, .09 PTSD symptoms .10 .05 .06 −.002, .19 Level 2 Group .15 .22 .50 −.29, .59 PTSD symptoms .32 .22 .15 −.11, .74 Variance components Level 1 Residual variance .99 .01 <.001 .97, 1.01 Level 2 Intercept variance .81 .13 <.001 .56, 1.06 Sleep quality Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged sleep quality −.20 .05 <.001 −.27, −.10 Lagged negative affect .01 .02 .81 −.09, .11 PTSD symptoms −.01 .01 .38 −.14, .05 Level 2 Group −.21 .34 .54 −.57, .30 PTSD symptoms −.03 .02 .09 −.79, .04 Variance components Level 1 Residual variance .69 .05 <.001 .93, 1.00 Level 2 Intercept variance .45 .12 <.001 .51, 1.03 Sleep efficiency Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged sleep efficiency −.22 .05 <.001 −.31, −.14 Lagged negative affect −.06 .05 .23 −.16, .04 PTSD symptoms .09 .05 .09 −.01, .19 Level 2 Group .04 .23 .86 −.41, .50 PTSD symptoms −.36 .22 .10 −.80, .07 Variance components Level 1 Residual variance .94 .02 <.001 .90, .99 Level 2 Intercept variance .89 .11 <.001 .67, 1.10 Midsleep timing Fixed effects Predictor Est SE p 95% CI (lower, upper) Level 1 Lagged midsleep timing .01 .05 .82 −.08, .10 Lagged negative affect −.09 .05 .07 −.19, .01 PTSD symptoms .03 .05 .62 −.07, .13 Level 2 Group .07 .23 .77 −.39, .53 PTSD symptoms .17 .23 .46 −.29, .63 Variance components Level 1 Residual variance .99 .01 <.001 .98, 1.01 Level 2 Intercept variance .95 .08 <.001 .80, 1.10 Open in a new tab Note . PTSD = Posttraumatic stress disorder. Level 1 (within-subject) variables were person-mean centered, such that deviations from 0 represent deviations at a given timepoint from one’s own average. Level 2 (between-subject) variables were grand-mean centered, such that deviations from 0 represent deviations from the sample average. Discussion Higher daily PTSD symptom severity is associated with adverse outcomes such as suicide ideation 13 . Identifying predictors of risk for increases in daily PTSD symptoms is needed to inform just-in-time interventions. Here we show that shorter sleep duration and longer sleep onset latency predict increased PTSD symptoms the following day, controlling for prior PTSD symptoms and negative affect, in sexual assault survivors with and without PTSD. These preliminary findings suggest that specific features of sleep (i.e., difficulties with sleep initiation and sleep duration) could be used to inform just-in-time interventions for individuals with PTSD. In sexual assault survivors, nights with shorter sleep duration were followed by days with higher PTSD symptoms. The finding replicates and extends prior research likewise demonstrating an effect of last night’s sleep duration on next-day PTSD symptoms in combat veterans 18 , 19 , first responders 20 , and mixed trauma-exposed samples 21 . We also found that night’s with longer sleep onset latency were followed by days with higher PTSD symptoms. Few studies have demonstrated an effect of sleep onset latency on next-day PTSD symptoms 21 , 31 , though group comparison studies have shown longer average sleep onset latency in those with PTSD versus healthy controls 32 , 33 . However, one recent study examining moderating effects of sex found that the association between longer sleep onset latency and higher next-day PTSD symptoms was only observed in female participants 21 . The high proportion of female participants in our study may have contributed to our ability to detect this effect. We also found that sexual assault survivors who reported longer sleep onset latency, more awakenings, lower sleep quality, and lower sleep efficiency on average reported higher momentary PTSD symptoms on average; however, these effects were no longer significant after accounting for diagnostic group. At the level of the individual, average sleep disruption may not account for unique variance in PTSD symptoms independent from other indicators of symptom severity. These findings stand in contrast to the results at the day level, where aspects of sleep disruption (shorter sleep duration, longer sleep onset latency) uniquely predict prospective change in PTSD symptom severity, highlighting the importance of ecological momentary assessment and examining daily effects for understanding the role of sleep disruption in PTSD symptoms. Notably, we found no significant reverse associations, such that higher PTSD symptoms on a given day did not significantly predict any aspect of the subsequent night’s sleep. Evidence for bidirectional relations between nightly sleep and daily PTSD symptoms is mixed 31 , and our findings suggest that the more robust effect is from sleep disruption to PTSD. There are several putative mechanisms by which sleep disruption may impact daily PTSD symptoms. Sleep is theorized to function to consolidate and organize information accumulated during the waking day through long-term synaptic potentiation, a process known as synaptic homeostasis 34 . In the absence of sufficient sleep, synaptic overload may then contribute to deficits in cognitive and emotional function due in part to decreased neuronal signal-to-noise ratios and reduced plasticity 34 . These cognitive and emotional impairments of sleep disruption have been well-documented, including in processes relevant to PTSD. For example, prior work has demonstrated that sleep loss results in deficits in inhibitory control 35 and memory encoding 36 as well as increased emotional reactivity to negative stimuli 37 and higher subjective stress in response to mild stressors 38 . Further, recent studies have demonstrated that nights with disrupted sleep are followed by days with reduced positive affect 39 – 41 . Thus, the neurophysiological consequences of sleep disruption may have downstream effects on cognitive and emotional function, which may in turn increase vulnerability for daily PTSD symptoms. Sleep disruption is a promising target for PTSD treatment. For example, recent findings indicate that cognitive behavior therapy for insomnia (CBTI) significantly reduces PTSD symptoms as a standalone treatment and results in greater symptom reductions when paired with cognitive processing therapy compared to cognitive processing therapy alone 7 . Evidence for predictive relations between last night’s sleep and next-day PTSD symptoms suggests that individuals with PTSD could use their sleep patterns to inform application of coping skills. Further, if our findings extend to objectively measured sleep, night-to-night variation in sleep may have utility to inform just-in-time interventions. Sleep wearables, which are widely adopted 42 , could be used to send providers real-time signals for risk management and/or be integrated into digital health treatments for PTSD. These possibilities highlight the considerable potential of sleep for the clinical management and treatment of PTSD. Our findings demonstrate that shorter sleep duration and longer sleep onset latency predict higher PTSD the following day, whereas higher daily PTSD symptoms did not predict the subsequent night’s sleep. Strengths of our study include extending findings on sleep and PTSD to an understudied sample (i.e., sexual assault survivors) and a robust modeling approach that controlled for prior PTSD symptoms and negative affect and tested reverse effects. However, our findings should be considered within the context of the study limitations. First, the pilot sample size may have limited our ability to detect effects of other aspects of sleep disruption on next-day PTSD symptoms, as well as potential reverse effects. Indeed, results of a post-hoc power analysis suggest observed power was 0.62 with 35 participants, though observed power should be interpreted with question given the known limitations of post-hoc power analyses. 43 , 44 Still, our findings offer preliminary evidence for predictive links between last night’s sleep and next-day PTSD symptoms in sexual assault survivors that require replication in larger samples. Second, the sample was relatively homogenous in terms of sex and race, which may limit the generalizability of these findings. Third, we did not include an objective measure of sleep, and replication using a measure such as actigraphy is needed. Fourth, one week is a relatively short sampling period for EMA, and a longer sampling period would provide more robust data. Fifth, part of data collection was completed during the COVID-19 pandemic, which may have influenced both sleep disruption and PTSD symptom severity. Finally, we did not assess nightmares in this study. Given the role of nightmares in PTSD 45 , it will be important to include nightmares in subsequent studies examining associations between last night’s sleep and next-day PTSD symptoms. Despite these limitations, our findings suggest a prospective relation between sleep disruption and PTSD symptoms that has the potential to be leveraged to treat PTSD. Acknowledgments. The authors would like to acknowledge Sarah Jessup, Alexa Garcia, Nicole Davies, Leanna Duong, Max Luber, Angelee Parmar, Maria Sanin, and Yunshu Yang for their assistance with data collection and Alyssa Week for her assistance with manuscript preparation Funding. This work was supported by the National Institute of Mental Health of the National Institutes of Health [F31MH113271 & K23MH137376]. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. It is subject to the NIH Public Access Policy. Through acceptance of this federal funding, NIH has been given a right to make this manuscript publicly available in PubMed Central upon the Official Date of Publication, as defined by NIH. Footnotes CRediT authorship contribution statement. Rebecca C. Cox: Conceptualization, Methodology, Formal analysis, Investigation, Data Curation, Writing-Original draft, Funding acquisition. Bunmi O. 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