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BackgroundObstructive sleep apnea (OSA) is often comorbid with both substance use disorders (SUD) and posttraumatic stress disorder (PTSD), yet frequently goes undiagnosed and untreated. We present data on the feasibility and acceptability of objective OSA diagnosis procedures, findings on OSA prevalence, and the relationship between OSA and baseline SUD/PTSD symptoms among veterans in residential treatment for comorbid PTSD/SUD.MethodsParticipants were 47 veterans admitted to residential PTSD/SUD treatment. Participants completed questionnaires assessing PTSD and sleep symptoms, and filled out a sleep diary for seven days. Apnea-hypopnea index (AHI) was recorded using the overnight Home Sleep Apnea test (HSAT; OSA was diagnosed with AHI ≥ 5).ResultsObjective OSA diagnostic testing was successfully completed in 95.7% of participants. Of the 45 veterans who went through HSAT, 46.7% had no OSA, 35.6% received a new OSA diagnosis, and 8.9% were previously diagnosed with OSA and were using positive airway pressure treatment (PAP); an additional 8.9% were previously diagnosed with OSA, reconfirmed with the HSAT, but were not using PAP. One hundred percent of respondents during follow-up deemed the testing protocol's usefulness as "Good" or "Excellent."ConclusionOSA diagnostic testing on the residential unit was feasible and acceptable by participants and was effective in diagnosing OSA. OSA testing should be considered for everyone entering a SUD and PTSD residential unit. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

AimsTo examine whether cognitive behavioral therapy for insomnia (CBT-I), delivered by telephone, improves sleep and non-sleep symptoms of Gulf War Illness (GWI).Main methodsEighty-five Gulf War veterans (21 women, mean age: 54 years, range 46-72 years) who met the Kansas GWI case definition, the Centers for Disease Control and Prevention (CDC) case definition for Chronic Multisymptom Illness (CMI), and research diagnostic criteria for insomnia disorder were randomly assigned to CBT-I or monitor-only wait list control. Eight weekly sessions of individual CBT-I were administered via telephone by Ph.D. level psychologists to study participants. Outcome measures included pre-, mid-, and post-treatment assessments of GWI and insomnia symptoms, subjective sleep quality, and continuous sleep monitoring with diary. Outcomes were re-assessed 6-months post-treatment in participants randomized to CBT-I.Key findingsCompared to wait list, CBT-I produced significant improvements in overall GWI symptom severity, individual measures of fatigue, cognitive dysfunction, depression and anxiety, insomnia severity, subjective sleep quality, and sleep diary outcome measures. The beneficial effects of CBT-I on overall GWI symptom severity and most individual GWI symptom measures were maintained 6-months after treatment.SignificanceGWI symptoms have historically been difficult to treat. Because CBT-I, which is associated with low stigma and is increasingly readily available to veterans, improved both sleep and non-sleep symptoms of GWI, these results suggest that a comprehensive approach to the treatment of GWI should include behavioral sleep interventions.

AimsTo examine whether cognitive behavioral therapy for insomnia (CBT-I), delivered by telephone, improves sleep and non-sleep symptoms of Gulf War Illness (GWI).Main methodsEighty-five Gulf War veterans (21 women, mean age: 54 years, range 46-72 years) who met the Kansas GWI case definition, the Centers for Disease Control and Prevention (CDC) case definition for Chronic Multisymptom Illness (CMI), and research diagnostic criteria for insomnia disorder were randomly assigned to CBT-I or monitor-only wait list control. Eight weekly sessions of individual CBT-I were administered via telephone by Ph.D. level psychologists to study participants. Outcome measures included pre-, mid-, and post-treatment assessments of GWI and insomnia symptoms, subjective sleep quality, and continuous sleep monitoring with diary. Outcomes were re-assessed 6-months post-treatment in participants randomized to CBT-I.Key findingsCompared to wait list, CBT-I produced significant improvements in overall GWI symptom severity, individual measures of fatigue, cognitive dysfunction, depression and anxiety, insomnia severity, subjective sleep quality, and sleep diary outcome measures. The beneficial effects of CBT-I on overall GWI symptom severity and most individual GWI symptom measures were maintained 6-months after treatment.SignificanceGWI symptoms have historically been difficult to treat. Because CBT-I, which is associated with low stigma and is increasingly readily available to veterans, improved both sleep and non-sleep symptoms of GWI, these results suggest that a comprehensive approach to the treatment of GWI should include behavioral sleep interventions.

Study objectivesOur objective was to examine the ability of a consumer-grade wearable device (Basis B1) with accelerometer and heart rate technology to assess sleep patterns compared with polysomnography (PSG) and research-grade actigraphy in healthy adults.MethodsEighteen adults underwent consecutive nights of sleep monitoring using Basis B1, actigraphy, and PSG; 40 nights were used in analyses. Discrepancies in gross sleep parameters and epoch-by-epoch agreements in sleep/wake classification were assessed.ResultsBasis B1 accuracy was 54.20 ± 8.20%, sensitivity was 98.90 ± 2.70%, and specificity was 8.10 ± 15.00%. Accuracy, sensitivity, and specificity for distinguishing between the different sleep stages were 60-72%, 48-62%, and 57-86%, respectively. Pearson correlations demonstrated strong associations between Basis B1 and PSG estimates of sleep onset latency and total sleep time; moderate associations for sleep efficiency, duration of light sleep, and duration of rapid eye movement sleep; and a weak association for duration of deep sleep. Basis B1 significantly overestimates total sleep time, sleep efficiency, and duration of light sleep and significantly underestimates wake after sleep onset and duration of deep sleep.ConclusionsBasis B1 demonstrated utility for estimates of gross sleep parameters and performed similarly to actigraphy for estimates of total sleep time. Basis B1 specificity was poor, and Basis B1 is not useful for the assessment of wake. Basis B1 accuracy for sleep stages was better than chance but is not a suitable replacement for PSG assessment. Despite low cost, ease of use, and attractiveness for patients, consumer devices are not yet accurate or reliable enough to guide treatment decision making in clinical settings.

Study objectivesInsomnia is highly co-occurring with both posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD). This is concerning since insomnia contributes to worse substance abuse and PTSD, and a host of negative health consequences. No study has tracked how sleep indices and insomnia change related to integrated PTSD and AUD treatment using evidence-based exposure therapy. This study examined how insomnia changes over time in a randomized control trial of two integrated PTSD and AUD treatments.MethodsParticipants were 119 adult veterans (90 % male) seeking treatment for AUD and PTSD at a large urban VA. Participants were randomized to either COPE (integrated treatment using prolonged exposure) or Seeking Safety (integrated therapy using cognitive behavioral, interpersonal techniques and case management). Assessments were done at pre- and post-treatment and include: Clinician Administered PTSD Scale, Timeline Follow-back calendar-assisted interview for AU, insomnia severity index (ISI), sleep diary and actigraphy for 7 days.ResultsISI showed significant decreases, but a majority remained above the clinical cutoff at post-treatment. Wake after sleep onset decreased, but only by 8 min, remaining above clinical thresholds. Decreases in PTSD, but not in heavy drinking, predicted change in ISI. No significant changes were observed in other sleep variables measured.ConclusionsFindings suggested some statistical improvements in sleep quality, but sleep indices remained above clinical cut-offs. This study provides evidence that insomnia is an independent disorder and not responsive to PTSD or AUD treatments alone. Sleep symptoms should be assessed and treated in patients with comorbid mental health conditions.

BACKGROUND:Posttraumatic stress disorder (PTSD) is associated with disturbed sleep and elevated levels of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Studies in animals and healthy humans have also shown that disrupted sleep elevates pro-inflammatory cytokines, including IL-6 and TNF-α. A better understanding of overnight cytokine levels and sleep might shed light on possible mechanisms for elevated inflammation in PTSD. Thus, we investigated overnight levels of IL-6 and TNF-α in individuals with and without PTSD while recording sleep polysomnography (PSG). METHOD:Serum samples were collected from otherwise healthy, medication-free participants with chronic PTSD (n = 44; 50% female; M age = 30.34 ± 8.11) and matched controls (n = 49; 53% female; M age = 30.53 ± 6.57) during laboratory PSG. Levels of IL-6 and TNF-α were measured at hours 0, 2, 4, 6, and 8 after typical sleep onset time using serial serum samples. Plasma IL-6 and TNF-α levels were quantified using enzyme-linked immunosorbent assays. RESULTS:Growth model analysis indicated a significantgroup by time interaction for IL-6 (t[247] = -2.92, p = .005) and a significant group by sex by time interaction for TNF-α (t[275] = 2.02, p = .04). PTSD positive men and women initially had higher IL-6 and TNF-α at sleep onset, but not at the end of their sleep cycle. Men with PTSD showed a peak of TNF-α at the end of the sleep cycle, whereas male control subjects demonstrated an inverted U-shaped profile. There were no significant differences in TNF-α levels overnight between women with and without PTSD. CONCLUSION:To our knowledge, this is the largest study to examine IL-6 overnight in a PTSD sample and the first study to examine overnight TNF-α in PTSD. Overnight IL-6 and TNF-α levels may be altered in individuals with PTSD compared to those without PTSD, and TNF-α trajectories also differed by sex. The current findings highlight the need to consider sex, sleep, time of day, and circadian variation when examining inflammation in PTSD. Additional research in broader study samples will be necessary to clarify associations between disrupted sleep, cytokines, and increased risk for disease in PTSD.

Background:Posttraumatic Stress Disorder (PTSD) is associated with a number of negative physical and mental health consequences. Fear conditioning plays an important mechanistic role in PTSD, and PTSD patients also show deficits in safety signal learning. Sleep, particularly REM sleep, is linked to improved safety learning and extinction processes in animal models and healthy humans. No studies have examined the link between REM sleep and safety signal learning or extinction memory in clinical populations. Methods:This study examined the relationship between REM sleep, safety signal learning, and extinction processes in veterans with PTSD (n = 13). Patients' overnight sleep was characterized in the laboratory via polysomnography (PSG). The next day, participants underwent a fear conditioning paradigm during which they acquired fear toward a visual cue. This testing session also included a visual cue that became a safety signal (CS-). Following conditioning, the veterans' sleep was monitored overnight again, after which they underwent extinction training. Following a third night of sleep, extinction recall and safety recall were tested. Bivariate correlations examined the relationship between the slope of safety signal learning and subsequent REM sleep, as well as the relationship between REM sleep and subsequent extinction recall and safety recall on the last day of testing. Results:Veterans learned to differentiate the CS+ and the CS- on the first day of testing. Veterans who underwent safety learning more quickly on the first day of testing showed more efficient REM sleep that night (r = .607, p = .028). On the second day of testing, the patients successfully underwent extinction learning. Patients with a higher percentage of REM sleep on the last night of the study showed more safety recall early on the last day of testing (r = .688, p = .009). Conclusion:To our knowledge, this was the first study to examine the relationship between objective sleep and fear-potentiated startle performance in veterans with PTSD. Study methods were well tolerated by participants, supporting feasibility of the experimental design. Results indicated REM sleep was associated with both initial safety learning and subsequent safety recall. Taken together with previous studies in healthy controls, these preliminary results provide additional evidence suggesting REM sleep could play a mechanistic role in the maintenance of PTSD and thus identify a modifiable biological process to target in treatment of PTSD. These findings should be replicated in larger samples.

BackgroundPosttraumatic Stress Disorder (PTSD) is associated with a number of negative physical and mental health consequences. Fear conditioning plays an important mechanistic role in PTSD, and PTSD patients also show deficits in safety signal learning. Sleep, particularly REM sleep, is linked to improved safety learning and extinction processes in animal models and healthy humans. No studies have examined the link between REM sleep and safety signal learning or extinction memory in clinical populations.MethodsThis study examined the relationship between REM sleep, safety signal learning, and extinction processes in veterans with PTSD (n = 13). Patients' overnight sleep was characterized in the laboratory via polysomnography (PSG). The next day, participants underwent a fear conditioning paradigm during which they acquired fear toward a visual cue. This testing session also included a visual cue that became a safety signal (CS-). Following conditioning, the veterans' sleep was monitored overnight again, after which they underwent extinction training. Following a third night of sleep, extinction recall and safety recall were tested. Bivariate correlations examined the relationship between the slope of safety signal learning and subsequent REM sleep, as well as the relationship between REM sleep and subsequent extinction recall and safety recall on the last day of testing.ResultsVeterans learned to differentiate the CS+ and the CS- on the first day of testing. Veterans who underwent safety learning more quickly on the first day of testing showed more efficient REM sleep that night (r = .607, p = .028). On the second day of testing, the patients successfully underwent extinction learning. Patients with a higher percentage of REM sleep on the last night of the study showed more safety recall early on the last day of testing (r = .688, p = .009).ConclusionTo our knowledge, this was the first study to examine the relationship between objective sleep and fear-potentiated startle performance in veterans with PTSD. Study methods were well tolerated by participants, supporting feasibility of the experimental design. Results indicated REM sleep was associated with both initial safety learning and subsequent safety recall. Taken together with previous studies in healthy controls, these preliminary results provide additional evidence suggesting REM sleep could play a mechanistic role in the maintenance of PTSD and thus identify a modifiable biological process to target in treatment of PTSD. These findings should be replicated in larger samples.

Study objectivesOur study aims were to examine (1) the association between fear of sleep and posttraumatic stress disorder (PTSD) symptoms, (2) the association between fear of sleep and subjective and objective insomnia symptoms and disruptive behaviors during sleep, and (3) whether fear of sleep decreases following cognitive behavioral therapy for insomnia (CBT-I).MethodsForty-five adults with PTSD and insomnia participated in the study. Fear of sleep was assessed using the Fear of Sleep Inventory; PTSD symptoms were assessed using the Clinician Administered PTSD Scale; and sleep disturbance symptoms were assessed using the Insomnia Severity Index, polysomnography, sleep diaries, and the Pittsburgh Sleep Quality Index Addendum for PTSD. Participants were randomly assigned to 8 weeks of CBT-I (n = 29) or a waitlist control condition (n = 16).ResultsGreater fear of sleep was associated with greater PTSD symptom severity, greater nightmare frequency, and greater hypervigilance intensity. Greater fear of sleep was associated with decreased wake after sleep onset (WASO), reduced total sleep time, and greater disruptive nocturnal behaviors. Following CBT-I, there was a significant reduction in fear of sleep compared to the waitlist condition. These improvements persisted 6 months later.ConclusionsFear of sleep was related to sleep disturbances specific to trauma rather than "classic" insomnia symptoms. Unexpectedly, greater fear of sleep was associated with reduced WASO. These results may be related to having a truncated sleep period and thus more consolidated sleep. Fear of sleep deceased following CBT-I despite not being a permissible target for this research protocol and not being related to insomnia symptoms.Clinical trial registrationRegistry: CinicalTrials.gov; Name: Treating People with Post-traumatic Stress Disorder with Cognitive Behavioral Therapy for Insomnia; Identifier: NCT00881647; URL: https://clinicaltrials.gov/ct2/show/NCT00881647.

Purpose of reviewComorbidity of posttraumatic stress disorder (PTSD) and insomnia, nightmares, and obstructive sleep apnea (OSA) is high. We review recent research on psychotherapeutic and pharmacological interventions for sleep disorders in PTSD.Recent findingsPTSD treatments decrease PTSD severity and nightmare frequency, but do not resolve OSA or insomnia. Research on whether insomnia hinders PTSD treatment shows mixed results; untreated OSA does interfere with PTSD treatment. Cognitive behavioral therapy for insomnia is the recommended treatment for insomnia; however, optimal ordering with PTSD treatment is unclear. PTSD treatment may be most useful for PTSD-related nightmares. CPAP therapy is recommended for OSA but adherence can be low. Targeted treatment of sleep disorders in the context of PTSD offers a unique and underutilized opportunity to advance clinical care and research. Research is needed to create screening protocols, determine optimal order of treatment, and elucidate mechanisms between sleep and PTSD treatments.