Treatment of Sleep Comorbidities in Posttraumatic Stress Disorder.
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ABSTRACT: Purpose of the review
Sleep disturbances, insomnia and recurrent nightmares in particular, are among the most frequently endorsed symptoms of posttraumatic stress disorder (PTSD). The present review provides a summary of the prevalence estimates and methodological challenges presented by sleep disturbances in PTSD, highlights the recent evidence for empirically supported psychotherapeutic and pharmacological interventions for comorbid sleep disturbances implicated in PTSD, and provides a summary of recent findings on integrated and sequential treatment approaches to ameliorate comorbid sleep disturbances in PTSD.Recent findings
Insomnia, recurrent nightmares, and other sleep disorders are commonly endorsed among individuals with PTSD; however, several methodological challenges contribute to the varying prevalence estimates. Targeted sleep-focused therapeutic interventions can improve sleep symptoms and mitigate daytime PTSD symptoms. Recently, attention has focused on the role of integrated and sequential approaches, suggesting that comprehensively treating sleep disturbances in PTSD is likely to require novel treatment modalities.Summary
Evidence is growing on the development, course, and treatment of comorbid sleep disturbances in PTSD. Further, interventions targeting sleep disturbances in PTSD show promise in reducing symptoms. However, longitudinal investigations and additional rigorous controlled trials with diverse populations are needed to identify key features associated with treatment response in order to alleviate symptoms.
SUBMITTER: Brownlow JA
PROVIDER: S-EPMC7864531 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Study objectivesCharacterize associations between sleep impairments and posttraumatic stress disorder (PTSD) symptoms, including anger, in service members seeking treatment for PTSD.MethodsNinety-three US Army personnel recruited into a PTSD treatment study completed the baseline assessment. State-of-the-science sleep measurements included 1) retrospective, self-reported insomnia, 2) prospective sleep diaries assessing sleep patterns and nightmares, and 3) polysomnography measured sleep architecture and obstructive sleep apnea-hypopnea severity. Dependent variables included self-report measures of PTSD severity and anger severity. Pearson correlations and multiple linear regression analyses examined if sleep symptoms, not generally measured in PTSD populations, were associated with PTSD and anger severity.ResultsAll participants met PTSD, insomnia, and nightmare diagnostic criteria. Mean sleep efficiency = 70%, total sleep time = 5.5 hours, obstructive sleep apnea/hypopnea (obstructive sleep apnea-hypopnea index ≥ 5 events/h) = 53%, and clinically significant anger = 85%. PTSD severity was associated with insomnia severity (β = .58), nightmare severity (β = .24), nightmare frequency (β = .31), and time spent in Stage 1 sleep (β = .27, all P < .05). Anger severity was associated with insomnia severity (β = .37), nightmare severity (β = .28), and obstructive sleep apnea-hypopnea during rapid eye movement sleep (β = .31, all P < .05).ConclusionsInsomnia and nightmares were related to PTSD and anger severity, and obstructive sleep apnea-hypopnea was related to anger. Better assessment and evidence-based treatment of these comorbid sleep impairments in service members with PTSD and significant anger should result in better PTSD, anger, and quality-of-life outcomes.Clinical trials registrationRegistry: ClinicalTrials.gov; Name: Treatment of Comorbid Sleep Disorders and Post Traumatic Stress Disorder; Identifier: NCT02773693; URL: https://clinicaltrials.gov/ct2/show/NCT02773693.CitationMiles SR, Pruiksma KE, Slavis D, et al. Sleep disorder symptoms are associated with greater posttraumatic stress and anger symptoms in US Army service members seeking treatment for posttraumatic stress disorder. J Clin Sleep Med. 2022;18(6):1617-1627.
| S-EPMC9163631 | biostudies-literature
Project description:Sleep disturbances (SDs) are among the most distressing and commonly reported symptoms in posttraumatic stress disorder (PTSD). Despite increased attention on sleep in clinical PTSD research, SDs remain difficult to treat. In Phase 2 trials, 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy has been shown to greatly improve PTSD symptoms. We hypothesized that MDMA-assisted psychotherapy would improve self-reported sleep quality (SQ) in individuals with PTSD and be associated with declining PTSD symptoms. Participants in four studies (n = 63) were randomized to receive 2-3 sessions of active MDMA (75-125 mg; n = 47) or placebo/control MDMA (0-40 mg, n = 16) during all-day psychotherapy sessions. The PSQI was used to assess change in SQ from baseline to the primary endpoint, 1-2 months after the blinded sessions. Additionally, PSQI scores were measured at treatment exit (TE) and 12-month follow-up. Symptoms of PTSD were measured using the CAPS-IV. At the primary endpoint, CAPS-IV total severity scores dropped more after active MDMA than after placebo/control (-34.0 vs. -12.4), p = .003. Participants in the active dose group showed more improvement in SQ compared to those in the control group (PSQI total score ΔM = -3.5 vs. 0.6), p = .003. Compared to baseline, SQ had improved at TE, p < .001, with further significant gains reported at 12-month follow-up (TE to 12-months ΔM = -1.0), p = .030. Data from these randomized controlled double-blind studies provide evidence for the beneficial effects of MDMA-assisted psychotherapy in treating SDs in individuals with PTSD.
| S-EPMC8453707 | biostudies-literature
Project description:ObjectivesSeveral medical and psychiatric disorders have stage-based treatment decision-making methods. However, international treatment guidelines for posttraumatic stress disorder (PTSD) fail to give specific treatment recommendations based on chronicity or stage of the disorder. There is convincing evidence of a finite range of PTSD symptom trajectories, implying that different phenotypes of the disorder can be distinguished, which are highly relevant for a staging typology of PTSD.MethodsState-of-the-art review building on prior work on staging models in other disorders as a mapping tool to identify and synthesize toward PTSD.ResultsWe propose a four-stage model of PTSD ranging from stage 0: trauma-exposed asymptomatic but at risk to stage 4: severe unremitting illness of increasing chronicity. We favor a symptom description in various chronological characteristics based on neurobiological markers, information processing systems, stress reactivity, and consciousness dimensions. We also advocate for a separate phenomenology of treatment resistance since this can yield treatment recommendations.ConclusionA staging perspective in the field of PTSD is highly needed. This can facilitate the selection of interventions that are proportionate to patients' current needs and risk of illness progression and can also contribute to an efficient framework to organize biomarker data and guide service delivery. Therefore, we propose that a neurobiologically driven trajectory-based typology of PTSD can help deduct several treatment recommendations leading to a more personalized and refined grid to strategize, plan and evaluate treatment interventions.
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Project description:ObjectiveIndividuals with posttraumatic stress disorder (PTSD) smoke at higher rates compared to the general population and experience significant barriers to initiating cessation treatment. Proactive outreach addresses these barriers by directly engaging with smokers and facilitating access to treatment. The objective of the present study was to evaluate a proactive outreach intervention for increasing rates of treatment utilization and abstinence among veteran smokers with and without PTSD.MethodThis is a secondary analysis of a randomized controlled trial conducted from 2013 to 2017 that demonstrated the effectiveness of proactive outreach among veterans using Veterans Affairs mental health care services. Electronic medical record data were used to identify participants with (n = 355) and without (n = 1,583) a diagnosis of PTSD. Logistic regressions modeled cessation treatment utilization (counseling, nicotine replacement therapy [NRT], and combination treatment) and abstinence (7-day point prevalence and 6-month prolonged at 6- and 12-month follow-ups) among participants randomized to proactive outreach versus usual care in the PTSD and non-PTSD subgroups, respectively.ResultsCompared to usual care, proactive outreach increased combined counseling and NRT utilization among participants with PTSD (odds ratio [OR] = 26.25, 95% confidence interval [3.43, 201.17]) and without PTSD (OR = 10.20, [5.21, 19.98]). Proactive outreach also increased 7-day point prevalence abstinence at 12 months among participants with PTSD (OR = 2.62, [1.16, 5.91]) and without PTSD (OR = 1.61, [1.11, 2.34]).ConclusionsProactive outreach increased treatment utilization and abstinence among smokers with and without PTSD. Smokers with PTSD may need additional facilitation to initiate cessation treatment but are receptive when it is offered proactively. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
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Project description:Emotion processing abnormalities and sleep pathology are central to the phenomenology of paediatric posttraumatic stress disorder, and sleep disturbance has been linked to the development, maintenance and severity of the disorder. Given emerging evidence indicating a role for sleep in emotional brain function, it has been proposed that dysfunctional processing of emotional experiences during sleep may play a significant role in affective disorders, including posttraumatic stress disorder. Here we sought to examine the relationship between sleep and emotion processing in typically developing youth, and youth with a diagnosis of posttraumatic stress disorder . We use high-density electroencephalogram to compare baseline sleep with sleep following performance on a task designed to assess both memory for and reactivity to negative and neutral imagery in 10 youths with posttraumatic stress disorder, and 10 age- and sex-matched non-traumatized typically developing youths. Subjective ratings of arousal to negative imagery (ΔArousal = post-sleep minus pre-sleep arousal ratings) remain unchanged in youth with posttraumatic stress disorder following sleep (mean increase 0.15, CI -0.28 to +0.58), but decreased in TD youth (mean decrease -1.0, 95% CI -1.44 to -0.58). ΔArousal, or affective habituation, was negatively correlated with global change in slow-wave activity power (ρ = -0.58, p = .008). When considered topographically, the correlation between Δslow-wave activity power and affective habituation was most significant in a frontal cluster of 27 electrodes (Spearman, ρ = -0.51, p = .021). Our results highlight the importance of slow-wave sleep for adaptive emotional processing in youth, and have implications for symptom persistence in paediatric posttraumatic stress disorder. Impairments in slow-wave activity may represent a modifiable risk factor in paediatric posttraumatic stress disorder.
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Project description:There is evidence that doxazosin is effective in the treatment of posttraumatic stress disorder (PTSD). Doxazosin is a "me-too" drug of prazosin. Doxazosin has an improved absorption profile and this likely minimizes the risk for unintended adverse hypotensive effects. The availability of doxazosin in the gastrointestinal therapeutic system (GITS) form permits a higher initial daily dose (4 mg/day) while avoiding significant first-dose side effects. The treatment of PTSD with prazosin has several disadvantages due to its short duration of action (6-8 hours), which results in multiple doses being required. Prazosin may wear off and this may lead to nightmares in the latter half of the sleep. Doxazosin has significant advantages over prazosin in clinical practice because it has a long half-life and requires only once-daily dosing. This may lead to better adherence and greater effectiveness in the treatment of PTSD.
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Project description:Patients with posttraumatic stress disorder (PTSD) exhibit an increased state of inflammation. Various animal models for PTSD have shown some of the same immune imbalances as have been shown in human subjects with PTSD, and some of these studies are discussed in this review. However, animal studies can only indirectly implicate immune involvement in PTSD in humans. This review of mainly studies with human subjects focuses on dissecting the immunological role in the pathogenesis of PTSD following initial trauma exposure. It addresses both the inflammatory state associated with PTSD and the immune imbalance between stimulatory and inhibitory immune mediators, as well as variables that can lead to discrepancies between analyses. The concept of immunological treatment approaches is proposed for PTSD, as new treatments are needed for this devastating disorder that is affecting unprecedented numbers of Veterans from the long-standing wars in the Middle East and which affects civilians following severe trauma.
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Project description:Purpose of reviewThis review aims to synthesize existing research regarding the definition of treatment resistance in posttraumatic stress disorder (PTSD), predictors of treatment non-response to first-line interventions, and emerging second-line PTSD treatment options into an accessible resource for the practicing clinician.Recent findingsThe concept of treatment resistance in PTSD is currently poorly defined and operationalized. There are no well-established predictors of treatment non-response utilized in routine clinical care, but existing research identifies several potential candidate markers, including male gender, low social support, chronic and early life trauma exposure, comorbid psychiatric disorders, severe PTSD symptoms, and poor physical health. The most promising available treatment options for PTSD patients non-responsive to first-line psychotherapies and antidepressants include transcranial magnetic stimulation and ketamine infusion. Methylenedioxymethamphetamine-assisted psychotherapy also appears promising but is only available in a research context. These options require careful consideration of risks and benefits for a particular patient.SummaryMore research is required to develop a robust, clinically-useful definition of treatment resistance in PTSD; identify reliable, readily assessable, and generalizable predictors of PTSD treatment non-response; and implement measurement and prediction in clinical settings to identify individuals unlikely to respond to first-line treatments and direct them to appropriate second-line treatments.
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| S-EPMC7076084 | biostudies-literature
Project description:Disturbed sleep is a core feature of posttraumatic stress disorder (PTSD), characterized in part by decreased delta power sleep that may result from stress-related alterations in corticotropin releasing factor (CRF), hypothalamic pituitary adrenal axis (HPA) regulation and glucocorticoid signaling. Overnight HPA axis response mediating sleep disturbances in men and women with PTSD was examined using a metyrapone challenge. Metyrapone blocks cortisol synthesis, removing negative feedback, and increases the release of hypothalamic CRF and pituitary adrenocorticotropic hormone (ACTH). Laboratory-based polysomnography was used to monitor the sleep of 66 medically healthy, medication-free men and pre-menopausal follicular phase women including 33 with chronic PTSD (16 women and 17 men) and 33 age- and sex-matched controls (14 women and 19 men) over 3 consecutive nights. Participants completed an overnight metyrapone challenge after an adaptation and baseline night of sleep and ACTH was obtained by repeated blood sampling. Metyrapone resulted in a greater increase in ACTH and greater decreases in cortisol and delta spectral power sleep in PTSD subjects compared to controls, and a greater increase in ACTH in women compared to men. There was no sex difference in metyrapone effects on delta power sleep, and no significant metyrapone by PTSD by sex interactions with either ACTH or delta power sleep. Regression analyses indicated that a greater increase in ACTH response was associated with a greater decrease in delta power sleep response in PTSD subjects, but no such relationship was found in controls. The PTSD group difference was similar in men and women. These results suggest that stress-related alterations of the HPA axis in PTSD may contribute to sleep difficulties. Therapeutics that target the HPA axis may offer promise as a potential future treatment for PTSD and related sleep difficulties.
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