The current report provides an updated review of sleep disturbance in posttraumatic stress disorder and anxiety-related disorders. First, this review provides a summary description of the unique and ...overlapping clinical characteristics and physiological features of sleep disturbance in specific DSM anxiety-related disorders. Second, this review presents evidence of a bidirectional relationship between sleep disturbance and anxiety-related disorders, and provides a model to explain this relationship by integrating research on psychological and neurocognitive processes with a current understanding of neurobiological pathways. A heuristic neurobiological framework for understanding the bidirectional relationship between abnormalities in sleep and anxiety-related brain pathways is presented. Directions for future research are suggested.
To investigate the objective sleep influencers behind older adult responses to subjective sleep measures, in this case, the Pittsburgh Sleep Quality Index (PSQI). Based on previous literature, we ...hypothesized that SE would be associated with PSQI reported sleep disruption. Furthermore, because SOL increases progressively with age and it tends to be easily remembered by the patients, we also expected it to be one of the main predictors of the perceived sleep quality in the elderly.
We studied 32 cognitively healthy community-dwelling older adults (age 74 ± 0.3 years) who completed an at-home sleep assessment (Zeo, Inc.) and the PSQI. Linear mixed models were used to analyze the association of the objective sleep parameters (measured by the Zeo) with the PSQI total score and sub-scores, adjusting for age, gender, years of education and likelihood of sleep apnea.
Objective sleep parameters did not show any association with the PSQI total score. We found that objective measures of Wake after sleep onset (WASO, % and min) were positively associated with the PSQI sleep disturbance component, while SE and Total Sleep Time (TST) were negatively associated with PSQI sleep disturbance. Lastly, objective SE was positively associated with PSQI SE.
Our findings showed that WASO, SE and TST, are associated with PSQI sleep disturbance, where the greater WASO, overall lower SE and less TST, were associated with increased subjective report of sleep disturbance. As expected, subjective (PSQI) and objective measures of SE were related. However, PSQI total score did not relate to any of the objective measures. These results suggest that by focusing on the PSQI total score we may miss the insight this easily administered self-report tool can provide. If interpreted in the right way, the PSQI can provide further insight into cognitively healthy older adults that have the likelihood of objective sleep disturbance.
Examine whether cognitive behavioral therapy for insomnia (CBT-I) improves sleep in posttraumatic stress disorder (PTSD) as well as nightmares, nonsleep PTSD symptoms, depression symptoms, and ...psychosocial functioning.
RANDOMIZED CONTROLLED TRIAL WITH TWO ARMS: CBT-I and monitor-only waitlist control.
Department of Veterans Affairs (VA) Medical Center.
Forty-five adults (31 females: mean age 37 y (22-59 y) with PTSD meeting research diagnostic criteria for insomnia, randomly assigned to CBT-I (n = 29; 22 females) or monitor-only waitlist control (n = 16; nine females).
Eight-session weekly individual CBT-I delivered by a licensed clinical psychologist or a board-certified psychiatrist.
Measures included continuous monitoring of sleep with diary and actigraphy; prepolysomnography and postpolysomnography and Clinician-Administered PTSD Scale (CAPS); and pre, mid, and post self-report questionnaires, with follow-up of CBT-I participants 6 mo later. CBT-I was superior to the waitlist control condition in all sleep diary outcomes and in polysomnography-measured total sleep time. Compared to waitlist participants, CBT-I participants reported improved subjective sleep (41% full remission versus 0%), disruptive nocturnal behaviors (based on the Pittsburgh Sleep Quality Index-Addendum), and overall work and interpersonal functioning. These effects were maintained at 6-mo follow-up. Both CBT-I and waitlist control participants reported reductions in PTSD symptoms and CAPS-measured nightmares.
Cognitive behavioral therapy for insomnia (CBT-I) improved sleep in individuals with posttraumatic stress disorder, with durable gains at 6 mo. Overall psychosocial functioning improved following CBT-I. The initial evidence regarding CBT-I and nightmares is promising but further research is needed. Results suggest that a comprehensive approach to treatment of posttraumatic stress disorder should include behavioral sleep medicine.
TRIAL NAME: Cognitive Behavioral Treatment Of Insomnia In Posttraumatic Stress Disorder. URL: http://clinicaltrials.gov/ct2/show/NCT00881647.
NCT00881647.
To test if posttraumatic stress disorder (PTSD) is associated with low brain gamma-aminobutyric acid (GABA) levels and if reduced GABA is mediated by poor sleep quality.
Laboratory study using in ...vivo proton magnetic resonance spectroscopy (1H MRS) and behavioral testing.
VA Medical Center Research Service, Psychiatry and Radiology.
Twenty-seven patients with PTSD (PTSD+) and 18 trauma-exposed controls without PTSD (PTSD-), recruited from United States Army reservists, Army National Guard, and mental health clinics.
None.
1H MRS at 4 Tesla yielded spectra from three cortical brain regions. In parieto-occipital and temporal cortices, PTSD+ had lower GABA concentrations than PTSD-. As expected, PTSD+ had higher depressive and anxiety symptom scores and a higher Insomnia Severity Index (ISI) score. Higher ISI correlated with lower GABA and higher glutamate levels in parieto-occipital cortex and tended to correlate with lower GABA in the anterior cingulate. The relationship between parieto-occipital GABA and PTSD diagnosis was fully mediated through insomnia severity. Lower N-acetylaspartate and glutamate concentrations in the anterior cingulate cortex correlated with higher arousal scores, whereas depressive and anxiety symptoms did generally not influence metabolite concentrations.
Low brain gamma-aminobutyric acid (GABA) concentration in posttraumatic stress disorder (PTSD) is consistent with most findings in panic and social anxiety disorders. Low GABA associated with poor sleep quality is consistent with the hyperarousal theory of both primary insomnia and PTSD. Our data demonstrate that poor sleep quality mediates low parieto-occipital GABA in PTSD. The findings have implications for PTSD treatment approaches.
Abstract Objective Experiencing potentially traumatic events across one’s lifecourse increases risk for poor physical health outcomes. Existing models emphasize the effects of any lifetime trauma ...exposure, risk accumulation (multiple traumas over time), and sensitive periods of exposure (specific exposure timepoints leading to lasting consequences). We examined how different indices of trauma exposure across the lifecourse were associated with later life arthritis, a common and debilitating health condition. Methods Data include 5,717 Health and Retirement Study participants (age mean = 65.3, SD = 12.9) who reported on lifetime adversity and trauma in 2006-2008. Lifetime trauma exposure was modeled as any trauma, accumulation of traumas, and lifecourse profiles (no exposure, childhood only, adulthood only, childhood and adulthood exposure). Outcomes included prevalent arthritis at baseline and incident arthritis across 12 years of follow-up. Covariate-adjusted generalized linear models for prevalence ratios (PR) and Cox proportional hazards models for hazard ratios (HR) were conducted. Results Any lifetime trauma was associated with both prevalent arthritis at baseline (PR = 1.13, 95%CI 1.05-1.22) and incident arthritis over 12 years (HR = 1.25, 95%CI 1.17-1.47). Greater trauma accumulation was significantly associated with both prevalent and incident arthritis. Childhood exposure was particularly strongly associated with prevalent and incident cases, with adulthood exposure being unassociated with incident arthritis. Across models, trauma exposure was associated with prevalent cases of both immune-related and osteoarthritis types. Conclusions Higher lifetime trauma burden, especially during childhood, may predispose individuals to arthritis later in life. Early intervention or prevention efforts should identify trauma as an important risk factor for musculoskeletal health across the lifecourse.
Fear extinction underlies prolonged exposure, one of the most well-studied treatments for posttraumatic stress disorder (PTSD). There has been increased interest in exploring pharmacological agents ...to enhance fear extinction learning in humans and their potential as adjuncts to PE. The objective of such adjuncts is to augment the clinical impact of PE on the durability and magnitude of symptom reduction. In this study, we examined whether hydrocortisone (HC), a corticosteroid, and D-Cycloserine (DCS), an N-methyl-D-aspartate receptor partial agonist, enhance fear extinction learning and consolidation in individuals with PTSD. In a double-blind placebo-controlled 3-group experimental design, 90 individuals with full or subsyndromal PTSD underwent fear conditioning with stimuli that were paired (CS+) or unpaired (CS-) with shock. Extinction learning occurred 72 h later and extinction retention was tested one week after extinction. HC 25 mg, DCS 50 mg or placebo was administered one hour prior to extinction learning. During extinction learning, the DCS and HC groups showed a reduced differential CS+/CS- skin conductance response (SCR) compared to placebo (b = -0.19, CI = -0.01 to -37, p = 0.042 and b = -0.25, CI = -08 to -0.43, p = 0.005, respectively). A nonsignificant trend for a lower differential CS+/CS- SCR in the DCS group, compared to placebo, (b = -0.25, CI = 0.04 to -0.55, p = 0.089) was observed at retention testing, one week later. A single dose of HC and DCS facilitated fear extinction learning in participants with PTSD symptoms. While clinical implications have yet to be determined, our findings suggest that glucocorticoids and NMDA agonists hold promise for facilitating extinction learning in PTSD.
•Lower cortisol levels predict a poorer clinical course of PTSD.•Elevated WBC, CRP, fibrinogen and ESR predict a poorer clinical course of PTSD.•Elevated WBC, CRP and fibrinogen predict a poorer ...clinical course of depression.
Prior research has focused largely on the pro-inflammatory states of PTSD and depression, with few studies evaluating the direction of inflammation’s association with these disorders. To clarify whether inflammation plays a role in the development of PTSD or depression, we assessed the predictive value of inflammatory biomarkers on the courses of these conditions in a cohort of Veterans.
This research was part of the Mind Your Heart Study, a prospective cohort study designed to examine PTSD-related health outcomes. Between 2008 and 2010, 746 San Francisco area Veterans Administration patients were enrolled. At baseline, inflammatory biomarkers were measured from fasting morning venous blood draws, and cortisol and catecholamine levels were measured from 24-hour urine samples. PTSD was diagnosed using the PTSD Checklist at baseline and annual follow-up. Depression was evaluated using the 9-item Patient Health Questionnaire at baseline and follow-up. Ordinal logistic regression models were used to assess the predictive value of baseline biomarker levels on clinically relevant courses of PTSD and depression categorized and ordered as none, resolved, developed, and chronic.
After adjustment for age and sex, elevated levels of white blood cell count (OR = 1.27(1.10–1.47), p = 0.001), C-reactive protein (OR = 1.20(1.04–1.39), p = 0.02), fibrinogen (OR = 1.19(1.03–1.38), p = 0.02), and ESR (OR = 1.17(1.00–1.36, p = 0.05), and decreased levels of urine cortisol (OR = 0.84(0.71–0.99), p = 0.04) were significant predictors of poorer courses of PTSD. Elevated levels of WBC count (OR = 1.31(1.14–1.50), p < 0.001), CRP (OR = 1.24(1.07–1.43), p = 0.003), fibrinogen (OR = 1.26(1.09–1.46), p = 0.002), and catecholamines (OR = 1.17(1.01–1.36), p = 0.04) were significant predictors of poorer courses of depression. After additionally controlling for physical activity, elevated WBC count (p = 0.002) and decreased levels of urine cortisol (p = 0.05) remained significant predictors of PTSD course, and elevated WBC count (p = 0.001), CRP (p = 0.03), and fibrinogen (p = 0.02) remained significant predictors of depression course. After adjusting for all significant variables, elevated WBC count (p = 0.02) was a significant predictor of a poorer course of PTSD, and elevated WBC count (p = 0.04) and platelet count (p = 0.03) were significant predictors of a poorer course of depression.
Increased levels of several inflammatory biomarkers were associated with significantly increased odds of clinically worse courses of PTSD and depression. Inflammation may be a target for prevention and treatment of these mental health disorders.
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