Relationships of posttraumatic stress symptoms and sleep measures to cognitive performance in young-adult African Americans.
TL;DR: There was an interaction of PTSD symptom severity and sleep duration on omission errors such that more than 7 hours 12 minutes of sleep mitigated attentional lapses that were associated with PTSD.
Abstract: Disturbed sleep is a prominent feature of posttraumatic stress disorder (PTSD). PTSD and disrupted sleep have been independently linked to cognitive deficits; however, synergistic effects of PTSD and poor sleep on cognition have not been investigated. The purpose of this study was to examine the effects of PTSD symptoms and objectively measured disruptions to sleep on cognitive function. Forty-four young-adult African American urban residents comprised the study sample. The Clinician-Administered PTSD Scale (CAPS; Blake et al., 1995) was utilized to determine the severity of PTSD symptoms. Participants underwent 2 consecutive nights of polysomnography. The Automated Neuropsychological Assessment Metrics (Reeves, Winter, Bleiberg, & Kang, 2007) was utilized to assess sustained attention and the Rey Auditory Verbal Learning Test (Schmidt, 1996) was used to evaluate verbal memory. PTSD symptom severity, r(42) = .40, p = .007, was significantly associated with omission errors on the sustained attention task, and sleep duration, r(42) = .41, p = .006, and rapid eye movement sleep, r(42) = .43, p = .003, were positively correlated with verbal memory. There was an interaction of PTSD symptom severity and sleep duration on omission errors such that more than 7 hours 12 minutes of sleep mitigated attentional lapses that were associated with PTSD.
Traditional and Simplified Chinese Abstracts by AsianSTSS
標題：非裔美國年輕人中創傷後壓力症和睡眠測量與認知表現的關係
撮要：睡眠困擾是創傷後壓力左(PTSD)的顯著病癥。PTSD和睡眠問題各自與認知受損有關，但PTSD和失眠對認知的協同效應則未有探討。本研究檢視PTSD症狀的影響和客觀地量度睡眠困擾對認知功能的效果。樣本是53名非裔美國年輕市區居民。醫生施行PTSD量表(CAPS)測量PTSD症狀的嚴重程度，而參加者亦會連續兩晚接受多重睡眠電圖測試。持續注意力會採用自動化神經心理評估指標來評核，而雷伊聽覺言語學習測試則評定言語記憶。PTSD症狀的嚴重程度 r(42)= .40, p= .007統計上顯著與持續注意力任務的遺漏錯誤相連，而睡眠持續時間r(42)= .41, p= .006和快速眼動睡眠r(42)= .43, p= .003均與言語記憶有正相連。PTSD症狀嚴重程度和睡眠持續時間對遺漏錯誤有相互影響，以致多於7小時12分的睡眠可減輕與PTSD相關的注意力失誤。
标题：非裔美国年轻人中创伤后压力症和睡眠测量与认知表现的关系
撮要：睡眠困扰是创伤后压力左(PTSD)的显著病症。PTSD和睡眠问题各自与认知受损有关，但PTSD和失眠对认知的协同效应则未有探讨。本研究检视PTSD症状的影响和客观地量度睡眠困扰对认知功能的效果。样本是53名非裔美国年轻市区居民。医生施行PTSD量表(CAPS)测量PTSD症状的严重程度，而参加者亦会连续两晚接受多重睡眠电图测试。持续注意力会采用自动化神经心理评估指标来评核，而雷伊听觉言语学习测试则评定言语记忆。PTSD症状的严重程度 r(42)= .40, p= .007统计上显著与持续注意力任务的遗漏错误相连，而睡眠持续时间r(42)= .41, p= .006和快速眼动睡眠r(42)= .43, p= .003均与言语记忆有正相连。PTSD症状严重程度和睡眠持续时间对遗漏错误有相互影响，以致多于7小时12分的睡眠可减轻与PTSD相关的注意力失误。
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TL;DR: Understanding sleep problems and their role in the development and maintenance of PTSD and TBI symptoms may lead to improvement in overall treatment outcomes while offering a non-stigmatizing entry in mental health services and make current treatments more comprehensive by helping to address a broader spectrum of difficulties.
106 citations
Cites background from "Relationships of posttraumatic stre..."
...One recent study by Brownlow, Brown, and Mellman (2014) demonstrated a relationship between sustained attention, verbal memory, and objectively measured sleep in PTSD. Interestingly, a full night’s sleep (approximately 7 hours or greater) mitigated attention errors in PTSD. Sleep problems and…...
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TL;DR: Sleep disturbance may be more than a mere epiphenomenon of PTSD, and the utility of targeting sleep disturbance in prevention and treatment is necessary to fully understand the likely bidirectional relationship between sleep disturbance and PTSD.
Abstract: Purpose of Review
The goal of this review is to integrate recent findings on sleep disturbance and PTSD, examine sleep disturbance as a causal factor in the development of PTSD, and identify future directions for research, treatment, and prevention.
44 citations
TL;DR: Evidence of dysregulated inflammation in PTSD is summarized and how the neurobiological underpinnings of PTSD, in the context of fear learning and extinction acquisition and recall, may interact with inflammation is explored.
Abstract: Compelling evidence from animal and human research suggest a strong link between inflammation and posttraumatic stress disorder (PTSD). Furthermore, recent findings support compromised neurocognitive function as a key feature of PTSD, particularly with deficits in attention and processing speed, executive function, and memory. These cognitive domains are supported by brain structures and neural pathways that are disrupted in PTSD and which are implicated in fear learning and extinction processes. The disruption of these supporting structures potentially results from their interaction with inflammation. Thus, the converging evidence supports a model of inflammatory dysregulation and cognitive dysfunction as combined mechanisms underpinning PTSD symptomatology. In this review, we summarize evidence of dysregulated inflammation in PTSD and further explore how the neurobiological underpinnings of PTSD, in the context of fear learning and extinction acquisition and recall, may interact with inflammation. We then present evidence for cognitive dysfunction in PTSD, highlighting findings from human work. Potential therapeutic approaches utilizing novel pharmacological and behavioral interventions that target inflammation and cognition also are discussed.
31 citations
TL;DR: Findings signify the relevance of sleep disturbances among trauma-exposed children, but type of trauma and characteristics of the traumatic event were largely unrelated to sleep problems on either caregiver's or children's reports.
26 citations
References
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TL;DR: The Clinician-Administered PTSD Scale (CAPS-1) is a structured interview for assessing core and associated symptoms of PTSD and is intended for use by experienced clinicians, and also can be administered by appropriately trained paraprofessionals.
Abstract: Several interviews are available for assessing PTSD. These interviews vary in merit when compared on stringent psychometric and utility standards. Of all the interviews, the Clinician-Administered PTSD Scale (CAPS-1) appears to satisfy these standards most uniformly. The CAPS-1 is a structured interview for assessing core and associated symptoms of PTSD. It assesses the frequency and intensity of each symptom using standard prompt questions and explicit, behaviorally-anchored rating scales. The CAPS-1 yields both continuous and dichotomous scores for current and lifetime PTSD symptoms. Intended for use by experienced clinicians, it also can be administered by appropriately trained paraprofessionals. Data from a large scale psychometric study of the CAPS-1 have provided impressive evidence of its reliability and validity as a PTSD interview.
4,643 citations
"Relationships of posttraumatic stre..." refers methods in this paper
...The CAPS (Blake et al., 1995) is a structured clinical interview designed to determine lifetime and current PTSD diagnostic status according to the Diagnostic and Statistical Manual of Mental Disorders (4th ed., DSM-IV; American Psychiatric Association, 1994)....
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...The index events were assessed using standard procedures for the Clinician-Administered PTSD Scale (CAPS; Blake et al., 1995)....
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...The CAPS (Blake et al., 1995) is a structured clinical interview designed to determine lifetime and current PTSD diagnostic status according to the Diagnostic and Statistical Manual of Mental Disorders (4th ed....
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...The Clinician-Administered PTSD Scale (CAPS; Blake et al., 1995) was utilized to determine the severity of PTSD symptoms....
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TL;DR: The effect size of all the risk factors was modest, but factors operating during or after the trauma, such as trauma severity, lack of social support, and additional life stress, had somewhat stronger effects than pretrauma factors.
Abstract: Meta-analyses were conducted on 14 separate risk factors for posttraumatic stress disorder (PTSD), and the moderating effects of various sample and study characteristics, including civilian/military status, were examined. Three categories of risk factor emerged: Factors such as gender, age at trauma, and race that predicted PTSD in some populations but not in others; factors such as education, previous trauma, and general childhood adversity that predicted PTSD more consistently but to a varying extent according to the populations studied and the methods used; and factors such as psychiatric history, reported childhood abuse, and family psychiatric history that had more uniform predictive effects. Individually, the effect size of all the risk factors was modest, but factors operating during or after the trauma, such as trauma severity, lack of social support, and additional life stress, had somewhat stronger effects than pretrauma factors.
4,488 citations
TL;DR: It appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults, and sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.
Abstract: OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h). CONCLUSIONS: Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.
2,694 citations
TL;DR: The familiar pick-a-point approach and the much less familiar Johnson-Neyman technique for probing interactions in linear models are described and macros for SPSS and SAS are introduced to simplify the computations and facilitate the probing of interactions in ordinary least squares and logistic regression.
Abstract: Researchers often hypothesize moderated effects, in which the effect of an independent variable on an outcome variable depends on the value of a moderator variable. Such an effect reveals itself statistically as an interaction between the independent and moderator variables in a model of the outcome variable. When an interaction is found, it is important to probe the interaction, for theories and hypotheses often predict not just interaction but a specific pattern of effects of the focal independent variable as a function of the moderator. This article describes the familiar pick-a-point approach and the much less familiar Johnson-Neyman technique for probing interactions in linear models and introduces macros for SPSS and SAS to simplify the computations and facilitate the probing of interactions in ordinary least squares and logistic regression. A script version of the SPSS macro is also available for users who prefer a point-and-click user interface rather than command syntax.
2,204 citations
"Relationships of posttraumatic stre..." refers methods in this paper
...The interaction effects were probed with Hayes and Matthes’ (2009) MODPROBE macro, which allowed modeling of the relationship between Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies....
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...To probe and interpret interaction effects, a macro developed by Hayes and Matthes (2009) was utilized....
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