Article

Psychological Stress Is Associated With Heightened Physiological Arousal During NREM Sleep in Primary Insomnia

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Abstract

The objective of this study was to evaluate cross-sectional relationships among symptoms of psychological stress, sleep, and physiological arousal during non-rapid eye movement (NREM) sleep in a sample of 30 patients with chronic, primary insomnia (mean age, 30.2 years, 60% female). Study measures included indexes of subjective stress, visually scored sleep, and physiological arousal during NREM sleep: quantitative electroencephalogram (QEEG) and quantitative electrocardiogram (QEKG) measures. Psychological stress was more strongly related to indexes of physiological arousal during NREM sleep than to visually scored measures of sleep. Higher levels of perceived stress were associated with decreased EEG delta power (rho = -0.50, p < .01) and increased EEG beta power (rho = 0.38, p < .05). Increased frequency of stress-related avoidance behaviors was associated with decreased EKG high-frequency power (rho = -0.46, p < .05). Although QEEG measures were significantly correlated with sleep maintenance (QEEG delta power rho = 0.45, p < .01; QEEG beta power rho = -0.54, p < .01) and time spent in delta sleep (QEEG delta power rho = 0.65, p < .001; QEEG beta power rho = -0.65, p < .001), QEKG measures were unrelated to visually scored measures of sleep. Perceived stress and stress-related avoidance behaviors were associated with multiple indexes of physiological arousal during NREM sleep in patients with chronic, primary insomnia.

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... Recently, a systematic review and meta-analysis by Clancy et al. [10] found an association between negative overthinking and insomnia. Negative overthinking is de ned as a repetitive thought process that may lead to cognitive arousal, worry, and intrusive thinking [11]. In addition, negative overthinking includes persistent worrying about future events and continual focus on painful past experiences or current negative feelings (i.e., rumination) [12]. ...
... Rumination is a maladaptive response that may impair problem solving [15,16], an especially necessary skill for adolescent-aged populations. Rumination also plays an important role in physiological arousal [11], which may lead to di culty falling asleep, reduced sleep quality, and shorter total sleep duration [14]. ...
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Objective Insomnia is the most common complaint in adolescents with mood disorders (MD). However, the psychopathological mechanisms associated with insomnia remain unclear. Therefore, we aimed to explore anxiety’s mediating role in the effect of rumination on insomnia in MD adolescents. Methods A total of 569 MD patients were recruited. Participants completed the Patient Health Questionnaire-9 (PHQ-9), 7-item Generalized Anxiety Disorder (GAD-7) scale, and Insomnia Severity Index (ISI) to self-assess their mood and insomnia symptoms. In addition, the 21-item Chinese version of the Ruminative Response Scale (RRS) was used to assess rumination specifically. Results The prevalence of insomnia in MD patients was 60.63%, with a higher prevalence in females (63.32%) vs. male patients(54.39%). MD patients with insomnia symptoms also scored higher on depression and anxiety symptom scales, as well as rumination, when compared to MD patients without insomnia. Depression-related rumination and anxiety were correlated with insomnia in MD patients. The AUCROC showed that the combination of depression-related rumination and anxiety could effectively distinguish patients with and without insomnia in MD adolescents. Furthermore, in adolescents with MD, depression-related rumination positively predicted anxiety and insomnia, and anxiety positively predicted insomnia. Finally, anxiety partially mediated the association between depression-related rumination and insomnia. Conclusion Our results suggest that depression-related rumination and anxiety are key riskfactors for insomnia in adolescents with MD. Furthermore, anxiety can exacerbate the effects of depression-related rumination on insomnia, suggesting that clinical interventions to reduce depression-related rumination and anxiety may be a viable consideration for insomnia in adolescents with MD.
... There is a clear neurobiological basis for predicting that an association between sleep and subjective stress should exist in individuals from the general population. Although a few studies have failed to identify any association, (Hisler and Krizan, 2017;Kramer et al., 2019;Veeramachaneni et al., 2019), most have identified a significant inverse association, whereby poorer sleep is associated with higher levels of subjective stress (e.g., Åkerstedt et al., 2015;Alfasi and Soffer-Dudek, 2018;Bani-Issa et al., 2020;Barber et al., 2010;Bidulescu et al., 2010;Cardoso et al., 2021;Cuadros et al., 2012;Doolin et al., 2018;Hall et al., 2007). A similar pattern has emerged in the literature focused on individuals with sleep disorders, with most studies finding poorer quality sleep is linked to greater stress (Basishvili et al., 2012;Chester and Dzierzewski, 2020;Giese et al., 2013;Lothian et al., 2016;Puzino et al., 2020;Vand et al., 2021;Veeramachaneni et al., 2019), and a smaller number finding no evidence of any association (Hall et al., 2000(Hall et al., , 2007. ...
... Although a few studies have failed to identify any association, (Hisler and Krizan, 2017;Kramer et al., 2019;Veeramachaneni et al., 2019), most have identified a significant inverse association, whereby poorer sleep is associated with higher levels of subjective stress (e.g., Åkerstedt et al., 2015;Alfasi and Soffer-Dudek, 2018;Bani-Issa et al., 2020;Barber et al., 2010;Bidulescu et al., 2010;Cardoso et al., 2021;Cuadros et al., 2012;Doolin et al., 2018;Hall et al., 2007). A similar pattern has emerged in the literature focused on individuals with sleep disorders, with most studies finding poorer quality sleep is linked to greater stress (Basishvili et al., 2012;Chester and Dzierzewski, 2020;Giese et al., 2013;Lothian et al., 2016;Puzino et al., 2020;Vand et al., 2021;Veeramachaneni et al., 2019), and a smaller number finding no evidence of any association (Hall et al., 2000(Hall et al., , 2007. However, what both of these literatures fail to clearly show is the typical magnitude of these effects, with the absolute magnitude of the associations reported across individual studies varying considerably. ...
Article
Prior research suggests that sleep is associated with increased subjective stress and aggression, but important questions remain about the typical magnitude of these relationships, as well as their potential moderators. We therefore conducted the first meta-analysis of this literature. Across 340 associational and experimental studies, significant associations were identified between sleep with both subjective stress (r =.307, p <.001) and aggression (r =.258, p <.001) in individuals from the general population, as well as between sleep with subjective stress (r =.425, p <.001) in individuals with sleep disorders. Experimental sleep restriction also led to increased subjective stress (g = 0.403, p =.017) and aggression (g = 0.330, p =.042). These findings suggest that poorer sleep is associated with - and leads to - heightened levels of subjective stress and aggression. These findings, and their implications, are discussed in relation to neurobiological literature, which highlights the complex interplay between metabolic activity in the brain, hormonal changes, and behavior.
... Few studies mentioned the increase in delta waves during chronic stress 9, 12, 21 . However, Neylan et al. and Hall et al. suggested a decrease in delta waves 29,30 . Like delta, theta also in some studies reported to not be a respondent of a stressor 9,24,25,31 . ...
... Now, beta waves are more involved in brain-specific tasks. Most of the studies reported an increase in beta oscillations at frontal, central, left occipital, anterior, right temporal and parietal temporal regions of the brain 18,20,[21][22][23]26,30 . Some detect a decline in this rhythm at the frontal and right hemispheric frontal site of the brain 8,9,17 . ...
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Background: The biological responses associated with stress originate in the brain and involve different physiological and physical effects. The direct effect of stress on cortical responses can be visualized by recording the brain’s electrical waves using an encephalograph. These waves are recorded by means of an electroencephalogram (EEG). EEG is the most commonly used neuroimaging technique to study the patterns of brainwaves and functioning of the brain. It also measures the variation of the electric field produced by neuronal activity a millisecond at a time. To systematically analyze published studies on the difference between brain wave patterns in terms of their frequencies among subjects with acute stress, chronic stress, and normal individuals. Methodology: The data from published studies was arranged quantitatively and qualitatively by producing a planned summary measure. Studies that focused on brain wave analysis of the EEG of healthy adult subjects with no history of mental illness or head injury were included in the review. The selected literature included many types of stressors that are acute or chronic, and that affected the neuronal electrical activity. The only electronic database utilized to identify relevant studies was PubMed. Result: Fifteen studies were included that were based on a variety of acute stressors to observe alterations in brain wave activity between stress-free and stressed states. These studies showed that stressors could be a causative factor to generate fluctuations in neuronal oscillations that also leads to significant psychological, physiological and neurobiological deteriorations to some extent. An additional sixteen studies were included, which showed the effect of chronic stress on the asymmetry of the amplitude in the frequencies of brain waves. Conclusion: The most common change observed was in the alpha frequency (8-13Hz), followed by changes in beta waves (13-30 Hz) and theta (4-8Hz). Though, there is not always the same resultant pattern of waves explored with even the same type of stressors due to interpersonal differences in response to a stressful situation.
... Subsequent to the stress induction, either only delta power decreased (Ackermann et al., 2019) or the decrease coincided with an increase in beta power (Wuyts et al., 2012;Beck et al., 2022). Increased beta power during sleep has been associated with poorer sleep quality, (Krystal and Edinger, 2008) hyperarousal in insomnia, (Riemann et al., 2010;Maes et al., 2014) and psychological stress burden (Hall et al., 2007) in a plethora of non-experimental studies. Noteworthy in the abovementioned experimental studies with PSD, two are based on a napping design (Ackermann et al., 2019;Beck et al., 2022) and two on an overnight sleep assessment (Wuyts et al., 2012;Kim et al., 2020). ...
Article
Objectives Evidence of the impact of chronic stress on sleep is abundant, yet experimental sleep studies with a focus on acute stress are scarce and the results are mixed. Our study aimed to fill this gap by experimentally investigating the effects of pre-sleep social stress on sleep dynamics during the subsequent night, as measured with polysomnography (PSG). Methods Thirty-four healthy individuals (65% females, Mage = 25.76 years SD = 3.35) underwent a stress-inducing (SC) or neutral control condition (CC) in virtual reality (VR). We used overnight EEG measurements to analyze the basic sleep parameters and power spectral density (PSD) across the sleep cycles, and measured heart rate and its variability (HRV), skin electrodermal activity (EDA), and salivary cortisol to capture physiological arousal during the VR task and the pre-sleep period. Results Following acute stress (SC), the amount of slow-wave sleep (SWS) was higher and N2 sleep lower relative to CC, specifically in the first sleep cycle. In SC, PSD was elevated in the beta-low (16–24 Hz) and beta-high (25–35 Hz) frequency ranges during both stages N2 and SWS over the entire night. Conclusions Sleep promoted adaptation to acute social stress by a longer duration of SWS in the subsequent sleep period, especially in early sleep. A similar homeostatic effect towards restorative sleep is well-evidenced in animal model stress studies but has not been previously reported in experimental human studies. Whether the high-frequency PSD activity during stages N2 and SWS also serves in the resolution of transient stress, remains open.
... Theta (~4-8 Hz) spectral power during REM sleep has been linked to emotional memory processing [16], and has been shown to be elevated in trauma-exposed individuals who were resilient to, compared to those diagnosed with, PTSD [17]. Beta spectral power (~16-30 Hz) has also been shown to be elevated in PTSD compared to those without PTSD [18][19][20][21], and has been theorized as a marker of disturbed sleep and hyperarousal [22][23][24][25]. Alongside these increases in high-frequency power, studies have also documented a reduction in low-frequency power (<4 Hz) that is consistent with reduced slow-wave sleep seen in patients [20,21,26]. ...
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The failure to retain memory for extinguished fear plays a major role in the maintenance of post-traumatic stress disorder (PTSD), with successful extinction recall necessary for symptom reduction. Disturbed sleep, a hallmark symptom of PTSD, impairs fear extinction recall. However, our understanding of the electrophysiological mechanisms underpinning sleep’s role in extinction retention remain underdetermined. We examined the relationship between the microarchitecture of sleep and extinction recall in healthy humans (n=71, both male and females included) and a pilot study in individuals with PTSD (n=12). Participants underwent a fear conditioning and extinction protocol over two days, with sleep recording occurring between conditioning and extinction. Twenty-four hours after extinction learning, participants underwent extinction recall. Power spectral density (PSD) was computed for pre- and post-extinction learning sleep. Increased beta band PSD (~17-26Hz) during pre-extinction learning sleep was associated with worse extinction recall in healthy participants (r=.41, p=.004). Beta PSD was highly stable across three nights of sleep (intraclass correlations (ICC)>0.92). Results suggest beta band PSD is elevated in PTSD, and is specifically implicated in difficulties recalling extinguished fear.
... Theoretically, ACT-based approaches may improve adherence to recommendations through multiple mechanisms. First, psychological flexibility predicts reduced insomnia severity and fewer avoidance behaviors that are linked to poor sleep (Hall et al., 2007;McCracken et al., 2011). Second, orientation to values and committed actions may help individuals to see beyond the initial discomfort associated with insomnia treatment recommendations. ...
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Objective: This randomized comparative effectiveness trial evaluated a novel insomnia treatment using acceptance and commitment therapy (ACT) among women veterans. Participants received either the acceptance and the behavioral changes to treat insomnia (ABC-I) or cognitive behavioral therapy for insomnia (CBT-I). The primary objectives were to determine whether ABC-I was noninferior to CBT-I in improving sleep and to test whether ABC-I resulted in higher treatment completion and adherence versus CBT-I. Method: One hundred forty-nine women veterans with insomnia disorder (Mage = 48.0 years) received ABC-I or CBT-I. The main sleep outcomes were Insomnia Severity Index (ISI), Pittsburgh Sleep Quality Index (PSQI), and sleep efficiency (SE) by actigraphy (objective) and sleep diary (subjective). Measures were collected at baseline, immediate posttreatment, and 3-month posttreatment follow-up. Treatment completion and adherence were assessed during the interventions. Results: Both interventions improved all sleep outcomes from baseline to immediate posttreatment and 3-month posttreatment follow-up. At immediate posttreatment, ABC-I was statically noninferior for sleep diary SE and objective SE, but noninferiority was not statistically confirmed for ISI or PSQI total scores. At 3-month posttreatment follow-up, ABC-I was noninferior for all four of the key outcome variables. There was not a statistically significant difference between the number of participants who discontinued CBT-I (11%) versus ABC-I (18%; p = .248) before completing treatment. ABC-I was superior to CBT-I for some adherence metrics. Conclusions: Overall, ABC-I was similar in effectiveness compared to CBT-I for the treatment of insomnia and may improve adherence to some behavioral elements of treatment. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
... For example, both selective serotonin reuptake inhibitors and tricyclic antidepressants are known to alter HRV in adults and adolescents 74,75 as well as psychostimulants, and interventions that increase HRV also improve sleep quality and stress-related cortisol responses. 76,77 The present study has several limitations. First, we could include only a limited number of studies in the metaanalyses, especially in relation to EDA. ...
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Objective To systematically investigate if there is a significant association between markers of autonomic functioning and emotional dysregulation (ED) in children and adolescents. Method Based on a pre-registered protocol (PROSPERO: CRD42021239635), we searched Pubmed, Web of Knowledge/Science, Ovid Medline, Embase and APA PsycInfo (21st April 2021) and included empirical studies reporting indices of autonomic nervous system (ANS) functioning in youths meeting DSM/ICD criteria for any psychopathological/neurodevelopmental condition and assessed for ED with a validated scale. Eligible outcomes included correlation coefficients between ED and ANS measures or differences in ANS measures between youths with and without ED. Study quality was assessed with the Appraisal tool for Cross-Sectional Studies (AXIS) and the Newcastle-Ottawa Scale (NOS) for cohort studies. Random-effects meta-analyses were used for data synthesis. Results Twelve studies (1016 participants) were included in the descriptive review and nine (567 participants) in the meta-analyses. We did not find evidence of a significant association between ED and altered cardiac or electrodermal functioning. However, exploratory meta-regressions suggested a possible association between reduced resting-state cardiac vagal control and increased ED. Conclusion Our study did not find evidence of an association between ED and autonomic dysfunction. However, we found preliminary evidence that reduced vagal control at rest might be a transdiagnostic marker of ED in young people. Additional future studies comparing autonomic measures in youths with and without ED are needed, and should also assess the effects of interventions for ED on ANS functioning.
... First, other characteristics relating to sleep-related metacognitive activity (e.g., beliefs about sleep; [8,58]), pre-sleep cognitive and somatic arousal (e.g., worries), and negative or positive emotions (e.g., [59]), not considered here, would help shed light on the role of thought control strategies at bedtime and sleep quality. In addition, because physiological arousal has been found to predict sleep disturbance [60,61], the perseverance of using a maladaptive strategy such as the worry strategy at bedtime can also be accompanied by physiological activation that can explain difficulty falling asleep (as reported above) and staying asleep throughout the night. Since sleep quality is also defined by other sleep indicators/parameters (e.g., nocturnal awakenings, nap frequency; [3]), future studies to better capture the nature of strategies should thus make the effort to consider a wider number of sleep quality indicators. ...
Article
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This study examined the associations between thought control strategies and subjective and objective sleep quality, across the adult lifespan. One hundred forty-nine individuals without insomnia (age range 18–86 years; M = 45.35, SD = 20.53) completed the Thought Control Questionnaire Insomnia–Revised for assessing sleep-related thought control strategies. Self-reported sleep quality was measured with the Pittsburgh Sleep Quality Index. Then, subjective and objective sleep parameters (i.e., total sleep time, sleep onset latency, sleep efficiency) were recorded through a sleep diary and an actigraph across 7 days. Results from linear mixed-effects models showed that a worry strategy was associated with longer subjective sleep latency and shorter subjective total sleeping time. An aggressive suppression strategy was associated with longer subjective total sleeping time. No such involvement of thought control strategies was detected for subjective sleep efficiency and all of the objective sleep parameters. Other individual differences (i.e., age, sex, circadian preference, self-reported sleep quality) also explained both subjective and objective sleep parameters, though to a different extent depending on the sleep parameter considered. The assessment of sleep-related thought control strategies, along with other individual characteristics, should be considered to account for individual differences in sleep quality and implement practices/interventions to support it in adulthood and older age.
... Acute insomnia follows a wide variety of stressors (Ellis et al., 2012) and risk of developing chronic insomnia is elevated in those showing strong sleep onset effects of acute stress of even a non-traumatic nature ("sleep reactivity") (Drake et al., 2011). In primary insomnia, ongoing stressors have been shown to additionally disrupt sleep, particularly delta frequencies in NREM (Hall et al., 2007). As noted above, trauma-induced insomnia can precede PTSD and hence the effects of sleep disturbance on fear generalization and extinction learning and memory may precede and contribute to development of the full complement of PTSD symptoms (Sinha, 2016). ...
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In Posttraumatic Stress Disorder (PTSD), fear and anxiety become dysregulated following psychologically traumatic events. Regulation of fear and anxiety involves both high-level cognitive processes such as cognitive reattribution and low-level, partially automatic memory processes such as fear extinction, safety learning and habituation. These latter processes are believed to be deficient in PTSD. While insomnia and nightmares are characteristic symptoms of existing PTSD, abundant recent evidence suggests that sleep disruption prior to and acute sleep disturbance following traumatic events both can predispose an individual to develop PTSD. Sleep promotes consolidation in multiple memory systems and is believed to also do so for low-level emotion-regulatory memory processes. Consequently sleep disruption may contribute to the etiology of PTSD by interfering with consolidation in low-level emotion-regulatory memory systems. During the first weeks following a traumatic event, when in the course of everyday life resilient individuals begin to acquire and consolidate these low-level emotion-regulatory memories, those who will develop PTSD symptoms may fail to do so. This deficit may, in part, result from alterations of sleep that interfere with their consolidation, such as REM fragmentation, that have also been found to presage later PTSD symptoms. Here, sleep disruption in PTSD as well as fear extinction, safety learning and habituation and their known alterations in PTSD are first briefly reviewed. Then neural processes that occur during the early post-trauma period that might impede low-level emotion regulatory processes through alterations of sleep quality and physiology will be considered. Lastly, recent neuroimaging evidence from a fear conditioning and extinction paradigm in patient groups and their controls will be considered along with one possible neural process that may contribute to a vulnerability to PTSD following trauma.
... except the correlation between centro-parietal and occipital Beta 3 and ΔLF for Tummo practice (r = 0.67, p = .049). The changes (increases) in LF are indicative of SNS activity (Kim et al., 2018;Reyes del Paso et al., 2013), and the significant correlation between Beta 3 activity and LF increases supports previous research suggesting the link between high Beta oscillations and autonomic arousal (Abhang et al., 2016;Hall et al., 2007), and further validate our HRV findings indicating a shift towards SNS activity during Tummo practice. ...
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Here we report meditative techniques, which modulate attentional control by arousal-driven influences and not by monitoring continuous thought processes as during mindfulness-related practices. We focus on Vajrayana (Tantric Buddhism) practices, during which a sequence of generation (self-visualization as a deity - Yidam) or completion with sign (inner heat -Tummo) stages necessarily precedes non-dual awareness (NDA) Tantric Mahamudra. We compared the electrocardiographic and electroencephalographic correlates of Mahamudra performed after rest (non-Tantric Mahamudra) with Mahamudra performed after Yidam (Tantric Mahamudra) in 16 highly experienced Vajrayana practitioners, 10 of whom also performed Tummo. Both Yidam and Tummo developed the state of PNS withdrawal (arousal) and phasic alertness, as reflected by HF HRV decreases and Alpha2 power increases, later neurophysiologically employed in Tantric Mahamudra. The latter led to the unique state of high cortical excitability, “non-selective” focused attention, and significantly reduced attentional control, quantified by power reductions in all frequency bands, except Theta. In contrast, similar to mindfulness-related practices, non-Tantric Mahamudra was performed in a state of PNS dominance (relaxation), tonic alertness, and active monitoring, as suggested by Alpha1 power increases and less pronounced decreases in other frequency bands. A neurobiological model of meditation is proposed, differentiating arousal-based and mindfulness-related practices.
... Theta power has been shown to be elevated in traumaexposed individuals who were resilient to, compared to those diagnosed with, PTSD (Cowdin et al., 2014; though see Denis et al., 2021). Similarly, electroencephalographic spectral power in in the beta frequency range (~20-30Hz) during sleep has also been shown to be elevated in PTSD compared to those without PTSD (de Boer et al., 2020;Germain et al., 2006;Wang et al., 2020;Woodward et al., 2000), and has been theorized as a marker of hyperarousal (Hall et al., 2007;Krystal et al., 2002;Perlis et al., 2001;Riedner et al., 2016;Spiegelhalder et al., 2012). In contrast however, beta power during sleep has also been associated with reduced risk of PTSD development (Mellman et al., 2007) and reduced symptomatology in healthy participants and those with PTSD . ...
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Background The failure to retain memory for extinguished fear plays a major role in the maintenance of post-traumatic stress disorder (PTSD), with successful extinction recall necessary for symptom reduction. Disturbed sleep, a hallmark symptom of PTSD, impairs fear extinction recall. However, our understanding of the electrophysiological mechanisms underpinning sleep’s role in extinction retention remain underdetermined. Methods We reanalyzed data from two existing datasets examining the relationship between the microarchitecture of sleep and extinction recall in healthy controls (Study 1, n = 46) and a pilot study in individuals with PTSD (Study 2, n = 12). In both studies, participants underwent a fear conditioning and extinction protocol over the course of two days, with polysomnography sleep recording occurring between conditioning and extinction. Twenty-four hours after extinction learning, participants underwent extinction recall. Power spectral density (PSD) was computed for NREM and REM sleep during both pre- and post-extinction learning. Results Increased PSD in frequencies spanning the canonical beta band during pre-extinction learning sleep were associated with worse extinction recall in healthy participants ( r = .41, p = .004). Beta PSD was shown to be highly stable across three nights of sleep (NREM intraclass correlation (ICC) = 0.93; REM ICC = 0.94). Individuals with PTSD were found to have increased beta PSD compared to healthy controls (NREM: p = .038; REM: p = .007), and beta PSD correlated with extinction recall in the PTSD group at a similar magnitude to controls ( r = .39). Conclusions The present findings suggest that beta band PSD may be a trait-like feature of the sleep EEG that is heightened in PTSD and associated with impaired fear extinction recall. Thus, beta PSD during sleep may reflect a trait marker for vulnerability to PTSD, specifically implicated in difficulties recalling extinguished fear.
... Third, the placebo effect in nausea was associated with reduced behavioral stress, a reduction in delta power in the FFT spectrum at electrode C4, and reduced activation in PFC regions in the placebo group. The central correlates have been linked to stress in previous studies (Hall et al., 2007;McEwen et al., 2015;Nater et al., 2006). ...
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Introduction Despite growing evidence validating placebo effects in nausea, little is known about the underlying cortical mechanisms in women and men. Therefore, the present study examined sex differences and electroencephalography (EEG) characteristics of the placebo effect on nausea. Methods On 2 consecutive days, 90 healthy subjects (45 females) were exposed to a nauseating visual stimulus. Nausea was continuously rated on an 11‐point numeric rating scale, and 32 EEG channels were recorded. On day 2, subjects were randomly allocated to either placebo treatment or no treatment: the placebo group received sham acupuncture, whereas the control group did not receive any intervention. Results In contrast to the control group, both sexes in the placebo group showed reduced signs for anticipatory nausea in the EEG, indexed by increased frontal lobe and anterior cingulate activity. Among women, the improvement in perceived nausea in the placebo group was accompanied by decreased activation in the parietal, frontal, and temporal lobes. In contrast, the placebo‐related improvement of perceived nausea in men was accompanied by increased activation in the limbic and sublobar (insular) lobes. Conclusion Activation of the parietal lobe in women during the placebo intervention may reflect altered afferent activity from gastric mechanoreceptors during nausea‐induced tachyarrhythmia, whereas in men, altered interoceptive signals in the insular cortex might play a role. Thus, the results suggest different cerebral mechanisms underlying the placebo effects in men and women, which could have implications for the treatment of nausea.
... Specifically, lower heart rate variability during sleep (represented by our BVP signal) was related to worse cognitive performance on tests of long-term memory, processing speed, working memory, and learning. This is consistent with reports that indicate that that high HR and low HRV is a general marker for disease (Bonnet & Arand, 2010;Fujiki et al., 2013;Palatini & Julius, 1997;Silvani, 2019;Stein & Kleiger, 1999;Stein & Pu, 2012; Task Force of the European Society of Cardiology and the North American Society of Pacing Electrophysiology, 1996;Tsuji et al., 1994), and that both low HRV (during the day and at night) is also associated with anxiety and stressors (Brosschot et al., 2007;Hall et al., 2007). In addition, increased arousal during sleep (represented by our EDA signal) was related to worse cognitive performance on a measure of executive function. ...
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Purpose/objective: While there is evidence in other clinical groups to suggest that sleep problems can negatively impact cognitive performance, this relationship has not yet been examined in people with spinal cord injury (SCI). Thus, we sought to examine the association between sleep and cognitive function in people with SCI. Research method/design: Over the course of 7 days, 167 individuals with SCI completed daily subjective ratings of sleep (sleep quality, number of hours slept per night, and bedtime variability) and wore a wrist-worn device that continuously monitored autonomic nervous system (ANS) activity (i.e., blood volume pulse [BVP] signal and electrodermal activity [EDA] signal). At the end of this home monitoring period, participants completed a subjective rating of cognition and six objective cognitive tests. A series of multivariable linear regressions were used to examine associations between eight measures of sleep/ANS activity during sleep and eight cognitive variables. Results: Subjective ratings of sleep were not related to either objective cognitive performance or self-reported cognitive function. However, there were some relationships between ANS activity during sleep and objective cognitive performance: lower BVP signal was associated with poorer performance on measures of processing speed, working memory, learning and long-term memory, and EDA signals were associated with poorer performance on a measure of executive function. Conclusions/implications: Future work is needed to better understand the relationship of sleep, especially sleep physiology, and cognitive functioning for individuals with SCI, and how that may be similar or different to relationships in the general population. (PsycInfo Database Record (c) 2022 APA, all rights reserved).
... Experimental studies inducing psychosocial stress and cognitive tasks in a laboratory directly before sleep and collecting objective polysomnographic data (Wuyts et al. 2012a;Ackermann et al. 2019), reported a prolonged sleep onset latency (SOL) and a decrease in low-/highfrequency power in the electroencephalogram (EEG) during nonrapid eye movement (NREM) sleep, which is a measure of objective sleep quality (e.g. Hall et al. 2007;Maes et al. 2014;Cordi et al. 2019;Hogan et al. 2020). These changes were limited to early periods of sleep and presleep stress did not affect sleep parameters during later sleep periods. ...
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The anticipation of a future stressor can increase worry and cognitive arousal and has a detrimental effect on sleep. Similarly, experiencing a stressful event directly before sleep increases physiological and cognitive arousal and impairs subsequent sleep. However, the effects of post- vs. pre-sleep stress on sleep and their temporal dynamics have never been directly compared. Here, we examined the effect of an anticipated psychosocial stressor on sleep and arousal in a 90-min daytime nap, in 33 healthy female participants compared to an anticipated within-subject relaxation task. We compared the results to an additional group (n = 34) performing the same tasks directly before sleep. Anticipating stress after sleep reduced slow-wave activity/beta power ratio, slow-wave sleep, sleep spindles, and slow-wave parameters, in particular during late sleep, without a concomitant increase in physiological arousal. In contrast, pre-sleep psychosocial stress deteriorated the same parameters during early sleep with a concomitant increase in physiological arousal. Our results show that presleep cognitions directly affect sleep in temporal proximity to the stressor. While physiological arousal mediates the effects of presleep stress on early sleep, we suggest that effects during late sleep originate from a repeated reactivation of mental concepts associated with the stressful event during sleep.
... This activity is the dominant rhythm of subjects who are alert or anxious or who have their eyes-open. It is the most frequently seen rhythm in normal adults and children and is associated with physiological arousal and psychological stress [33]. This activity is closely linked to motor behavior and is generally attenuated during active movement [34]. ...
Thesis
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The aim of this thesis is to move one step forward towards the concept of electroencephalographic (EEG) systems that can achieve the same objectives as high-density EEG with a minimum required number of channels. This requires EEG signal analysis, computational intelligence, and optimization techniques that can systematically identify the minimum number of channels that fulfills the objectives currently achieved with high-density EEG systems. Achieving this goal will pave the way towards the hardware-software realization of user-centric, easy-to-use, readily affordable EEG systems for universal applications. Enabling portability while ensuring performance of comparable or higher quality than that of high-density EEG will expand the accessibility of EEG to non-traditional users and personal applications moving EEG out of the lab. The application horizon will be expanded from experimental research to clinical use, to the gaming industry, intelligence and security sectors, education and daily use by people for self-knowledge. The methods proposed in the thesis comprise the combination of feature extraction techniques and channel selection algorithms with optimization techniques that allow extracting the most essential information from a minimum set of required EEG channels that were tested in two cases-studies: Epileptic seizure classification, and EEG-based biometric systems. The Discrete Wavelet Transform (DWT) and Empirical Mode Decomposition (EMD) were used to decompose EEG signals into different frequency bands and then four features were computed for each sub-band, the Teager and Instantaneous energies and the Higuchi and Petrosian fractal dimensions. For the optimization stage, non-dominated sorting genetic algorithms (NSGA) were used for channel selection, using binary values to represent the channels in the chromosomes, $1$ if the channel is used in the classification and optimization process, and $0$ if not. Additional genes to represent important parameters for the classifiers were added using integer and decimal values. For Case-study 1, NSGA-III selected one or two channels from a set of 22 for epileptic seizure classification, obtaining an accuracy of up to 0.98 and 1.00, respectively, using EMD/DWT-based features. For Case-study 2, a task-independent, resting-state-based biometric system using Local Outlier Factor (LOF)- and DWT-based features showed a True Acceptance Rate (TAR) of up to 0.993±0.01 and a True Rejection Rate (TRR) of up to 0.941±0.002 using only three channels selected by NSGA-III from a set of 64. The results presented herein can be considered to be a first proof-of-concept, showing that it is possible to reduce the number of required EEG channels for classification tasks and opens the way to explore these methods on other neuroparadigms. This will lead to reduced real-time computational costs for EEG signal processing, removing task-irrelevant and redundant information, as well as reducing the preparation time for use of the EEG headsets. The results of such a reduction in the number of required EEG channels will make possible a low-power hardware design, expanding the range of EEG-based applications from clinical diagnosis and research to health-care, to non-medical applications that can improve our understanding of cognitive processes, learning and education and to the discovery of current hidden/unknown properties behind ordinary human activity and ailments.
... Discrimination, defined as differential treatment, particularly that which is considered to be unfair, is commonly considered to be a source of psychosocial stress 15,16 ; and stress is associated with sleep disturbances 17 . There is a growing evidence base linking discrimination stress to sleep disturbances 8,[18][19][20] . ...
Article
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Self-reported experiences of discrimination and sleep dysfunction have both been shown to adversely impact biological functioning; however, few studies have examined how they are jointly associated with health. The current study draws from two samples of the Midlife in the United States (MIDUS) data (n=617 participants; 59.8% female; 72.3% White and 27.7% African American; Age: Mean=52.6, SD = 12.22) to identify latent profiles of sleep (duration, variability, onset latency, naps) and discrimination (everyday, lifetime, impact). Associations with latent profiles of biomarkers of inflammation (CRP, fibrinogen, IL-6,) and endocrine stress (cortisol, epinephrine, norepinephrine) were examined. Three profiles were identified for sleep/discrimination (good, fair, poor) and for biomarkers (average, high inflammation, high neuroendocrine). Chi-square analyses indicated that adults in the good sleep/low discrimination profile were more likely to be in the average biomarker profile but less likely to be in the high inflammation profile. Adults in the fair sleep/moderate discrimination risk profile were more likely to be in the high inflammation profile. Adults in the poor sleep/high discrimination risk profile were less likely to be in the average biomarker profile but more likely to be in the high inflammation profile. The current study identified configurations of sleep and discrimination among midlife adults which were associated with profiles of biological risk. The findings provide implications for identifying individuals who may be at increased risk of developing stress-related tertiary outcomes of morbidity and disease.
... Focusing on this sleep-dependent anxiolytic mechanism, reductions in NREM SWA have been observed in primary insomnia 59 and further associated with aberrantly high sympathetic autonomic activity 60 . Conversely, NREM SWS reflects a homoeostatic state of marked parasympathetic dominance 61 , coupled with a reduction in central autonomic network activity within the brain. ...
Article
Full-text available
A Correction to this paper has been published: https://doi.org/10.1038/s41562-019-0754-8.
... However, none of those study designs featured a significant delay between intention encoding and retrieval/execution, and in most cases, both phases of the PM process were instantiated under stressful conditions. Although a relatively large literature examines relations between the experience of chronic daytime stress and sleep disruption (Hall et al., 2007;Mezick et al., 2009;Hall et al., 2017), few studies have examined whether cognitive processes are affected by the experience of laboratory-induced stress immediately before bedtime (and none have examined whether next-day retrieval/execution of a PM intention encoded prior to sleep is affected by such an experience). This question is of interest because self-reported bedtime stress affects sleep quality negatively (Åkerstedt et al., 2012), and laboratory-induced acute psychosocial stress experienced immediately prior to a nap increases sleep latency and decreases slow-wave activity (Ackermann et al., 2019). ...
Article
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The cognitive construct of prospective memory (PM) refers to the capacity to encode, retain and execute delayed intentions (e.g. to remember to buy milk on the way home). Although previous research suggests that PM performance is enhanced by healthy sleep, conclusions tend to be drawn based on designs featuring ecologically unnatural manipulations (e.g. total sleep deprivation). This study investigates whether a more common everyday experience (bedtime stress) affects next-day PM performance and, in so doing, also contributes to the heretofore inconsistent literature on stress and PM. Forty young adults received PM task instructions and were then assigned to either a stress condition (exposure to a laboratory-based stress-induction manipulation; n = 20, 9 women) or a non-stress condition (exposure to a non-stressful control manipulation; n = 20, 12 women). After completing the experimental manipulation, all participants had their objective sleep quality measured over a full night of polysomnographic monitoring. Upon awakening, they completed the PM task. Analyses detected significant between-group differences in terms of stress outcomes, sleep quality and PM performance: Participants exposed to the manipulation experienced heightened signs of stress (captured using a composite variable that included self-report, psychophysiological and endocrinological measures), had longer sleep latencies and poorer sleep depth and displayed significantly longer reaction times to PM cues. An interaction between experimental condition (being exposed to the stressor) and disrupted sleep (longer sleep latency) significantly predicted poorer next-day PM reaction time. We interpret these findings as indicating that bedtime stress, which leads to heightened presleep arousal, affects sleep processes and, consequently, the deployment of attentional resources during next-day execution of a delayed intention.
... Moreover, pharmacological inhibition of orexin neurons in LH blocks analgesia induced by restraint in rats [200]. In addition, facing an stressful experience has been widely shown to increase the general wakefulness [201,202]. Now, we need to discuss how the modulatory role of orexin system comes into play when an organism needs to efficiently cope with the stressor stimuli. ...
... Cross-sectional, longitudinal, and experimental studies suggest that stressor exposure is a precipitating factor for the development of sleep disturbances (12, 13). The association between stressor exposure and increased subjective and objective measures of sleep quality has been shown across a range of psychosocial stressors (14)(15)(16)(17)(18)(19)(20). Daily diary studies also indicate that perceived stress on a given day predicts lower sleep efficiency and sleep satisfaction that night (21,22). ...
Article
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Background Disrupted sleep quality is one of the proposed mechanisms through which chronic stress may lead to depression. However, there exist significant individual differences in sleep reactivity, which is the extent to which one experiences sleep disturbances in response to stress. Purpose The aim of the current study was to investigate whether low high-frequency heart rate variability (HRV), as a psychophysiological marker of poor emotional and physiological arousal regulation, predicts stress-related sleep disturbances associated with greater risk of depression symptoms. Methods Using a chronic caregiving stress model, 125 mothers of adolescents with developmental disorders and 97 mothers of typically developing adolescents had their resting HRV and HRV reactivity recorded and completed a measure of depressive symptoms, as well as a 7 day sleep diary to assess their sleep quality. A moderated mediation model tested whether sleep quality mediated the association between chronic stress exposure and depressive symptoms and whether HRV moderated this mediation. Results After controlling for participant age, body mass index, ethnicity, socioeconomic status, and employment status, poor sleep quality mediated the association between chronic stress and depressive symptoms. Resting HRV moderated this indirect effect such that individuals with lower HRV were more likely to report poorer sleep quality in the context of chronic stressor exposure, which, in turn, was related to greater depressive symptoms. Conclusions Lower HRV, a potential biomarker of increased sleep reactivity to stress, is associated with greater vulnerability to stress-related sleep disturbances, which, in turn, increases the risk for elevated depressive symptoms in response to chronic stress.
... We also surpass the current benchmark of 71.41% by Saeed et al. (2015) by almost 10 %. An analysis of the spectral power between more and less stressed persons in the four identified EEG subbands revealed strong differences (Table 4) Although our findings of decreased spectral power in the High-Beta in highly stressed participants are in line with the results of a negative correlation between the PSS score and the spectral power in alpha and beta bands (Hamid et al. 2010), our findings did not confirm that perceived stress was associated with decreased spectral power in the delta band and an increased EEG beta power (Hall et al. 2007). Also, our evaluation partially confirms that chronic stress leads to increased spectral power in the prefrontal cortex (Peng et al. 2013;Goodman et al. 2013), which can be found in the Mid-Delta sub-band. ...
Conference Paper
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While there are several works that diagnose acute stress using electroencephalographic recordings and machine learning, there are hardly any works that deal with chronic stress. Currently, chronic stress is mainly determined using questionnaires, which are, however, subjective in nature. While chronic stress has negative influences on health, it also greatly influences decision-making processes in humans. In this paper we propose a novel machine learning approach based on the fine-graded spectral analysis of resting-state EEG recordings, to diagnose chronic stress. By using this new machine learning approach, we achieve a very good balanced accuracy of 81.33%, outperforming the current benchmark by 10%. Our algorithm allows an objective assessment of chronic stress, is accurate, robust, fast and cost-efficient and substantially contributes to decision-making research, as well as Information Systems research in healthcare.
... In the forward direction, perceived stress predicted all insomnia symptoms, indicating long-term consequences for all aspects of insomnia, in addition to the immediate effects found in previous studies (Åkerstedt, Orsini, et al., 2012;Hall et al., 2007). Similarly, work F I G U R E 3 Best-fitting structural equation model of work demands and three components of insomnia: difficulties initiating sleep, difficulties maintaining sleep, and non-restorative sleep. ...
Article
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Work stress and poor sleep are closely related in cross‐sectional data, but evidence from prospective data is limited. We analysed how perceived stress and work stressors (work demands, decision authority and workplace social support) are related to key dimensions of insomnia over time, using structural equation modelling. Biennial measurements from a large sample of the working population in Sweden enabled us to analyse both the relationship from stress to sleep as well as that from sleep to stress. Overall, we found reciprocal relations between insomnia and all four stress measures. However, looking at the relation between each dimension of insomnia and each stress measure, there were some differences in direction of effects. In the direction from stress to sleep, all work stressors as well as perceived stress predicted both difficulties initiating sleep and difficulties maintaining sleep. The same was found for non‐restorative sleep, with the exception for decision authority. In the opposite direction, difficulties maintaining sleep predicted increased levels of work demands and perceived stress. Difficulties initiating sleep stood out among the insomnia symptoms as not predicting any of the stress measures, while non‐restorative sleep was the only symptom predicting all stress measures. The results advance the understanding of the stress−sleep relationship and indicate a potential vicious circle between insomnia and perceived stress as well as work stressors, suggesting that the workplace could be an arena for interventions to alleviate insomnia.
... Focusing on this sleep-dependent anxiolytic mechanism, reductions in NREM SWA have been observed in primary insomnia 59 and further associated with aberrantly high sympathetic autonomic activity 60 . Conversely, NREM SWS reflects a homoeostatic state of marked parasympathetic dominance 61 , coupled with a reduction in central autonomic network activity within the brain. ...
Article
Full-text available
Are you feeling anxious? Did you sleep poorly last night? Sleep disruption is a recognized feature of all anxiety disorders. Here, we investigate the basic brain mechanisms underlying the anxiogenic impact of sleep loss. Additionally, we explore whether subtle, societally common reductions in sleep trigger elevated next-day anxiety. Finally, we examine what it is about sleep, physiologically, that provides such an overnight anxiety-reduction benefit. We demonstrate that the anxiogenic impact of sleep loss is linked to impaired medial prefrontal cortex activity and associated connectivity with extended limbic regions. In contrast, non-rapid eye movement (NREM) slow-wave oscillations offer an ameliorating, anxiolytic benefit on these brain networks following sleep. Of societal relevance, we establish that even modest night-to-night reductions in sleep across the population predict consequential day-to-day increases in anxiety. These findings help contribute to an emerging framework explaining the intimate link between sleep and anxiety and further highlight the prospect of non-rapid eye movement sleep as a therapeutic target for meaningfully reducing anxiety.
... Psychological flexibility can be a strong predictor of insomnia severity, sleep problems, low sleep efficiency, and fatigue 14 . The number of avoidance behaviors is directly related to sleep disturbances 15 . ...
Article
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Background: We aimed to perform a cluster analysis on sleep quality and insomnia severity in addition to predicting the clusters based on personality traits, experiential avoidance, stress, anxiety, depression, and dysfunctional beliefs and attitudes about sleep. Study design: A cross-sectional study. Methods: This study was conducted on earthquake victim in Kermanshah (western Iran) in 2017. Data collection began 15 d after the earthquake and lasted for 2 weeks. First, 1002 copies of the questionnaire were distributed and, finally, analyses were performed for 778 individuals. Data analysis was conducted using cluster analysis. Results: Based on sleep quality and insomnia severity, four clusters were formed, and a correlation existed between some personality traits, psychological distress, experiential avoidance, and dysfunctional beliefs and attitudes about sleep with unhealthy clusters (P<0.05). The summary of the model showed the sufficient fit of the model (P<0.0005) and that it could predict 22.8%-42.4% of the variance of unhealthy clusters. Conclusion: Dysfunctional beliefs and attitudes about sleep, experiential avoidance, stress, anxiety, depression, and personality traits could contribute to sleep problems and reduce sleep quality in earthquake victims.
... Previous studies have identified the unique role of psychological stress on suboptimal sleep. 31 The mediation role of sleep between environmental factors and ADHD warrant further investigation. ...
Article
Background: This study aims to study prospectively specific sleep patterns and risk of ADHD after adjusting for potential confounders such as obstructive sleep apnoea (OSA) and methylphenidate use. / Methods: A population-representative sample of 514 Chinese preschool children was recruited when in kindergarten (K3). Parents reported on their socioeconomic status and children’s sleep duration. The cohort was reassessed 3 years later when the children were in Grade 3 (P3). Parents reported on children’s sleep patterns and ADHD symptoms. Information on OSA diagnosis and methylphenidate use was retrieved from health records. / Results: Among the 514 parent–child dyads (mean [SD] age, 5.52 [0.33] years), 411 were reassessed (80.0% retention; 9.35 [0.33] years) at follow-up. There were no significant baseline differences between follow-up and drop-out groups. A gradient relationship was observed between probable ADHD in P3 and sleep duration in K3. The risk of probable ADHD was 15.5 per 100 for children with <8 h of sleep in K3, whereas it was 1.1 per 100 for children with 11–12 h of sleep in K3. The adjusted risk ratio was 14.19 (p = 0.02). / Conclusions: Sleep deprivation in early childhood is associated with higher risk of ADHD in middle childhood.
... Sleep is also a complex health behavior that is influenced by psychological processes such as anxiety and stress (Hall et al., 2007;Lev Ari & Shulman, 2012), environmental features such as noise and crowding (Brouillette, Horwood, Constantin, Brown, & Ross, 2011;Street et al., 2018), as well as physiological influences such as pubertal development (Dewald et al., 2010;Knutson, 2005). As such, sleep, like other health behaviors, may be particularly sensitive to sociocultural differences. ...
Article
This study investigates the same‐day associations between discrimination and sleep among 350 adolescents ages 13–15 (M = 14.29, SD = 0.65; Asian = 41%, Black = 22%, Latinx = 37%). Assessing sleep duration, sleep onset latency, and wake minutes after sleep onset using wrist actigraphy, Black adolescents slept 35 min less than Asian and 36 min less than Latinx youth. Black adolescents suffered the most wake minutes after sleep onset, followed by Latinx and Asian youth. Latinx youth reported the highest levels of sleep disturbance, whereas Asian youth reported the highest levels of daytime dysfunction. Daily discrimination was associated with lower levels of same‐night sleep onset latency, more sleep disturbance, more next‐day daytime dysfunction, and higher next‐day daytime sleepiness.
... Previous studies have identified the unique role of psychological stress on suboptimal sleep. 31 The mediation role of sleep between environmental factors and ADHD warrant further investigation. ...
Article
Background: This study aims to study prospectively specific sleep patterns and risk of ADHD after adjusting for potential confounders such as obstructive sleep apnoea (OSA) and methylphenidate use. Methods: A population-representative sample of 514 Chinese preschool children was recruited when in kindergarten (K3). Parents reported on their socioeconomic status and children's sleep duration. The cohort was reassessed 3 years later when the children were in Grade 3 (P3). Parents reported on children's sleep patterns and ADHD symptoms. Information on OSA diagnosis and methylphenidate use was retrieved from health records. Results: Among the 514 parent-child dyads (mean [SD] age, 5.52 [0.33] years), 411 were reassessed (80.0% retention; 9.35 [0.33] years) at follow-up. There were no significant baseline differences between follow-up and drop-out groups. A gradient relationship was observed between probable ADHD in P3 and sleep duration in K3. The risk of probable ADHD was 15.5 per 100 for children with <8 h of sleep in K3, whereas it was 1.1 per 100 for children with 11-12 h of sleep in K3. The adjusted risk ratio was 14.19 (p = 0.02). Conclusions: Sleep deprivation in early childhood is associated with higher risk of ADHD in middle childhood.
... There are also stress-related links between social support and health behaviors (i.e., stress prevention and stress-buffering models; Gore, 1981;Lin, 1986). These models are particularly important to consider because high stress has been linked to less healthy behaviors including poorer diet, less exercise, and sleep quality, as well as greater alcohol consumption and smoking (Cohen & Lichtenstein, 1990;Hall, Thayer, et al., 2007;Ng & Jeffrey, 2003). Consistent with this pathway, researchers found that tangible support decreased the association between financial stress and alcohol involvement (Peirce, Frone, et al., 1996; also see Wills & Cleary, 1996). ...
Chapter
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Social support is defined as the perceived or actual receipt of social resources (e.g., tangible, emotional) and is one of the most reliable predictors of disease morbidity and mortality. In this chapter, the evidence linking social support to disease is reviewed along with the presentation of a theoretical model which highlights the social, psychological, behavioral, and biological pathways potentially responsible for such links. Important unresolved issues are also raised such as the distinction between perceived and received support, the importance of modeling antecedent processes and change over time, and cultural/technological influences on support processes. Studies attempting to utilize the epidemiological evidence to produce effective support intervention that impact health are also reviewed. Finally, the future of social support research/interventions along with their policy implications is discussed and highlights the tremendous progress in the field and potential impact of social support to help individuals live healthier and happier lives.
... 22 Delta EEG activity has been observed to be increased in women with preeclampsia, 23 and is decreased overnight in the nonpregnant population after disruption of SWS 24 or a daytime nap. 25 Beta EEG activity is associated with high levels of perceived stress and increased at or around sleep onset and during NREM sleep in patients with insomnia. [26][27][28] Only one small study (n = 9) using spectral analysis 4 in healthy pregnant women reported that delta, theta, and alpha bands were reduced, but high frequencies such as beta band did not change across pregnancy. Pregnant women are susceptible to sleep disturbances caused by sleep apnea, periodic limb movements, or difficulty maintaining sleep 1,29,30 that result in reduction in the percentage of SWS. ...
Article
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Study objectives: Few studies have objectively evaluated sleep characteristics during pregnancy or investigated the relationship between altered spectral electroencephalogram (EEG) bands and sleep-disordered breathing (SDB). The study aimed to describe changes in sleep as measured by polysomnography (PSG) and spectral EEG bands during pregnancy and to examine the relationship between delta power in non-rapid eye movement (NREM) sleep and SDB. Methods: This is a secondary analysis of a prospective study. One hundred twenty-three women underwent full PSG in early pregnancy, and 97 repeated PSG in late pregnancy. Spectral analysis of the EEG in NREM sleep was performed. We used linear and logistic mixed-model regression to analyze the sleep measures and linear regression to explore the association between delta power and apnea-hypopnea index (AHI) changes during pregnancy. Results: In late pregnancy, women had shorter sleep duration, poorer sleep efficiency, more awakenings, more stage N2 sleep, less slow wave sleep, less REM sleep, higher AHI, and higher periodic limb movement index compared to early pregnancy. The percentage of stage N1 sleep, sleep latency, REM sleep latency, and arousal index frequency did not change. Regarding EEG-spectra, delta and theta powers decreased, but beta-2 power increased during pregnancy. In multivariable analyses, greater reduction of delta power was associated with larger increases in AHI (β [95% confidence interval] = -0.038 [-0.073, -0.002], P = .040). Estimates suggest that each one-unit increase in AHI reduces delta power by 4% in late pregnancy. Conclusions: PSG-measured sleep characteristics change during pregnancy. Delta power decreases when the severity of SDB increases during pregnancy.
... Another treatment target is to increase engagement in value driven behaviours. This may prevent unhelpful efforts to cope with sleep disturbances, such as staying in bed to gain more sleep and daytime napping, which unintentionally perpetuate the problem (Dalrymple, Fiorentino, Politi, & Posner, 2010;Hall et al., 2007). ...
Article
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Background: For patients with chronic pain the prevalence of insomnia is 5–8 times higher as compared to the general population. Acceptance and Commitment Therapy (ACT) has gained strong empirical support in the treatment of chronic pain and is today increasingly used in pain clinics. However, no ACT-consistent treatment for insomnia in chronic pain has yet been empirically evaluated, although preliminary data show a relation between acceptance and aspects of insomnia. The aim of this clinical pilot study was to develop and evaluate the feasibility and preliminary outcome of an acceptance-based behavioural group treatment protocol for insomnia in patients with chronic pain. Methods: Patients with chronic pain who had completed an ACT program to improve behavioural flexibility and functioning, and continued to have poor sleep to an extent that met the diagnostic criteria for insomnia, were considered eligible for participation in an acceptance-based behavioural group treatment for insomnia. Sixteen patients were enrolled in the study. Feasibility and treatment effects (primary outcome measure: Insomnia Severity Index, ISI) were assessed pre- and post treatment, as well as three months post- treatment. Results: There was a satisfying degree of retention and treatment compliance. On average patients participated in 5.31 (SD=0.70) out of six group sessions and completed 4.63 (SD = 0.62) of the five homework assignments. Overall, the completion rate of planned assessments was acceptable. However, assessment of sleep diary data at follow-up had 37.5% missing data and the recruitment rate averaged one patient per month. Significant improvements were seen in most outcomes, and results were maintained at follow-up, with large effects on primary outcome (ISI) at post-treatment g′= 2.02, 95% CI [0.90–3.14], and at follow-up g′= 1.69, 95% CI [.59, 2.78]. At follow-up twelve (75.0%) of the patients were classified as responders, of which five (31.2%) were remitters. Conclusion: Results overall showed a satisfying degree of feasibility with regards to retention, treatment compliance and completion of planned assessments. Changes in procedure are required in order to optimise recruitment rate. The treatment is potentially promising in terms of improved sleep for patients with longstanding pain. Larger, randomised controlled studies are needed to evaluate the treatment.
Article
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Currently, there is limited evidence regarding various neurophysiological responses to strength exercise and the influence of the adopted practice schedule. This study aimed to assess the acute systemic effects of snatch training bouts, employing different motor learning models, on skill efficiency, electric brain activity (EEG), heart rate variability (HRV), and perceived exertion as well as mental demand in novices. In a within-subject design, sixteen highly active males (mean age: 23.13 ± 2.09 years) randomly performed snatch learning bouts consisting of 36 trials using repetitive learning (RL), contextual interference (blocked, CIb; and serial, CIs), and differential learning (DL) models. Spontaneous resting EEG and HRV activities were recorded at PRE and POST training bouts while measuring heart rate. Perceived exertion and mental demand were assessed immediately after, and barbell kinematics were recorded during three power snatch trials performed following the POST measurement. The results showed increases in alpha, beta, and gamma frequencies from pre-to post-training bouts in the majority of the tested brain regions (p values ranging from < 0.0001 to 0.02). The CIb model exhibited increased frequencies in more regions. Resting time domain HRV parameters were altered following the snatch bouts, with increased HR (p < 0.001) and decreased RR interval (p < 0.001), SDNN, and RMSSD (p values ranging from < 0.0001 to 0.02). DL showed more pronounced pulse-related changes (p = 0.01). Significant changes in HRV frequency domain parameters were observed, with a significant increase in LFn (p = 0.03) and a decrease in HFn (p = 0.001) registered only in the DL model. Elevated HR zones (> HR zone 3) were more dominant in the DL model during the snatch bouts (effect size = 0.5). Similarly, the DL model tended to exhibit higher perceived physical (effect size = 0.5) and mental exertions (effect size = 0.6). Despite the highest psycho-physiological response, the DL group showed one of the fewest significant EEG changes. There was no significant advantage of one learning model over the other in terms of technical efficiency. These findings offer preliminary support for the acute neurophysiological benefits of coordination-strength-based exercise in novices, particularly when employing a DL model. The advantages of combining EEG and HRV measurements for comprehensive monitoring and understanding of potential adaptations are also highlighted. However, further studies encompassing a broader range of coordination-strength-based exercises are warranted to corroborate these observations. CITATION: Ammar A, Boujelbane MA, Simak ML et al. Unveiling the acute neurophysiological responses to strength training: An exploratory study on novices performing weightlifting bouts with different motor learning models.
Article
Different psychological chronic pain treatments benefit some individuals more than others. Understanding the factors that are associated with treatment response - especially when those factors differ between treatments - may inform more effective patient-treatment matching. This study aimed to identify variables that moderate treatment response to four psychological pain interventions in a sample of adults with low back pain or chronic pain associated with multiple sclerosis, spinal cord injury, acquired amputation, or muscular dystrophy (N = 173). The current study presents the results from secondary exploratory analyses using data from a randomized controlled clinical trial which compared the effects of four sessions of cognitive therapy (CT), hypnosis focused on pain reduction (HYP), hypnosis focused on changing pain-related cognitions and beliefs (HYP-CT), and a pain education control condition (ED). The analyses tested the effects of seven potential treatment moderators. Measures of primary (pain intensity) and secondary (pain interference, depression severity) outcome domains were administered before and after the pain treatments, and potential moderators (catastrophizing, hypnotizability, and EEG-assessed oscillation power across five bandwidths) were assessed at pre-treatment. Moderator effects were tested fitting regression analyses to pre- to post-treatment changes in the three outcome variables. The study findings, while preliminary, support the premise that pre-treatment measures of hypnotizability and EEG brain activity predict who is more (or less) likely to respond to different psychological pain treatments. If additional research replicates the findings, it may be possible to better match patients to their more individually suitable treatment, ultimately improving pain treatment outcomes. PERSPECTIVE: Pre-treatment measures of hypnotizability and EEG-assessed brain activity predicted who was more (or less) likely to respond to different psychological pain treatments. If these findings are replicated in future studies, they could inform the development of patient-treatment matching algorithms.
Article
Although cognitive behavioral therapy for insomnia (CBT-I) is an effective treatment of insomnia, difficulties exist with adherence to recommendations and premature discontinuation of treatment does occur. The current article aims to review existing research on acceptance and commitment therapy (ACT)-based interventions, demonstrate differences and similarities between ACT for insomnia and CBT-I, and describe treatment components and mechanisms of ACT that can be used to treat insomnia disorder.
Chapter
This up-to-date, superbly illustrated book is a practical guide to the effective use of neuroimaging in the patient with sleep disorders. There are detailed reviews of new neuroimaging techniques – including CT, MRI, advanced MR techniques, SPECT and PET – as well as image analysis methods, their roles and pitfalls. Neuroimaging of normal sleep and wake states is covered plus the role of neuroimaging in conjunction with tests of memory and how sleep influences memory consolidation. Each chapter carefully presents and analyzes the key findings in patients with sleep disorders indicating the clinical and imaging features of the various sleep disorders from clinical presentation to neuroimaging, aiding in establishing an accurate diagnosis. Written by neuroimaging experts from around the world, Neuroimaging of Sleep and Sleep Disorders is an invaluable resource for both researchers and clinicians including sleep specialists, neurologists, radiologists, psychiatrists, psychologists.
Chapter
This up-to-date, superbly illustrated book is a practical guide to the effective use of neuroimaging in the patient with sleep disorders. There are detailed reviews of new neuroimaging techniques – including CT, MRI, advanced MR techniques, SPECT and PET – as well as image analysis methods, their roles and pitfalls. Neuroimaging of normal sleep and wake states is covered plus the role of neuroimaging in conjunction with tests of memory and how sleep influences memory consolidation. Each chapter carefully presents and analyzes the key findings in patients with sleep disorders indicating the clinical and imaging features of the various sleep disorders from clinical presentation to neuroimaging, aiding in establishing an accurate diagnosis. Written by neuroimaging experts from around the world, Neuroimaging of Sleep and Sleep Disorders is an invaluable resource for both researchers and clinicians including sleep specialists, neurologists, radiologists, psychiatrists, psychologists.
Chapter
This up-to-date, superbly illustrated book is a practical guide to the effective use of neuroimaging in the patient with sleep disorders. There are detailed reviews of new neuroimaging techniques – including CT, MRI, advanced MR techniques, SPECT and PET – as well as image analysis methods, their roles and pitfalls. Neuroimaging of normal sleep and wake states is covered plus the role of neuroimaging in conjunction with tests of memory and how sleep influences memory consolidation. Each chapter carefully presents and analyzes the key findings in patients with sleep disorders indicating the clinical and imaging features of the various sleep disorders from clinical presentation to neuroimaging, aiding in establishing an accurate diagnosis. Written by neuroimaging experts from around the world, Neuroimaging of Sleep and Sleep Disorders is an invaluable resource for both researchers and clinicians including sleep specialists, neurologists, radiologists, psychiatrists, psychologists.
Chapter
This up-to-date, superbly illustrated book is a practical guide to the effective use of neuroimaging in the patient with sleep disorders. There are detailed reviews of new neuroimaging techniques – including CT, MRI, advanced MR techniques, SPECT and PET – as well as image analysis methods, their roles and pitfalls. Neuroimaging of normal sleep and wake states is covered plus the role of neuroimaging in conjunction with tests of memory and how sleep influences memory consolidation. Each chapter carefully presents and analyzes the key findings in patients with sleep disorders indicating the clinical and imaging features of the various sleep disorders from clinical presentation to neuroimaging, aiding in establishing an accurate diagnosis. Written by neuroimaging experts from around the world, Neuroimaging of Sleep and Sleep Disorders is an invaluable resource for both researchers and clinicians including sleep specialists, neurologists, radiologists, psychiatrists, psychologists.
Chapter
This up-to-date, superbly illustrated book is a practical guide to the effective use of neuroimaging in the patient with sleep disorders. There are detailed reviews of new neuroimaging techniques – including CT, MRI, advanced MR techniques, SPECT and PET – as well as image analysis methods, their roles and pitfalls. Neuroimaging of normal sleep and wake states is covered plus the role of neuroimaging in conjunction with tests of memory and how sleep influences memory consolidation. Each chapter carefully presents and analyzes the key findings in patients with sleep disorders indicating the clinical and imaging features of the various sleep disorders from clinical presentation to neuroimaging, aiding in establishing an accurate diagnosis. Written by neuroimaging experts from around the world, Neuroimaging of Sleep and Sleep Disorders is an invaluable resource for both researchers and clinicians including sleep specialists, neurologists, radiologists, psychiatrists, psychologists.
Article
Background: Native Americans (NAs) are more likely to experience chronic pain than non-Hispanic Whites (NHWs); however, the proximate causes predisposing NAs to chronic pain remain elusive. Likely due to centuries of adversity, discrimination, and marginalization, NAs report greater psychological stress than NHWs, which may place them at risk for sleep problems, a well-established risk factor for chronic pain onset. Purpose: This study examined the effects of psychological stress and sleep problems on subjective and physiological measures of pain processing in NAs and NHWs. Methods: Structural equation modeling was used to determine whether ethnicity (NA or NHW) was associated with psychological stress or sleep problems and whether these variables were related to conditioned pain modulation of pain perception (CPM-pain) and the nociceptive flexion reflex (CPM-NFR), temporal summation of pain (TS-pain) and NFR (TS-NFR), and pain tolerance in a sample of 302 (153 NAs) pain-free participants. Results: NAs experienced more psychological stress (Estimate = 0.027, p = .009) and sleep problems (Estimate = 1.375, p = .015) than NHWs. When controlling for age, sex, physical activity, BMI, and general health, NA ethnicity was no longer related to greater sleep problems. Psychological stress was also related to sleep problems (Estimate = 30.173, p = <.001) and psychological stress promoted sleep problems in NAs (indirect effect = 0.802, p = .014). In turn, sleep problems were associated with greater TS-pain (Estimate = 0.714, p = .004), but not other pain measures. Conclusions: Sleep problems may contribute to chronic pain risk by facilitating pain perception without affecting facilitation of spinal neurons or endogenous inhibition of nociceptive processes. Since psychological stress promoted pain facilitation via enhanced sleep problems, efforts to reduce psychological stress and sleep problems among NAs may improve health outcomes.
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Sleep disturbances are common in post-traumatic stress disorder (PTSD), although which sleep microarchitectural characteristics reliably classify those with and without PTSD remains equivocal. Here, we investigated sleep microarchitectural differences (i.e., spectral power, spindle activity) in trauma-exposed individuals that met ( n = 45) or did not meet ( n = 52) criteria for PTSD and how these differences relate to post-traumatic and related psychopathological symptoms. Using ecologically-relevant home sleep polysomnography recordings, we show that individuals with PTSD exhibit decreased beta spectral power during NREM sleep and increased fast sleep spindle peak frequencies. Contrary to prior reports, spectral power in the beta frequency range (20.31–29.88 Hz) was associated with reduced PTSD symptoms, reduced depression, anxiety and stress and greater subjective ability to regulate emotions. Increased fast frequency spindle activity was not associated with individual differences in psychopathology. Our findings may suggest an adaptive role for beta power during sleep in individuals exposed to a trauma, potentially conferring resilience. Further, we add to a growing body of evidence that spindle activity may be an important biomarker for studying PTSD pathophysiology.
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Background Mental disorders are prevalent and cause considerable burden of disease. Exercise has been shown to be efficacious to treat major depressive disorders, insomnia, panic disorder with and without agoraphobia and post traumatic stress disorder (PTSD). Methods This pragmatic, two arm, multi-site randomised controlled trial will evaluate the efficacy and cost-effectiveness of the manualized, group-based six-months exercise intervention “ImPuls”, among physically inactive patients with major depressive disorders, insomnia, panic disorder, agoraphobia and PTSD within a naturalistic outpatient context in Germany. A minimum of 375 eligible outpatients from 10 different study sites will be block- randomized to either ImPuls in addition to treatment as usual (TAU) or TAU only. ImPuls will be conducted by trained exercise therapists and delivered in groups of six patients. The program will combine (a) moderate to vigorous aerobic exercise carried out two-three times a week for at least 30 min with (b) behavior change techniques for sustained exercise behavior change. All outcomes will be assessed pre-treatment, post-treatment (six months after randomization) and at follow-up (12 months after randomization). Primary outcome will be self-reported global symptom severity assessed with the Brief Symptom Inventory (BSI-18). Secondary outcomes will be accelerometry-based moderate to vigorous physical activity, self-reported exercise, disorder-specific symptoms, quality-adjusted life years (QALY) and healthcare costs. Intention-to-treat analyses will be conducted using mixed models. Cost-effectiveness and cost-utility analysis will be conducted using incremental cost-effectiveness and cost-utility ratios. Discussion Despite its promising therapeutic effects, exercise programs are currently not provided within the outpatient mental health care system in Germany. This trial will inform service providers and policy makers about the efficacy and cost-effectiveness of the group-based exercise intervention ImPuls within a naturalistic outpatient health care setting. Group-based exercise interventions might provide an option to close the treatment gap within outpatient mental health care settings. Trial registration The study was registered in the German Clinical Trials Register (ID: DRKS00024152 , 05/02/2021).
Chapter
This chapter introduces quantitative electroencephalographic (QEEG) literature about normal and pathological sleep. It starts by introducing QEEG methods with a particular focus about power spectrum, functional connectivity analyses (i.e., coherence and phase synchronization), and source localization methods. It then illustrates the QEEG literature, from a power spectrum and a functional connectivity point of view, both about normal sleep process and pathological sleep conditions such as primary insomnia, sleep-related breathing disorders (e.g., obstructive sleep apnea syndrome), sleep parasomnias, and those occurring in neuropsychiatric and neurodegenerative diseases. Finally, the chapter provides a discussion about the clinical implications and future directions about sleep-related QEEG research.
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Abstract Background Exercise efficaciously reduces disorder-specific symptoms of psychiatric disorders. The current study aimed to examine the efficacy of a group exercise intervention on global symptom severity and disorder-specific symptoms among a mixed outpatient sample. Methods Groups of inactive outpatients, waiting for psychotherapy, with depressive disorders, anxiety disorders, insomnia, and attention-deficit/hyperactivity disorders were randomized to a manualized 12-week exercise intervention, combining moderate to vigorous aerobic exercise with techniques for sustainable exercise behaviour change (n = 38, female = 71.1% (n = 27), M age = 36.66), or a passive control group (n = 36, female = 75.0% (n = 27), M age = 34.33). Primary outcomes were global symptom severity and disorder-specific symptoms, measured with the Symptom Checklist-90-Revised and Pittsburgh Sleep Quality Index pre- and post-treatment. Secondary outcome was the self-reported amount of exercise (Physical Activity, Exercise, and Sport Questionnaire), measured pre-treatment, intermediate-, and post-treatment. Intention-to-treat analyses were conducted using linear mixed models. Linear regressions were conducted to examine the effect of the change of exercise behaviour on the change of symptoms. Results The intervention significantly improved global symptom severity (d = 0.77, p = .007), depression (d = 0.68, p = .015), anxiety (d = 0.87, p = .002), sleep quality (d = 0.88, p = .001), and increased the amount of exercise (d = 0.82, p
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Objectives Starting in adolescence, female sex is a strong risk factor for the development of insomnia. Reasons for this are unclear but could involve altered stress reactivity and/or autonomic nervous system (ANS) dysregulation, which are strongly associated with the pathophysiology of insomnia. We investigated sex differences in the effect of stress on sleep and ANS activity in adolescents, using the first night in the laboratory as an experimental sleep-related stressor. Design Repeated measures (first night vs. a subsequent night) with age (older/younger) and sex (males/females) as between factors. Setting Recordings were performed at the human sleep laboratory at SRI International. Participants One hundred six healthy adolescents (Age, mean ± SD: 15.2 ± 2.0 years; 57 boys). Measures Polysomnographic sleep, nocturnal heart rate (HR), and frequency-domain spectral ANS HR variability (HRV) indices. Results Boys and girls showed a first-night effect, characterized by lower sleep efficiency, lower %N1 and %N2 sleep, more wake after sleep onset and %N3 sleep, altered sleep microstructure (increased high-frequency sigma and Beta1 electroencephalographic activity), and reduced vagal activity (P < .05) on the first laboratory night compared to a subsequent night. The first night ANS stress effect (increases in HR and suppression in vagal HRV during rapid eye movement sleep) was greater in girls than boys (P < .05). Conclusions Sleep and ANS activity were altered during the first laboratory night in adolescents, with girls exhibiting greater ANS alterations than boys. Findings suggest that girls may be more vulnerable than boys to sleep-specific stressors, which could contribute to their increased risk for developing stress-related sleep disturbances.
Article
This study analysed heart rate variability (HRV) parameters in selected intervals of a 24-hour recording session. The study was conducted with eight young and eight old, clinically-healthy geldings. HRV measurements were taken with Polar RS800CX instruments. The recordings were then analysed with Kubios HRV software. The following time intervals were identified: 24 hours, 15 hours of the day (light period), 9 hours of the night in total, and in subsequent hours of the night. During each interval, the following time analysis parameters were investigated: heart rate (beats per minute; HR), verified beat-to-beat times (NN), standard deviation of the NN intervals (SDNN), and the square radical of the mean sum of the squares of differences between the adjacent NN intervals (rMSSD). The following HRV frequency parameters were also investigated: total power of the spectrum (TP), high-frequency spectrum (HF), low-frequency spectrum (LF) and LF/HF ratio. It was found that geriatric horses had higher HRs, but reduced some HRV parameters compared to young horses. Noticeable changes were least evident after midnight, especially between 01h00 and 04h00.
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Associations have been found between perseverative cognition (PC: worry and rumination) and somatic markers of ill-health. Further studies have reported associations between sleep and both PC and poorer health. As such, sleep disturbance may represent a pathway between PC and ill-health. Therefore, studies assessing the relationship between PC and sleep in non-clinical populations were synthesized. Meta-analyses (k = 55) revealed small- to medium-sized associations between higher PC and poorer sleep quality (SQ, r = -0.28), shorter total sleep time (TST, r = -0.15) and longer sleep onset latency (SOL, r = -0.16). Variations included associations between SQ and rumination (r = -.33) and worry (r = -.23). Associations were stronger in studies measuring SQ via self-report rather than actigraphy, and where SOL and TST outcomes were cross-sectional. Associations with SOL were stronger when outcomes were from non-diary studies and when trait, rather than state PC, was measured, but weaker where studies incorporated more measures of PC. Effect sizes were generally larger where studies were higher quality and being female may act as a protective factor between PC and longer SOL. Therefore, there is a consistent association between PC and sleep which may partially explain the link between PC and ill-health.
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The term “acute insomnia” has been part of the language of sleep medicine since the late 1970s. Despite that, a comprehensive research agenda on the topic has only recently been advanced. This has prevented a clinical viewpoint on the assessment and management of acute insomnia. Although there is a cognitive behavioral therapy for insomnia focused intervention, designed to circumvent the transition from acute insomnia to insomnia disorder, the results from trials undertaken have been variable and limited by small sample sizes. There is much work to be done regarding the assessment, diagnosis, and management of acute insomnia.
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The development of a 21-item self-report inventory for measuring the severity of anxiety in psychiatric populations is described. The initial item pool of 86 items was drawn from three preexisting scales: the Anxiety Checklist, the Physician’s Desk Reference Checklist, and the Situational Anxiety Checklist. A series of analyses was used to reduce the item pool. The resulting Beck Anxiety Inventory (BAI) is a 21-item scale that showed high internal consistency (α = .92) and test—retest reliability over 1 week, r (81) = .75. The BAI discriminated anxious diagnostic groups (panic disorder, generalized anxiety disorder, etc.) from nonanxious diagnostic groups (major depression, dysthymic disorder, etc). In addition, the BAI was moderately correlated with the revised Hamilton Anxiety Rating Scale, r (150) = .51, and was only mildly correlated with the revised Hamilton Depression Rating Scale, r (153) = .25.
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It was hypothesized that the metabolic effects of caffeine, which can be objectively measured (i.e. physiological, "arousal"), could be used to develop a physiological arousal model of chronic insomnia in a group of normal young adults. Twelve normal young adult males participated for 11 nights after laboratory adaptation. Subjects received 400 mg of caffeine three times a day for 7 nights and days. As predicted, the use of caffeine resulted in increased metabolic rate. Sleep efficiency was significantly reduced by caffeine and multiple sleep latency tests (MSLTs) were significantly increased. Some adaptation to the metabolic, sleep efficiency, and MSLT effects of caffeine was seen over the week of administration. Withdrawal effects (i.e. rebound sleep or sleepiness) were not seen for metabolic, MSLT or sleep variables. The data indicated that caffeine was effective in producing significant metabolic and sleep effects and that those effects were related. The results were consistent with the interpretation that a chronic decrease in sleep efficiency associated with increased physiological arousal, although producing subjective dysphoria, does not produce a physiological sleep debt.
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The noise sensitivities for nine different QRS detection algorithms were measured for a normal, single-channel lead II, synthesized ECG corrupted with five different types of synthesized noise. The noise types were electromyographic interference, 60 Hz powerline interference, baseline drift due to respiration, abrupt baseline shift, and a composite noise constructed from all of the other noise types. The percentage of QRS complexes detected, the number of false positives, and the detection delay were measured. None of the algorithms were able to detect all QRS complexes without any false positives for all of the noise types at the highest noise level. Algorithms based on amplitude and slope had the highest performance for EMG-corrupted ECG. An algorithm using a digital filter had the best performance for the composite noise corrupted data.
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To investigate individual differences in REM sleep drive and function, a factorial design that manipulated type of experimental presleep stimulation (insolvable, solvable, or no problems), personality (repressor or sensitizer), and sleep manipulation (REM deprivation or nondeprivation) was used. Data were obtained from 169 18–28 yr old male undergraduates who completed the Neuroticism scale of the Maudsley Personality Inventory as a measure of repression–sensitization. REM drive was assessed in terms of initial REM sleep onset and inter-REM interval throughout the night; REM function was assessed in terms of postsleep mood (Multiple Affect Adjective Check List) and anagram performance. Results reveal REM drive to be an interactive function of personality and presleep stimulation, but there was little evidence of an adaptive function for REM sleep. (22 ref)
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Spectral analysis was used to assess heart rate variability in consecutive 5-min epochs during the night in 12 normal adults. Simultaneous time coding of EEG and digitized EKG allowed examination of heart rate variability as a function of sleep stage, time of night and presence of EEG arousal. The results replicated previous studies in showing increases in high frequency components and decreases in low frequency components of heart rate variability across NREM sleep stages and opposite changes in REM sleep and wake. These results are consistent with sympathetic nervous system activation during REM sleep and wake periods. The shift in heart rate variability seen during REM sleep began in NREM sleep several minutes prior to standardly scored REM and often continued beyond the end of REM sleep. EEG arousals during Stage 2 and to some extent REM sleep were also associated with changes in heart rate variability which were consistent with sympathetic activation. An examination of beat to beat intervals in proximity to EEG arousals showed heart rate acceleration at least 10 beats prior to the EEG arousal. The arousal data along with Stage 2 sleep transition data support the contention that increases in central nervous system sympathetic activity precede and possibly play a role in the initiation of REM sleep and arousals during sleep.
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Although four meta-analytic reviews support the efficacy of pharmacotherapy and behavior therapy for the treatment of insomnia, no meta-analysis has evaluated whether these treatment modalities yield comparable outcomes during acute treatment. The authors conducted a quantitative review of the literature on the outcome of the two treatments to compare the short-term efficacy of pharmacotherapy and behavioral therapy in primary insomnia. They identified studies from 1966 through 2000 using MEDLINE, psycINFO, and bibliographies. Investigations were limited to studies using prospective measures and within-subject designs to assess the efficacy of benzodiazepines or benzodiazepine receptor agonists or behavioral treatments for primary insomnia. Benzodiazepine receptor agonists included zolpidem, zopiclone, and zaleplon. Behavioral treatments included stimulus control and sleep restriction therapies. Twenty-one studies summarizing outcomes for 470 subjects met inclusion criteria. Weighted effect sizes for subjective measures of sleep latency, number of awakenings, wake time after sleep onset, total sleep time, and sleep quality before and after treatment were moderate to large. There were no differences in magnitude between pharmacological and behavioral treatments in any measures except latency to sleep onset. Behavior therapy resulted in a greater reduction in sleep latency than pharmacotherapy. Overall, behavior therapy and pharmacotherapy produce similar short-term treatment outcomes in primary insomnia.
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The objectives of this study were to: 1) demonstrate the feasibility of combining polysomnography and SPECT neuroimaging to study NREM sleep in primary insomnia and 2) evaluate possible functional CNS abnormalities associated with insomnia. Patients with insomnia and good sleeper controls were studied polysomnographically for three nights with a whole brain SPECT Scan of NREM sleep on Night 3. Groups were screened for medical/psychiatric history, substance use, and matched on age, body mass index, and education. Sleep Research Laboratory and Nuclear Medicine Center Nine females, 5 patients with chronic psychophysiologic insomnia and 4 healthy good sleepers (mean age 36 years, SD 12, range 27-55). N/A. Tomographs of regional cerebral blood flow during the 1st NREM sleep cycle were successfully obtained. Contrary to our expectations, patients with insomnia showed a consistent pattern of hypoperfusion across all 8 pre-selected regions of interest, with particular deactivation in the basal ganglia (p=.006). The frontal medial, occipital, and parietal cortices also showed significant decreases in blood flow compared to good sleepers (p<.05). Subjects with insomnia had decreased activity in the basal ganglia relative to the frontal lateral cortex, frontal medial cortex, thalamus, occipital and parietal cortices (p<.05). This study demonstrated the feasibility of combining neuroimaging and polysomnography to study cerebral activity in chronic insomnia. These preliminary results suggest that primary insomnia may be associated with abnormal central nervous system activity during NREM sleep that is particularly linked to basal ganglia dysfunction.
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To determine whether the frequency spectrum of the sleep EEG is a physiologic correlate of 1) the degree to which individuals with persistent primary insomnia (PPI) underestimate their sleep time compared with the traditionally scored polysomnogram (PSG) and 2) the sleep complaints in PPI subjects who have relatively long traditionally scored PSG sleep times and relatively greater underestimation of sleep time. We compared EEG frequency spectra from REM and NREM sleep in PPI subjects subtyped as subjective insomnia sufferers (those with relatively long total sleep time and relative underestimation of sleep time compared with PSG), and objective insomnia sufferers (those with relatively short PSG total sleep time) with EEG frequency spectra in normals. We also studied the correlation between these indices and the degree of underestimation of sleep. Further, we determined the degree to which sleep EEG indexes related to sleep complaints. Duke University Medical Center Sleep Laboratory. Normal (N=20), subjective insomnia (N=12), and objective insomnia (N=18) subjects. N/A. Lower delta and greater alpha, sigma, and beta NREM EEG activity were found in the patients with subjective insomnia but not those with objective insomnia, compared with the normal subjects. These results were robust to changes in the subtyping criteria. No effects were found for REM spectral indexes. Less delta non- REM EEG activity predicted greater deviation between subjective and PSG estimates of sleep time across all subjects. For the subjective insomnia subjects, diminished low-frequency and elevated higher frequency non- REM EEG activity was associated with their sleep complaints. NREM EEG frequency spectral indexes appear to be physiologic correlates of sleep complaints in patients with subjective insomnia and may reflect heightened arousal during sleep.
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This study examined how sleep loss affects neurophysiologic signals related to attention and working memory. Subjective sleepiness, resting-state electroencephalogram, and behavior and electroencephalogram during performance of working-memory tasks were recorded in a within-subject, repeated-measures design. Data collection occurred in a computerized laboratory setting. Participants: Sixteen healthy adults (mean age, 26 years; 8 female) Interventions: Data from alert daytime baseline tests were compared with data from tests during a late-night, extended-wakefulness session that spanned up to 21 hours of sleep deprivation. Alertness measured both subjectively and electrophysiologically decreased monotonically with increasing sleep deprivation. A lack of alertness-related changes in electroencephalographic measures of the overall mental effort exerted during task execution indicated that participants attempted to maintain high levels of performance throughout the late-night tests. Despite such continued effort, responses became slower, more variable, and more error prone within 1 hour after participants' normal time of sleep onset. This behavior failure was accompanied by significant degradation of event-related brain potentials related to the transient focusing of attention. Moderate sleep loss compromises the function of neural circuits critical to subsecond attention allocation during working-memory tasks, even when an effort is made to maintain wakefulness and performance. Multivariate analyses indicate that combinations of working-memory-related behavior and neurophysiologic measures can be sensitive enough to permit reliable detection of such effects of sleep loss in individuals. Similar methods might prove useful for assessment of functional alertness in patients with sleep disorders.
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This study examined the impact of a workplace-based stress management program on blood pressure (BP), emotional health, and workplace-related measures in hypertensive employees of a global information technology company. Thirty-eight (38) employees with hypertension were randomly assigned to a treatment group that received the stress-reduction intervention or a waiting control group that received no intervention during the study period. The treatment group participated in a 16-hour program, which included instruction in positive emotion refocusing and emotional restructuring techniques intended to reduce sympathetic nervous system arousal, stress, and negative affect, increase positive affect, and improve performance. Learning and practice of the techniques was enhanced by heart rate variability feedback, which helped participants learn to self-generate physiological coherence, a beneficial physiologic mode associated with increased heart rhythm coherence, physiologic entrainment, parasympathetic activity, and vascular resonance. BP, emotional health, and workplace-related measures were assessed before and 3 months after the program. Three months post-intervention, the treatment group exhibited a mean adjusted reduction of 10.6 mm Hg in systolic BP and of 6.3 mm Hg in diastolic BP. The reduction in systolic BP was significant in relation to the control group. The treatment group also demonstrated improvements in emotional health, including significant reductions in stress symptoms, depression, and global psychological distress and significant increases in peacefulness and positive outlook. Reduced systolic BP was correlated with reduced stress symptoms. Furthermore, the trained employees demonstrated significant increases in the work-related scales of workplace satisfaction and value of contribution. Results suggest that a brief workplace stress management intervention can produce clinically significant reductions in BP and improve emotional health among hypertensive employees. Implications are that such interventions may produce a healthier and more productive workforce, enhancing performance and reducing losses to the organization resulting from cognitive decline, illness, and premature mortality.
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The purpose of this study was to determine the consistency of situational insomnia across several stressful conditions, including the first night in the sleep laboratory, phase advance of sleep time by 3 hours, phase advance of sleep time by 6 hours, and administration of 400 mg of caffeine. The impact of situational insomnia on alertness, metabolic rate, and cardiac measures on the following day was also measured. Subjects spent 5 to 7 nights and the following days in the laboratory. Standard polysomnographic recordings were made on each night. On each day, subjects had a Multiple Sleep Latency Test, performance testing, and metabolic and heart-rate observation periods. Fifty adult normal sleepers. Subjects had 1 night with their sleep phase advanced by 3 hours, 1 night with sleep phase advanced by 6 hours, and 1 night with the administration of 400 mg of caffeine 30 minutes prior to lights out. Sleep efficiency was reduced and variability was increased in each of the stressful conditions, as predicted. Those subjects with the greatest sleep efficiency on the adaptation night (top 25%) were compared with those subjects with the lowest sleep efficiency on the adaptation night (bottom 25%). Those subjects with the poorest sleep on the adaptation night (situational insomnia) had normal sleep on the baseline night that followed but had significantly reduced sleep efficiency when their sleep was advanced or they were given caffeine. Those same subjects had a significant decrease on their Multiple Sleep Latency Test on the day following the 6-hour advance and a significant increase in their Multiple Sleep Latency Test on the day following caffeine administration. The good sleepers had no significant change in their Multiple Sleep Latency Test during any of the study conditions. In terms of demographic variables, the situational insomnia group used less alcohol and tended to include a higher percentage of men. The situational insomnia group also had an elevated heart rate and increased low-frequency and decreased high-frequency electrocardiographic spectral power compared to the good sleepers. Significant differences were not found on personality or historical reports of poor sleep. Normal young adults have a consistent response to various types of situational stress. Those individuals who respond with poor sleep may display increased sleepiness associated with their poor sleep but may also be more sensitive to the effects of caffeine. These individuals have cardiac changes consistent with sympathetic nervous system activation, and they may be at risk for developing insomnia and other associated disorders.
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To determine the presence of a hypothesized trait vulnerability to sleep disturbance and hyperarousal. Polysomnographic assessment of sleep in response to stress during a first night in the laboratory and subsequent physiologic arousal. One hundred and four individuals (46% men, mean age 40.4 +/- 12.9 years) drawn from a population-based sample. Individuals were exposed to a first night in the laboratory. Participants completed a Likert-scale questionnaire, consisting of 27 items, that assesses sleep disturbance in response to commonly experienced stressful situations. Factor analytic techniques identified a single 9-item factor that was representative of the construct of "stress-related" vulnerability to sleep disturbance. Reliability of the resulting 9-item scale was high (Cronbach's alpha = .83). Individuals with higher scores on this scale, the Ford Insomnia Response to Stress Test (FIRST; median split), had a lower sleep efficiency (P = .001), as well as an increased latency to stage 1 sleep (P = .001) and persistent sleep (P = .002) on the first night of nocturnal polysomnography. Moreover, these high-scoring individuals showed increased arousal as evidenced by an elevated sleep latency on the Multiple Sleep Latency Test compared to individuals with low FIRST scores. Importantly, after controlling for current and past insomnia, the differences between individuals scoring high and low on the FIRST in terms of nocturnal sleep and daytime arousal remained significant. Other stages of sleep (stage 2, slow-wave, and rapid eye movement sleep) were not different between the groups. These results showing a relationship between FIRST scores and nocturnal polysomnography and Multiple Sleep Latency Test scores have 3 potential implications: (1) the data demonstrate a characteristic that relates to vulnerability to stress-related sleep disturbance as manifested by a first night in the laboratory; (2) the elevated latencies on the Multiple Sleep Latency Test in these individuals, despite significantly disturbed sleep, support the notion of physiologic hyperarousal in these individuals and suggests they may be predisposed to developing chronic primary insomnia; and (3) the vulnerability identified may underlie vulnerability to transient sleep disturbance associated with other sleep-disruptive factors.
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• Subjects with a primary complaint of insomnia (N = 124) were evaluated with Minnesota Multiphasic Personality Inventories (MMPIs). A high percentage of subjects (85%) had one or more MMPI scales elevated to a pathological degree. The scales most elevated were, in order, 2 (depression), 7 (psychasthenia), and 3 (conversion hysteria). A striking finding was the preponderance of depression. This was indicated by the frequency in which scale 2 was elevated above 70, the frequency in which this scale had the highest elevation, and the frequency of MMPI code types that included scale 2. Four common MMPI code types representing various types of depression were noted, indicating considerable homogeneity for code types in this sample. The predominant personality styles in this sample were characterized by the internalization of psychological disturbances rather than by acting out or aggression. We propose that this internalization produces a state of constant emotional arousal and resultant physiological activation and that this process is a psychophysiological mechanism underlying insomnia.
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The conceptual and practical aspects of the assessment of insomnia are described. A rationale is presented for the categorization of case material into a schema of predisposing conditions, precipitating circumstances and perpetuating factors. The application of this method is illustrated with an ‘expectable’ case. Following the discussion of the case, the features of a patient's history most likely to result in the greatest diagnostic yield are described and indications for specialized polysomnographic recording are reviewed. Finally, the common insomnia disorders are described employing the Association of Sleep Disorders Centers Nosology.
Article
SUMMARY  Increasingly, there is a need in both research and clinical practice to document and quantify sleep and waking behaviors in a comprehensive manner. The Pittsburgh Sleep Diary (PghSD) is an instrument with separate components to be completed at bedtime and waketime. Bedtime components relate to the events of the day preceding the sleep, waketime components to the sleep period just completed. Two-week PghSD data is presented from 234 different subjects, comprising 96 healthy young middle-aged controls, 37 older men, 44 older women, 29 young adult controls and 28 sleep disorders patients in order to demonstrate the usefulness, validity and reliability of various measures from the instrument. Comparisons are made with polysomnographic and actigraphic sleep measures, as well as personality and circadian type questionnaires. The instrument was shown to have sensitivity in detecting differences due to weekends, age, gender, personality and circadian type, and validity in agreeing with actigraphic estimates of sleep timing and quality. Over a 12–31 month delay, PghSD measures of both sleep timing and sleep quality showed correlations between 0.56 and 0.81 (n= 39, P < 0.001).
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In the present study, we evaluate the temporal and stagewise distribution of high frequency EEG activity (HFA) in primary and secondary insomnia. Three groups (n=9 per group) were compared: primary insomnia (PI), Insomnia secondary to major depression (MDD), and good sleeper controls (GS). Groups were matched for age, sex and body mass. Average spectral profiles were created for each sleep epoch. Grand averages were created for each NREM cycle and each stage of sleep after removing waking and movement epochs and epochs containing micro or miniarousals. It was found that HFA (in terms of relative power) tends to increase across NREM cycles, occurs maximally during stage 1 and during REM sleep, and that both these effects are exaggerated in patients with PI. In addition, HFA was found to be inversely associated with Delta activity and the three groups in our study appear to exhibit characteristic Delta/Beta patterns. Our data are consistent with the perspective that HFA is related to CNS arousal to the extent that Beta/Gamma activity occurs maximally during shallow stages of sleep and maximally in subjects with PI.
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Thirty-eight female good sleepers were instructed to go to sleep as quickly as possible in a daytime nap session under one of three instructional sets designed to manipulate the likelihood of cognitive intrusions. Subjects informed that they would be required to present a speech after their sleep period and told the topic of the speech required significantly longer to fall asleep and obtained less sleep than subjects in two control conditions. Analysis of heart rate and skin conductance measures failed to support the mediational role of autonomic activity in retarding sleep-onset.
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The authors investigated the neurobiological basis of poor sleep and daytime fatigue in insomnia. [(18)F]Fluorodeoxyglucose positron emission tomography was used to assess regional cerebral glucose metabolism of seven patients with insomnia and 20 healthy subjects. Compared with healthy subjects, patients with insomnia showed greater global cerebral glucose metabolism during sleep and while awake, a smaller decline in relative metabolism from waking to sleep states in wake-promoting regions, and reduced relative metabolism in the prefrontal cortex while awake. Subjectively disturbed sleep in patients with insomnia is associated with greater brain metabolism. The inability to fall asleep may be related to a failure of arousal mechanisms to decline in activity from waking to sleep states. Further, daytime fatigue may reflect decreased activity in the prefrontal cortex resulting from inefficient sleep.
Article
The present study investigated autonomic activity during NREM and REM sleep stages and wakefulness by spectral analysis of heart rate variability. The results demonstrated that NREM sleep in humans was characterized by a widely different autonomic activation pattern than REM sleep: high parasympathetic activity was found in NREM, while REM was characterized by attenuated vagal tone, and augmented sympathetic activity. The overall pattern during wakefulness showed an intermediate position between NREM and REM patterns; parasympathetic activity was lower than in NREM and higher than in REM, with an opposite trend for sympathetic activity.
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Clinical, field, and experimental studies of response to potentially stressful life events give concordant findings: there is a general human tendency to undergo episodes of intrusive thinking and periods of avoidance. A scale of current subjective distress, related to a specific event, was based on a list of items composed of commonly reported experiences of intrusion and avoidance. Responses of 66 persons admitted to an outpatient clinic for the treatment of stress response syndromes indicated that the scale had a useful degree of significance and homogeneity. Empirical clusters supported the concept of subscores for intrusions and avoidance responses.
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Subjects with a primary complaint of insomnia (N = 124) were evaluated with Minnesota Multiphasic Personality Inventories (MMPIs). A high percentage of subjects (85%) had one or more MMPI scales elevated to a pathological degree. The scales most elevated were, in order. 2 (depression), 7 (psychasthenia), and 3 (conversion hysteria). A striking finding was the preponderance of depression. This was indicated by the frequency in which scale 2 was elevated above 70, the frequency in which this this scale had the highest elevation, and the frequency of MMPI code types that included scale 2. Four common MMPI code types representing various types of depression were noted, indicating considerable homogeneity for code types in this sample. The predominant personality styles in this sample were characterized by the internalization of psychological distrubances rather than by acting out or aggression. We propose that this internalization produces a state of constant emotional arousal and resultant physiological activation and that this process is a psychophysiological mechansim underlyling insomnia.
Article
Seventy volunteers had 3 nights of sleep recordings during a period of marital separation, and 61 returned for repeat studies 1 year later. At that time, the divorce was final for 42. Forty of the volunteers were depressed when first screened, and 30 were not. Initially all those undergoing marital separation had less delta sleep than an age-matched married comparison sample. Delta increased at followup for those whose divorce was completed. Rapid eye movement (REM) latency was reduced and REM percent was elevated only in the depressed. Among the not depressed, those whose divorces remained incomplete at the followup had lower delta, higher REM percent, and shorter REM latency than did those whose divorces were finalized. This suggests that prolonged emotional stress may put these subjects at some risk for a mood disorder.
Article
A stress-support model incorporating indicators of life events, social support and SCL-90 measures of psychological distress was hypothesized to affect both reported and objective (somnographic) sleep. To determine the effects of these antecedents on sleep among 69 mid-life women, two models were tested, using both partial correlations and path analysis. Of all the measures of life events and social support examined in this study only negative LEs and contacts with non-supportive persons were associated (positively) with psychological distress, differentially explaining between 9% and 19% of the variance in each of five SCL-90 subscales. Both negative life events and contacts with non-supportive persons influenced depression and the SCL-90 PST index, whereas only negative life events affected anxiety, phobic anxiety and paranoid ideation. Anxiety, depression and the PST index, as indicators of psychological distress, had direct inverse effects on reported sleep with significant adjusted R2 values ranging from 10% to 16%. The model did not hold for somnographic sleep. The factors which are likely to contribute to the absence of an observed relationship between psychological distress and somnographic sleep are discussed.
Article
The present report describes the development of the Penn State Worry Questionnaire to measure the trait of worry. The 16-item instrument emerged from factor analysis of a large number of items and was found to possess high internal consistency and good test-retest reliability. The questionnaire correlates predictably with several psychological measures reasonably related to worry, and does not correlate with other measures more remote to the construct. Responses to the questionnaire are not influenced by social desirability. The measure was found to significantly discriminate college samples (a) who met all, some, or none of the DSM-III-R diagnostic criteria for generalized anxiety disorder and (b) who met criteria for GAD vs posttraumatic stress disorder. Among 34 GAD-diagnosed clinical subjects, the worry questionnaire was found not to correlate with other measures of anxiety or depression, indicating that it is tapping an independent construct with severely anxious individuals, and coping desensitization plus cognitive therapy was found to produce significantly greater reductions in the measure than did a nondirective therapy condition.
Article
Despite the prevalence of sleep complaints among psychiatric patients, few questionnaires have been specifically designed to measure sleep quality in clinical populations. The Pittsburgh Sleep Quality Index (PSQI) is a self-rated questionnaire which assesses sleep quality and disturbances over a 1-month time interval. Nineteen individual items generate seven "component" scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. The sum of scores for these seven components yields one global score. Clinical and clinimetric properties of the PSQI were assessed over an 18-month period with "good" sleepers (healthy subjects, n = 52) and "poor" sleepers (depressed patients, n = 54; sleep-disorder patients, n = 62). Acceptable measures of internal homogeneity, consistency (test-retest reliability), and validity were obtained. A global PSQI score greater than 5 yielded a diagnostic sensitivity of 89.6% and specificity of 86.5% (kappa = 0.75, p less than 0.001) in distinguishing good and poor sleepers. The clinimetric and clinical properties of the PSQI suggest its utility both in psychiatric clinical practice and research activities.
Article
In 57 normal subjects (age 20-60 years), we analyzed the spontaneous beat-to-beat oscillation in R-R interval during control recumbent position, 90 degrees upright tilt, controlled respiration (n = 16) and acute (n = 10) and chronic (n = 12) beta-adrenergic receptor blockade. Automatic computer analysis provided the autoregressive power spectral density, as well as the number and relative power of the individual components. The power spectral density of R-R interval variability contained two major components in power, a high frequency at approximately 0.25 Hz and a low frequency at approximately 0.1 Hz, with a normalized low frequency:high frequency ratio of 3.6 +/- 0.7. With tilt, the low-frequency component became largely predominant (90 +/- 1%) with a low frequency:high frequency ratio of 21 +/- 4. Acute beta-adrenergic receptor blockade (0.2 mg/kg IV propranolol) increased variance at rest and markedly blunted the increase in low frequency and low frequency:high frequency ratio induced by tilt. Chronic beta-adrenergic receptor blockade (0.6 mg/kg p.o. propranolol, t.i.d.), in addition, reduced low frequency and increased high frequency at rest, while limiting the low frequency:high frequency ratio increase produced by tilt. Controlled respiration produced at rest a marked increase in the high-frequency component, with a reduction of the low-frequency component and of the low frequency:high frequency ratio (0.7 +/- 0.1); during tilt, the increase in the low frequency:high frequency ratio (8.3 +/- 1.6) was significantly smaller. In seven additional subjects in whom direct high-fidelity arterial pressure was recorded, simultaneous R-R interval and arterial pressure variabilities were examined at rest and during tilt. Also, the power spectral density of arterial pressure variability contained two major components, with a relative low frequency:high frequency ratio at rest of 2.8 +/- 0.7, which became 17 +/- 5 with tilt. These power spectral density components were numerically similar to those observed in R-R variability. Thus, invasive and noninvasive studies provided similar results. More direct information on the role of cardiac sympathetic nerves on R-R and arterial pressure variabilities was derived from a group of experiments in conscious dogs before and after bilateral stellectomy. Under control conditions, high frequency was predominant and low frequency was very small or absent, owing to a predominant vagal tone. During a 9% decrease in arterial pressure obtained with IV nitroglycerin, there was a marked increase in low frequency, as a result of reflex sympathetic activation.(ABSTRACT TRUNCATED AT 400 WORDS)
Article
This paper presents evidence from three samples, two of college students and one of participants in a community smoking-cessation program, for the reliability and validity of a 14-item instrument, the Perceived Stress Scale (PSS), designed to measure the degree to which situations in one's life are appraised as stressful. The PSS showed adequate reliability and, as predicted, was correlated with life-event scores, depressive and physical symptomatology, utilization of health services, social anxiety, and smoking-reduction maintenance. In all comparisons, the PSS was a better predictor of the outcome in question than were life-event scores. When compared to a depressive symptomatology scale, the PSS was found to measure a different and independently predictive construct. Additional data indicate adequate reliability and validity of a four-item version of the PSS for telephone interviews. The PSS is suggested for examining the role of nonspecific appraised stress in the etiology of disease and behavioral disorders and as an outcome measure of experienced levels of stress.
Article
A survey of 296 insomniacs sought to clarify the relative influence of somatic versus cognitive arousal - the causes assumed in the two main competing theories of insomnia. Subjects averaged 46 years in age, had endured sleep complaints an average of 11 years, and needed 89 minutes, on the average, to fall asleep. Most subjects blamed insomnia on cognitive arousal rather than somatic factors, both factors, or neither. On separate complaint ratings, cognitive surpassed somatic arousal for all subjects combined and for those who complained of both forms of disturbance. The results suggest that intrusive cognitions are far more prevalent than somatic factors in creating insomnia and need to be emphasized in treatment development.
Article
Because of the role of psychological factors in insomnia, the shortcomings of hypnotic medications, and patients' greater acceptance of nonpharmacological treatments for insomnia, the authors conducted a meta-analysis to examine the efficacy and durability of psychological treatments for the clinical management of chronic insomnia. A total of 59 treatment outcome studies, involving 2,102 patients, were selected for review on the basis of the following criteria: 1) the primary target problem was sleep-onset, maintenance, or mixed insomnia, 2) the treatment was nonpharmacological, 3) the study used a group design, and 4) the outcome measures included sleep-onset latency, time awake after sleep onset, number of nighttime awakenings, or total sleep time. Psychological interventions, averaging 5.0 hours of therapy time, produced reliable changes in two of the four sleep measures examined. The average effect sizes (i.e., z scores) were 0.88 for sleep latency and 0.65 for time awake after sleep onset. These results indicate that patients with insomnia were better off after treatment than 81% and 74% of untreated control subjects in terms of sleep induction and sleep maintenance, respectively. Stimulus control and sleep restriction were the most effective single therapy procedures, whereas sleep hygiene education was not effective when used alone. Clinical improvements seen at treatment completion were well maintained at follow-ups averaging 6 months in duration. The findings indicate that nonpharmacological interventions produce reliable and durable changes in the sleep patterns of patients with chronic insomnia.
Article
This research examines longitudinal data on psychosocial status andpolysomnographic sleep collected annually from 57 healthy, community-residing elders aged 61-89. Cluster analysis of variables reflecting sleep continuity and architecture at the baseline assessment was used to identify three groups of elders: those whose sleep was either (a) superior to all remaining respondents across a variety of measures, (b) marred only by significantly reduced sleep efficiency relative to other respondents, or (c) poorer than all other respondents in multiple areas. Cross-validation procedures suggested that the three-group cluster solution was stable and replicable over persons and over time. Subsequent multivariate analyses indicated that recent life events, as well as psychosocial stability and support variables at baseline, distinguished between the sleep pattern groups. Moreover, sleep pattern group membership itself predicted subjects' subsequent sleep characteristics and psychosocial status at follow-up. Implications of these results for conceptualizing psychosocial factors that affect, and are ultimately affected by, sleep disturbances in late life are discussed
Article
In this study, we compared repeated measures of electroencephalographic (EEG) sleep and subjective sleep quality in nondepressed, spousally bereaved elders and a healthy control group, in order to search for possible psychobiological correlates of bereavement not confounded by concurrent major depression. Laboratory-based EEG sleep studies and measures of subjective sleep quality (Pittsburgh Sleep Quality Index [PSQI]) were repeated at 3, 6, 11, 18, and 23 months after spousal bereavement in a study group of 27 elderly volunteers. Data were compared with similar measures from a control group of 27 nonbereaved subjects recorded on three occasions 1 year apart. Repeated-measures analysis of variance (ANOVA), using age as a covariate, examined effects due to time on selected variables in the bereaved group, as well as effects due to group, time, and group-by-time interactions in the experimental and control subjects. Bereaved and control groups showed consistent differences over time in the phasic measures of rapid eye movement (REM) sleep (higher in bereaved subjects during the first and third REM sleep periods), but were similar on all other EEG sleep measures over the 2 years of observation. The bereaved showed a small decline in the percentage of slow-wave sleep over 2 years, but measures of sleep efficiency, REM latency, and delta sleep ratio were stable and did not differ from values seen in control subjects. Bereaved and control subjects were also similar on subjective sleep quality. During successful adaptation to the loss of a spouse, and in the absence of major depression, spousal bereavement is associated with elevation in the phasic measures of REM sleep but does not appear to be associated with other physiologic sleep changes typical of major depression when studied at 3 to 23 months after the event. Although this observation does not preclude the possibility of significant sleep disturbance nearer the time of the event, it suggests that preservation of normal sleep following a major negative life event may be an important correlate of the resilience seen in successful aging. The elevation in REM density may provide a psychobiological correlate of bereavement not confounded by concurrent major depression.
Article
Autonomic characteristics of generalized anxiety disorder (GAD) and worry were examined using measures of heart period variability. The cardiorespiratory responses of 34 GAD clients and 32 nonanxious control subjects were recorded during resting baseline, relaxation, and worry periods. Results indicated differences between GAD subjects and controls as well as among baseline, relaxation, and worry periods. GAD clients exhibited shorter cardiac interbeat intervals (IBIs) and lower high frequency spectral power across all task conditions. Relative to baseline and relaxation conditions, worry was associated with (1) shorter IBIs, (2) smaller mean successive differences (MSD) of the cardiac IBIs, and (3) lower high frequency spectral power. These findings suggest that GAD and its cardinal feature (worry), are associated with lower cardiac vagal control. The findings of the present study provide evidence for the utility of further exploration of the role of autonomic nervous system activity in GAD.
Article
Synopsis The psychometric properties of the 28- and 30-item versions of the Inventory of Depressive Symptomatology, Clinician-Rated (IDS-C) and Self-Report (IDS-SR) are reported in a total of 434 (28-item) and 337 (30-item) adult out-patients with current major depressive disorder and 118 adult euthymic subjects (15 remitted depressed and 103 normal controls). Cronbach's α ranged from 0·92 to 0·94 for the total sample and from 0·76 to 0·82 for those with current depression. Item total correlations, as well as several tests of concurrent and discriminant validity are reported. Factor analysis revealed three dimensions (cognitive/mood, anxiety/arousal and vegetative) for each scale. Analysis of sensitivity to change in symptom severity in an open-label trial of fluoxetine ( N = 58) showed that the IDS-C and IDS-SR were highly related to the 17-item Hamilton Rating Scale for Depression. Given the more complete item coverage, satisfactory psychometric properties, and high correlations with the above standard ratings, the 30-item IDS-C and IDS-SR can be used to evaluate depressive symptom severity. The availability of similar item content for clinician-rated and self-reported versions allows more direct evaluations of these two perspectives.
Article
Owing to the use of scalp electrodes in human sleep recordings, cortical EEG signals are inevitably intermingled with the electrical activity of the muscle tissue on the skull. Muscle artifacts are characterized by surges in high frequency activity and are readily identified because of their outlying high values relative to the local background activity. To detect bursts of myogenic activity a simple algorithm is introduced that compares high frequency activity (26.25-32.0 Hz) in each 4-s epoch with the activity level in a local 3-min window. A 4-s value was considered artifactual if it exceeded the local background activity by a certain factor. Sensitivity and specificity of the artifact detection algorithm were empirically adjusted by applying different factors as artifact thresholds. In an analysis of sleep EEG signals recorded from 25 healthy young adults 2.3% (SEM: 0.16) of all 4-s epochs during sleep were identified as artifacts when a threshold factor of four was applied. Contamination of the EEG by muscle activity was more frequent towards the end of non-REM sleep episodes when EEG slow wave activity declined. Within and across REM sleep episodes muscle artifacts were evenly distributed. When the EEG signal was cleared of muscle artifacts, the all-night EEG power spectrum showed significant reductions in power density for all frequencies from 0.25-32.0 Hz. Between 15 and 32 Hz, muscle artifacts made up a substantial part (20-70%) of all-night EEG power density. It is concluded that elimination of short-lasting muscle artifacts reduces the confound between cortical and myogenic activity and is important in interpreting quantitative EEG data. Quantitative approaches in defining and detecting transient events in the EEG signal may help to determine which EEG phenomena constitute clinically significant arousals.
Article
In previous sleep studies, it has been demonstrated that Poincare plots of RR intervals, which provide a beat to beat dynamic measure of heart rate variability, have distinctive and characteristic patterns according to sleep stages. This study was designed to evaluate the temporal relationship between heart rate variability and sleep electroencephalographic activity (EEG) by using the Pearson's interbeat autocorrelation coefficients of RR intervals derived from the Poincare plots. The coefficients were calculated in 12 subjects over each minute and were related to the profiles of EEG mean frequency (0.5-35 Hz) computed using a Fast Fourier Transformation algorithm. Overnight profiles of interbeat autocorrelation coefficients and of EEG mean frequency were found to be related with highly significant cross-correlation coefficients ranging between 0.216 and 0.638 (P < 0.001). The variations in heart rate variability preceded changes in brain activity by 1-2 min. These results demonstrate that beat to beat heart rate variability and EEG activity are closely linked during sleep in normal man.
Article
A number of paradoxes are apparent in the assessment and treatment of psychophysiological insomnia and sleep state misperception. Three of these paradoxes exist as discrepancies between polysomnographic (PSG) measures and the subjective impressions regarding sleep quality and quantity. The remaining incongruity exists largely within the objective domain. In the case of subjective-objective discrepancies, patients with insomnia: (1) frequently identify themselves as having been awake when awakened from PSG defined sleep; (2) tend to overestimate sleep latency and underestimate total sleep time as compared with PSG measures; (3) appear to derive more benefit from pharmacotherapy that can be explained by objective gains. The remaining paradox pertains to the observation that hypnotic medications, by and large, do not normalize sleep architecture or produce a more 'sleep-like' EEG. In this paper, we review possible explanations for these various paradoxes, introduce a new perspective and suggest possible research avenues. The model introduced is based on the observation that beta and/or gamma activity (which have been found to be associated with cognitive processes) is enhanced in insomnia at or around sleep onset. We propose that this kind of high frequency EEG activity may interfere with the normal establishment of sleep onset-related mesograde amnesia. As a result, the patient with insomnia maintains a level of information and/or memory processing that blurs the phenomenological distinction between sleep and wakefulness and influences retrospective judgments about sleep initiation and duration.
Article
We describe the methods for power spectral analysis (PSA) of sleep electroencephalogram (EEG) data at a large clinical and research sleep laboratory. The multiple-bedroom, multiple-polygraph design of the sleep laboratory poses unique challenges for the quantitative analysis of the data. This paper focuses on the steps taken to ensure that our PSA results are not biased by the particular bedroom or polygraph from which the data were acquired. After describing the data acquisition system hardware, we present our signal amplitude calibration procedure and our methods for performing PSA. We validate the amplitude calibration procedure in several experiments using PSA to establish tolerances for data acquisition from multiple bedrooms and polygraphs. Since it is not possible to acquire identical digitized versions of an EEG signal using different sets of equipment, the best that can be achieved is data acquisition that is polygraph-independent within a known tolerance. We are able to demonstrate a tolerance in signal amplitude of +/- 0.25% when digitizing data from different bedrooms. When different data acquisition hardware is used, the power tolerance is approximately +/- 3% for frequencies from 1 to 35 Hz. The power tolerance is between +/- 3 and +/- 7% for frequencies below 1 Hz and frequencies between 35 and 50 Hz. Additional data demonstrate that variability due to the hardware system is small relative to the inherent variability of the sleep EEG. The PSA results obtained in one location can be replicated elsewhere (subject to known tolerances) only if the data acquisition system and PSA method are adequately specified.
Article
Sleep is not a uniform state but is characterized by the cyclic alternation between rapid eye movement (REM) and non-REM sleep with a periodicity of 90–110 min. This cycle length corresponds to one of the oscillations in electroencephalographic (EEG) activity in the delta frequency band (0.5–3.5 Hz), which reflect the depth of sleep. To demonstrate the intimate link between EEG and neuroendocrine rhythmic activities in man, we adopted a procedure permitting simultaneous analysis of sleep EEG activity in the delta band and of two activating systems: the adrenocorticotropic system and the autonomic nervous system. Adrenocorticotropic activity was evaluated by calculating the cortisol secretory rate in blood samples taken at 10-min intervals. Autonomic activity was estimated by two measures of heart rate variability: 1) by the ratio of low-frequency (LF) to high-frequency (HF) power from spectral analysis of R-R intervals; and 2) by the interbeat autocorrelation coefficient of R-R intervals (rRR intervals between two successive cardiac beats). The results revealed that oscillations in delta wave activity, adrenocorticotropic activity, and autonomic activity are linked in a well-defined manner. Delta wave activity developed when cortisol secretory rates had returned to low levels and sympathetic tone was low or decreasing, as reflected by a low LF/HF ratio and by low levels in rRR. Conversely, the decrease in delta wave activity occurred together with an increase in the LF/HF ratio and in rRR. REM sleep was associated with a decrease in cortisol secretory rates preceding REM sleep onset, whereas the LF/HF ratio and rRR remained high. These results demonstrate a close coupling of adrenocorticotropic, autonomic, and EEG ultradian rhythms during sleep in man. They suggest that low neuroendocrine activity is a prerequisite for the increase in slow wave activity.
Article
Previous studies have not evaluated the clinical correlates of the electroencephalographic spectral profile in patients with insomnia. In the preliminary study described here, we evaluated the extent to which symptoms of stress and depression are associated with subjective sleep complaints and quantitative measures of sleep in individuals with chronic insomnia. Subjects were 14 healthy adults who met criteria for primary insomnia as specified in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders. Measures of stress, depression, and subjective sleep quality were collected before subjects participated in a two-night laboratory sleep series. We hypothesized that elevated symptoms of stress and depression would be associated with subjective sleep complaints and electroencephalographic evidence of hyperarousal during sleep. Hyperarousal during sleep was defined as decreases in delta power and elevations in alpha and beta power throughout non-rapid eye movement sleep, and symptoms of stress were defined as the tendency to experience stress-related intrusive thoughts and the interaction between intrusion tendency and the number of recent stressful events (subjective stress burden). A stronger tendency to experience stress-related intrusive thoughts was associated with greater sleep complaints and a trend toward higher beta power, whereas increases in subjective stress burden were associated with decreases in delta power. In addition, elevations in subclinical symptoms of depression were associated with greater sleep complaints and elevations in alpha power. Observed relationships among symptoms of stress, depression, subjective sleep complaints, and electroencephalographic power may be relevant to the discrepancy between subjective and objective measures of sleep in patients with insomnia and may be more broadly applicable to sleep complaints in association with stressful life events and major depression.
Article
Work stress has repeatedly been associated with an increased risk for cardiovascular disease. This study tested whether this relationship could be explained by exaggerated cardiovascular reactivity to work or impaired recovery in leisure time. Vagal tone was assessed as a possible determinant of these work stress effects. Participants included 109 male white-collar workers (age, 47.2+/-5. 3) who were monitored on 2 workdays and 1 nonworkday for ambulatory blood pressure, heart rate, and heart rate variability. Chronic work stress was defined according to Siegrist's model as (1) high imbalance, a combination of high effort and low reward at work, or (2) high overcommitment, an exhaustive work-related coping style indexing the inability to unwind. All findings were adjusted for possible differences in posture and physical activity between the work stress groups. High imbalance was associated with a higher heart rate during work and directly after work, a higher systolic blood pressure during work and leisure time, and a lower 24-hour vagal tone on all 3 measurement days. Overcommitment was not associated with an unfavorable ambulatory profile. Logistic regression analysis revealed that heart rate [odds ratio 1-SD increase 1.95 (95% CI, 1.02 to 3.77)] and vagal tone [odds ratio 1-SD decrease 2.67 (95% CI, 1.24 to 5.75)] were independently associated with incident mild hypertension. Surprisingly, the values during sleep were more predictive for mild hypertension than the values during work. The results from the present study suggest that the detrimental effects of work stress are partly mediated by increased heart rate reactivity to a stressful workday, an increase in systolic blood pressure level, and lower vagal tone.
Article
This paper critically reviews the evidence base for previously reported conceptual models of the development and persistence of insomnia. Although a number of perspectives have some empirical support, no one approach emerges as preeminent. Importantly, the efficacy of any particular psychological intervention cannot be taken as confirmation of presumed, underlying mechanisms. An integrated psychobiological inhibition model of insomnia is developed that accounts for the research data. The model views insomnia as arising from inhibition of de-arousal processes associated with normal sleep. It is proposed that sleep homeostatic and circadian factors are compromised by impairment of the automaticity and plasticity associated with good sleep, and that cognitive/affective processes activate the clinical complaint of insomnia. Common pathways for the action of cognitive-behavioral interventions are identified, and a research agenda is set for further conceptual and clinical study.
Article
To date there have been seven studies which find that beta EEG is elevated at around sleep onset and during polysomnographic sleep in patients with insomnia. These findings suggest that insomnia may be characterized by central nervous system (CNS) hyperarousal. In this article, the seven studies are critically reviewed, two theoretical perspectives on beta EEG are presented, and the concept of hyperarousal as a three component process is discussed.
Article
Although stress is often presumed to cause sleep disturbances, little research has documented the role of stressful life events in primary insomnia. The present study examined the relationship of stress and coping skills, and the potential mediating role of presleep arousal, to sleep patterns in good sleepers and insomnia sufferers. The sample was composed of 67 participants (38 women, 29 men; mean age, 39.6 years), 40 individuals with insomnia and 27 good sleepers. Subjects completed prospective, daily measures of stressful events, presleep arousal, and sleep for 21 consecutive days. In addition, they completed several retrospective and global measures of depression, anxiety, stressful life events, and coping skills. The results showed that poor and good sleepers reported equivalent numbers of minor stressful life events. However, insomniacs rated both the impact of daily minor stressors and the intensity of major negative life events higher than did good sleepers. In addition, insomniacs perceived their lives as more stressful, relied more on emotion-oriented coping strategies, and reported greater presleep arousal than good sleepers. Prospective daily data showed significant relationships between daytime stress and nighttime sleep, but presleep arousal and coping skills played an important mediating role. The findings suggest that the appraisal of stressors and the perceived lack of control over stressful events, rather than the number of stressful events per se, enhance the vulnerability to insomnia. Arousal and coping skills play an important mediating role between stress and sleep. The main implication of these results is that insomnia treatments should incorporate clinical methods designed to teach effective stress appraisal and coping skills.
Article
The level of EEG slow-wave activity (SWA) is determined by the duration of prior sleep and waking. SWA is a marker of nonREM sleep intensity and may serve as an indicator of sleep homeostasis. The two-process model of sleep regulation posits the interaction of the homeostatic Process S and the circadian Process C. Also models of neurobehavioral functions (three-process model; interactive models of alertness and cognitive throughput) are based on the concept of an interaction between homeostatic and circadian factors. Whether the interaction is linear or non-linear is still unresolved. Models may serve as a guiding principle for specifying the relationship between processes occurring at the macroscopic and microscopic level of analysis.
Article
The present study aimed to provide an empirical test of the proposal that catastrophic worry about the consequences of not sleeping is common among patients with primary insomnia and serves to maintain the sleep disturbance. It was predicted that relative to good sleepers, patients with primary insomnia would catastrophize more and that catastrophizing would be associated with increased negative affect and increased perception of threat. A 'catastrophizing interview' was administered to 30 patients with primary insomnia and 30 good sleepers. Consistent with the predictions, the insomnia patients generated more catastrophes about the consequences of not sleeping and gave higher likelihood ratings than good sleepers. For the insomnia group, but not the good sleepers, the catastrophizing interview was associated with increased anxiety and discomfort. The limitations of the study, possibilities for future research, and clinical implications of these findings are discussed.
Article
There is growing interest in insomnia both from the perspective of recent advances in clinical management as well as research aimed at elucidating its pathophysiology. This theoretical overview of insomnia describes the negative impact, etiological considerations, and pharmacological and behavioral treatments for the disorder, with an emphasis on areas receiving increased research attention. Insomnia, the most prevalent sleep disorder, affects 10-15% of the general population. In population-based studies severe insomnia has been shown to last for a median of 4 years. In addition, insomnia has a significant negative impact on an individual's work, physical, and social performance as well as overall quality of life. Furthermore, the economic cost of insomnia related to lost productivity, work-related accidents, absenteeism, and health-care costs are enormous. There is increasing evidence linking the precipitation of insomnia to stress, and converging evidence from cognitive, endocrine, neurological, and behavioral domains provide clear evidence for hyper-arousal in insomnia. However, there remains no consensus regarding the specific etiological mechanisms of this disorder. Although the pathophysiology of primary insomnia remains an enigma, numerous treatments both pharmacological and behavioral have been developed and found to be efficacious in controlled studies. Despite the wide availability of pharmacological treatments and increased knowledge of behavioral interventions, the vast majority of individuals with insomnia do not appear to be receiving adequate treatment. The inadequate treatment of insomnia leads to several important and under-recognized consequences including subsequent development of psychiatric disease and increased substance use.
Article
Although stress can elicit profound and lasting effects on sleep, the pathways whereby stress affects sleep are not well understood. In this study, we used autoregressive spectral analysis of the electrocardiogram (EKG) interbeat interval sequence to characterize stress-related changes in heart rate variability during sleep in 59 healthy men and women. Participants (N = 59) were randomly assigned to a control or stress condition, in which a standard speech task paradigm was used to elicit acute stress in the immediate presleep period. EKG was collected throughout the night. The high frequency component (0.15-0.4 Hz Eq) was used to index parasympathetic modulation, and the ratio of low to high frequency power (0.04-0.15 Hz Eq/0.15-0.4 Hz Eq) of heart rate variability was used to index sympathovagal balance. Acute psychophysiological stress was associated with decreased levels of parasympathetic modulation during nonrapid eye movement (NREM) and rapid eye movement sleep and increased levels of sympathovagal balance during NREM sleep. Parasympathetic modulation increased across successive NREM cycles in the control group; these increases were blunted in the stress group and remained essentially unchanged across successive NREM periods. Higher levels of sympathovagal balance during NREM sleep were associated with poorer sleep maintenance and lower delta activity. Changes in heart rate variability associated with acute stress may represent one pathway to disturbed sleep. Stress-related changes in heart rate variability during sleep may also be important in association with chronic stressors, which are associated with significant morbidity and increased risk for mortality.