Article

The effects of presleep stress on sleep-onset insomnia

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Abstract

10 sleep-onset (SO) insomniacs and 11 noninsomniacs (18–21 yrs old) slept undisturbed for 3 nights but were exposed to brief cognitive stressors before SO on the next 2 nights. Significant between-group differences were found in responses to the cognitive stressors on self-report but not objective measures of SO latency (SOL). Noninsomniac Ss evidenced an increase and insomniac Ss a decrease in SOL on stress nights. Insomniac Ss demonstrated a significantly higher mean heart-rate response before and after the stressors. A variable expressing the relationship between objective and subjective measures of SOL (pseudoidiopathic dimension) for each S was not significantly related to Ss' responses to stress. Results are inconsistent with the hypothesized role of presleep stress in SO insomnia but are consistent with other studies indicating higher levels of physiological arousal of insomniac vs noninsomniac Ss. (22 ref)

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... The physiological hyperarousal hypothesis (Monroe, 1967) originates from physiological differences between good and poor sleepers, namely greater autonomic activity pre-sleep and during sleep, and higher mean heart and pulse rates, rectal body temperature, and phasic vasoconstriction presleep in poor sleepers relative to good sleepers. However, attempts to empirically separate good sleepers from poor sleepers on the basis of physiological measures, have not convincingly supported heightened physiological arousal as a primary cause of insomnia (Haynes, Adams & Franzen, 1981); subsequent investigations have not found reliable physiological differences (Frankel, Buchbinder, Coursey, & Syder, 1973;Johns, Gay, Marston, & Bruce, 1971). Some have not found a relationship between physiological arousal and sleep-onset latency (Brownman & Tepas, 1976;Freedman & Papsdorf, 1976;Borkovec, Grayson, O'Brien, & Weerts, 1979). ...
... In some studies, pre-sleep cognitive arousal has been linked to sleep variables like sleep onset latency (Nicassio, Mendlowitz, Fussell & Petras, 1985;Sanavio, 1988;Wicklow & Espie, 2000), while other studies have not found a link (Haynes, Adams, & Franzen, 1981). In the validation studies of the Pre-Sleep Arousal Scale (PSAS; Nicassio, Mendlowitz, Fussell & Petras, 1985), both somatic and cognitive subscales correlated highly with sleep onset latency and total sleep time on subjective sleep diaries. ...
... Sleep has much inter-subject and inter-night variability (Speilman, Yang, & Glovinsky, 2001; see also Agnew, Webb, & William, 1966;Hauri & Olmstead, 1989), so it is possible that a The finding that changes occurred in pre-sleep cognitive arousal, but not sleep indices, implies that pre-sleep arousal may have little or no effect on sleep disruption. Pre-sleep cognitive arousal has often been strongly linked to sleep variables like sleep onset latency (Nicassio, Mendlowitz, Fussell & Petras, 1985;Sanavio, 1988;Wicklow & Espie, 2000), while other studies have not (Haynes, Adams, & Franzen, 1981). The present study would not support a significant relationship between cognitive arousal and rated sleep, although this conclusion is tempered by the fact that the sleep analyses were under-powered. ...
... The manual search of reference lists of relevant papers and reviews identified three papers [53, 64,72]. Three additional studies [79][80][81] were added to explain the transition from "poor" sleepers to clinically defined insomniacs. The vast majority of these articles (n = 366) were excluded by title or abstract alone (see Fig 1) ...
... Studies without specific diagnostic criteria for insomnia disorder. In studies without specific diagnostic criteria for insomnia disorder, physiological differences during sleep were investigated between the "poor" and "good" sleeper groups [79], as well as subjects with sleep- onset insomnia [80,81]. Monroe [79] reported significantly higher HR 30 minutes before sleep in "poor" sleepers as compared to "good" sleepers. ...
... Freedman et al. [81] found that sleep-onset insomniacs had increased HR prior to sleep, but not during sleep. Similarly, Haynes et al. [80] reported that sleep-onset insomniacs showed a mean HR 4.6 beats per minute, significantly higher than that of non-insomniacs, whilst the effects of pre-sleep cognitive stress were examined. Haynes et al. [80], concluded that insomniacs show higher levels of physiological arousal compared to non-insomniac subjects. ...
Article
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Background Insomnia disorder is a widespread sleep disorder with a prevalence of approximately 10%. Even though the link between insomnia and cardiovascular activity is not exactly clear, it is generally assumed that cardiovascular autonomic modifications could occur as a result of sleeplessness, or, alternatively, that autonomic alterations could be an expression of a hyper-arousal state. This review investigates whether cardiovascular measures are different between insomniacs and controls. Methods Electronic databases were systematically searched, and 34 studies were identified. Heart rate variability features, the association of cardiac and EEG activity, physiologic complexity measures, and cardiovascular activity, assessed by measures such as pre-ejection time, blood pressure, and heart rate dynamics were studied. Given the heterogeneity of the studies, a narrative synthesis of the findings was performed. Results This review study found overall differences in cardiovascular activity between insomniacs and controls in most of the observational studies (21/26), while the expression of cardiovascular regulation varied between the examined insomniac groups. All the studies that investigated the association of cardiac activity and EEG power reported an altered relation between autonomic activity and EEG parameters in insomniacs. Conclusion Autonomic regulation tends to be consistent between insomniacs, as long as they are grouped according to their respective phenotype, as shown in the insomnia subgroup with objectively short sleep duration. Our hypothesis is that these differences in the expression of cardiovascular activity could be explained by the heterogeneity of the disorder. Therefore, the determination of insomnia phenotypes, and the study of cardiovascular measures, rather than heart rate variability alone, will give more insight into the link between insomnia and cardiovascular regulation. This study suggests that cardiovascular activity differs between insomniacs and controls. These new findings are of interest to clinicians and researchers for a more accurate insomnia assessment, and the development of personalized technological solutions in insomnia.
... In addition, It is possible that individuals reporting long sleep durations may actually have reduced objective total sleep time while reporting subjectively increased sleep duration (by reporting time in bed rather than actual time asleep). [10]; [9]; [18]; [15]; [14]; [41]; [42]; [43]; [44]; [45]; [46]; [47]; [48]; [49]; [50]; [51]; [50]; [48]; [52] Exercise [53] HR/Symp no [13]; [12] [54]; [55]; [56] Lormetaze-difference pam [57] Zopiclone [57] Blood Pressure (Increased) ...
... [49] Other studies have found differences in heart rate at sleep onset in insomnia patients compared with controls. [44], [43] Additional studies have shown evidence of elevated cardiac activity in insomnia patients where significant differences in heart rate were not found. For example, in a recent study, Cellini et al [51] found a 9 ...
Chapter
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It is well-known that insomnia is not the same as sleep restriction for a number of reasons including the fact that many insomnia patients underestimate their total sleep time, which may actually be close to normal. However, many patients with insomnia actually do have a chronic reduction in their objective total sleep time. This review will focus on the medical implications of chronic partial sleep restriction in normal individuals and the extent to which these findings are consistent with pathology found in patients with insomnia. Specifically, chronic partial sleep deprivation is associated with movement toward abnormal blood glucose and insulin; movement toward abnormal cardiovascular outcomes including elevated hsCRP; movement towards inflammation based on IL-6; movement toward decreased immunity based on NK-cells and decreased response to influenza vaccination; and movement toward weight imbalance based upon leptin. These data suggest that insomnia patients with reduced total sleep time should be at least at the same level of risk as normal individuals with a few nights of sleep restriction. A number of relevant abnormalities, including increased cortisol, sympathetic activity, blood pressure, and metabolic rate with some evidence of abnormal glycemic control and inflammation have been found in insomnia patients. Such data suggest that treatment for insomnia should involve normalization of objective total sleep time, and that such therapy should also reduce the incidence of the above abnormalities. However, cognitive behavioral treatments for insomnia, for example, are based on the use of sleep restriction as a treatment. Our understanding of the relationship between pathology stemming from chronic partial sleep deprivation and that seen in insomnia with decreased objective total sleep time suggest that sleep restriction as a treatment for insomnia could actually increase risks, as indicated in recent performance data.
... Addressing the issue of attentional bias toward relevant topics, Haynes et al. (1981) observed that engagement with a challenging mental arithmetic problem reduced subjective sleep latency among insomniacs (Haynes et al., 1981). Similarly, practicing crossword puzzles, reading, and listening to audiobooks could provide sufficient distraction so that the patient would no longer attend to or think about their inability to sleep. ...
... Addressing the issue of attentional bias toward relevant topics, Haynes et al. (1981) observed that engagement with a challenging mental arithmetic problem reduced subjective sleep latency among insomniacs (Haynes et al., 1981). Similarly, practicing crossword puzzles, reading, and listening to audiobooks could provide sufficient distraction so that the patient would no longer attend to or think about their inability to sleep. ...
Article
Full-text available
Insomnia is a widespread neuropsychological sleep-related disorder known to result in various predicaments including cognitive impairments, emotional distress, negative thoughts, and perceived sleep insufficiency besides affecting the incidence and aggravation of other medical disorders. Despite the available insomnia-related theoretical cognitive models, clinical studies, and related guidelines, an evidence-based conceptual framework for a personalized approach to insomnia seems to be lacking. This study proposes a conceptual cognitive framework (CCF) providing insight into cognitive mechanisms involved in the predisposition, precipitation, and perpetuation of insomnia and consequent cognitive deficits. The current CCF for insomnia relies on evaluative conditional learning and appraisal which generates negative valence (emotional value) and arousal (cognitive value). Even with the limitations of this study, the suggested methodology is well-defined, reproducible, and accessible can help foster future high-quality clinical databases. During clinical insomnia but not the neutral one, negative mood (trait-anxiety) causes cognitive impairments only if mediating with a distorted perception of insomnia (Ind-1 = 0.161, 95% CI 0.040–0.311). Further real-life testing of the CCF is intended to formulate a meticulous, decision-supporting platform for clinical interventions. Furthermore, the suggested methodology is expected to offer a reliable platform for CCF-development in other cognitive impairments and support the causal clinical data models. It may also improve our knowledge of psychological disturbances and complex comorbidities to help design rehabilitation interventions and comprehensive frameworks in line with the “preventive medicine” policies.
... For example, one study found that although a mathematical task delayed sleep onset in healthy subjects, when presented to insomniacs the same task actually improved sleep onset latency. It was suggested that the experimental manipulation may have created a distraction from usually sleep-laden cognitions (Espie, 2007;Haynes, Adams and Franzen, 1981). ...
... The gratitude exercise could serve as a diversion from these maladaptive coping mechanisms by broadening cognitive activity, and therefore distracting from usual patterns of ruminative thinking. Findings from previous research illustrate a comparable process, whereby an arithmetic task reduced sleep onset latency in a group of poor sleepers as it served to distract them from usually sleep-laden cognitions (Espie, 2007;Haynes, Adams and Franzen, 1981). ...
... An activity recorder (Actigraphy) [41] that records activity during sleep worn on the wrist or ankle 2. Polysomnography ( [42] test, which is a medical examination that measures the physiological changes by measuring EEG [43] , EMG, EEG, ECG, snoring, and respiration, that is used to diagnose a disorder 3. A sleep diary is used to measure the patient's sleep habits, sleep hygiene, and sleep problems for 2 weeks and to evaluate the progress of the treatment. We will measure the following sleep variables: total sleep time, [44,45] sleep onset latency, [36,37,45] wake after sleep onset, and sleep efficiency [46] by using the above tools. b. ...
... There is no restriction. Outcomes -Effect on sleep time (total sleep time, [35] sleep onset latency, [36,37] wake after sleep onset, [38] sleep efficiency) -Effect on quality of sleep (Pittsburgh Sleep Quality, [39] comparisons or control; duration of the intervention and main outcomes; and adverse effects. Two independent researchers will then organize and code the extracted data using Excel 2007 (Microsoft, Redmond, WA) that will then be shared among researchers using Dropbox (Dropbox, Inc., CA) folders. ...
Article
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Introduction: This systematic review protocol describes the methods that will be used to evaluate the efficacy and safety of mindfulness meditation and cognitive behavioral therapy programs as a psychological intervention for insomnia disorders. Methods and analysis: We will search the following 11 electronic databases without language or publication status restrictions: MEDLINE, the Cochrane Central Register of Controlled Trials, EMBASE, Allied and Complementary Medicine Database, Cumulative Index to Nursing and Allied Health Literature, and PsycARTICLES. Furthermore, we will also search 5 Korean-language databases (Oriental Medicine Advanced Searching Integrated System, Korean studies Information Service System, Research Information Service System, Korean Medical Database, and Korea Citation Index). The study selection and data extraction will be performed independently by 2 authors. The study quality assessment and evaluation of the quality of evidence for the main findings will be performed independently by 2 authors using the Cochrane tool for assessing risk of bias and predefined criteria (the Grading of Recommendations Assessment, Development, and Evaluation approach). Data synthesis and analysis will be performed using RevMan Version 5.3. Data will be synthesized by either a fixed effects or random effects model according to a heterogeneity test or the number of studies included in the meta-analysis. If any plan for documenting important protocol amendments changes, the researchers will have a revision agreement and then register the modification in the International Prospective Register of Systematic Reviews (PROSPERO). Ethics and dissemination: Ethical approval will not be required because individual patient data are not included and because this protocol is for a systematic review. The findings of this systematic review will be disseminated through conference presentations.PROSPERO registration number: CRD42018111217.
... According to the account that the cognitive space is limited, the cognitive task will occupy sufficient cognitive space to keep the individual from re-engaging in the personally relevant negative intrusive thought. So, the adoption of a cognitive task can interrupt and suppress the unwanted thought [11,[13][14][15][16]. And then the problem of long sleep onset latency [17] will be solved for the maintenance of suppression for intrusive thought [15]. ...
... So, the adoption of a cognitive task can interrupt and suppress the unwanted thought [11,[13][14][15][16]. And then the problem of long sleep onset latency [17] will be solved for the maintenance of suppression for intrusive thought [15]. ...
Article
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The difficulty of switching off unwanted pre-sleep cognitive activities always causes most people with insomnia unable to fall asleep. Previous studies suggested that manipulating pre-sleep thoughts with cognitive task could change sleep onset latency. The interaction effect of cognitive task and unwanted thoughts is a mixed effect in which each mechanism alone is not completely understood. The present study tries to explore the mixed effect and extract the single effect from it. Seven people with insomnia were investigated and the general cognitive task controlled internally by insomniacs themselves was replaced with an audio task in which the participants have to react distinctively to two different auditory stimuli. The reaction time for which reflected the interaction effect was recorded and then analyzed by the autocorrelation and partial autocorrelation method. A general decline tendency which is called decline effect was observed in the single effect and for most insomniacs the length of the decline effect was around 4 or 5 seconds. In addition, it indicated that such decline effect could be a potential candidate for investing the correlation between cognitive load and interaction effect.
... In weiteren experimentellen Untersuchungen konnte gezeigt werden, dass Insomniker von einer experimentell induzierten Lenkung der Aufmerksamkeit weg vom Schlaf sowohl in ihrer subjektiven als auch in ihrer objektiven Schlafqualität profitierten. Verwendete Manipulationen waren die Imagination einer interessanten und einnehmenden Erinnerung (Harvey & Payne, 2002) sowie das Lösen mittelschwerer arithmetischer Aufgaben (Haynes, Adams & Franzen, 1981). ...
Article
Full-text available
Cognitive behaviour therapy provides a range of interventions to treat nonrestorative sleep, though their effect sizes are smaller than those reported for mood disorders and anxiety disorders. Based on current models explaining the etiology of non-restorative sleep, we introduce possible contributions derived from motivational and volitional theory and discuss possible differential strategies treating sleep disorders to improve treatment outcomes. Suggestions are illustrated using case studies. Patients with good action control may benefit especially from stimulus control whereas for patients with less action control (state-oriented individuals) such techniques may be contraindicated. State-oriented individuals may benefit more from a therapy focused on overcoming characteristic cognitive and affective dysregulation.
... In weiteren experimentellen Untersuchungen konnte gezeigt werden, dass Insomniker von einer experimentell induzierten Lenkung der Aufmerksamkeit weg vom Schlaf sowohl in ihrer subjektiven als auch in ihrer objektiven Schlafqualität profitierten. Verwendete Manipulationen waren die Imagination einer interessanten und einnehmenden Erinnerung (Harvey & Payne, 2002) sowie das Lösen mittelschwerer arithmetischer Aufgaben (Haynes, Adams & Franzen, 1981). ...
Article
Full-text available
Zur Behandlung nicht erholsamen Schlafes bietet die kognitive Verhaltenstherapie eine Reihe von Interventionen an, deren Wirksamkeit jedoch geringer ist als die für affektive Störungen und Angststörungen. Auf der Grundlage bestehender aktueller Ätiologiemodelle wird der mögliche Beitrag motivations- und volitionspsychologischer Ansätze zur Verbesserung der Wirksamkeit der Behandlung von Schlafstörungen diskutiert. Hieraus werden differentielle Behandlungsstrategien abgeleitet und durch Fallbeispiele illustriert. Während Betroffene mit guten Selbststeuerungskompetenzen (Handlungsorientierte) insbesondere von Methoden der Stimuluskontrolle profitieren sollten, könnten für Menschen mit weniger guten Selbststeuerungskompetenzen (Lageorientierte) Methoden der Stimuluskontrolle kontraindiziert sein. Sie könnten eher von einer Überwindung charakteristischer kognitiver und affektiver Dysregulation profitieren. Cognitive behavior therapy provides a range of interventions to treat non-restorative sleep, though their effect sizes are smaller than those reported for mood disorders and anxiety disorders. Based on current models explaining the etiology of non-restorative sleep, we introduce possible contributions derived from motivational and volitional theory and discuss possible differential strategies treating sleep disorders to improve treatment outcomes. Suggestions are illustrated with case studies. Patients with good action control may benefit especially from stimulus control whereas for patients with less action control (state-oriented individuals) such techniques may be contraindicated. State-oriented individuals may benefit more from a therapy focused on overcoming characteristic cognitive and affective dysregulation.
... Four studies demonstrated significantly elevated heart rate in insomniacs or poor sleepers compared with normal sleepers during the pre-sleep period or in response to stress. 91,181,283,284 Other investigations revealed no significant difference in heart rate. 183,263 Core temperature was significantly increased during sleep in three studies, 176,183,263 while others failed to demonstrate significant elevation in insomniacs. ...
... The assumption was that the threat created more worry in the insomniacs, and that this increased physiological arousal and delayed sleep onset. The one study of pre-sleep stress that gives slightly contradictory results is that of Haynes, Adams and Franzen (1981) who found that a pre-sleep mental arithmetic task let to decreases in sleep-onset latency in insomniacs. However, in this study, the experimental conditions were confounded with order effects. ...
Working Paper
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A cognitive model of sleep onset was developed in 1994/5 by Watts and Barnard, using the Interacting Cognitive Subsystems framework (ICS). The model was presented by Barnard at the Annual Conference of the British Psychological Society in 1996. This working paper describes that model in detail. In a context where there has been a growing acknowledgement of the complexity of the onset process, ICS is well-suited to capturing the far-reaching cognitive changes that take place, and to integrate experiential and tacit aspects of cognition. During the process of sleep onset, it is argued that the overall pattern of mental processing activity alters from one in which the underlying information processing mechanism is configured for action in the world, to a state in which processes are configured for rest and the maintenance of low-level vigilance to significant changes in sensation and proprioception. Whilst there may be many different specific routes to the latter state, the core theory of sleep onset holds that there are three cognitive way points shared by all routes to deep sleep. Systematic passage through these way points is perturbed in insomnia. Such perturbations are related both to patterns of recurrent mentation and to an association of that mentation with affect. Implications are discussed for the classification of insomnia, and for the formulation of cognitive processes involved in the treatment of insomnia.
... In the current study, the strongest clinical factor associated with pre-sleep cognitive arousal was sleep reactivity, followed by insomnia severity and arousability, which is consistent with previous studies and conceptual models of the diathesis and pathophysiology of insomnia (Fernández-Mendoza et al., 2010;Jarrin, Chen, Ivers, & Morin, 2014;LeBlanc et al., 2009;. Traits such as sleep reactivity and arousability are believed to identify individual differences predisposing individuals to the development of chronic insomnia (Coren, 1990;Fernández-Mendoza et al., 2010;LeBlanc et al., 2009), while pre-sleep cognitive arousal has been consistently identified as one of the most significant perpetuating factors of chronic insomnia (Gross & Borkovec, 1982;Harvey, 2002;Hauri, 1969;Haynes, Adams, & Franzen, 1981;Lichstein & Rosenthal, 1980;Wicklow & Espie, 2000). This study reinforces the concept that trait vulnerability (sleep reactivity) and cognitive arousal do jointly contribute to insomnia even once it has become a chronic disorder. ...
Conference Paper
Introduction Traits related to a weakened sleep system (i.e., sleep reactivity) and hyperreactive arousal system (i.e., arousability) are considered key predisposing factors for insomnia. However, it is still difficult to predict who will develop clinical insomnia and who amongst those presenting with insomnia express specific traits that may require specific treatment needs. Methods Participants included 500 adults (41.8% female, 39.1 ± 15.9 years old) who completed the Arousal Predisposition Scale (APS, arousability), Ford Insomnia Response to Stress Test (FIRST, sleep reactivity), Insomnia Severity Index (ISI), Profile of Mood States (POMS-A, anxiety; POMS-D, depression), and NEO personality inventory (NEO-N, neuroticism; NEO-E, extraversion). Structural equation modelling was used to conduct confirmatory factor analysis (CFA) of the APS and mediation analyses. Receiver operating characteristic analysis was used to determine the predictive value for identifying insomnia risk. Results CFA identified two APS dimensions of emotional reactivity (APS-ER) and trait anxiety (APS-TA) with adequate goodness-of-fit (TLI=0.95, CFI=0.96, RMSEA=0.05). APS-ER was independently associated with FIRST (β=0.45; p<0.001), while APS-TA (β=-0.02; p=0.587) and NEO-N (β=0.08; p=0.06) were not. FIRST partially mediated the relationship between APS-ER with ISI (95%CI=0.12–0.25, p<0.001).An APS score 32 points or higher (84% sensitivity, 65% specificity) identified individuals with high sleep reactivity with an area under the curve (AUC) of 0.79 (95% CI 0.74–0.83). APS-ER performed significantly better (AUC 0.81 [95% CI 0.77–0.85]) than did APS-TA (AUC 0.65 [95% CI 0.59–0.70]; p<0.05). Conclusion Emotional reactivity was strongly associated with sleep reactivity. In fact, sleep reactivity partially explained the association of emotional reactivity with insomnia severity. Trait anxiety appears to be a predisposing factor for the comorbidity of insomnia with anxiety disorders, rather than a specific diathesis for insomnia. The APS and FIRST can help clinicians identify which patients carry insomnia-specific predisposing traits, which may require targeted behavioral sleep medicine treatments. Support (If Any):
... 21,22 Some studies have shown increased sleeping heart rate in insomniacs. 23,24 Insomniacs have higher ACTH and cortisol secretion, 25 metabolic rate, 26 and global cerebral glucose metabolism during sleep and awake 27 compared with normal controls. Several factors in COPD may alter the sympathovagal balance with a resultant increase in sympathetic activity. ...
Article
Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality and may frequently be complicated by sleep disorders. Insomnia and obstructive sleep apnea are commonly encountered in patients with COPD. Nocturnal hypoxemia is also prevalent in COPD may occur despite adequate awake oxygenation and can be especially severe in rapid eye movement sleep. Additionally, several factors-some of them unique to COPD-can contribute to sleep-related hypoventilation. Recognition of hypoventilation can be vital as supplemental oxygen therapy itself can acutely worsen hypoventilation and lead to disastrous consequences. Finally, accruing data establish an association between restless leg syndrome and COPD-an association that may be driven by hypoxemia and/ or hypercapnia. Comorbid sleep disorders portend worse sleep quality, diminished quality of life, and multifarious other adverse consequences. The awareness and knowledge regarding sleep comorbidities in COPD has continued to evolve over past many years. There are still several lacunae, however, in our understanding of the etiologies, impact, and therapies of sleep disorders, specifically in patients with COPD. This review summarizes the latest concepts in prevalence, pathogenesis, diagnosis, and management of diverse sleep disorders in COPD. © 2015 American Academy of Sleep Medicine.
... Symptoms of cognitive arousal include sustaining thoughts, worry and a "racing/ overactive mind" before going to bed (Smith, Perlis, Carmody, Smith, & Giles, 2001). Previous studies have consistently associated cognitive hyperarousal with both subjectively and objectively measured sleeponset latency (SOL), and it has been identified as one of the most significant perpetuating factors of chronic insomnia (Gross & Borkovec, 1982;Harvey, 2002;Hauri, 1969;Haynes, Adams, & Franzen, 1981;Lichstein & Rosenthal, 1980;Wicklow & Espie, 2000). ...
Article
Self‐reported somatic arousal remains a challenging clinical construct, particularly because only a subset of patients report symptoms such as racing heart, palpitations or increased body temperature interfering with their sleep. It is unclear whether self‐reported somatic arousal is a marker of hyperarousal or co‐morbid clinical anxiety in individuals with insomnia. Participants included 196 young adults aged 20.2 ± 1.0 years old who were predominantly females (75%). About 39% of the sample reported subthreshold insomnia, and about 8% reported clinically significant insomnia, based on their Insomnia Severity Index. Participants completed the Pre‐Sleep Arousal Scale, Beck Anxiety Inventory, Beck Depression Inventory, Arousal Predisposition Scale, and Ford Insomnia Response to Stress Test. Multivariable stepwise regression assessed which factors were independently associated with pre‐sleep cognitive (Pre‐Sleep Arousal Scale‐Cognitive) and somatic (Pre‐Sleep Arousal Scale‐Somatic) arousal. Receiver‐operating characteristic analysis assessed the predictive value to identify clinically significant anxiety (Beck Anxiety Inventory ≥ 20), insomnia (Insomnia Severity Index ≥ 15) and arousability (Arousal Predisposition Scale ≥ 32). Beck Anxiety Inventory (β = 0.42) was the best single correlate of Pre‐Sleep Arousal Scale‐Somatic, while Insomnia Severity Index (β = 0.33) was of Pre‐Sleep Arousal Scale‐Cognitive. A Pre‐Sleep Arousal Scale‐Somatic score of 12 or more identified those with clinically significant anxiety with 65% specificity and 65% sensitivity, while a cut‐off score of 14 increased its sensitivity (86%). Self‐reported pre‐sleep somatic arousal may be an index of co‐morbid clinical anxiety in individuals with insomnia. These findings aid clinicians with assessment and treatment, particularly in the absence of clinical guidelines indicating when somatically focused relaxation techniques should be included as part of multicomponent cognitive behavioural treatment of insomnia.
... Two previous studies have looked at stress during cognitive performance in insomnia patients compared to controls, and both have reported significantly increased heart rate in the insomnia patients. 1,3 However, in one study, 3 the control subjects had an increase in heart rate on the second study night and also had increased sleep latency (not found in the insomnia patients compared to their previous nights). Such data imply that the stress of the constant routine situation might have had more impact on the control subjects than on the insomnia subjects and could also have accounted for their higher than expected mean heart rate. ...
... Arousal can also influence the duration of sleep. For instance, heightened arousal associated with states of anxiety has been show to increase sleep onset latency and decrease reports of restful sleep (Haynes et al., 1981;Tang and Harvey, 2004). The phase of circadian rhythms during sleep bouts also modulates sleep propensity and thus influences sleep duration (Dijk and Czeisler, 1994;Dijk and Franken, 2005). ...
... In the current study, the strongest clinical factor associated with pre-sleep cognitive arousal was sleep reactivity, followed by insomnia severity and arousability, which is consistent with previous studies and conceptual models of the diathesis and pathophysiology of insomnia (Fernández-Mendoza et al., 2010;Jarrin, Chen, Ivers, & Morin, 2014;LeBlanc et al., 2009;. Traits such as sleep reactivity and arousability are believed to identify individual differences predisposing individuals to the development of chronic insomnia (Coren, 1990;Fernández-Mendoza et al., 2010;LeBlanc et al., 2009), while pre-sleep cognitive arousal has been consistently identified as one of the most significant perpetuating factors of chronic insomnia (Gross & Borkovec, 1982;Harvey, 2002;Hauri, 1969;Haynes, Adams, & Franzen, 1981;Lichstein & Rosenthal, 1980;Wicklow & Espie, 2000). This study reinforces the concept that trait vulnerability (sleep reactivity) and cognitive arousal do jointly contribute to insomnia even once it has become a chronic disorder. ...
Article
Background: In contrast to pre-sleep cognitive arousal, self-reported pre-sleep somatic arousal is a rather elusive construct for which little validity has been provided. Thus, the clinical significance of somatic symptoms during the pre-sleep period remains unknown. Participants: 248 patients (45.0 ± 16.7 years old, 65.3% female) with a diagnosis of chronic insomnia disorder, out of 388 consecutive patients evaluated at the Behavioral Sleep Medicine (BSM) program of Penn State Hershey Sleep Research & Treatment Center. Methods: Participants completed the Pre-sleep Arousal Scale assessing cognitive (PSAS-C) and somatic (PSAS-S) arousal as well as the Insomnia Severity Index (ISI), Ford Insomnia Response to Stress Test (FIRST), Arousal Predisposition Scale (APS), and Depression Anxiety Stress Scale (DASS). Multivariable stepwise regression assessed which clinical factors were independently associated with greater PSAS-C and PSAS-S scores. Receiver operating characteristic analysis determined the predictive value for identifying sleep reactivity (FIRST≥18) and clinical anxiety (DASS-A ≥ 10) and clinically useful cutoff scores. Results: The strongest correlates of PSAS-S were DASS-A (β = 0.64) and chronic pain (β = 0.11), while those of PSAS-C were FIRST (β = 0.29) and a history of stroke (β = 0.10). A PSAS-S score of 14.8 (AUC = 0.87, 95%CI = 0.83–0.91) and a PSAS-C score of 24.5 (AUC = 0.82, 95%CI = 0.76–0.88) showed the best balance in specificity and sensitivity to identify clinical anxiety and sleep reactivity, respectively. Conclusions: Self-reported pre-sleep somatic symptoms are a marker of comorbid anxiety and, potentially chronic pain, impacting nighttime sleep. The optimal cutoff scores of 14 and 20 proposed herein can help clinicians with case formulation, with tailoring BSM treatments and their targets.
... Individuals with high metabolic rates may suffer higher oxidative damage under increased reactive oxidative species production during activity (Larcombe, Coffey, Bann, Alexander, & Arnold, 2010;Urso & Clarkson, 2003) suggesting that 'fast' individuals may experience higher baseline levels of stress than 'slow' individuals. Both activity (Driver, Meintjes, Rogers, & Shapiro, 1988;Driver & Taylor, 2000;Horne & Staff, 1983) and stress (Haynes, Adams, & Franzen, 1981;Sadeh, Keinan, & Daon, 2004;Waters, Adams, Binks, & Varnado, 1993) are known to play roles in shaping subsequent sleep patterns, and indeed, one putative function of sleep is cellular repair of damage caused by metabolic stress (Savage & West, 2007;Xie et al., 2013). However, most sleep behaviours in great tits had only low repeatability. ...
Article
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Ecologists have recently begun to recognize sleep as a behaviour that is important in animal ecology. The first steps have been taken to characterize sleep in free-living birds, but it is unclear to what extent these results can be generalized between species. To describe sleep behaviour in the wild, we videorecorded great tits, Parus major, in their roosting boxes during two consecutive winters and individuals in captivity for comparison. Here, we examined endogenous and exogenous correlates of sleep behaviour in free-living great tits and addressed the potential confounding issues of studying avian sleep in captivity. Like that in blue tits, Cyanistes caeruleus, sleep behaviour in great tits was strongly related to season, and was affected by sex, age and the environment. Although literature suggests relationships between sleep and risk-taking behaviours, possibly arising from stable differences in physiological state, sleep behaviour appeared to be plastic in great tits, and was not predicted by between-individual variation in exploratory tendencies. Captive tits initiated sleep later than wild individuals, even under natural photoperiodic conditions, suggesting that captivity alters timing and duration of sleep in great tits. Long-term repeatability in sleep behaviour was low for all variables, except morning latency (high repeatability) and evening box entry time, evening latency and frequency of awakenings (no detectable repeatability). Variation in sleep behaviour may largely represent within-individual differences in daily sleep requirements. Our study describes how different observable components of sleep are intercorrelated by providing evidence for significant within-individual correlations between sleep behaviours, which represent the integration of plasticity between traits. Consistent with low repeatability, low between-individual correlations suggest substantial behavioural plasticity in sleep, rather than a correlational structure leading to clear sleep 'syndromes'. Our study provides quantitative evidence for the factors producing phenotypic plasticity in behavioural sleep in an ecological context.
... 23 Objective and subjective sleep latency measures have been related to decreases in cortisol response to stress, sleep-wake problems, increased sleep latencies and increased daytime sleepiness. [24][25] In the current study, we conceptualize TBI as an acute stressor on the biology of the human body via a physical trauma to the brain. Additionally, we utilize the terms "subjective stress" to characterize self-reported psychological status, post-injury, and "cortisol actigraphy" as objective (i.e., biological) measures of stress and sleep. ...
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This study sought to address the complex interplay between both biological and psychological perceptions of stress and sleep in the acute stages following a mild traumatic brain injury. A secondary goal was to identify potential targets for intervention. Eleven acutely injured youth (mean age 12 years) were studied at home with overnight actigraphy, salivary cortisol and melatonin assays, and subjective ratings of stress and fatigue (injured group). Nine matched control youth also were assessed (control group). Results suggested longer sleep latencies (time to fall asleep) and higher levels of fatigue in the injured group exist (p = 0.025 and p = 0.004, respectively). In the injured group, stress and sleep onset were significantly related with most subjects meeting criteria for Acute Stress Disorder. Melatonin levels were lower at bedtime in the injured group. Saliva samples were collected via passive drool at three time points: ∼1 hour before bed (“bedtime” or T1), immediately upon waking (time 2: T2), and 30 minutes post-waking (time 3: T3). Overnight increases in cortisol (T1 to T2) were greater for the injured group; however, post-sleep changes in cortisol (T2 to T3) were reversed with control concentrations increasing. These findings are unique in using actigraphy and salivary hormone levels in an acutely injured youth while in their homes. The differences in sleep latency and the presence of injury-related stress point to potential treatment targets in acute concussion.
... Stress is also associated with sleep disturbance, shorter sleep duration, nighttime awakening, and insomnia [152,153]. Changes in daily schedules due to confinement may also contribute to poor sleep quality due to disruptions in circadian rhythms which may already be disrupted in older adults [154]. Indeed, recent data from individuals quarantined during the COVID-19 outbreak in China reported anxiety correlated with stress resulting in reduced sleep quality [155], while an Italian study [156] reported lower sleep quality despite participants spending more time in bed. ...
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The COVID-19 pandemic is an extraordinary global emergency that has led to the implementation of unprecedented measures in order to stem the spread of the infection. Internationally, governments are enforcing measures such as travel bans, quarantine, isolation, and social distancing leading to an extended period of time at home. This has resulted in reductions in physical activity and changes in dietary intakes that have the potential to accelerate sarcopenia, a deterioration of muscle mass and function (more likely in older populations), as well as increases in body fat. These changes in body composition are associated with a number of chronic, lifestyle diseases including cardiovascular disease (CVD), diabetes, osteoporosis, frailty, cognitive decline, and depression. Furthermore, CVD, diabetes, and elevated body fat are associated with greater risk of COVID-19 infection and more severe symptomology, underscoring the importance of avoiding the development of such morbidities. Here we review mechanisms of sarcopenia and their relation to the current data on the effects of COVID-19 confinement on physical activity, dietary habits, sleep, and stress as well as extended bed rest due to COVID-19 hospitalization. The potential of these factors to lead to an increased likelihood of muscle loss and chronic disease will be discussed. By offering a number of home-based strategies including resistance exercise, higher protein intakes and supplementation, we can potentially guide public health authorities to avoid a lifestyle disease and rehabilitation crisis post-COVID-19. Such strategies may also serve as useful preventative measures for reducing the likelihood of sarcopenia in general and in the event of future periods of isolation.
... (4) Total sleep time (TST) [24] : insufficient sleep if total sleep time was lower than. [25] (5) Sleep onset latency (SOL) [26,27] : insufficient sleep when the elevation delay time was more than 30 minutes. (6) Wake-up Sleep On Time (WASO) [28] : If the awakening time was >30 minutes after the elevation, the sleep is considered insufficient. ...
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Background: This systematic review investigated the clinical effects of inhalation aromatherapy for the treatment of sleep problems such as insomnia. Methods: Studies on sleep problems and inhalation aromatherapy, published in Korean and international journals, were included in the meta-analysis. Five domestic and international databases, respectively each, were used for the literature search. Keywords included sleep disorder, sleep problems, insomnia, and aroma inhalation, and the related literature was further searched. After the screening, selected articles were assessed for their quality and conducted the risk of bias using RevMan 5.0, a systematic literature review was then conducted. A meta-analysis comparing the averages was conducted on studies that reported numerical values. Additionally, meta-analysis of variance and meta-regression analyses were performed. Results: Meta-analysis of the 34 studies using the random-effects model revealed that the use of aromatherapy was highly effective in improving sleep problems such as insomnia, including quantitative and qualitative sleep effects (95% confidence interval [CI], effect sizes = 0.6491). Subgroup analysis revealed that the secondary outcomes including stress, depression, anxiety, and fatigue were significantly effective. The single aroma inhalation method was more effective than the mixed aroma inhalation method. Among the single inhalation methods, the lavender inhalation effect was the greatest. Conclusion: Inhalation aromatherapy is effective in improving sleep problems such as insomnia. Therefore, it is essential to develop specific guidelines for the efficient inhalation of aromatherapy. Ethics and dissemination: Ethical approval is not required because individual patient data are not included. The findings of this systematic review were disseminated through peer-reviewed publications or conference presentations. Prospero registration number: CRD42020142120.
... 40 A recent study using the Multiple Sleep Latency Test (MSLT) as a measure of physiologic hyperarousal has shown that patients with insomnia who had an MSLT score higher than 14 minutes and those who had an MSLT score higher than 17 minutes had 3.3-fold and 4.3-fold odds, respectively, of high blood pressure, whereas insomnia with a MSLT of 8 to 14 minutes was not significantly associated with high blood pressure (OR = 1.17). 41 Several studies have shown an elevated resting HR or blunted HRV in patients with insomnia (Table 84-3), 40,[42][43][44][45][46][47][48] with the latter suggesting a shift of the sympathovagal balance toward a predominance of sympathetic modulation during both wake and nighttime. 10 However, these findings have been inconsistent. ...
Chapter
This chapter is focused on insomnia and three specific health outcomes: cardiovascular disease and diabetes (hereafter referred to as cardiometabolic disease) and all-cause mortality. Epidemiologic and experimental studies support an association of insomnia with clinical (e.g., hypertension) and subclinical (e.g., heart rate variability [HRV]) cardiovascular risk factors as well as cardiovascular disease per se. Emerging data suggest that the association of insomnia with cardiovascular morbidity is more pronounced when insomnia is associated with objectively measured short sleep duration or other measures of physiologic arousal, including elevated heart rate, blunted HRV, and longer latencies in MSLT. Available evidence—especially epidemiologic research—has linked insomnia to poor metabolic function, ranging from overt metabolic disease (i.e., type 2 diabetes) to subclinical manifestations (e.g., metabolic syndrome, insulin resistance) that are risk factors for future diabetes. These studies also suggest that the metabolic risk is greatest among individuals with insomnia and short sleep duration. However, clinical studies involving small samples of adults diagnosed with chronic insomnia have largely failed to corroborate the epidemiologic findings, and studies that have experimentally induced poor sleep quality may generalize to other sleep disorders (e.g., sleep-disordered breathing) as well as insomnia. The association between insomnia and mortality is rather modest based on studies that have used insomnia symptoms not associated with any severity or chronicity criteria. Furthermore, in these studies, the lack of objective polysomnographic measures raises the question of whether this association is confounded by the presence of other sleep pathology, such as sleep apnea. More recent studies that have used more stringent criteria and polysomnographic measures suggest that mortality in insomnia is marked and significant, particularly in men and in those with short sleep duration. Candidate pathways through which insomnia adversely affects health include changes in physiology (e.g., increased inflammation, endocrine dysregulation, autonomic imbalance) and poor health behaviors (e.g., physical inactivity and caffeine, alcohol, and nicotine use) observed in association with chronic insomnia. More research is needed to determine whether interventions that reduce symptoms of insomnia are associated with concomitant improvements in physiology (e.g., decreased inflammation, normalization of cortisol and adrenocorticotropic hormone, increased heart failure or HRV) or health behaviors (e.g., increased physical activity, improved diet, decreased alcohol, nicotine, and caffeine use). Also unclear is whether any improvements in physiology and health behaviors associated with improvements in insomnia would attenuate the long-term risk associated with chronic insomnia disorder.
... Predisposing factors are present before insomnia is manifested, and it is hypothesized that they interact with precipitating factors, i.e. stressful life events over time, to increase the risk of insomnia. Mounting evidence confirms that higher levels of stress are indeed associated with more disrupted sleep [116][117][118][119][120][121][122], both of which are associated with immune and neuroendocrine dysregulation and increased morbidity [22,123,124]. Within this context, sleep disorders during pregnancy may be considered a stress response to an increased level of stress in pregnancy (Fig. 2). ...
... Insomnia disorder is the most common sleep disorder (Basiri et al., 2017), characterized by difficulties in initiating and maintaining sleep, despite ample opportunity to sleep (Renom-Guiteras et al., 2014). One of the most prominent models playing a key role in explaining the pathophysiology of insomnia is the hyperarousal model (Riemann and Perlis, 2009), which has been characterized by significantly higher sympathetic and lower parasympathetic activity during sleep (Varkevisser, Van Dongen, & Kerkhof, 2005), decreased heart rate variability (Spiegelhalder et al, 2011;Bonnet & Arand, 1995;Haynes et al., 1981;Stepanski et al., 1994), increases in body temperature (Chiu et al., 2000), and increases in the basal metabolic rate (Bonnet & Arand, 1995). ...
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Insomnia is a common disease that negatively affects patients both mentally and physically. While insomnia disorder is mainly characterized by hyperarousal, a few studies that have directly intervened with cortical arousal. This study was conducted to investigate the effect of a neurofeedback protocol for reducing cortical arousal on insomnia compared to cognitive-behavioral treatment for insomnia (CBT-I). Seventeen adults with insomnia, free of other psychiatric illnesses, were randomly assigned to neurofeedback or CBT-I. All participants completed questionnaires on insomnia [Insomnia Severity Index (ISI)], sleep quality [Pittsburgh Sleep Quality Index (PSQI)], and dysfunctional cognition [Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS-16)]. The neurofeedback group showed decreases in beta waves and increases in theta and alpha waves in various areas of the electroencephalogram (EEG), indicating lowered cortical arousal. The ISI and PSQI scores were significantly decreased, and sleep efficiency and sleep satisfaction were increased compared to the pre-treatment scores in both groups. DBAS scores decreased only in the CBT-I group (NF p = 0.173; CBT-I p = 0.012). This study confirmed that neurofeedback training could alleviate the symptoms of insomnia by reducing cortical hyperarousal in patients, despite the limited effect in reducing cognitive dysfunction compared to CBT-I.
... 41,42 Experimental studies have also confirmed that pre-sleep stress can increase physiological arousal at bedtime for insomniac and non-insomniac subjects. 43 If a person experiences stress without coping with it appropriately, internal conflicts can worsen and he or she can repeatedly ruminate on past situations. Such series of psychological reactions are likely to result in insomnia by increasing arousal. ...
Article
Objective: Among various causes of insomnia, stress is the most common and representative cause. Insomnia is also known to negatively affect the quality of life (QoL). The objective of this study was to explore the effect of stress on QoL and the mediating role of insomnia symptoms in the relationship between stress and QoL. Methods: In this study, the mediating effect of insomnia symptoms on the relationship between stress and QoL was analyzed by enrolling 3,714 participants from the Ansung and Ansan cohorts of the Korea Association Resource project from 2001 to 2004. These cohort participants were asked about how much they felt stressed during their everyday life. Insomnia symptoms were evaluated by asking participants whether they had trouble sleeping such as difficulty in falling asleep, disrupted sleep, and early morning awakening due to the lack of a validated questionnaire for this cohort. QoL was evaluated using the World Health Organization QoL Scale Brief Version. Results: In total, stress was positively associated with insomnia symptoms, which in turn predicted QoL. The same result could be derived from subgroup analysis according to sex, and it was confirmed that insomnia symptoms acted as a mediating factor more significantly in female than in male. Conclusion: In this study, insomnia symptoms were confirmed to act as a significant mediating factor between stress and QoL, suggesting that insomnia symptoms should be actively identified and controlled to alleviate the negative effect of stress on QoL in clinical practice.
... Dodds et al. [12] studied recent literature on heart rate with insomnia and discovered that several studies reported significant differences between the participants with insomnia and good sleepers, especially for the middle and elderage groups. Haynes et al. [13] studied 10 sleep-onset young insomniacs and 11 non-insomniacs who have been identified as good sleepers and observed that the insomniac subjects demonstrated a significantly higher mean heart-rate response than non-insomniacs during the period of before and after the lights off. The increase in the heart rate during sleep was also reported by Bonnet and Arand [14] in a study of 12 young adults with insomnia compared with 12 controls. ...
Article
Insomnia, whether situational or chronic, affects over a third of the general population in today's society. However, given the lack of non-contact and non-inductive quantitative evaluation approaches, most insomniacs are often unrecognized and untreated. Although Polysomnography (PSG) is considered as one of the assessment methods, it is poorly tolerated and expensive. In this paper, with the recent development of Internet-of-Things devices and edge computing techniques, we propose a detrended fractal dimension (DFD) feature for the analysis of heart-rate signals, which can be easily acquired by many wearables, of good sleepers and insomniacs. This feature was derived by calculating the fractal dimension (FD) of detrended signals. For the trend component removal, we improved the null space pursuit algorithm and proposed an adaptive trend extraction algorithm. The experimental results demonstrated the efficacy of the proposed DFD index through numerical statistics and significance testing for healthy and insomnia groups, which renders it a potential biomarker for insomnia assessment and management.
... Stress also interacts with sleep (Åkerstedt et al., 1994;Kim & Dimsdale, 2007); stress is associated with insomnia, greater symptoms of sleep disturbance, and shorter sleep duration, and precipitates frequent episodes of nighttime awakening, both in healthy adults and in those with HF (Hall et al., 2015;Haynes et al., 1981;Mezick et al., 2009;Redeker et al., 2019;Zoccola et al., 2009). More specifically, in one study, individuals with high perceived stress exhibited worse nighttime sleep and daytime problems (i.e., shorter sleep duration, worse sleep quality, a greater likelihood of sleep apnea, sleepiness, and fatigue) and an increased cardiovascular risk profile (i.e., higher body mass index and inflammation) compared to those with low stress, outlining a potential mechanistic pathway from perceived stress to cardiovascular disease (Kashani et al., 2012). ...
Article
Objective/Background: Sleep disturbance is prevalent among patients with heart failure (HF) and is associated with increased morbidity and mortality. Stress also affects health and quality of life among patients with cardiovascular disease and likely plays a prominent role in HF. However, little is known about the associations between stress and sleep among HF patients. Participants: One hundred fifty-three stable New York Heart Association (NYHA) Classification I–IV HF patients with at least low symptoms of insomnia (Mage:63.0 ± 12.8, 42% Women). Methods: We examined baseline stress, sleep disturbance, and sleep-related characteristics from a randomized controlled trial of cognitive behavioral therapy for insomnia, including the Perceived Stress Scale, Insomnia Severity Index, Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, Sleep Disturbance Questionnaire, Dysfunctional Beliefs about Sleep Scale, PROMIS Cognitive Ability, SF-36 Mental Health, and wrist actigraphy. We used Pearson correlations and general linear models to assess stress-sleep associations, including the potential moderating effects of sex and symptom severity (NYHA). Results: There were moderate-to-large correlations between stress and self-reported sleep disturbance, dysfunctional beliefs about sleep, cognitive ability, and mental health (p’s < 0.01). High stress was associated with more objectively-measured (i.e., actigraph-assessed) awakenings and sleep fragmentation among women than men (β = − 0.04, p < 0.01; β = − 0.71, p = 0.04). Relationships between stress and objectively-measured sleep did not vary by symptom severity. Conclusions: Perceived stress is related to sleep disturbance among HF patients, and effects may be sex-dependent. Subsequent research should determine the temporal links between sleep and stress, and optimal opportunities for intervention among HF patients.
Article
Good sleepers and patients with insomnia symptoms (poor sleepers) were tracked with two measures of arousal; conventional polysomnography (PSG) for electroencephalogram (EEG) assessed cortical arousals, and a peripheral arterial tonometry device was used for the detection of peripheral nervous system (PNS) arousals associated with vasoconstrictions. The relationship between central (cortical) and peripheral (autonomic) arousals was examined by evaluating their close temporal dynamics. Cortical arousals almost invariably were preceded and followed by peripheral activations, while large peripheral autonomic arousals were followed by cortical arousals only half of the time. The temporal contiguity of these two types of arousals was altered in poor sleepers, and poor sleepers displayed a higher number of cortical and peripheral arousals compared with good sleepers. Given the difference in the number of peripheral autonomic arousals between good and poor sleepers, an evaluation of such arousals could become a means of physiologically distinguishing poor sleepers.
Article
Animal and human studies have shown that disorders of the autonomic nervous system may influence sleep physiology. Conversely, sleep disorders may be associated with autonomic dysfunctions. The current review describes the clinical presentation, supposed pathogenetic mechanisms and the diagnostic and prognostic implications of impaired cardiovascular autonomic control in sleep disorders. This dysfunction may result from a common pathogenetic mechanism affecting both autonomic cardiovascular control and sleep, as in fatal familial insomnia, or it may be mainly caused by the sleep disorder, as observed in obstructive sleep apnoea. For other sleep disorders, like primary insomnia, restless legs syndrome, narcolepsy type 1 and rapid eye movement sleep behaviour disorder, the causal link with the autonomic dysfunction and its possible impact on health remains unsettled. Given its clinical implications, most of the data available suggest that a systematic assessment of the association between sleep disorders and impaired autonomic control of the cardiovascular system is warranted. Understanding the mechanism of this association may also yield insights into the interaction between the autonomic nervous system and sleep. Copyright © 2015 Elsevier Ltd. All rights reserved.
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The purpose of this research was to examine the relationship between rumination, worry, pre-sleep arousal, and sleep quality. The participants were 202 young adults who completed questionnaires on sleep quality, trait rumination, and worry. After factor analysis of rumination and worry scales, three factors were found and which were positively correlated with pre-sleep cognitive arousal and sleep quality. The results of structural equation model analysis suggested that pre-sleep arousal is a mediator of the effects of repetitive thought on sleep quality. Dwelling on the negative and worry engagement can predict higher pre-sleep arousal which can predict poor sleep quality. Pre-sleep arousal is the key factor in the relationship between repetitive thought and sleep quality.
Chapter
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Insomnia, nightmares, or nocturnal panic attacks are prominent features of sleep disturbance that spans across many anxiery disorders. In a meta-analysis of 177 studies, Benca and colleagues (1992) reported that individuals with an anxiery disorder take longer ro get to sleep at the beginning of the night, experience more awakenings during rhe night, obtain less sleep overall, and exhibit poorer sleep efficienry, relative to nonpatients. More recently, a review of dre literature by Papadimitriou and Linkowski 2005) suggesrs rhat the major findings reported bv Benca et al. have held over the ensuing decade. \,foreover, Papadimitriou and Linkowski (2005) tbund an especially strong association beween sleep disturbance and several anxiety disorders, including panic disorder, generalized anxiery disorder (GAD), obsessive-compulsive disorder, and posttraumatic stress disorder (PTSD). Afthough-ort of the evidence to date is based on samples of aduhs in their rriddle years, there is also evidence ofan association)erween sleep disturbance and anxiety disorders in ;hildren and adolescence (Forbes et al., 2006), as well as among older adults (Spira, Friedman, Flint, & Sheikh,2005). The first aim of this chapter is to highlight the potential importance of sleep problems in individuals with anxiery disorders. W'e argue that disturbed sleep not only impairs the qualiry of a patientt life but may also contribute to rhe maintenance of the anxiety disorder. Our second aim is to review the evidence base for rrearing parienrs who sufFer from comorbid sleep disturbance and anxiery disorder. As will become evident throughout the chapter, there is a dearth of evidence that specifically delineates the relationship berween sleep disturbance and anxiery disorder and thus several ofour proposals are based on evidence from healthy nonpatients or patienrs with other clinical disorders. 'We raise this caveat at
Chapter
Over the last few years, articles in both the medical literature and popular press stressing the negative consequences of using hypnotic medication may have made physicians unjustifiably hesitant to prescribe these drugs (Kales & Kales, 1984). Frequently, such articles contend that sleeping pills are prescribed too often. However, these concerns may be exaggerated, as illustrated by the following data.
Article
Study objectives: Obstructive sleep apnea (OSA) and posttraumatic stress disorder (PTSD) are common in United States veterans. These conditions often coexist and symptoms overlap. Previous studies reported improvement in PTSD symptoms with continuous positive airway pressure (CPAP) therapy for comorbid OSA but its effect has not been assessed in a non-PTSD cohort. We have prospectively assessed the effect of CPAP therapy on clinical symptom improvement as a function of CPAP compliance levels among PTSD and non-PTSD veterans. Methods: Veterans in whom OSA was newly diagnosed were enrolled in our study (n = 192). Assignment to PTSD and non-PTSD cohorts was determined by chart review. Each patient completed the military version of the PTSD Checklist (PCL), Epworth Sleepiness Scale (ESS), and reported nightmare frequency (NMF) at baseline and 6 months after CPAP therapy. CPAP adherence was objectively documented from machine compliance data. Results: We had complete data for 177 veterans (PTSD n = 59, non-PTSD n = 118) for analysis. The mean ages were 51.24 years in the PTSD cohort and 52.36 years in the non-PTSD cohort (P = .30). In the PTSD cohort, the mean total PCL score (baseline = 66.06, post-CPAP = 61.27, P = .004, d = -0.34) and NMF (baseline = 4.61, post-CPAP = 1.49, P = .0001, d = -0.51) decreased after 6 months of CPAP treatment. Linear regression analysis showed that the CPAP compliance was the only significant predictor for these changes among veterans with PTSD (PCL score: P = .033, R2 = .65; NMF; P = .03, R2 = .61). Further analysis by CPAP compliance quartiles in this cohort (Q1 = 0% to 25%, Q2 = 26% to 50%, Q3 = 51% to 75%, Q4> 75%) revealed that mean total PCL score declined in Q2 (change = -3.91, P = .045, d = 0.43), Q3 (change = -6.6, P = .002, d = 0.59), and Q4 (change = -7.94, P = .037, d = 0.49). In the non-PTSD cohort, the PCL score increased despite CPAP therapy in lower CPAP compliance quartiles Q1 (change = 8.71, P = .0001, d = 0.46) and Q2 (change = 4.51, P = .046, d = 0.27). With higher CPAP compliance (in Q3 and Q4) in this cohort, the mean total PCL scores slightly improved with CPAP but they were not statistically significant (P> .05). Conclusions: CPAP treatment reduces total PCL score and NMF in veterans with PTSD and OSA. Those with overt PTSD respond to even lower CPAP compliance, whereas non-PTSD patients require higher compliance to achieve any symptom improvement. Poor CPAP compliance results in increased PCL score in non-PTSD veterans and may lead to overt PTSD if the OSA remains undertreated.
Chapter
Sleep taken at regular intervals has been an indispensable part of human and virtually all mammalian life. Yet its ephemeral and delicate nature remains poised to introduce the pain of insomnia when strained by momentous, but more often, trivial irritants. An extra sip of coffee, an awkward glance by a supervisor, or a barely audible noise in the home at bedtime may steal sleep from us. Left in its place is frustration and the nagging heritage of inadequate sleep that haunts us the next day.
Chapter
Insomnia is a clinical problem that has proved difficult to define. Generally considered to be a complaint or symptom rather than a disorder, insomnia can result from one or more of a multitude of causes. The current nosology of the American Sleep Disorder Association (ASDA) includes over 40 diagnostic classifications that could potentially relate to insomnia complaints; however, the term insomnia actually identifies only a handful of these diagnoses (American Sleep Disorders Association, 1990).
Chapter
Although most people occasionally suffer from disturbed sleep, to the person suffering from chronic or severe insomnia the bed may become a battlefield; a nightly struggle ensues in which the sufferer attempts to force what comes naturally to others. As a biological imperative, sleep’s absence may result in physical, cognitive, and emotional consequences. In this volume covering various types of psychological disorders, it is evident that few problems exist in isolation. Insomnia is a prime example of how physical, behavioral, and cognitive factors can interact to produce distressing symptoms. As we shall see, insomnia can co-occur with other disorders as one of several symptoms, or it can stand alone as a presenting problem of substantial magnitude. We begin by describing insomnia and its correlates and then review methods for distinguishing it from related disorders. We then review several treatment options that may be used to improve sleep, as assessed by both objective measures of sleep duration and the subjective experience of the patient. We conclude with a case example in hope of clarifying the use of the methods described.
Article
This pilot study aimed to improve sleep in college students. The National Institutes of Health have identified sleep as an important health issue. Twenty percent of college students report that sleep difficulties affect academic performance and that these difficulties are not easy to handle. Educational interventions to improve sleep have been successful in other populations. The study took place in a small, private, residential liberal arts college in Southern New England among first year college students. After obtaining Institution Review Board approval and informed consent, a convenience sample of 56 students participated in an experimental design study. The control and experimental groups took a baseline survey by Survey Monkey using the Pittsburgh Sleep Quality Index and the Sleep Hygiene Practices Scale. They then participated in different discussion sessions. The control group discussion focused on general health issues and the experimental group focused on sleep issues. Subsequently each group received two emails a week for the remainder of the semester. The intervention group emails contained a sleep tip and linked to an educational blog site on sleep. The control group had a general health email linked to various health web sites. Two more surveys were obtained at one month and two months. Repeated measures ANOVA were performed and showed no significant difference among or between the groups. Sleep quality declined at the end of the semester. This pilot study begins to explore a new method of sleep health interventions in college students.
Chapter
Primary insomnia has been previously viewed first as a symptom of mental disorders and more recently as a type of behavior disorder. However, increasing evidence has shown that objective primary insomnia is associated with activation or pathology in whole body and brain metabolic systems, the cardiovascular system, and the endocrine system. Data have shown the appearance of pathophysiology prior to and leading to the development of changes in cognitive and mood function. Pathophysiology has also been shown in an animal model that suggested specific brain arousal areas impacted and treatment by modification of those brain arousal sites. Primary objective insomnia is a significant risk for important medical pathology including hypertension, diabetes, depression, and mortality. Recognition of primary insomnia as a significant medical risk means that treatment of insomnia should be directed toward measurement and reduction of this risk. Current data suggest that reduction in risk is best accomplished by increasing total sleep time above 7 h. However, research showing the success of these changes in diagnosis, treatment goals, and treatment outcomes requires significant research emphasis.
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Der Schlaf ist lebenswichtig für uns, jedoch merken wir dies meist erst dann, wenn es Probleme mit dem Schlafen gibt. Auswirkungen von mangelndem oder schlechtem Schlaf sind oftmals Konzentrationsschwierigkeiten, Stimmungseinbußen oder Stimmungsschwankungen aber auch Arbeitsunfälle. Zwischen 20 und 30 % der Allgemeinbevölkerung weisen Schlafprobleme auf und ca. 10 % leiden unter einer behandlungsbedürftigen Schlafstörung. Die größte Gruppe der Schlafstörungen sind die Insomnien. Daher wird die hypnotherapeutische Vorgehensweise bei Insomnien hier besonders behandelt und in Augenschein genommen. Zum anderen wird das Restless Legs Syndrom hier vorgestellt und ein hypnotherapeutischer Ansatz dargestellt. Alle hypnotherapeutischen Strategien wurden wissenschaftlich untersucht und publiziert und können somit als wissenschaftlich fundiert gelten.
Article
Bedtime worry, including worrying about incomplete future tasks, is a significant contributor to difficulty falling asleep. Previous research showed that writing about one’s worries can help individuals fall asleep. We investigated whether the temporal focus of bedtime writing—writing a to-do list versus journaling about completed activities—affected sleep onset latency. Fifty-seven healthy young adults (18–30) completed a writing assignment for 5 min prior to overnight polysomnography recording in a controlled sleep laboratory. They were randomly assigned to write about tasks that they needed to remember to complete the next few days (to-do list) or about tasks they had completed the previous few days (completed list). Participants in the to-do list condition fell asleep significantly faster than those in the completed-list condition. The more specifically participants wrote their to-do list, the faster they subsequently fell asleep, whereas the opposite trend was observed when participants wrote about completed activities. Therefore, to facilitate falling asleep, individuals may derive benefit from writing a very specific to-do list for 5 min at bedtime rather than journaling about completed activities.
Article
The role of presleep cognition in insomnia was studied in normal sleepers and insomniacs with either (1) psychophysiological insomnia, an objective disorder of initiating and maintaining sleep (DIMS), or (2) DIMS without objective findings (subjective insomnia), as defined by two nights’ polysomnographic baseline data. During the experimental night in the sleep laboratory, 24 subjects were interviewed at intervals during the presleep/sleep-onset period. Judges’ ratings of subjects’ spontaneous reports and subjects’ responses to questionnaire items were analyzed for cognitive quality. Objective insomniacs had more frequent cognitive activity than the subjective insomniacs. Both insomnia groups reported more negative thoughts than the controls. Cognitive hyperarousal as a factor in objective insomnia was not clearly supported.
Article
Insomnia is the most prevalent sleep disorder, particularly among middle and older aged adults, and is associated with a variety of negative health consequences, including higher risk for cardiovascular disease. Unfortunately, the mechanisms linking insomnia with cardiovascular risk remain largely unknown, thus limiting targeted therapeutic interventions. The hyperarousal hypothesis has attracted the most support, positing that insomnia is a result of multisystem over-activation, including sympathetic hyperactivity, which promotes wakefulness and blocks the occurrence of sleep at the desired time. The results from literature in support of this hypothesis are inconclusive and mainly relay on studies that used methods to assess sympathetic activity lacking in specificity and reproducibility. The present review aims at summarizing the primary findings on autonomic nervous system regulation in insomnia while highlighting the advantages and limitations of the methods mainly used to support the increase in sympathetic function in insomnia. Collectively, this review aims to provide novel perspectives on conceptualizing insomnia and suggest innovative approaches to help elucidate the relationship between insomnia and autonomic nervous system activity.
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Insomnia is a widespread neuropsychological sleep-related disorder known to result in various predicaments including cognitive impairments, emotional distress, negative thoughts, and perceived sleep insufficiency besides affecting the incidence and aggravation of other medical disorders. Despite the available insomnia-related theoretical cognitive models, clinical studies, and related guidelines, an evidence-based conceptual framework for a personalized approach to insomnia seems to be lacking. This study proposes a conceptual cognitive framework providing insight into cognitive mechanisms involved in the predisposition, precipitation, and perpetuation of insomnia and consequent cognitive deficits. The current Conceptual Cognitive Framework (CCF) for insomnia relies on evaluative conditional learning and appraisal which generates negative valence (emotional value) and arousal (cognitive value). Even with the limitations of this study, the suggested methodology is well-defined, reproducible, and accessible can help foster future high-quality clinical databases. During clinical insomnia but not the neutral one, negative mood (trait-anxiety) causes cognitive impairments only if mediating with a distorted perception of insomnia (Ind-1=0.161,95%CI 0.040-0.311). Further real-life testing of the CCF is intended to formulate a meticulous, decision-supporting platform for clinical interventions. Furthermore, the suggested methodology is expected to offer a reliable platform for CCF-development in other cognitive impairments and support the causal clinical data models. It may also improve our knowledge of psychological disturbances and complex comorbidities to help design rehabilitation interventions and comprehensive frameworks in line with the ‘preventive medicine’ policies.
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Objective The COVID-19 pandemic has strongly affected daily habits and psychological wellbeing, and many studies point to large modifications in several sleep and sleep-related domains. Nevertheless, pre-sleep arousal during the pandemic has been substantially overlooked. Since hyperarousal represents one of the main factors for the development and the perpetuation of chronic insomnia disorder, the assessment of variables associated with high levels of pre-sleep arousal during the pandemic is clinically relevant. The study aimed to assess the prevalence and predictors of perceived sleep quality and pre-sleep arousal in an Italian sample during the COVID-19 lockdown. Methods We used an online survey to collect self-reported sociodemographic, environmental, clinical, sleep, and sleep-related data. Our final sample included 761 participants. Results Beyond a high frequency of poor sleep quality, depressive and stress symptoms, our results show that almost half of the sample suffered from clinically relevant levels of at least one component (i.e., cognitive, somatic) of pre-sleep arousal. Subjects with greater pre-sleep arousal exhibited poorer sleep quality. Also, sleep quality was strongly associated with somatic and cognitive pre-sleep arousal. Regarding the predictors of sleep and sleep-related measures, depressive and event-related stress symptoms were the main factors associated with both poor sleep quality and pre-sleep arousal components. Moreover, specific sociodemographic and environmental variables were uniquely related to sleep quality, cognitive or somatic pre-sleep arousal. Conclusions These findings suggest that the assessment of specific sleep-related factors (i.e., pre-sleep arousal), together with more global measures of sleep quality, may be crucial to depict the complex impact of the pandemic on sleep, and to help prevent and counteract the spread of insomnia symptoms.
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Insônia é um transtorno que envolve dificuldade em dormir, em manter-se dormindo ou em ter um sono restaurador. Esta revisão reúne informações que buscam explicar a insônia, incluindo aquelas que estudam os aspectos psicológicos e os neurobiológicos. A insônia tem sido definida em termos psicológicos (componentes cognitivos, tais como preocupações e ruminação e aspectos comportamentais, tais como o condicionamento clássico) e em termos fisiológicos (taxa metabólica aumentada, com tônus muscular, frequência cardíaca e temperatura aumentados). Do ponto de vista neurobiológico, há duas perspectivas: uma propondo que a insônia ocorre em associação com uma falha na inibição da vigília e outra que considera o hiperalerta como tendo um papel importante na fisiologia do sono. São apresentadas também as estratégias não farmacológicas desenvolvidas para lidar com os diferentes aspectos da insônia.
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