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Diagnostic and Statistical Manual criteria for insomnia related impairment in daytime functioning: Polysomnographic correlates in older adults
Abstract
Diagnosis of insomnia disorder by the Diagnostic and Statistical Manual (DSM)-IV, and as proposed by the DSM-V, includes criteria for impairment in occupational- or social functioning due to sleep complaints. This study evaluated the clinical and polysomnographic correlates of impairment in daytime functioning in older adults with insomnia.
In older adults with DSM-IV chronic insomnia (n=68), clinical and demographic information, and measures of health functioning, medical co-morbidity, and polysomnographic sleep were obtained. Four questions that evaluated difficulties or distress in occupational- or social functioning related to sleep complaints were used to code DSM threshold criteria for impairment in daytime functioning. Stepwise regression was used to identify predictors of impairment in daytime functioning.
Impairment in daytime functioning was significantly associated with younger age (p<0.05), and the amount of wake time after sleep onset as assessed by polysomnography (p<0.001), controlling for health functioning and minority racial status.
Amount of wake time after sleep onset uniquely contributes to criteria symptoms of impairment in daytime functioning among older adults with insomnia. Treatments that target sleep maintenance have the potential to improve social and occupational functioning in older adults with sleep complaints.
... However, this evidence has been relatively mixed (Riedel & Lichstein, 2000), and the nature of the relationship between nocturnal insomnia symptoms and daytime impairment has not been fully explored (Shekleton, Rogers, & Rajaratnam, 2010). Specifically, the factors that may explain the links between disturbed sleep and different types of impairment are unknown (Kierlin, Olmstead, Yokomizo, Nicassio, & Irwin, 2012). For example, quantitative measures of nocturnal insomnia symptom severity and frequency may be differentially associated with various types of daytime impairment. ...
... Recent studies have begun to elucidate these associations by examining specific factors that may explain the impact of insomnia on daytime impairment. For example, daytime impairment has been shown to vary as a function of global measures of insomnia severity (Szelenberger & Niemcewicz, 2000), global sleep dissatisfaction (Ohayon et al., 2012), difficulty resuming sleep (Ohayon, 2009), and polysomnography-determined amount of wake time after sleep onset (Kierlin et al., 2012). Taken together, these findings suggest that separate aspects of insomnia may have independent effects on daytime functioning domains. ...
This study examined the associations between reported quantitative sleep measures and multiple daytime impairment domains. We collected data from a subsample of adults (n = 513) from the Colorado Longitudinal Twin Study and Community Twin Study. Results revealed that greater insomnia symptom frequency (days per week) significantly predicted greater global sleep-related functional impairment and depressive symptoms. Sleep onset latency was also positively associated with depressive symptoms. Receiver operating characteristic curve analyses indicated 3-4 nights per week and 36-40 min provided optimal sensitivity and specificity for impairment. Thus, insomnia frequency and sleep latency are critical in understanding the impact of insomnia on multiple impairment domains. Using functional impairment as criterion, these findings also support the use of specific quantitative cutoffs for sleep measures in diagnostic systems.
... Furthermore, there appears to be a hierarchical order regarding which sleep items are most associated with daytime consequences, a cardinal component of insomnia disorder; these sleep items follow the following ranking; self-reported dissatisfaction, complaints of nonrestorative sleep, difficulty resuming or maintaining sleep, and difficulty initiating sleep [53]. Additionally, objective EEG data suggest that higher amount of wake after sleep onset (WASO) is associated with greater impairments in daytime functioning [54]. ...
Thermoregulation and sleep are tightly coordinated, with evidence that impairments in thermoregulation as well as increases in ambient temperature increase the risk of sleep disturbance. As a period of rest and low demand for metabolic resources, sleep functions to support host responses to prior immunological challenges. In addition by priming the innate immune response, sleep prepares the body for injury or infection which might occur the following day. However when sleep is disrupted, this phasic organization between nocturnal sleep and the immune system becomes misaligned, cellular and genomic markers of inflammation are activated, and increases of proinflammatory cytokines shift from the nighttime to the day. Moreover, when sleep disturbance is perpetuated due to thermal factors such as elevated ambient temperature, the beneficial crosstalk between sleep and immune system becomes further imbalanced. Elevations in proinflammatory cytokines have reciprocal effects and induce sleep fragmentation with decreases in sleep efficiency, decreases in deep sleep, and increases in rapid eye movement sleep, further fomenting inflammation and inflammatory disease risk. Under these conditions, sleep disturbance has additional potent effects to decrease adaptive immune response, impair vaccine responses, and increase vulnerability to infectious disease. Behavioral interventions effectively treat insomnia and reverse systemic and cellular inflammation. Further, insomnia treatment redirects the misaligned inflammatory- and adaptive immune transcriptional profiles with the potential to mitigate risk of inflammation-related cardiovascular, neurodegenerative, and mental health diseases, as well as susceptibility to infectious disease.
... Sleep deficits can be extremely debilitating, causing dysphoria and daytime impairment at any age. In older adults in particular, sleep fragmentation predicts worse daytime functioning, including cognitive and social impairment 79 . Given the importance of sleep in cognitive and emotional functions, these results highlight an important factor driving variation in sleep and cognition throughout the lifespan that suggest age-appropriate and trauma informed treatment of sleep problems [80][81][82][83][84][85][86][87][88] . ...
Sleep quality varies widely across individuals, especially during normal aging, with impaired sleep contributing to deficits in cognition and emotional regulation. Sleep can also be impacted by a variety of adverse events, including childhood adversity. Here we examined how early life adverse events impacted later life sleep structure and physiology using an animal model to test the relationship between early life adversity and sleep quality across the life span. Rat pups were exposed to an Adversity-Scarcity model from postnatal day 8–12, where insufficient bedding for nest building induces maternal maltreatment of pups. Polysomnography and sleep physiology were assessed in weaning, early adult and older adults. Early life adversity induced age-dependent disruptions in sleep and behavior, including lifelong spindle decreases and later life NREM sleep fragmentation. Given the importance of sleep in cognitive and emotional functions, these results highlight an important factor driving variation in sleep, cognition and emotion throughout the lifespan that suggest age-appropriate and trauma informed treatment of sleep problems.
... Further, the strength and quality of assessment of sleep disturbance (ie, validated questionnaire vs single item) contribute to heterogeneity of effects linking sleep to immune outcomes; stronger effects are found when questionnaires are used ). Yet, when use of validated questionnaires is not possible, it is important to note that certain single items predict daytime consequences, a necessary criterion for the diagnosis of insomnia (Kierlin et al, 2012). These predictive items show the following hierarchical order: self-reported dissatisfaction with sleep, complaints of non-restorative sleep, difficulty resuming or maintaining sleep, and difficulty initiating sleep (Ohayon et al, 2012). ...
Sleep disturbances including insomnia independently contribute to risk of inflammatory disorders, and major depressive disorder. This review and overview provides an integrated understanding of the reciprocal relationships between sleep and the innate immune system and considers the role of sleep in the nocturnal regulation of the inflammatory biology dynamics, the impact of insomnia complaints, extremes of sleep duration, and experimental sleep deprivation on genomic, cellular, and systemic markers of inflammation, and the influence of sleep complaints and insomnia on inflammaging and molecular processes of cellular aging. Clinical implications of this research include discussion of the contribution of sleep disturbance to depression and especially inflammation-related depressive symptoms. Reciprocal action of inflammatory mediators on the homeostatic regulation of sleep continuity and sleep macrostructure; and the potential of interventions that target insomnia to reverse inflammation are reviewed. Togther, interactions between sleep and inflammatory biology mechanisms underscores the implications of sleep disturbance for inflammatory disesease risk, and provides a map to guide the development of treatments that modulate inflammation, improve sleep, and promote sleep-health.Neuropsychopharmacology accepted article preview online, 11 August 2016. doi:10.1038/npp.2016.148.
... Sleep disturbance when combined with short duration are thought to be particularly caustic for health outcomes (4,(117)(118)(119)(120), although studies of inflammation have predominantly examined sleep disturbance and sleep duration in separate models. Sleep fragmentation, as opposed to shortened sleep amounts, might also contribute to sleep disturbance, and such disruption of sleep continuity is uniquely associated with daytime dysfunction (121) and increases rates of mortality (1). ...
Sleep disturbance is associated with inflammatory disease risk and all-cause mortality. Here, we assess global evidence linking sleep disturbance, sleep duration, and inflammation in adult humans.
A systematic search of English language publications was performed, with inclusion of primary research articles that characterized sleep disturbance and/or sleep duration or performed experimental sleep deprivation and assessed inflammation by levels of circulating markers. Effect sizes (ES) and 95% confidence intervals (CI) were extracted and pooled using a random effect model.
A total of 72 studies (n > 50,000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα). Sleep disturbance was associated with higher levels of CRP (ES .12; 95% CI = .05-.19) and IL-6 (ES .20; 95% CI = .08-.31). Shorter sleep duration, but not the extreme of short sleep, was associated with higher levels of CRP (ES .09; 95% CI = .01-.17) but not IL-6 (ES .03; 95% CI: -.09 to .14). The extreme of long sleep duration was associated with higher levels of CRP (ES .17; 95% CI = .01-.34) and IL-6 (ES .11; 95% CI = .02-20). Neither sleep disturbances nor sleep duration was associated with TNFα. Neither experimental sleep deprivation nor sleep restriction was associated with CRP, IL-6, or TNFα. Some heterogeneity among studies was found, but there was no evidence of publication bias.
Sleep disturbance and long sleep duration, but not short sleep duration, are associated with increases in markers of systemic inflammation.
Copyright © 2015 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
... Patients in the study by Perrier et al. (2014) were slightly younger (mean age approximately 49 vs 61 years old) and showed significantly worse sleep than normal sleepers the night before testing as measured by polysomnography (sleep efficiency 74% vs 81%) than in the study by Leufkens et al. (2014). A recent study showed that complaints of daytime impairment were more pronounced in young than in older insomnia patients (Kierlin, Olmstead, Yokomizo, Nicassio, & Irwin, 2012). Moreover impairment is more likely to be associated with more severe insomnia. ...
Insomniacs report decreased performance in daily routines, which may have detrimental consequences for car driving. We compared changes over time in driving performance (measured as Standard Deviation of Lateral Position-SDLP) and background EEG between 20 untreated insomnia patients (52-70 years old) and 21 normal sleepers (54-73 years old) during a one hour on-the-road driving test after a normal night of sleep, in the morning. SDLP did not differ between groups and increased slightly over time to similar degrees in both groups. EEG alpha and beta power were lower in insomniacs as compared to normal sleepers. Alpha and beta power slightly reduced during driving in normal sleepers but remained at a constant low level in insomniacs. Changes in EEG power and SDLP were not related. It is concluded that on-the-road driving performance does not differ between older insomniacs and older normal sleepers and that changes in spectral EEG measures of cortical arousal and in driving performance are not related.
Copyright © 2015. Published by Elsevier B.V.
... However, a limitation of the study is the relatively small sample size of participants that may have prevented us from being able to assess whether young persons with insomnia experienced more impairments than older persons, as suggested by another study. 67 Because most patients with insomnia are treated with hypnotics, further research is needed to study this population to assess whether the treatment has beneficial or deleterious effects on driving performance. This question remains to be addressed, as it has been clearly shown that hypnotics impair driving performance after a single intake in healthy young or older subjects, 17,19 or after 1 w of treatment in patients with insomnia, 16 but the effects of long-term treatment with hypnotics have not yet been studied. ...
Study objectives:
To evaluate driving performance and psychomotor vigilance in patients with primary insomnia.
Design:
After 1 night of polysomnography, participants performed a 1-h simulated monotonous driving task and a psychomotor vigilance task (PVT). Self-ratings of sleepiness, mood, and driving performance were completed.
Setting:
This study was conducted at the CHU of Caen Sleep Unit and the University of Caen.
Participants:
Twenty-one primary insomnia patients and 16 good sleepers.
Interventions:
Not applicable.
Measurements and results:
Results revealed a larger standard deviation of lateral position (P = 0.023) and more lane crossings (P = 0.03) in insomnia patients than in good sleepers. Analyses of effect of time on task performance showed that the impairment in patients occurred after 20 min of driving, which was not the case for good sleepers. No difference between groups was found for the PVT, neither for the mean reaction time (RT) (P = 0.43) nor the number of lapses (P = 0.21) and the mean slowest 10% 1/RT (P = 0.81). Patients rated their sleepiness level higher (P = 0.06) and their alertness level lower (P = 0.007) than did good sleepers (P = 0.007). The self-evaluation of the driving performance was not different between groups (P = 0.15).
Conclusions:
These findings revealed that primary insomnia is associated with a performance decrement during a simulated monotonous driving task. We also showed that patients are able to drive safely only for a short time. It appears advisable for clinicians to warn patients about their impaired driving performance that could lead to an increased risk of driving accidents.
... Patients in the study by Perrier et al. (2014) were slightly younger (mean age approximately 49 vs 61 years old) and showed significantly worse sleep than normal sleepers the night before testing as measured by polysomnography (sleep efficiency 74% vs 81%) than in the study by Leufkens et al. (2014). A recent study showed that complaints of daytime impairment were more pronounced in young than in older insomnia patients (Kierlin, Olmstead, Yokomizo, Nicassio, & Irwin, 2012). Moreover impairment is more likely to be associated with more severe insomnia. ...
Introduction
Insomnia patients consistently self-reported daytime fatigue and cognitive impairments which could contribute to traffic crashes. However, the model of hyperarousal was proposed to explain the lack of objective evidence of cognitive dysfunction in patients with primary insomnia because of the contribution of psychological and physiological arousal to daytime functioning. In this case it is not clear that insomnia patients could suffer from sleepiness which could contribute to traffic crashes. Electroencephalography recordings during driving were previously used to assess sleepiness and fatigue during a driving task. It appeared that an increase in the theta, alpha and beta band is linked to a higher fatigue. We expected that insomnia patients will not have a decrement in their driving performance associated with EEG correlates of less fatigue. The purpose of the present study was thus to compare the electroencephalographic correlates of sleepiness and fatigue during a driving task in insomniac patients and in good sleepers.
Materials and methods
Nineteen older insomniacs and nineteen older good sleepers were included in the study (aged between 55–75 years). After a sleep recording night in the sleep unit, the participants performed an on-the-road highway driving task in the morning. The vehicle’s speed and lateral position were continuously recorded. Electroencephalography was also recorded during the driving task. The main driving parameter was the standard deviation of the lateral position (SDLP), which is an index of weaving; the standard deviation of speed (SDS) was also quantified. The fatigue EEG correlates were assessed by quantification of the absolute power spectra in the theta, alpha and beta bands.
Results
Results for the SDLP and the SDS reveal that driving performance was not impaired in the insomnia group in comparison to the good sleepers group. Preliminary analysis of EEG recordings reveal that good sleepers had a higher power spectrum in the theta, alpha and beta bands.
Conclusion
It is concluded that older chronic insomnia patients appear to be able to successfully perform a one hour highway driving task in real traffic. EEG results suggested that insomniacs were less fatigued than good sleepers which could explain the lack of difference in the driving performance. This could be in line with the hyperarousal model proposed to explain to lack of cognitive dysfunction in insomnia patients.
Acknowledgements
We want to thanks Anita Van Oers for the driving data analyses, Henk Brauers and Jo Gorissen as driving instructors and student assistants for the help in the data collection.
Insomnia is a common disorder that results in short sleep at night along with daytime symptoms, for example, fatigue, lethargy, poor concentration, cognitive problems, and mood alteration to name a few. These symptoms may, at times, be so severe that they can be mistaken for a number of psychiatric disorders, for example, depression and somatic symptoms disorders. Moreover, insomnia also increases the risk for cognitive impairment and dementia. Fibromyalgia and chronic fatigue syndrome are other common presentations of chronic insomnia. Many patients with chronic insomnia try to self-medicate using addictive substances, for example, alcohol that may culminate in alcohol use disorder. A number of patients continue hypnotic medications beyond the prescription period and a proportion of them increase the dose, thus clinically presenting with benzodiazepine use disorder, according to the present classification system. A careful assessment of these patients may unmask the underlying chronic insomnia. Optimal treatment of insomnia using behavioral and pharmacological measures can improve the prognosis.KeywordsChronic insomniaDepressionAnxietyFatigueCognitive behavior therapy
Insomnia is a disorder characterized by difficulty falling asleep and poor sleep continuity and is associated with increased risks for physical and cognitive decline. Insomnia with short sleep duration is considered the most biologically severe phenotype of the disorder. Evidence suggests that short-chain fatty acids (SCFAs), the main byproducts of fiber fermentation in the gut, may affect sleep via gut–brain communications. This study explores associations between SCFAs and sleep continuity and compares SCFA concentrations in short vs. normal sleep insomnia phenotypes in older adults. Fifty-nine participants with insomnia symptoms (≥ 65 years), completed 2 weeks of objective sleep monitoring (actigraphy), and were divided into short and normal sleep duration phenotypes via cluster analysis. Sleep measures included total sleep time (TST), sleep onset latency (SOL), sleep efficiency (SE), and wake after sleep onset (WASO). Stool samples were collected and fecal SCFA concentrations were determined by gas-chromatography-mass-spectrometry (GCMS). Higher concentrations of acetate, butyrate, and propionate, and total SCFAs, were associated with lower SE and longer SOL after controlling for Body Mass Index (BMI). Concentrations were higher in the short sleep duration phenotype. Age, BMI, TST, and SOL explained 40.7% of the variance in total SCFAs. Findings contribute to understanding pathways along the gut–brain axis and may lead to the use of SCFAs as biomarkers of insomnia phenotypes.
ABSTRACT
Context: Sleep disturbances and cognitive dysfunction are consistently reported as extremely troublesome aspects of psychotic illnesses. While sleep disturbances are not included in definitions of psychosis they are associated with poor levels of daily function and impaired social recovery. Despite sleep problems being documented as co-occurring with psychosis, including during the prodrome phase and following symptomatic recovery, sleep remains unexamined as a potential therapeutic target pathway for social recovery. Specific areas of cognition are known to be associated with psychosis, sleep deficits and daily function, yet these have not been tested as possible mediators to improve daily function and social recovery through the effective treatment of sleep. A well-validated web-based CBT intervention to reduce insomnia (Sleepio) has potential to overcome resource-based barriers of treating sleep disruptions in early psychosis.
Hypotheses: The primary hypothesis is that improved sleep (increase in SCI-8 score, adjusted difference (AD) ≥4.2) in those utilising Sleepio + treatment as usual (TAU), compared with TAU alone, will be associated with improved daily function (lower WSAS score, adjusted difference (AD) ≥1.7) by the end of the 8-week intervention period. Secondary hypotheses are: 1) Improvements in sleep (increase in SCI-8 score) will be associated with improved social recovery (increased hours on TUS-SH , adjusted difference (AD) ≥4 per week) by the end of the follow-up period, 8-weeks after completion of intervention. 2) Changes in social recovery (TUS-SH) following changes in sleep (SCI-8) will be partially mediated by changes in specific areas of cognition; i.e. attention, memory, executive function and social/emotional (measured by Cantab cognitive tests). 3) Changes in social recovery (TUS-SH) following changes in sleep (SCI-8) will be partially mediated by changes in daily function (lower WSAS score). 4) Sleep diaries and actigraphy results will be strongly correlated and provide subjective and objective validation of sleep quality based on SCI-8 scores.
Methods: Stage one: two surveys will be distributed through REDCap to assess perception of sleep problems and their treatment in patients with psychosis. Stage two: A minimum of 43 participants in early psychosis (EP) will be recruited through CAMEO early intervention services. These participants will be randomised into two groups with three measurement points covering insomnia and sleep quality (SCI-81, PSQI & ISI ); depression (PHQ-9 ); cognition (CANTAB ); symptom level (GAF-S ), daily function (WSAS2) and Social Recovery (TUS-SH3). Two additional measurement points will occur mid-treatment and mid-follow-up to allow for mediation analysis. Participants will receive either the Sleepio online intervention + treatment as usual (TAU) or TAU alone over an 8-week period. Actigraphy watches (objective measure) will be provided for three one-week periods to validate sleep diaries (subjective measure). Stage three: A follow-up period will be conducted for an additional 8 weeks (week 9 through 16). The original TAU group will be offered the intervention during this period.
Impetuses and Impact: CRISP is predicated on findings from the National EDEN (NEDEN) study, which provided strong evidence that duration of sleep was significantly associated with the level of social recovery at 1-year follow-up. This analysis was prompted by conversations with experts by experience, many of which continue to advise on the current study through a Lived Experience Advisory Group (LEAG). This research will not only test the effectiveness of improving daily function by improving sleep, it will also explore its impact on the resistant area of social recovery in a population heavily burdened by sleep disruptions and social inequalities. Potentially uncovering a viable method to improve functional outcomes, by overcome barriers for the treatment of sleep in early psychosis through a validated intervention that is web-based and readily available. What is discovered about the relationship between sleep and social recovery, as well as the mediating effects of cognition may act as pilot data for future research.
Background
Facial emotion perception (FEP) is pivotal for discriminating salient emotional information. Accumulating data indicate that FEP responses, particularly to sad emotional stimuli, are impaired in depression. This study tests whether sleep disturbance and inflammation, two risk factors for depression, contribute to impaired FEP to sad emotional stimuli.
Methods
In older adults (N=40, 71.7±6.8y, 56.4% female), disturbance of sleep maintenance (i.e., wake time after sleep onset [WASO]) was evaluated by polysomnography. In the morning, plasma concentrations of two markers of systemic inflammation were evaluated (i.e., interleukin [IL]-6, tumor necrosis factor [TNF]-α), followed by two FEP tasks, which assessed delays in emotion recognition (ER) and ratings of perceived emotion intensity (EI) in response to sad facial emotional stimuli, with exploration of FEP responses to happiness and anger. Linear regression models tested whether WASO, IL-6, and TNF-α would be associated with impaired FEP of sad emotional stimuli. In addition, moderation tests examined whether inflammation would moderate the link between sleep disturbance and impaired FEP of sad emotional stimuli.
Results
Longer WASO predicted longer ER delays (p<0.05) and lower EI ratings in response to sad faces (p<0.01). Further, higher TNF-α (p<0.05) but not IL-6 predicted longer ER delays for sad faces, whereas higher IL-6 (p<0.01) but not TNF-α predicted lower EI ratings for sad faces. Finally, TNF-α moderated the relationship between longer WASO and longer ER delays for sad faces (p<0.001), while IL-6 moderated the relationship between longer WASO and lower EI ratings for sad faces (p<0.01). Neither sleep nor inflammatory measures were associated with FEP responses to happiness or anger.
Conclusion
In older adults, disturbance of sleep maintenance is associated with impaired FEP of sad emotion, a relationship that appears to be moderated by inflammation. These data indicate that sleep disturbance and inflammation converge into impaired FEP associated with late-life depression.
The association between psychopathology and poor sleep has long been recognized. The current review focuses on the association between the most prevalent sleep disorders (insomnia, sleep-related breathing disorders and restless legs syndrome) and four major psychiatric disorders: alcohol dependence, schizophrenia, depression and anxiety disorders. Decreased total sleep time and increased sleep onset latency as measured by polysomnography as well an increase of the prevalence of insomnia has been reported in all of these psychiatric disorders. Furthermore, sleep disturbance is a risk factor for their development. Cognitive-behavioral therapy for insomnia has been shown to have a positive impact on both sleep and symptoms of depression and anxiety. Whether adequate treatment of sleep disorders can prevent the incidence of psychiatric disorders, remains to be investigated.
The frequencies of five common sleep complaints--trouble falling asleep, waking up, awaking too early, needing to nap and not feeling rested--were assessed in over 9,000 participants aged 65 years and older in the National Institute on Aging's multicentered study entitled "Established Populations for Epidemiologic Studies of the Elderly" (EPESE). Less than 20% of the participants in each community rarely or never had any complaints, whereas over half reported at least one of these complaints as occurring most of the time. Between 23% and 34% had symptoms of insomnia, and between 7% and 15% percent rarely or never felt rested after waking up in the morning. In multivariate analyses, sleep complaints were associated with an increasing number of respiratory symptoms, physical disabilities, nonprescription medications, depressive symptoms and poorer self-perceived health. Sleep disturbances, particularly among older persons, oftentimes may be secondary to coexisting diseases. Determining the prevalence of specific sleep disorders, independent of health status, will require the development of more sophisticated and objective measures of sleep disturbances.
To evaluate the validity of the Cumulative Illness Rating Scale (CIRS) in a geriatric institutional population by examining its associations with mortality, hospitalization, medication usage, laboratory findings and disability.
A validation of the CIRS using self- and physician-report surveys, with archival data drawn from medical charts and facility records.
Long-term care facility with skilled nursing and congregate apartments.
Four hundred thirty-nine facility residents selected on the basis of completeness of self-report data and physician ratings.
Composite measures of illness severity and comorbidity, based on physicians' CIRS ratings; time to death or acute hospitalization after assessment; medication use, drawn from pharmacy records; medical chart data on laboratory tests; self-reported functional disability.
CIRS illness severity and comorbidity indices, as well as individual CIRS items, were significantly associated with mortality, acute hospitalization, medication usage, laboratory test results, and functional disability. The CIRS showed good divergent validity vis a vis functional disability in predicting mortality and hospitalization.
The CIRS appears to be a valid indicator of health status among frail older institution residents. The illness severity and comorbidity composites performed equally well in predicting longitudinal outcomes. Item-level analyses suggest that the CIRS may be useful in developing differential illness profiles associated with mortality, hospitalization, and disability.
Nonrestorative sleep (NRS) has been little studied in the general population, even though this symptom has an important role in several medical conditions such as heart disease, fibromyalgia, and chronic fatigue syndrome, as well as various sleep disorders.
A total of 25,580 individuals (age range, 15-100 years) from the noninstitutionalized general population representative of 7 European countries (France, the United Kingdom, Germany, Italy, Portugal, Spain, and Finland) were interviewed by telephone using the Sleep-EVAL system. Nonrestorative sleep was analyzed in relationship to sociodemographic determinants, environmental factors, life habits, health, sleep-wake schedule, and psychological factors.
The prevalence of NRS was 10.8% (95% confidence interval, 10.4%-11.2%) in the sample, was higher in women than in men (12.5% vs 9.0%; P<.001), and decreased with age. The United Kingdom (16.1%) and Germany (15.5%) had the highest prevalence of NRS and Spain (2.4%), the lowest. In multivariate analyses, several factors were positively associated with NRS. The most important were younger age, dissatisfaction with sleep, difficulty getting started in the morning, stressful life, presence of anxiety, bipolar or a depressive disorder, and having a physical disease. When compared with subjects who have difficulty initiating or maintaining sleep (without NRS), subjects with NRS reported more frequently a variety of daytime impairment (irritability, physical, and mental fatigue) and consulted a physician twice as frequently for their sleeping difficulties than did other subjects with insomnia.
Nonrestorative sleep is a frequent symptom in the general population, but its prevalence largely varies between countries. It is often associated with mental disorders and characteristics of sleep deprivation (such as extra sleep time on weekends). Nonrestorative sleep affected more frequently the active classes of the population and caused greater daytime impairment than difficulty initiating or maintaining sleep.
Meta-analyses support the effectiveness of behavioral interventions for the treatment of insomnia, although few have systematically evaluated the relative efficacy of different treatment modalities or the relation of old age to sleep outcomes. In this meta-analysis of randomized controlled trials (k = 23), moderate to large effects of behavioral treatments on subjective sleep outcomes were found. Evaluation of the moderating effects of behavioral intervention type (i.e., cognitive-behavioral treatment, relaxation, behavioral only) revealed similar effects for the 3 treatment modalities. Both middle-aged adults and persons older than 55 years of age showed similar robust improvements in sleep quality, sleep latency, and wakening after sleep onset. A research agenda is recommended to examine the mechanisms of action of behavioral treatments on sleep with increased attention to the high prevalence of insomnia in older individuals.
The prevalence of sleep-related breathing disorder (SRBD) and insomnia symptoms increases considerably with advancing age, but little is known about their cooccurrence and their effects on daytime functioning when present together.
Older adults with (cases, n = 99) and without (controls, n = 100) symptoms of insomnia underwent 2 nights of in-laboratory polysomnography, daytime nap, and neurobehavioral testing and completed study questionnaires. Predictors of SRBD were identified (apnea-hypopnea index [indicating number of events per hour], > or =15). Participants were divided into 4 groups--with and without insomnia and with and without SRBD--and the groups were compared on measures of daytime functioning.
Cases had a lower rate of SRBD (29.3%) than controls (38.0%). Body mass index (calculated as weight in kilograms divided by height in meters squared) of 30 or higher, neck circumference greater than 15.5 inches, and a history of "loud snoring" or "stops breathing, chokes, or struggles for breath" were independently predictive of SRBD in participants with insomnia symptoms. Having both insomnia symptoms and SRBD was associated with significantly lower daytime functioning and longer psychomotor reaction times compared with having neither condition.
Because insomnia comorbid with SRBD is associated with the greatest functional impairment, and SRBD is commonly found in the elderly population, health care providers should also consider SRBD in elderly patients with insomnia symptoms.
Objective.
—To evaluate the efficacy of benzodiazepines and zolpidem tartrate in chronic insomnia based on a quantitative review of literature.Data Sources.
—Articles from 1966 to 1996 were identified using MEDLINE, by a manual review of relevant journals, and from bibliographies of identified articles.Study Selection.
—Studies using randomized, double-blind, placebo-controlled, parallel or crossover designs with benzodiazepines or zolpidem in adults younger than 65 years with chronic insomnia (modified Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for primary insomnia) were selected for review. Self-report and polysomnographic measures of sleep-onset latency, total sleep time, number of awakenings, and sleep quality were selected as outcomes.Data Extraction.
—Twenty-two studies met the selection criteria. A combined test of P values was performed, pooling broadly from the 22 studies to determine whether medication was superior to placebo. A combined test of effect sizes was performed on the subset of studies that reported effect size information to determine the magnitude of medication effect.Data Synthesis.
—A homogeneous sample of studies summarized 1894 patients treated for a median duration of 7 days. The combined test of P values demonstrated that medication was superior to placebo in all 4 outcome measures. Treatment response was moderate in magnitude by the combined test of effect sizes.Conclusions.
—Benzodiazepines and zolpidem produced reliable improvements in commonly measured parameters of sleep in patients with chronic insomnia. Relative to the chronic and recurring course of insomnia, both the limited duration of treatments studied and the lack of follow-up data from controlled trials represent challenges for developing evidence-based guidelines for the use of hypnotics in the management of chronic insomnia.
Sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. Given sex differences in the prevalence of inflammatory disorders with stronger associations in females, this study was undertaken to test the effects of sleep loss on cellular mechanisms that contribute to proinflammatory cytokine activity. In 26 healthy adults (11 females; 15 males), monocyte intracellular proinflammatory cytokine production was repeatedly assessed at 08:00, 12:00, 16:00, 20:00, and 23:00 h during a baseline period and after partial sleep deprivation (awake from 23:00 to 3.00 h). In the morning after a night of sleep loss, monocyte production of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) differentially changed between the two sexes. Whereas both females and males showed a marked increase in the lipopolysaccharide (LPS) — stimulated production of IL-6 and TNF-α in the morning immediately after PSD, production of these cytokines during the early- and late evening was increased in the females as compared to decreases in the males. Sleep loss induces a functional alteration of monocyte proinflammatory cytokine responses with females showing greater cellular immune activation as compared to changes in males. These results have implications for understanding the role of sleep disturbance in the differential risk profile for inflammatory disorders between the sexes.
To explore how insomnia symptoms are hierarchically organized in individuals reporting daytime consequences of their sleep disturbances.
This is a cross-sectional study conducted in the general population of the states of California, New York, and Texas. The sample included 8937 individuals aged 18 years or older representative of the general population. Telephone interviews on sleep habits and disorders were managed with the Sleep-EVAL expert system and using DSM-IV and ICSD classifications. Insomnia symptoms and global sleep dissatisfaction (GSD) had to occur at least three times per week for at least three months.
A total of 26.2% of the sample had a GSD. Individuals with GSD reported at least one insomnia symptom in 73.1% of the cases. The presence of GSD in addition to insomnia symptoms considerably increased the proportion of individuals with daytime consequences related to insomnia. In the classification trees performed, GSD arrived as the first predictor for daytime consequences related to insomnia. The second predictor was nonrestorative sleep followed by difficulty resuming sleep and difficulty initiating sleep.
Classification trees are a useful way to hierarchically organize symptoms and to help diagnostic classifications. In this study, GSD was found to be the foremost symptom in identifying individuals with daytime consequences related to insomnia.
Nocturnal awakenings are one of the most prevalent sleep disturbances in the general population. Little is known, however, about the frequency of these episodes and how difficulty resuming sleep once awakened affects subjective sleep quality and quantity.
This is a cross-sectional telephone study with a representative sample consisting of 8937 non-institutionalized individuals aged 18 or over living in Texas, New York and California. The interviews included questions on sleeping habits, health, sleep and mental disorders. Nocturnal awakenings were evaluated according to their frequency per week and per night, as well as their duration.
A total of 35.5% of the sample reported awakening at least three nights per week. Of this 35.5%, 43% (15.2% of the total sample) reported difficulty resuming sleep once awakened. More than 80% of subjects with insomnia symptoms (difficulty initiating or maintaining sleep or non-restorative sleep) also had nocturnal awakenings. Difficulty resuming sleep was associated with subjective shorter sleep duration, poorer sleep quality, greater daytime impairment, greater consultations for sleep disturbances and greater likelihood of receiving a sleep medication.
Nocturnal awakenings disrupt the sleep of about one-third of the general population. Using difficulty resuming sleep identifies individuals with significant daytime impairment who are most likely to seek medical help for their sleep disturbances. In the absence of other insomnia symptoms, nocturnal awakenings alone are unlikely to be associated with daytime impairments.
The widespread use of standardized health surveys is predicated on the largely untested assumption that scales constructed from those surveys will satisfy minimum psychometric requirements across diverse population groups. Data from the Medical Outcomes Study (MOS) were used to evaluate data completeness and quality, test scaling assumptions, and estimate internal-consistency reliability for the eight scales constructed from the MOS SF-36 Health Survey. Analyses were conducted among 3,445 patients and were replicated across 24 subgroups differing in sociodemographic characteristics, diagnosis, and disease severity. For each scale, item-completion rates were high across all groups (88% to 95%), but tended to be somewhat lower among the elderly, those with less than a high school education, and those in poverty. On average, surveys were complete enough to compute scales scores for more than 96% of the sample. Across patient groups, all scales passed tests for item-internal consistency (97% passed) and item-discriminant validity (92% passed). Reliability coefficients ranged from a low of 0.65 to a high of 0.94 across scales (median = 0.85) and varied somewhat across patient subgroups. Floor effects were negligible except for the two role disability scales. Noteworthy ceiling effects were observed for both role disability scales and the social functioning scale. These findings support the use of the SF-36 survey across the diverse populations studied and identify population groups in which use of standardized health status measures may or may not be problematic.
To evaluate the efficacy of benzodiazepines and zolpidem tartrate in chronic insomnia based on a quantitative review of literature.
Articles from 1966 to 1996 were identified using MEDLINE, by a manual review of relevant journals, and from bibliographies of identified articles.
Studies using randomized, double-blind, placebo-controlled, parallel or crossover designs with benzodiazepines or zolpidem in adults younger than 65 years with chronic insomnia (modified Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for primary insomnia) were selected for review. Self-report and polysomnographic measures of sleep-onset latency, total sleep time, number of awakenings, and sleep quality were selected as outcomes.
Twenty-two studies met the selection criteria. A combined test of Pvalues was performed, pooling broadly from the 22 studies to determine whether medication was superior to placebo. A combined test of effect sizes was performed on the subset of studies that reported effect size information to determine the magnitude of medication effect.
A homogeneous sample of studies summarized 1894 patients treated for a median duration of 7 days. The combined test of P values demonstrated that medication was superior to placebo in all 4 outcome measures. Treatment response was moderate in magnitude by the combined test of effect sizes.
Benzodiazepines and zolpidem produced reliable improvements in commonly measured parameters of sleep in patients with chronic insomnia. Relative to the chronic and recurring course of insomnia, both the limited duration of treatments studied and the lack of follow-up data from controlled trials represent challenges for developing evidence-based guidelines for the use of hypnotics in the management of chronic insomnia.
To increase both the within- and between-researcher agreement in sleep stage identification and to foster the development of computer algorithms for automatic analyses of sleep, a need for additional definitions was recognized. In 1991, the Subcommittee for Automatic Sleep Staging (SASS) was formed by the JSSR. The Subcommittee comprised 53 investigators and seven project leaders selected for their skill in scoring sleep records: S. Sugita (Chair), M. Okawa (co-Chair), T. Kobayashi, T. Hori, A. Miyasita, S. Shirakawa and Y. Atsumi. In 1995, based on their 5 year discussions, the Subcommittee proposed supplementary definitions and amendments for the Standard Scoring System to the JSSR. These proposals were reported in the JSSR Newsletter (1996; No. 13, February 1, pages 5–13).
Inflammation is associated with increased risk of cardiovascular disorders, arthritis, diabetes mellitus, and mortality. The effects of sleep loss on the cellular and genomic mechanisms that contribute to inflammatory cytokine activity are not known.
In 30 healthy adults, monocyte intracellular proinflammatory cytokine production was repeatedly assessed during the day across 3 baseline periods and after partial sleep deprivation (awake from 11 pm to 3 am). We analyzed the impact of sleep loss on transcription of proinflammatory cytokine genes and used DNA microarray analyses to characterize candidate transcription-control pathways that might mediate the effects of sleep loss on leukocyte gene expression.
In the morning after a night of sleep loss, monocyte production of interleukin 6 and tumor necrosis factor alpha was significantly greater compared with morning levels following uninterrupted sleep. In addition, sleep loss induced a more than 3-fold increase in transcription of interleukin 6 messenger RNA and a 2-fold increase in tumor necrosis factor alpha messenger RNA. Bioinformatics analyses suggested that the inflammatory response was mediated by the nuclear factor kappaB inflammatory signaling system as well as through classic hormone and growth factor response pathways.
Sleep loss induces a functional alteration of the monocyte proinflammatory cytokine response. A modest amount of sleep loss also alters molecular processes that drive cellular immune activation and induce inflammatory cytokines; mapping the dynamics of sleep loss on molecular signaling pathways has implications for understanding the role of sleep in altering immune cell physiologic characteristics. Interventions that target sleep might constitute new strategies to constrain inflammation with effects on inflammatory disease risk.
We investigated the prevalence and correlates of sleep complaints in a large well-characterized population.
The Atherosclerosis Risk in Communities Study is a prospective population-based study of cardiovascular disease. Using this well-characterized cohort, we undertook a cross-sectional epidemiologic analysis of correlates of 3 sleep complaints that are commonly included in insomnia definitions. We hypothesized that different sleep complaints included under the rubric of "insomnia" would have different correlates. Using multivariate regression analysis we predicted the likelihood of endorsing the symptoms of difficulty falling asleep, difficulty staying asleep, and nonrestorative sleep by age, sex, alcohol intake, smoking, diabetes, heart disease, menopausal status, hypnotic use, hypertension, depression, education level, income, body mass index, respiratory symptoms, and pulmonary function.
North American communities.
13,563 participants aged 47 to 69 years.
None.
The prevalences of sleep complaints were 22%, 39%, and 35% for difficulty falling asleep, difficulty staying asleep, and nonrestorative sleep, respectively. In contrast to previous reports, we found that Black race was associated with reduced risk of sleep complaints. We also found that increasing age was associated with difficulty staying asleep but not with difficulty falling asleep or nonrestorative sleep. Medical illness, depression, lower socioeconomic status, and unhealthy behaviors were associated with increased risk of sleep complaints, which varied by risk factor.
In a well-characterized population-based study, specific sleep complaints have differing covariates. It is likely that difficulty falling asleep and difficulty staying asleep have different causes and outcomes. Sleep difficulties do not appear to be associated with black race per se.
Sleep complaintsamongelderly persons: communities
- Dj Foley
- Aa Monjan
- Brown
- Sl
- Em Simonsick
- Rb Wallace
- Blazer
Foley DJ, Monjan AA, Brown SL, Simonsick EM, Wallace RB, Blazer DG. Sleep complaintsamongelderly persons: communities. Sleep 1995;18:425–32.
Structured Clinical Interview for DSM-IV Axis I Disorders – Patient edition State Psychiatric Institute
- First Mb
- Spitzer Rl
- M Gibbon
- Williams
First MB, Spitzer RL, Gibbon M, and Williams JB, Structured Clinical Interview for DSM-IV Axis I Disorders – Patient edition, Version 2.0, New York: NY, New York: State Psychiatric Institute; 1996.
Structured Clinical Interview for DSM-IV Axis I Disorders. Patient Edition, Version 2.0. New York State Psychiatric Institute
- M B First
- R L Spitzer
- M Gibbon
- J B Williams
First, MB.; Spitzer, RL.; Gibbon, M.; Williams, JB. Structured Clinical Interview for DSM-IV Axis
I Disorders. Patient Edition, Version 2.0. New York State Psychiatric Institute; New York, New
York: 1996.