Showing papers on "Polysomnography published in 2009"

Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults.

Abstract: Background Obstructive sleep apnea (OSA) is a common chronic disorder that often requires lifelong care. Available practice parameters provide evidence-based recommendations for addressing aspects of care. Objective This guideline is designed to assist primary care providers as well as sleep medicine specialists, surgeons, and dentists who care for patients with OSA by providing a comprehensive strategy for the evaluation, management and long-term care of adult patients with OSA. Methods The Adult OSA Task Force of the American Academy of Sleep Medicine (AASM) was assembled to produce a clinical guideline from a review of existing practice parameters and available literature. All existing evidence-based AASM practice parameters relevant to the evaluation and management of OSA in adults were incorporated into this guideline. For areas not covered by the practice parameters, the task force performed a literature review and made consensus recommendations using a modified nominal group technique. Recommendations Questions regarding OSA should be incorporated into routine health evaluations. Suspicion of OSA should trigger a comprehensive sleep evaluation. The diagnostic strategy includes a sleep-oriented history and physical examination, objective testing, and education of the patient. The presence or absence and severity of OSA must be determined before initiating treatment in order to identify those patients at risk of developing the complications of sleep apnea, guide selection of appropriate treatment, and to provide a baseline to establish the effectiveness of subsequent treatment. Once the diagnosis is established, the patient should be included in deciding an appropriate treatment strategy that may include positive airway pressure devices, oral appliances, behavioral treatments, surgery, and/or adjunctive treatments. OSA should be approached as a chronic disease requiring long-term, multidisciplinary management. For each treatment option, appropriate outcome measures and long-term follow-up are described.

Quantifying the risk of neurodegenerative disease in idiopathic REM sleep behavior disorder

Abstract: Objective Idiopathic REM sleep behavior disorder (RBD) is a potential preclinical marker for the development of neurodegenerative diseases, particularly Parkinson disease (PD) and Lewy body dementia. However, the long-term risk of developing neurodegeneration in patients with idiopathic RBD has not been established. Obtaining an accurate picture of this risk is essential for counseling patients and for development of potential neuroprotective therapies. Methods We conducted a follow-up study of all patients seen at the sleep disorders laboratory at the Hopital du Sacre Coeur with a diagnosis of idiopathic RBD. Diagnoses of parkinsonism and dementia were defined according to standard criteria. Survival curves were constructed to estimate the 5-, 10-, and 12-year risk of developing neurodegenerative disease. Results Of 113 patients, 93 (82%) met inclusion criteria. The mean age of participants was 65.4 years and 75 patients (80.4%) were men. Over the follow-up period, 26/93 patients developed a neurodegenerative disorder. A total of 14 patients developed PD, 7 developed Lewy body dementia, 4 developed dementia that met clinical criteria for AD, and 1 developed multiple system atrophy. The estimated 5-year risk of neurodegenerative disease was 17.7%, the 10-year risk was 40.6%, and the 12-year risk was 52.4%. Conclusions Although we have found a slightly lower risk than other reports, the risk of developing neurodegenerative disease in idiopathic REM sleep behavior disorder is substantial, with the majority of patients developing Parkinson disease and Lewy body dementia.

Cognitive behavioral therapy, singly and combined with medication, for persistent insomnia: a randomized controlled trial.

Abstract: Context Cognitive behavioral therapy (CBT) and hypnotic medications are efficacious for short-term treatment of insomnia, but few patients achieve complete remission with any single treatment. It is unclear whether combined or maintenance therapies would enhance outcome. Objectives To evaluate the added value of medication over CBT alone for acute treatment of insomnia and the effects of maintenance therapies on long-term outcome. Design, Setting, and Patients Prospective, randomized controlled trial involving 2-stage therapy for 160 adults with persistent insomnia treated at a university hospital sleep center in Canada between January 2002 and April 2005. Interventions Participants received CBT alone or CBT plus 10 mg/d (taken at bedtime) of zolpidem for an initial 6-week therapy, followed by extended 6-month therapy. Patients initially treated with CBT attended monthly maintenance CBT for 6 months or received no additional treatment and those initially treated with combined therapy (CBT plus 10 mg/d of zolpidem) continued with CBT plus intermittent use of zolpidem or CBT only. Main Outcome Measures Sleep onset latency, time awake after sleep onset, total sleep time, and sleep efficiency derived from daily diaries (primary outcomes); treatment response and remission rates derived from the Insomnia Severity Index (secondary outcomes). Results Cognitive behavioral therapy used singly or in combination with zolpidem produced significant improvements in sleep latency, time awake after sleep onset, and sleep efficiency during initial therapy (all P Conclusion In patients with persistent insomnia, the addition of medication to CBT produced added benefits during acute therapy, but long-term outcome was optimized when medication is discontinued during maintenance CBT. Trial Registration clinicaltrials.gov Identifier: NCT00042146

Insomnia with objective short sleep duration is associated with a high risk for hypertension.

Abstract: INSOMNIA IS, BY FAR, THE MOST COMMONLY ENCOUNTERED SLEEP DISORDER IN MEDICAL PRACTICE. HOWEVER, RELATIVELY LITTLE IS KNOWN about the mechanisms, causes, clinical course, and consequences of this highly prevalent chronic condition.1,2 Many studies have established that insomnia is highly comorbid with psychiatric disorders and is a risk factor for the development of depression, anxiety, and suicide.1,2 However, in contrast to the other most common sleep disorder, sleep disordered breathing (SDB), chronic insomnia has not been linked with significant medical morbidity, e.g., cardiovascular disorders. Few studies that have examined the association of chronic insomnia with hypertension have reported modest and inconsistent effects of little or no clinical significance.3–6 In fact, Kripke et al. found a reduced mortality rate for those individuals complaining of sleep difficulties after 6 years of follow-up.7 Most, but not all, studies have reported that insomnia is associated with an overall hypersecretion of ACTH and cortisol, suggesting an activation of the hypothalamic-pituitary-adrenal (HPA) axis in these patients.8–11 Given the well-established association of hypercortisolemia with significant medical morbidity, e.g., hypertension, metabolic syndrome, osteoporosis,12 the paucity of data linking insomnia with these medical disorders is a paradox. In our studies, we observed and reported that the activation of the HPA axis in insomnia was strongly and positively correlated with objective indices of sleep disturbance.8,9 Specifically, hypercortisolemia was found primarily in insomniacs who demonstrated short sleep duration in the sleep laboratory but not in those whose objective sleep duration was similar to that of normal sleepers. Similarly, earlier studies have shown higher autonomic activation, including heart rate, 24-h metabolic rate, and impaired heart rate variability, in insomniacs selected based on objective polysomnographic criteria.13–16 Based on these observations, we speculate that objective short sleep duration may be an index of the biological severity of the disorder and that insomniacs with short sleep duration are at high risk for adverse medical outcomes. To test this hypothesis, we examined the joint effect of the complaints of chronic insomnia and poor sleep (a milder form of insomnia), and objective sleep duration on the prevalent hypertension in a large cross-sectional population-based sample from central Pennsylvania. We hypothesized that chronic insomnia is associated with a significant risk of hypertension, and that the comorbidity of insomnia and hypertension is enhanced by objective short sleep duration.

The New AASM Criteria for Scoring Hypopneas: Impact on the Apnea Hypopnea Index

Abstract: POLYSOMNOGRAPHY (PSG) IS PERFORMED FOR A WIDE VARIETY OF INDICATIONS, MOST COMMONLY FOR INVESTIGATION OF OBSTRUCTIVE SLEEP APNEA (OSA). OSA is characterized by repeated episodes of upper airway obstruction resulting in cessation (apnea) or reduction (hypopnea) in airflow during sleep. The apnea hypopnea index (AHI), a count of the number of apneas and hypopneas per hour of sleep, is the key measure used for case identification, for quantifying disease severity, and for defining disease prevalence in normal and clinical populations. Despite the importance of this measure, inter-laboratory variations in apnea and, in particular, hypopnea definition have been reported.1,2 Differences in hypopnea definition relate to the degree of airflow reduction and/or oxygen desaturation required and the requirement for associated EEG arousal. The effect of varying definitions of hypopnea on AHI has been examined in a number of studies3–6 and the importance of standardizing the hypopnea definition, and thereby reducing inter-laboratory variability in AHI, has been recognized.3,5,7,8 In 1999, the American Academy of Sleep Medicine (AASM) produced a consensus report,9 targeted at clinical research rather than clinical practice,10 recommending standardized scoring criteria for a range of respiratory events. These guidelines (also known as “Chicago Criteria”) described 2 types of hypopneas: (i) Those with a > 50% decrease in a valid measure of airflow without a requirement for associated oxygen desaturation or arousal, and (ii) Those with a lesser airflow reduction in association with oxygen desaturation of > 3% or an arousal. The lack of clinical practice guidelines was addressed in 2001 when the AASM, via the Clinical Practices Review Committee, published a position paper11 which described a hypopnea as an abnormal respiratory event lasting ≥ 10 sec with ≥ 30% reduction in thoracoabdominal movement or airflow, and with ≥ 4% oxygen desaturation. This is currently the approved hypopnea definition for the Centers for Medicare and Medicaid Services in the United States to determine eligibility for treatment funding.12 Nevertheless, in 2005 the AASM, via the Practice Parameters Committee, reported that, “Several clinical definitions of hypopnea are in clinical use and there is no clear consensus.”13 In a further attempt to improve standardization, the AASM recently published the Manual for the Scoring of Sleep and Associated Events.14 In this manual there is a “recommended” and an “alternative” hypopnea definition; and either can be used at the discretion of the clinician or investigator. The recommended definition is the same as the definition published in the AASM 2001 position paper: hypopnea scoring requires ≥ 30% reduction in nasal pressure signal excursions from baseline and associated ≥ 4% desaturation from pre-event baseline. The alternative definition requires ≥ 50% reduction in nasal pressure signal excursions and associated ≥ 3% desaturation or arousal. Introduction of new standards is likely to lead to a period when individual laboratories assess and change their practices and when different laboratories use different methodologies. This study aims to assist in interpretation of clinical or research results in this setting. Specifically, this study examines the impact of the 2 recently published hypopnea definitions on the AHI, compared to the previously published “Chicago” hypopnea definition, and subsequently examines the impact on the measured prevalence of OSA in a cohort of patients presenting for diagnosis or exclusion of obstructive sleep apnea. Compared to similar previous studies3–6 it is unique in its focus on published standard hypopnea definitions.

Sleep in Children With Attention-Deficit/Hyperactivity Disorder: Meta-Analysis of Subjective and Objective Studies

Abstract: Objective To perform a meta-analysis of subjective (i.e., based on questionnaires) and objective (i.e., using poly-somnography or actigraphy) studies comparing sleep in children with attention-deficit/hyperactivity disorder (ADHD) versus controls. Method We searched for subjective and objective sleep studies (1987–2008) in children with ADHD (diagnosed according to standardized criteria). Studies including subjects pharmacologically treated or with comorbid anxiety/depressive disorders were excluded. Results Sixteen studies, providing 9 subjective and 15 objective parameters and including a total pooled sample of 722 children with ADHD versus 638 controls, were retained. With regard to subjective items, the meta-analysis indicated that children with ADHD had significantly higher bedtime resistance ( z = 6.94, p z = 9.38, p z = 2.15, p = .031), difficulties with morning awakenings ( z = 5.19, p z = 2.05, p = .040), and daytime sleepiness ( z = 1.96, p = .050) compared with the controls. As for objective parameters, sleep onset latency (on actigraphy), the number of stage shifts/hour sleep, and the apnea-hypopnea index were significantly higher in the children with ADHD compared with the controls ( z = 3.44, p = .001; z = 2.43, p = .015; z = 3.47, p = .001, respectively). The children with ADHD also had significantly lower sleep efficiency on polysomnography ( z = 2.26, p = .024), true sleep time on actigraphy ( z = 2.85, p = .004), and average times to fall asleep for the Multiple Sleep Latency Test ( z = 6.37, p Conclusions The children with ADHD are significantly more impaired than the controls in most of the subjective and some of the objective sleep measures. These results lay the groundwork for future evidence-based guidelines on the management of sleep disturbances in children with ADHD.

Sleep disordered breathing in children in a general population sample: prevalence and risk factors.

Abstract: THE PREVALENCE OF SLEEP DISORDERED BREATHING (SDB) IN CHILDREN, BASED ON OBJECTIVE FINDINGS, HAS BEEN ESTIMATED IN SEVERAL STUDIES.1–10 These prevalence estimates have varied widely from 0.7% to 13.0%. This wide range of prevalence is at least partially due to the fact that SDB in children was defined based on an assortment of methods of assessing for the presence of SDB. These methods included: only hemoglobin oxygen saturation (SpO2)2,8; SpO2 + airflow3,4; and SpO2 + airflow + effort.5,7,9 Only 3 of these studies used a full polysomnogram (PSG),1,6,10 however, the number of subjects evaluated in these PSG studies was very small (N = 12–50). The majority of these studies had relatively narrow age ranges,2–4,6–10 while others had relatively wide age ranges.1,5 Some of these studies were primarily focused on ages < 6 years 2–4,8 while others included subjects as old as 18 years.1,5 Another limitation of the available studies is that they have not systematically assessed a wide range of risk factors that may contribute to SDB in children. This may reflect the paucity studies large enough to evaluate potential variables. Thus, the objectives of this study were (1) to establish the prevalence of SDB based on cutoff points of respiratory events that we have previously observed to be associated with a clinically significant risk (i.e., elevated systolic blood pressure), and (2) to identify independent risk factors for SDB. This study is based on the largest population-based sample of elementary school-aged children available to date.

Obstructive Sleep Apnea Among Obese Patients With Type 2 Diabetes

Abstract: OBJECTIVE To assess the risk factors for the presence and severity of obstructive sleep apnea (OSA) among obese patients with type 2 diabetes. RESEARCH DESIGN AND METHODS Unattended polysomnography was performed in 306 participants. RESULTS Over 86% of participants had OSA with an apnea-hypopnea index (AHI) ≥5 events/h. The mean AHI was 20.5 ± 16.8 events/h. A total of 30.5% of the participants had moderate OSA (15 ≤ AHI <30), and 22.6% had severe OSA (AHI ≥30). Waist circumference (odds ratio 1.1; 95% CI 1.0–1.1; P = 0.03) was significantly related to the presence of OSA. Severe OSA was most likely in individuals with a higher BMI (odds ratio 1.1; 95% CI 1.0–1.2; P = 0.03). CONCLUSIONS Physicians should be particularly cognizant of the likelihood of OSA in obese patients with type 2 diabetes, especially among individuals with higher waist circumference and BMI.

Sleep habits and susceptibility to the common cold.

Abstract: Background Sleep quality is thought to be an important predictor of immunity and, in turn, susceptibility to the common cold. This article examines whether sleep duration and efficiency in the weeks preceding viral exposure are associated with cold susceptibility. Methods A total of 153 healthy men and women (age range, 21-55 years) volunteered to participate in the study. For 14 consecutive days, they reported their sleep duration and sleep efficiency (percentage of time in bed actually asleep) for the previous night and whether they felt rested. Average scores for each sleep variable were calculated over the 14-day baseline. Subsequently, participants were quarantined, administered nasal drops containing a rhinovirus, and monitored for the development of a clinical cold (infection in the presence of objective signs of illness) on the day before and for 5 days after exposure. Results There was a graded association with average sleep duration: participants with less than 7 hours of sleep were 2.94 times (95% confidence interval [CI], 1.18-7.30) more likely to develop a cold than those with 8 hours or more of sleep. The association with sleep efficiency was also graded: participants with less than 92% efficiency were 5.50 times (95% CI, 2.08-14.48) more likely to develop a cold than those with 98% or more efficiency. These relationships could not be explained by differences in prechallenge virus-specific antibody titers, demographics, season of the year, body mass, socioeconomic status, psychological variables, or health practices. The percentage of days feeling rested was not associated with colds. Conclusion Poorer sleep efficiency and shorter sleep duration in the weeks preceding exposure to a rhinovirus were associated with lower resistance to illness.

Sleep duration and biomarkers of inflammation.

Abstract: MOUNTING EVIDENCE FROM BOTH OBSERVATIONAL AND EXPERIMENTAL RESEARCH SUGGESTS SLEEP DURATION PLAYS AN IMPORTANT ROLE IN HEALTH. Studies suggest both short and extended durations of sleep are associated with increased risk for all-cause mortality, coronary heart disease, diabetes, and obesity.1–5 The mechanisms by which altered sleep duration affects health are unclear, but experimental studies suggest altered sleep may impact levels of cytokines known to be important in regulating inflammation. Experimental sleep deprivation has been shown to acutely elevate pro-inflammatory cytokine levels including C-reactive protein (CRP) and interleukin-6 (IL-6).6–8 However, it is not clear whether this pro-inflammatory effect observed with short-term sleep deprivation experiments persists chronically. While one week of modest sleep restriction has been associated with elevations in IL-6 and tumor necrosis factor alpha (TNFα),9 a large population based study found no relationship between habitual sleep duration in the long term and CRP levels.10 Because chronic elevations in cytokines such as CRP and IL-6 are associated with an increased risk of adverse health outcomes such as diabetes and heart disease,11–13 any effect of sleep duration on regulation of these cytokines could have important long-term health effects. In this study, we sought to use a well-characterized cohort with standardized polysomnography (PSG) that allowed careful adjustment for sleep apnea severity, to examine whether an association exists between sleep duration and inflammatory mediators that might explain the associations between sleep duration and disease.

Updated systematic review of tonsillectomy and adenoidectomy for treatment of pediatric obstructive sleep apnea/hypopnea syndrome.

Abstract: Objective Perform an updated systematic review and meta-analysis to determine the cure rate of tonsillectomy and adenoidectomy (T&A) for pediatric obstructive sleep apnea/hypopnea syndrome (OSAHS). Methods A systematic review was performed to identify English-language studies that evaluate the treatment of pediatric (age Results The meta-analysis included 1079 subjects (mean sample size of 42 patients) with a mean age of 6.5 years. The effect measure was the percentage of pediatric patients with OSAHS who were successfully treated (k = 22 studies) with T&A based on preoperative and postoperative PSG data. Random-effects model estimated the treatment success of T&A was 66.3 percent, when cure was defined per each individual study. When “cure” was defined as an apnea-hypopnea index (AHI) of Conclusions Contrary to popular belief, meta-analysis of current literature demonstrates that pediatric sleep apnea is often not cured by T&A. Although complete resolution is not achieved in most cases, T&A still offers significant improvements in AHI, making it a valuable first-line treatment for pediatric OSAHS.

Portuguese-language version of the Epworth sleepiness scale: validation for use in Brazil

Abstract: Objective: The aim of this study was to develop a Portuguese-language version of the Epworth sleepiness scale (ESS) for use in Brazil. Methods: The steps involved in creating the ESS in Brazilian Portuguese (ESS-BR) were as follows: translation; back-translation; comparison (by a committee) between the translation and the back-translation; and testing in bilingual individuals. The ESS-BR was applied to a group of patients who were submitted to overnight polysomnography in order to identify obstructive sleep apnea-hypopnea syndrome (OSAHS), insomnia and primary snoring. A control group was composed of subjects with a history of normal sleep habits, without reported snoring. Results: A total of 114 patients and 21 controls were included. The 8-item scores of the ESS-BR had an overall reliability coefficient of 0.83. The study group was composed of 59 patients with OSAHS, 34 patients with primary snoring and 21 patients with insomnia. One-way ANOVA demonstrated significant differences in ESS-BR scores among the four diagnostic groups (p 0.05). The ESS-BR scores were significantly higher for OSAHS patients and for primary snorers than for controls (p < 0.05). In addition, the scores for OSAHS patients were significantly higher than were those for primary snorers (p < 0.05). Conclusions: The results of the present study demonstrate that the ESS-BR is a valid and reliable instrument for the assessment of daytime sleepiness, equivalent to its original version when applied to individuals who speak Brazilian Portuguese.

Prospective study of sleep-disordered breathing and hypertension: The sleep heart health study

Abstract: Rationale: Cross-sectional epidemiologic studies show an association between sleep-disordered breathing and hypertension, but only one cohort study has examined sleep-disordered breathing as a risk factor for incident hypertension. Objectives: To examine whether sleep-disordered breathing increases the risk of incident hypertension among persons 40 years of age and older. Methods: In a prospective cohort study, we analyzed data from 2,470 participants who at baseline did not have hypertension, defined as blood pressure of at least 140/90 mm Hg or taking antihypertensive medication. The apnea-hypopnea index (AHI), the number of apneas plus hypopneas per hour of sleep, was measured by overnight in-home polysomnography. We estimated odds ratios for developing hypertension during 5 years of follow-up according to baseline AHI. Measurements and Main Results: The odds ratios for incident hypertension increased with increasing baseline AHI; however, this relationship was attenuated and not statistically significant after adjustment for baseline body-mass index. Although not statistically significant, the observed association between a baseline AHI greater than 30 and future hypertension (odds ratio, 1.51; 95% confidence interval, 0.93–2.47) does not exclude the possibility of a modest association. Conclusions: Among middle-aged and older persons without hypertension, much of the relationship between AHI and risk of incident hypertension was accounted for by obesity. After adjustment for body mass index, the AHI was not a significant predictor of future hypertension, although a modest influence of an AHI greater than 30 on hypertension could not be excluded.

Association between sleep and blood pressure in midlife: the CARDIA sleep study.

Abstract: Nearly one-third of Americans have high blood pressure,1 and worldwide 7 million deaths are attributed to high blood pressure each year.2 Recently, two large epidemiologic studies reported an association between self-reported sleep duration and the prevalence or incidence of hypertension.3, 4 Identifying a novel lifestyle risk factor for high blood pressure could lead to new interventions to prevent or reduce high blood pressure. Laboratory studies of short-term sleep deprivation have suggested potential mechanisms for a causal link between sleep loss and hypertension. Partial sleep deprivation is associated with increased sympathetic activity estimated from measures of heart rate variability.5, 6 Other studies have observed increased blood pressure after a night of partial 7, 8 or total sleep deprivation.9 Thus, sleep loss may lead to increased sympathetic nervous activity which could cause high blood pressure if sleep loss were chronic. On a population level, previous epidemiologic studies have observed associations between shorter sleep duration and increased blood pressure.3, 4, 10-13 However, most of these studies were cross-sectional and relied on self-reported usual sleep duration, which is only moderately correlated with objectively-measured sleep duration.14, 15 Furthermore, the possible role of sleep quality independent of sleep duration as a risk factor for high blood pressure has not been explored in adults. The goal of our study was to determine if objectively-measured sleep duration or quality predicted 5-year incidence of hypertension and changes in systolic and diastolic blood pressure in a community-based sample of persons in early middle age.

Sleep classification according to AASM and Rechtschaffen & Kales: effects on sleep scoring parameters.

Abstract: FOR APPROXIMATELY 40 YEARS THE ONLY WIDELY ACCEPTED STANDARD FOR DESCRIBING THE HUMAN SLEEP PROCESS WAS THE MANUAL OF SLEEP CLASSIFICATION by Rechtschaffen and Kales.1 On the basis of these scoring rules, sleep recordings are divided into 7 discrete stages (wake, stage 1, stage 2, stage 3, stage 4, stage REM, and movement time). Even though in many cases this standard is useful, the rules of Rechtschaffen and Kales have also been criticized for leaving plenty of room for subjective interpretation, which leads to a great variability in the visual evaluation of sleep stages.2,3 Last but not least, the standard rules were developed for young healthy adults4,5 and do not necessarily directly apply to elderly subjects and patients. The American Academy of Sleep Medicine (AASM)6 modified the standard guidelines for sleep classification by Rechtschaffen and Kales and developed a new guideline for terminology, recording method, and scoring rules for sleep-related phenomena. The manual is the result of a review of literature, analysis and consensus which addresses 7 topics: digital analysis and reporting parameters, visual scoring, arousal, cardiac and respiratory events, movements and pediatric scoring. One of the major changes is a change in terminology: in the AASM classification, sleep stages S1 to S4 are referred to as N1, N2, and N3, with N3 reflecting slow wave sleep (SWS, RK stage REM is referred to as stage R. According to the AASM manual, a minimum of 3 EEG derivations, sampling activity from the frontal, central, and occipital regions, has to be recorded. The recommended derivations are F4-M1, C4-M1, and O2-M1 (right-sided active electrodes and a reference over the left mastoid, rather than the ear).7 The new manual also deals with the definition of the sleep-wake transition, sleep spindles, K-complexes, slow wave sleep, and REM sleep, as well as arousals and major body movements. In summary, the major changes of the new manual comprise EEG derivations, the merging of stages 3 and 4 into N3, the abolition of stage “movement time,” the simplification of many context rules as well as the recommendation of sampling rates and filter settings for polysomnographic (PSG) reporting and for user interfaces of computer-assisted sleep analysis.6 To date there are no studies evaluating the effects of the new standard on sleep scoring data. The aim of the present investigation was to describe in detail differences between visual sleep scoring according to the Rechtschaffen and Kales classification and scoring based on the new AASM guidelines in normal subjects of different age groups and sleep-disturbed patients.

Race and Financial Strain are Independent Correlates of Sleep in Midlife Women: The SWAN Sleep Study

Abstract: MOUNTING EVIDENCE SUGGESTS THAT SLEEP DIFFERS SIGNIFICANTLY ACROSS RACIAL AND ETHNIC GROUPS IN WAYS THAT MAY BE IMPORTANT TO health and functioning.1–5 Most consistent among these effects is a marked decrease in laboratory-assessed slow wave sleep and a concomitant increase in stages 1 and 2 of NREM sleep in African Americans compared to Caucasians.3–7 Other dimensions of sleep shown to differ between African Americans and Caucasians include sleep duration, continuity and subjective sleep quality, although these relationships are not as strong and consistent as those observed for sleep architecture.8 Far fewer studies have compared sleep across other racial and ethnic groups. Hale and Do9 evaluated data from 32,749 respondents to the 1990 health promotion supplement of the National Health Interview Survey (NHIS) and found that, compared to Caucasians, the prevalence of short sleepers (< 6 hours/night) was higher among all racial and ethnic minorities surveyed including African Americans, Hispanics and non-Hispanic “others.” As measured by one night of in-home polysomnography (PSG) collected in the population-based Sleep Heart Health Study (SHHS), Redline and colleagues reported that American Indians and African Americans had lighter sleep than Caucasians, Hispanics, or Asian Americans.10 Despite growing evidence that sleep differs by race and/or ethnic minority status, few studies have evaluated possible causes or correlates of these differences. It has been suggested that socioeconomic status (SES), which is closely tied to race and ethnic minority status in many countries, including the United States, may play an important role in the relationship between minority racial/ethnic status and disturbed sleep.5,6,11 Indeed, a number of studies have reported significant associations among subjective sleep complaints and various indices of SES including lower education, occupational status and income, although these studies did not evaluate the influence of race on the SES-sleep relationship.12–17 Three recent studies reported that both race/ethnicity and traditional measures of SES, income, and education, were significant correlates of behavioral or PSG-assessed indices of sleep.2,6,18 For instance, Mezick and colleagues evaluated the independent effects of race and SES on sleep in a cohort of midlife men and women who were self-identified as either non-Hispanic Caucasian or African American. Lower SES, as measured by a composite score of income and education, was associated with greater PSG-assessed wakefulness after sleep onset, after adjusting for other confounding variables, including race. Sleep quality, duration, and architecture were unrelated to SES in the Mezick et al., study. These studies provide some support for the hypothesis that certain dimensions of sleep may be related to traditional markers of SES, independent of race. The extent to which other dimensions of SES affect, or are affected by, sleep have received less empirical attention. We have hypothesized that financial strain, which is a key chronic stressor associated with lower SES, may be a sensitive marker of the SES-sleep relationship.11 We reported that financial strain, operationalized as difficulties with paying for basics like food and housing, was a significant correlate of increased subjective sleep quality complaints in a sample of 462 midlife women, one-third of whom were African American.11 In multivariate models, financial strain attenuated the relationship between income and sleep quality, which is consistent with the hypothesis that stress pathways are important to the SES-sleep relationship. Stress pathways by which financial strain might interfere with sleep include increased worries and negative affect, as well as endocrine and autonomic dysregulation.19–24 More recently, we demonstrated that chronic and ongoing financial strain was associated with significant decreases in PSG-assessed sleep efficiency in a large sample of community-dwelling elders, after adjusting for a host of variables known to impact sleep in late life.25 Although these studies suggest that financial strain may be an important correlate of sleep, the extent to which financial strain plays a role in the SES-sleep or race-sleep relationship has not been evaluated. The present study evaluated relationships among race and markers of SES in relation to sleep in a multiracial sample of midlife women enrolled in the SWAN Sleep Study, which was designed to characterize sleep during the menopausal transition. Sleep during the menopausal transition provides an opportune model for evaluating the influence of race and SES on sleep because subjective sleep complaints and some sleep disorders are much more frequent in perimenopausal and menopausal women.26–30 Moreover, sleep disturbances that arise during the menopausal transition may be a marker for the development of later chronic health conditions and declines in general health and functioning occurring in the postmenopausal years. SWAN Sleep Study participants included African American, Caucasian, and Chinese women. Measures of sleep were subjective sleep quality, as measured by the validated Pittsburgh Sleep Quality Index (PSQI),31 and indices of sleep duration, continuity, and architecture including NREM electroencephalographic (EEG) power, as measured by multinight in-home PSG. We hypothesized that African American race would be associated with worse sleep, compared to Caucasian and Chinese participants. We further hypothesized that markers of SES, as measured by educational attainment and financial strain, would affect the race-sleep relationship. Specifically, we hypothesized that lower educational attainment and financial strain would attenuate observed relationships among race and sleep after adjusting for other factors that might confound relationships among race, SES, and sleep in midlife women.

Long-term homeostasis of extracellular glutamate in the rat cerebral cortex across sleep and waking states.

Abstract: Neuronal firing patterns, neuromodulators, and cerebral metabolism change across sleep waking states, and the synaptic release of glutamate is critically involved in these processes. Extrasynaptic glutamate can also affect neural function and may be neurotoxic, but whether and how extracellular glutamate is regulated across sleep-waking states is unclear. To assess the effect of behavioral state on extracellular glutamate at high temporal resolution, we recorded glutamate concentration in prefrontal and motor cortex using fixed-potential amperometry in freely behaving rats. Simultaneously, we recorded local field potentials (LFP) and electroencephalograms (EEG) from contralateral cortex. We observed dynamic, progressive changes in the concentration of glutamate that switched direction as a function of behavioral state. Specifically, the concentration of glutamate increased progressively during waking (0.329 ± 0.06 %/min) and rapid eye movement (REM) sleep (0.349 ±0.13 %/min). This increase was opposed by a progressive decrease during non-REM (NREM) sleep (0.338 ± 0.06 %/min). During a 3-hr sleep deprivation period, glutamate concentrations initially exhibited the progressive rise observed during spontaneous waking. As sleep pressure increased, glutamate concentrations ceased to increase and began decreasing despite continuous waking. During NREM sleep, the rate of decrease in glutamate was positively correlated with sleep intensity, as indexed by LFP slow wave activity. The rate of decrease doubled during recovery sleep after sleep deprivation. Thus, the progressive increase in cortical extrasynaptic glutamate during EEG-activated states is counteracted by a decrease during NREM sleep that is modulated by sleep pressure. These results provide evidence for a long-term homeostasis of extracellular glutamate across sleep-waking states.

Nocturnal Arrhythmias Across a Spectrum of Obstructive and Central Sleep-Disordered Breathing in Older Men: Outcomes of Sleep Disorders in Older Men (MrOS Sleep) Study

Abstract: .001, respectively). The highest RDI quartile was associated with increased odds of AF (odds ratio [OR], 2.15; 95% confidence interval [CI], 1.19-3.89) and CVE (OR, 1.43; 95% CI, 1.12-1.82) compared with the lowest quartile. An increasing OSA quartile was significantly associated with increasing CVE (P value for trend, .01) but not AF.Centralsleepapneawasmorestronglyassociatedwith AF(OR,2.69;95%CI,1.61-4.47)thanCVE(OR,1.27;95% CI, 0.97-1.66). Hypoxia level was associated with CVE (P value for trend, .001); those in the highest hypoxia category had an increased odds of CVE (OR, 1.62; 95% CI, 1.23-2.14) compared with the lowest quartile.

Cognitive behavioral therapy for patients with primary insomnia or insomnia associated predominantly with mixed psychiatric disorders: a randomized clinical trial.

Abstract: CHRONIC INSOMNIA IS A SERIOUS FORM OF SLEEP DISTURBANCE ASSOCIATED WITH REDUCED QUALITY OF LIFE, INCREASED RISKS FOR SERIOUS PSYCHIATRIC illness, and enhanced healthcare utilization among millions worldwide.1–3 Insomnia may present either as a primary sleep disorder or as a disorder comorbid with another sleep, medical, or psychiatric disorder or a combination thereof. Both primary insomnia (PI) and comorbid insomnia (CMI) are relatively common maladies, but CMI is more prevalent than PI in both clinical venues4,5 and the general population at large.6 Moreover, CMI may be more persistent and have even more serious consequences than PI. Recent data,7 for example, show that insomnia sufferers with comorbid gastrointestinal problems, chronic pain, hypertension, or problems with breathing or urination report more chronic insomnia than do those without such conditions. Furthermore, when insomnia occurs comorbid with a psychiatric illness such as major depression, it complicates disease management and often remains as a residual symptom that enhances risk for both suicide and relapse.8,9 In view of these considerations, patients who present with insomnia and particularly those with CMI warrant early and effective treatment. Pharmacotherapy with benzodiazepine receptor agonists or sedating antidepressants currently remains the most common treatment offered to patients with insomnia.10 However, cognitive behavioral therapy (CBT), designed to address sleep-disruptive beliefs and habits, has become an increasingly well-regarded insomnia treatment.10 Results of meta-analyses (e.g., Smith, et al.11) and head-to-head comparisons12 suggest CBT produces short-term sleep improvements that compare favorably to those achieved with various forms of pharmacotherapy. Furthermore, sleep improvements following CBT appear to endure long after treatment is completed,13 and limited data suggest that patients prefer CBT over treatment with sleep medications.14 Given such observations, CBT has become a popular alternative for insomnia management. Most evidence supporting the efficacy of CBT comes from studies conducted with patients with PI, although there is some limited evidence supporting use of this treatment with CMI as well. Some uncontrolled case series or clinic-based studies have suggested the efficacy of CBT among patients with CMI and mixed psychiatric and medical conditions.15 Other case series or quasi-experimental studies have suggested CBT may be efficacious for treating insomnia in such specific patient groups as those with chronic pain,16 cancer,17 posttraumatic stress disorder,18 and clinical depression19 and those with mixed serious mental disorders.20 In addition, a number of small to moderately sized, single-site, randomized clinical trials have suggested that CBT is efficacious for patients with insomnia and comorbid chronic peripheral pain syndromes,21 treated breast cancer,22 fibromyalgia23, mixed medical disorders,24 mixed psychiatric and medical disorders,25 and alcoholism.26 Despite these findings, it is yet to be determined whether patients with PI or CMI show similar improvement from an equal and standard dose of CBT intervention. The current study tested the relative efficacy of CBT against a sleep hygiene control treatment (SH) in patients with PI and in a group of patients with CMI composed predominantly of individuals with mixed comorbid psychiatric disorders. The study hypotheses predicted that CBT would produce significantly greater short- and longer-term improvements in insomnia symptoms than would sleep hygiene in the sample as a whole. The data obtained were also examined to assess the relative efficacy of CBT in the PI and CMI groups considered separately.

Cross-sectional and longitudinal associations between objectively measured sleep duration and body mass index: the CARDIA Sleep Study.

Abstract: Numerous studies have found an association between shorter sleep duration and higher body mass index (BMI) in adults. Most previous studies have been cross-sectional and relied on self-reported sleep duration, which may not be very accurate. In the Coronary Artery Risk Development in Young Adults (CARDIA) Sleep Study (2000-2006), the authors examine whether objectively measured sleep is associated with BMI and change in BMI. They use several nights of wrist actigraphy to measure sleep among participants in an ongoing cohort of middle-aged adults. By use of linear regression, the authors examine whether average sleep duration or fragmentation is associated with BMI and 5-year change in BMI, adjusting for confounders. Among 612 participants, sleep duration averaged 6.1 hours and was grouped into 4 categories. Both shorter sleep and greater fragmentation were strongly associated with higher BMI in unadjusted cross-sectional analysis. After adjustment, BMI decreased by 0.78 kg/m(2) (95% confidence interval: -1.6, -0.002) for each increasing sleep category. The association was very strong in persons who reported snoring and weak in those who did not. There were no longitudinal associations between sleep measurements and change in BMI. The authors confirmed a cross-sectional association between sleep duration and BMI using objective sleep measures, but they did not find that sleep predicted change in BMI. The mechanism underlying the cross-sectional association is not clear.