Showing papers on "Polysomnography published in 2005"
TL;DR: In men, severe obstructive sleep apnoea-hypopNoea significantly increases the risk of fatal and non-fatal cardiovascular events and CPAP treatment reduces this risk.
4,132 citations
TL;DR: The obstructive sleep apnea syndrome significantly increases the risk of stroke or death from any cause, and the increase is independent of other risk factors, including hypertension.
Abstract: background Previous studies have suggested that the obstructive sleep apnea syndrome may be an important risk factor for stroke. It has not been determined, however, whether the syndrome is independently related to the risk of stroke or death from any cause after adjustment for other risk factors, including hypertension. methods In this observational cohort study, consecutive patients underwent polysomnography, and subsequent events (strokes and deaths) were verified. The diagnosis of the obstructive sleep apnea syndrome was based on an apnea–hypopnea index of 5 or higher (five or more events per hour); patients with an apnea–hypopnea index of less than 5 served as the comparison group. Proportional-hazards analysis was used to determine the independent effect of the obstructive sleep apnea syndrome on the composite outcome of stroke or death from any cause. results Among 1022 enrolled patients, 697 (68 percent) had the obstructive sleep apnea syndrome. At baseline, the mean apnea–hypopnea index in the patients with the syndrome was 35, as compared with a mean apnea–hypopnea index of 2 in the comparison group. In an unadjusted analysis, the obstructive sleep apnea syndrome was associated with stroke or death from any cause (hazard ratio, 2.24; 95 percent confidence interval, 1.30 to 3.86; P=0.004). After adjustment for age, sex, race, smoking status, alcohol-consumption status, body-mass index, and the presence or absence of diabetes mellitus, hyperlipidemia, atrial fibrillation, and hypertension, the obstructive sleep apnea syndrome retained a statistically significant association with stroke or death (hazard ratio, 1.97; 95 percent confidence interval, 1.12 to 3.48; P=0.01). In a trend analysis, increased severity of sleep apnea at baseline was associated with an increased risk of the development of the composite end point (P=0.005). conclusions The obstructive sleep apnea syndrome significantly increases the risk of stroke or death from any cause, and the increase is independent of other risk factors, including hypertension.
2,766 citations
TL;DR: These practice parameters are an update of the previously-published recommendations regarding the indications for polysomnography and related procedures in the diagnosis of sleep disorders.
Abstract: These practice parameters are an update of the previously-published recommendations regarding the indications for polysomnography and related procedures in the diagnosis of sleep disorders. Diagnostic categories include the following: sleep related breathing disorders, other respiratory disorders, narcolepsy, parasomnias, sleep related seizure disorders, restless legs syndrome, periodic limb movement sleep disorder, depression with insomnia, and circadian rhythm sleep disorders. Polysomnography is routinely indicated for the diagnosis of sleep related breathing disorders; for continuous positive airway pressure (CPAP) titration in patients with sleep related breathing disorders; for the assessment of treatment results in some cases; with a multiple sleep latency test in the evaluation of suspected narcolepsy; in evaluating sleep related behaviors that are violent or otherwise potentially injurious to the patient or others; and in certain atypical or unusual parasomnias. Polysomnography may be indicated in patients with neuromuscular disorders and sleep related symptoms; to assist in the diagnosis of paroxysmal arousals or other sleep disruptions thought to be seizure related; in a presumed parasomnia or sleep related seizure disorder that does not respond to conventional therapy; or when there is a strong clinical suspicion of periodic limb movement sleep disorder. Polysomnography is not routinely indicated to diagnose chronic lung disease; in cases of typical, uncomplicated, and noninjurious parasomnias when the diagnosis is clearly delineated; for patients with seizures who have no specific complaints consistent with a sleep disorder; to diagnose or treat restless legs syndrome; for the diagnosis of circadian rhythm sleep disorders; or to establish a diagnosis of depression.
1,883 citations
TL;DR: In this article, the authors did an observational study to compare incidence of fatal and non-fatal cardiovascular events in simple snorers, patients with untreated obstructive sleep apnoea-hypopnoeas, patients treated with CPAP, and healthy men recruited from the general population.
Abstract: Summary Background The effect of obstructive sleep apnoea-hypopnoea as a cardiovascular risk factor and the potential protective effect of its treatment with continuous positive airway pressure (CPAP) is unclear. We did an observational study to compare incidence of fatal and non-fatal cardiovascular events in simple snorers, patients with untreated obstructive sleep apnoea-hypopnoea, patients treated with CPAP, and healthy men recruited from the general population. Methods We recruited men with obstructive sleep apnoea-hypopnoea or simple snorers from a sleep clinic, and a population-based sample of healthy men, matched for age and body-mass index with the patients with untreated severe obstructive sleep apnoea-hypopnoea. The presence and severity of the disorder was determined with full polysomnography, and the apnoea-hypopnoea index (AHI) was calculated as the average number of apnoeas and hypopnoeas per hour of sleep. Participants were followed-up at least once per year for a mean of 10·1 years (SD 1·6) and CPAP compliance was checked with the built-in meter. Endpoints were fatal cardiovascular events (death from myocardial infarction or stroke) and non-fatal cardiovascular events (non-fatal myocardial infarction, non-fatal stroke, coronary artery bypass surgery, and percutaneous transluminal coronary angiography). Findings 264 healthy men, 377 simple snorers, 403 with untreated mild-moderate obstructive sleep apnoea-hypopnoea, 235 with untreated severe disease, and 372 with the disease and treated with CPAP were included in the analysis. Patients with untreated severe disease had a higher incidence of fatal cardiovascular events (1·06 per 100 person-years) and non-fatal cardiovascular events (2·13 per 100 person-years) than did untreated patients with mild-moderate disease (0·55, p=0·02 and 0·89, p Interpretation In men, severe obstructive sleep apnoea-hypopnoea significantly increases the risk of fatal and non-fatal cardiovascular events. CPAP treatment reduces this risk.
1,042 citations
TL;DR: People with obstructive sleep apnea have a peak in sudden death from cardiac causes during the sleeping hours, which contrasts strikingly with the nadir of sudden death at this period in people without obstructiveSleep apnea and in the general population.
Abstract: Background The risk of sudden death from cardiac causes in the general population peaks from 6 a.m. to noon and has a nadir from midnight to 6 a.m. Obstructive sleep apnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleep. Methods We reviewed polysomnograms and the death certificates of 112 Minnesota residents who had undergone polysomnography and had died suddenly from cardiac causes between July 1987 and July 2003. For four intervals of the day, we compared the rates of sudden death from cardiac causes among people with obstructive sleep apnea and the following: the rates among people without obstructive sleep apnea, the rates in the general population, and the expectations according to chance. For each interval, we assessed the median apnea–hypopnea index and the relative risk of sudden death from cardiac causes. We similarly analyzed sudden death from cardiac causes during...
930 citations
TL;DR: These data demonstrate a strong association between moderate to severe sleep-disordered breathing and prevalent stroke, independent of confounding factors and provide the first prospective evidence that sleep- Disordered breathing precedes stroke and may contribute to the development of stroke.
Abstract: Rationale: Sleep-disordered breathing has been linked to stroke in previous studies. However, these studies either used surrogate markers of sleep-disordered breathing or could not, due to cross-sectional design, address the temporal relationship between sleep-disordered breathing and stroke.
Objectives: To determine whether sleep-disordered breathing increases the risk for stroke.
Methods: We performed cross-sectional and longitudinal analyses on 1,475 and 1,189 subjects, respectively, from the general population. Sleep-disordered breathing was defined by the apnea–hypopnea index (frequency of apneas and hypopneas per hour of sleep) obtained by attended polysomnography. The protocol, including polysomnography, risk factors for stroke, and a history of physician-diagnosed stroke, was repeated at 4-yr intervals.
Measurements and Main Results: In the cross-sectional analysis, subjects with an apnea–hypopnea index of 20 or greater had increased odds for stroke (odds ratio, 4.33; 95% confidence interval, 1.32–14.24; p = 0.02) compared with those without sleep-disordered breathing (apnea–hypopnea index, <5) after adjustment for known confounding factors. In the prospective analysis, sleep-disordered breathing with an apnea–hypopnea index of 20 or greater was associated with an increased risk of suffering a first-ever stroke over the next 4 yr (unadjusted odds ratio, 4.31; 95% confidence interval, 1.31–14.15; p = 0.02). However, after adjustment for age, sex, and body mass index, the odds ratio was still elevated, but was no longer significant (3.08; 95% confidence interval, 0.74–12.81; p = 0.12).
Conclusions: These data demonstrate a strong association between moderate to severe sleep-disordered breathing and prevalent stroke, independent of confounding factors. They also provide the first prospective evidence that sleep-disordered breathing precedes stroke and may contribute to the development of stroke.
895 citations
TL;DR: In this paper, a comprehensive review of the relationship between sleep and depression is presented, focusing on the relationships between sleep disturbance and depression, and focusing on sleep-related hypotheses explaining the pathophysiology of depression.
Abstract: Background Of all the psychiatric disorders associated with insomnia, depression is the most common. It has been estimated that 90% of patients with depression complain about sleep quality. Since the first reports of short rapid eye movement (REM) latency in depressed patients and of the effect of sleep deprivation on depression in the 1970s, numerous sleep studies have provided extensive observations and theoretical hypotheses concerning the etiology and pathophysiology of depression. The aim of this review is to summarize knowledge regarding the relationships between sleep and depression. Data sources and selection MEDLINE and PsycINFO searches of the literature published in English or French between 1964 and 2005 that examined the relationships between sleep disturbance and depression were conducted. Search terms used were depression, depressive disorder, affective disorder, mood disorders, seasonal affective disorder, sleep, sleep disorders, insomnia, REM, polysomnography, sleep deprivation, electroencephalography, PET, SPECT, and fMRI. Data synthesis Two hundred five papers were identified and selected and then integrated into the following categories: sleep architecture, antidepressive therapies, age- and gender-associated differences, functional imaging results, and sleep-related hypotheses explaining the pathophysiology of depression. Conclusion Numerous studies provide findings indicating the remarkable relationship between sleep alterations and depression. Although the existing hypotheses are not likely to explain all aspects of the sleep alterations in depression, each may be worth being maintained for refinements of pathophysiologic models of depression as new data accumulate. Further research taking into account the heterogeneity of depressive disorder and linking the different areas of research is needed to develop more comprehensive theoretical models and new therapies for depression.
886 citations
TL;DR: The hypothesis that sleep duration is associated with obesity in a large longitudinally monitored United States sample supports earlier experimental sleep studies and provides a basis for future studies on weight control interventions that increase the quantity and quality of sleep.
Abstract: Study objectives Sleep deprivation has been hypothesized to contribute toward obesity by decreasing leptin, increasing ghrelin, and compromising insulin sensitivity. This study examines cross-sectional and longitudinal data from a large United States sample to determine whether sleep duration is associated with obesity and weight gain. Design Longitudinal analyses of the 1982-1984, 1987, and 1992 NHANES I Followup Studies and cross-sectional analysis of the 1982-1984 study. Setting Probability sample of the civilian noninstitutionalized population of the United States. Participants Sample sizes of 9,588 for the cross-sectional analyses, 8,073 for the 1987, and 6,981 for the 1992 longitudinal analyses. Measurements and results Measured weight in 1982-1984 and self-reported weights in 1987 and 1992. Subjects between the ages of 32 and 49 years with self-reported sleep durations at baseline less than 7 hours had higher average body mass indexes and were more likely to be obese than subjects with sleep durations of 7 hours. Sleep durations over 7 hours were not consistently associated with either an increased or decreased likelihood of obesity in the cross-sectional and longitudinal results. Each additional hour of sleep at baseline was negatively associated with change in body mass index over the follow-up period, but this association was small and statistically insignificant. Conclusions These findings support the hypothesis that sleep duration is associated with obesity in a large longitudinally monitored United States sample. These observations support earlier experimental sleep studies and provide a basis for future studies on weight control interventions that increase the quantity and quality of sleep.
874 citations
TL;DR: Investigating the prevalence and incidence of type II diabetes in subjects with SDB found diabetes is more prevalent in SDB and this relationship is independent of other risk factors, however, it is not clear that SDB is causal in the development of diabetes.
Abstract: Rationale: Cross-sectional association has been reported between sleep-disordered breathing (SDB) and insulin resistance, but no prospective studies have been performed to determine whether SDB is causal in the development of diabetes.Objectives: The purpose of our study was to investigate the prevalence and incidence of type II diabetes in subjects with SDB and whether an independent relationship exists between them.Methods: A cross-sectional and longitudinal analysis was performed in 1,387 participants of the Wisconsin Sleep Cohort. Full polysomnography was used to characterize SDB. Diabetes was defined in two ways: (1) physician-diagnosis alone or (2) for those with glucose measurements, either fasting glucose ⩾ 126 mg/dl or physician diagnosis.Measurements and Main Results: There was a greater prevalence of diabetes in subjects with increasing levels of SDB. A total of 14.7% of subjects with an apnea–hypopnea index (AHI) of 15 or more had a diagnosis of diabetes compared with 2.8% of subjects with an ...
737 citations
TL;DR: It appears that the presence of EDS is more strongly associated with depression and metabolic factors than with sleep-disordered breathing or sleep disruption per se, and patients with a complaint of E DS should be thoroughly assessed for depression and obesity/diabetes independent of whether sleep- disordered breathing is present.
Abstract: Design and Setting: We examined this question in the Penn State cohort (a random sample of 16,583 men and women from central Pennsylvania, ranging in age from 20 to 100 yr) A random subset of thiscohort(n1,741)wasfurtherevaluatedforonenightinthesleep laboratory Main Outcome Measure: The main measure was a complaint of EDS Results: The final logistic regression model indicated depression was the most significant risk factor for EDS followed by body mass index, age, typical sleep duration, diabetes, smoking, and finally sleep apnea The strength of the association with EDS decreased with increasing age, whereas the association of depression with EDS was stronger in the young EDS is more prevalent in the young (30 yr), suggesting the presence of unmet sleep needs and depression, and in theveryold(75yr),suggestingincreasingmedicalillnessandhealth problems EDS was associated with a reduced report of typical sleep duration without any association with objective polysomnographic measures Conclusions: It appears that the presence of EDS is more strongly associated with depression and metabolic factors than with sleepdisordered breathing or sleep disruption per se Our findings suggest that patients with a complaint of EDS should be thoroughly assessed for depression and obesity/diabetes independent of whether sleepdisordered breathing is present (J Clin Endocrinol Metab 90: 4510–4515, 2005)
635 citations
TL;DR: Middle-aged patients with OSA who are free of overt cardiovascular diseases have early signs of atherosclerosis, and all vascular abnormalities correlated significantly with the severity of the OSA, which supports the hypothesis that OSA plays an independent role in Atherosclerosis progression.
Abstract: Background: Obstructive sleep apnea (OSA) is associated with several cardiovascular diseases. However, the mechanisms are not completely understood. Recent studies have shown that OSA is associated with multiple markers of endothelial damage. We hypothesized that OSA affects functional and structural properties of large arteries, contributing to atherosclerosis progression. Methods and Measurements: Twelve healthy volunteers, 15 patients with mild to moderate OSA, and 15 with severe OSA matched for age, sex, and body mass index were studied by using (1) full standard overnight polysomnography; (2) carotid-femoral pulse wave velocity with a noninvasive automatic device; and (3) a high-definition echo-tracking device to measure intima-media thickness, diameter, and distensibility. All participants were free of hypertension, diabetes, and smoking, and were not on any medications. Patients with OSA were naive to treatment. Main Results: Significant differences existed between control subjects and patients wit...
TL;DR: In this paper, the authors performed a longitudinal cohort study of the cardiovascular consequences of sleep apnea in diverse US communities and found that moderate changes in weight were related to an increase or decrease in sleep disordered breathing.
Abstract: Background The relationship of weight changes to the incidence, progression, and remission of sleep-disordered breathing (SDB) is not well defined. This study aims to determine the relationship between change in weight and progression or remission of SDB by polysomnography. Methods We performed a longitudinal cohort study of the cardiovascular consequences of sleep apnea in diverse US communities. Sleep apnea and polysomnographic indicators of SDB were assessed 5 years apart. Results A total of 2968 men and women (mean age, 62 years) participated in the study. Men were more likely to have an increase in Respiratory Disturbance Index (RDI) with a given increase in weight than were women, and this was not explained by differences in starting weight, waist circumference, age, or ethnicity. In a linear regression analysis, both men and women had a greater increase in RDI with weight gain than a decrease in RDI with weight loss. In a categorical analysis of larger degrees of change, this sex difference was also evident. Associations were similar in diverse ethnic groups. However, SDB progressed over time, even in those with stable weight. Conclusion Modest changes in weight were related to an increase or decrease in SDB, and this association was stronger in men than in women.
TL;DR: The data support a protective effect of CPAP therapy against death from cardiovascular disease in patients with OSAS.
TL;DR: In this article, a review of the epidemiology, clinical presentation, and diagnosis of obstructive sleep apnea is presented, focusing on the neurocognitive sequelae of the disorder.
Abstract: Obstructive sleep apnea remains an important public health problem because of its neurocognitive sequelae This review covers the epidemiology, clinical presentation, and diagnosis of obstructive s
TL;DR: Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence as well as aspects of sleep homeostasis.
Abstract: STUDY OBJECTIVES:
To examine the effects of total sleep deprivation on adolescent sleep and the sleep electroencephalogram (EEG) and to study aspects of sleep homeostasis.
DESIGN: Subjects were studied during baseline and recovery sleep after 36 hours of wakefulness.
SETTING: Four-bed sleep research laboratory.
PARTICIPANTS: Seven prepubertal or early pubertal children (pubertal stage Tanner 1 or 2 = Tanner 1/2; mean age 11.9 years, SD +/- 0.8, 2 boys) and 6 mature adolescents (Tanner 5; 14.2 years, +/- 1.4, 2 boys).
INTERVENTIONS: Thirty-six hours of sleep deprivation.
MEASUREMENTS: All-night polysomnography was performed. EEG power spectra (C3/A2) were calculated using a Fast Fourier transform routine.
RESULTS:
In both groups, sleep latency was shorter, sleep efficiency was higher, non-rapid eye movement (NREM) sleep stage 4 was increased, and waking after sleep onset was reduced in recovery relative to baseline sleep. Spectral power of the NREM sleep EEG was enhanced after sleep deprivation in the low-frequency range (1.6-3.6 Hz in Tanner 1/2; 0.8-6.0 Hz in Tanner 5) and reduced in the sigma range (11-15 Hz). Sleep deprivation resulted in a stronger increase of slow-wave activity (EEG power 0.6-4.6 Hz, marker for sleep homeostatic pressure) in Tanner 5 (39% above baseline) than in Tanner 1/2 adolescents (18% above baseline). Sleep homeostasis was modeled according to the two-process model of sleep regulation. The build-up of homeostatic sleep pressure during wakefulness was slower in Tanner 5 adolescents (time constant of exponential saturating function 15.4 +/- 2.5 hours) compared with Tanner 1/2 children (8.9 +/- 1.2 hours). In contrast, the decline of the homeostatic process was similar in both groups.
CONCLUSION:
Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence.
TL;DR: Treatment with 200 mg of modafinil reduced the extreme sleepiness that was observed in patients with shift-work sleep disorder and resulted in a small but significant improvement in performance as compared with placebo, however, the residual sleepiness in the treated patients underscores the need for the development of interventions that are even more effective.
Abstract: background Patients with shift-work sleep disorder chronically have excessive sleepiness during night work and insomnia when attempting to sleep during the day. We evaluated the use of modafinil for treating sleepiness in patients with this disorder. methods In a three-month, double-blind trial, we randomly assigned 209 patients with shiftwork sleep disorder to receive either 200 mg of modafinil or placebo before the start of each shift. Assessments were performed with the use of the nighttime Multiple Sleep Latency Test, the Clinical Global Impression of Change, the Psychomotor Vigilance Test, diaries of patients, and daytime polysomnography. After randomization, we conducted monthly assessments. results Treatment with modafinil, as compared with placebo, resulted in a modest improvement from baseline in mean (±SEM) nighttime sleep latency (the interval between the time a person attempts to fall asleep and the onset of sleep) (1.7±0.4 vs. 0.3±0.3 minutes, respectively; P=0.002), and more patients had improvement in their clinical symptoms (74 percent vs. 36 percent, respectively; P<0.001). Patients who were receiving modafinil also had a reduction in the frequency and duration of lapses of attention during nighttime testing of their performance on the Psychomotor Vigilance Test (change from baseline, a reduction in lapse frequency of 2.6 vs. an increase of 3.8, respectively; P<0.001), and proportionally fewer patients reported having had accidents or near accidents while commuting home (29 percent vs. 54 percent, respectively; P<0.001). Despite these benefits, patients treated with modafinil continued to have excessive sleepiness and impaired performance at night. Modafinil did not adversely affect daytime sleep as compared with placebo. Headache was the most common adverse event. conclusions Treatment with 200 mg of modafinil reduced the extreme sleepiness that we observed in patients with shift-work sleep disorder and resulted in a small but significant improvement in performance as compared with placebo. However, the residual sleepiness that was observed in the treated patients underscores the need for the development of interventions that are even more effective.
TL;DR: The severity of OSA is independently associated with oxidative stress, and among various sleep-disordered breathing parameters, ODI is most closely related to oxidative stress.
TL;DR: Evidence-based knowledge of pediatric obstructive sleep apnea syndrome (OSAS) is reviewed to review the clinical symptoms, syndromes, polysomnographic findings and variables, and treatment options, and the authors' recommendations are reviewed.
Abstract: Objective To review evidence-based knowledge of pediatric obstructive sleep apnea syndrome (OSAS). Data Sources and Extraction We reviewed published articles regarding pediatric OSAS; extracted the clinical symptoms, syndromes, polysomnographic findings and variables, and treatment options, and reviewed the authors’ recommendations. Data Synthesis Orthodontic and craniofacial abnormalities related to pediatric OSAS are commonly ignored, despite their impact on public health. One area of controversy involves the use of a respiratory disturbance index to define various abnormalities, but apneas and hypopneas are not the only abnormalities obtained on polysomnograms, which can be diagnostic for sleep-disordered breathing. Adenotonsillectomy is often considered the treatment of choice for pediatric OSAS. However, many clinicians may not discern which patient population is most appropriate for this type of intervention; the isolated finding of small tonsils is not sufficient to rule out the need for surgery. Nasal continuous positive airway pressure can be an effective treatment option, but it entails cooperation and training of the child and the family. A valid but often overlooked alternative, orthodontic treatment, may complement adenotonsillectomy. Conclusions Many complaints and syndromes are associated with pediatric OSAS. This diagnosis should be considered in patients who report the presence of such symptoms and syndromes.
TL;DR: This study shows that severe OSAH may mimick the symptoms of RBD and that VPSG is mandatory to establish the diagnosis of R BD, and identify or exclude other causes of dream-enacting behaviors.
Abstract: Objective To describe the clinical and video-polysomnographic (VPSG) features of a group of subjects with severe obstructive sleep apnea/hypopnea (OSAH) mimicking the symptoms of REM sleep behavior disorder (RBD). Design Evaluation of clinical and VPSG data. Setting University hospital sleep laboratory unit. Participants Sixteen patients that were identified during routine first evaluation visits. Patients' PSG measures were compared with those of 20 healthy controls and 16 subjects with idiopathic RBD of similar age and sex distribution and apnea/hypopnea index lower than 10. Interventions NA. Results Sixteen subjects were identified presenting with dream-enacting behaviors and unpleasant dreams suggesting the diagnosis of RBD, in addition to snoring and excessive daytime sleepiness. VPSG excluded RBD showing REM sleep with atonia and without increased phasic EMG activity, and was diagnostic of severe OSAH with a mean apnea-hypopnea index of 67.5 +/- 18.7 (range, 41-105) demonstrating that the reported abnormal sleep behaviors occurred only during apnea-induced arousals. Continuous positive airway pressure therapy eliminated the abnormal behaviors, unpleasant dreams, snoring and daytime hypersomnolence. Conclusions Our study shows that severe OSAH may mimick the symptoms of RBD and that VPSG is mandatory to establish the diagnosis of RBD, and identify or exclude other causes of dream-enacting behaviors.
TL;DR: REM sleep behavior disorder-related symptoms and neurophysiologic features are qualitatively similar in RBD subjects with the idiopathic form, multiple system atrophy (MSA), and Parkinson disease (PD), suggesting a more severe dysfunction in the structures that modulate REM sleep.
Abstract: Objective: To compare the clinical and video-polysomnographic (VPSG) characteristics of idiopathic REM sleep behavior disorder (RBD) vs the RBD seen in multiple system atrophy (MSA) and Parkinson disease (PD). Methods: Clinical features and VPSG measures were evaluated in 110 consecutive nondemented subjects (26 MSA, 45 PD, and 39 idiopathic RBD) free of psychoactive medications referred for suspected RBD to our sleep unit over a 5-year period, with extended follow-up (mean 26.9 ± 21.3 months). Results: Across the three groups studied, logistic regression analysis demonstrated that there were no differences in the quality of RBD symptoms (e.g., nature of unpleasant dream recall or behaviors witnessed by bed partners), most PSG variables, abnormal behaviors captured by VPSG, and clinical response to clonazepam. When compared to subjects with PD, however, patients with MSA had a significantly shorter duration of disease, a higher REM sleep without atonia percentage, a greater periodic leg movement index, and less total sleep time. Subjects with idiopathic RBD, as compared to those with either MSA or PD, were more often male, had greater self-reported clinical RBD severity, and were more often aware of their abnormal sleep behaviors. Conclusions: REM sleep behavior disorder (RBD)-related symptoms and neurophysiologic features are qualitatively similar in RBD subjects with the idiopathic form, multiple system atrophy (MSA), and Parkinson disease (PD). Polysomnographic abnormalities associated with RBD in the setting of MSA are greater than in PD, suggesting a more severe dysfunction in the structures that modulate REM sleep.
TL;DR: At the time ofOSAS diagnosis, women with OSAS are more likely to be treated for depression, to have insomnia, and to have hypothyroidism than are men with the same degree of OSAS.
Abstract: Study objectives Obstructive sleep apnea syndrome (OSAS) results from recurrent episodes of breathing cessation during sleep. Epidemiologic studies have shown that OSAS is more prevalent in men than women (4% vs 2%). Previous studies have explored gender-related differences in upper airway anatomy and function, hormone physiology, and polysomnographic findings. The aim of this study is to assess differences in clinical presentation between women and men with OSAS. Design Retrospective chart review analysis. Setting Tertiary university-based medical center Participants 130 randomly selected women with OSAS matched individually with 130 men with OSAS for age, body mass index, apnea-hypopnea index, and Epworth Sleepiness Scale score. Interventions N/A. Measurements and results Data were obtained from questionnaires and in-laboratory polysomnographic studies. There were no differences between the genders for age (48.0 +/- 1.1 years [mean +/- SEM] for women vs 47.6 +/- 1.0 years for men), body mass index (40.4 +/- 0.7 kg/m2 for women vs 40.0 +/- 0.6 kg/m2 for men), apnea-hypopnea index (36.8 +/- 3.3/hour for women vs 36.0 +/- 3.0/hour for men), or Epworth Sleepiness Scale score (12.45 +/- 0.53 for women vs 12.84 +/- 0.47 for men). Although snoring and sleepiness were similarly common in women and men, women more often described their main presenting symptoms as insomnia (odds ratio: 4.20; 95% confidence interval: 1.54-14.26) and were much more likely to have a history of depression (odds ratio: 4.60; 95% confidence interval: 1.71-15.49) and hypothyroid disease (odds ratio: 5.60; 95% confidence interval: 2.14-18.57). Women presented less often with a primary complaint of witnessed apnea (odds ratio: 0.66; 95% confidence interval: 0.38-1.12), consumed less caffeine per day (3.3 cups in women vs 5.2 cups in men; P = .0001), and admitted to less alcohol consumption (odds ratio: 0.36; 95% confidence interval: 0.18-0.70). Conclusions At the time of OSAS diagnosis, women with OSAS are more likely to be treated for depression, to have insomnia, and to have hypothyroidism than are men with the same degree of OSAS.
TL;DR: Cognitive-behavioral therapy represents a promising intervention for sleep disturbance in FM patients and larger clinical trials of this intervention with FM patients seem warranted.
Abstract: Background Insomnia is common and debilitating to fibromyalgia (FM) patients. Cognitive-behavioral therapy (CBT) is effective for many types of patients with insomnia, but has yet to be tested with FM patients. This study compared CBT with an alternate behavioral therapy and usual care for improving sleep and other FM symptoms. Methods This randomized clinical trial enrolled 47 FM patients with chronic insomnia complaints. The study compared CBT, sleep hygiene (SH) instructions, and usual FM care alone. Outcome measures were subjective (sleep logs) and objective (actigraphy) total sleep time, sleep efficiency, total wake time, sleep latency, wake time after sleep onset, and questionnaire measures of global insomnia symptoms, pain, mood, and quality of life. Results Forty-two patients completed baseline and continued into treatment. Sleep logs showed CBT-treated patients achieved nearly a 50% reduction in their nocturnal wake time by study completion, whereas SH therapy– and usual care–treated patients achieved only 20% and 3.5% reductions on this measure, respectively. In addition, 8 (57%) of 14 CBT recipients met strict subjective sleep improvement criteria by the end of treatment compared with 2 (17%) of 12 SH therapy recipients and 0% of the usual care group. Comparable findings were noted for similar actigraphic improvement criteria. The SH therapy patients showed favorable outcomes on measures of pain and mental well-being. This finding was most notable in an SH therapy subgroup that self-elected to implement selected CBT strategies. Conclusions Cognitive-behavioral therapy represents a promising intervention for sleep disturbance in FM patients. Larger clinical trials of this intervention with FM patients seem warranted.
TL;DR: Comorbid conditions, including respiratory disease, sleep restriction, insomnia, and nocturnal leg complaints, are important risk factors for sleepiness in individuals with moderate to severe sleep-disordered breathing.
Abstract: Population-based studies suggest that complaints of sleepi-ness are absent in many individuals with sleep-disordered breathing. Weinvestigated the prevalence of sleepiness as well as factors associatedwith sleepiness in individuals with moderate to severe sleep-disorderedbreathing (apnea-hypopnea index >15).
TL;DR: At the doses tested, caffeine, dextroamphetamine, and modafinil are equally effective for approximately 2–4 h in restoring simple psychomotor performance and objective alertness.
Abstract: Stimulants may provide short-term performance and alertness enhancement during sleep loss. Caffeine 600 mg, d-amphetamine 20 mg, and modafinil 400 mg were compared during 85 h of total sleep deprivation to determine the extent to which the three agents restored performance on simple psychomotor tasks, objective alertness and tasks of executive functions. Forty-eight healthy young adults remained awake for 85 h. Performance and alertness tests were administered bi-hourly from 8:00 hours day 2 to 19:00 hours day 5. At 23:50 hours on day 4 (after 64 h awake), subjects ingested placebo, caffeine 600 mg, dextroamphetamine 20 mg, or modafinil 400 mg (n=12 per group). Performance and alertness testing continued, and probe tasks of executive function were administered intermittently until the recovery sleep period (20:00 hours day 5 to 8:00 hours day 5). Bi-hourly postrecovery sleep testing occurred from 10:00 hours to 16:00 hours day 6. All three agents improved psychomotor vigilance speed and objectively measured alertness relative to placebo. Drugs did not affect recovery sleep, and postrecovery sleep performance for all drug groups was at presleep deprivation levels. Effects on executive function tasks were mixed, with improvement on some tasks with caffeine and modafinil, and apparent decrements with dextroamphetamine on others. At the doses tested, caffeine, dextroamphetamine, and modafinil are equally effective for approximately 2-4 h in restoring simple psychomotor performance and objective alertness. The duration of these benefits vary in accordance with the different elimination rates of the drugs. Whether caffeine, dextroamphetamine, and modafinil differentially restore executive functions during sleep deprivation remains unclear.
TL;DR: Double-blind, placebo-controlled trials will be needed to corroborate current findings and solidly establish antiinflammatory strategies, such as leukotriene modifiers, as therapeutic alternatives in children with SDB too mild to justify referral for adenotonsillectomy.
Abstract: Background: Children with mild sleep-disordered breathing (SDB), who may not be recommended for adenotonsillectomy, frequently exhibit neurocognitive and behavioral morbidity, and may benefit from alternative therapeutic interventions, such as leukotriene modifier therapy. Methods: Twenty-four children with SDB completed an open-label intervention study for 16 weeks with daily montelukast therapy. Sleep studies and adenoid size estimates from lateral X-ray films of the neck were obtained before and after treatment. In a parallel study, adenoid and tonsillar tissues from children with obstructive sleep apnea or recurrent throat infections were subjected to quantitative polymerase chain reaction, immunohistochemistry, and Western blotting for gene and protein expression of leukotriene receptors LT1-R and LT2-R, and for concentrations of LTB4 and LTC4/D4/E4. Results: Montelukast treatment induced significant reductions in adenoid size and respiratory-related sleep disturbances, which were absent in 16 children with SDB who did not receive treatment. LT1-R and LT2-R mRNA was similarly abundant in adenoid tissues, but increased LT1-R and LT2-R protein expression and higher levels of LTB4 and LTC4/D4/E4 emerged in children with obstructive sleep apnea. Conclusions: Oral therapy with a leukotriene modifier appears to be associated with improved breathing during sleep. Double-blind, placebo-controlled trials will be needed to corroborate current findings and solidly establish antiinflammatory strategies, such as leukotriene modifiers, as therapeutic alternatives in children with SDB too mild to justify referral for adenotonsillectomy.
TL;DR: Thirty percent of stable MMT patients have CSA, a minority of which can be explained by blood methadone concentration, and other physiologic variables may also play a role in the pathogenesis of CSA in M MT patients, and further research is indicated.
TL;DR: The development and optimization of an automatic classification system that is based on one central EEG channel, two EOG channels and one chin EMG channel and proved the high reliability and validity of the Somnolyzer 24 × 7 and demonstrated its applicability in clinical routine and sleep studies.
Abstract: To date, the only standard for the classification of sleep-EEG recordings that has found worldwide acceptance are the rules published in 1968 by Rechtschaffen and Kales. Even though several attempts have been made to automate the classification process, so far no method has been published that has proven its validity in a study including a sufficiently large number of controls and patients of all adult age ranges. The present paper describes the development and optimization of an automatic classification system that is based on one central EEG channel, two EOG channels and one chin EMG channel. It adheres to the decision rules for visual scoring as closely as possible and includes a structured quality control procedure by a human expert. The final system (Somnolyzer 24 x 7) consists of a raw data quality check, a feature extraction algorithm (density and intensity of sleep/wake-related patterns such as sleep spindles, delta waves, SEMs and REMs), a feature matrix plausibility check, a classifier designed as an expert system, a rule-based smoothing procedure for the start and the end of stages REM, and finally a statistical comparison to age- and sex-matched normal healthy controls (Siesta Spot Report). The expert system considers different prior probabilities of stage changes depending on the preceding sleep stage, the occurrence of a movement arousal and the position of the epoch within the NREM/REM sleep cycles. Moreover, results obtained with and without using the chin EMG signal are combined. The Siesta polysomnographic database (590 recordings in both normal healthy subjects aged 20-95 years and patients suffering from organic or nonorganic sleep disorders) was split into two halves, which were randomly assigned to a training and a validation set, respectively. The final validation revealed an overall epoch-by-epoch agreement of 80% (Cohen's kappa: 0.72) between the Somnolyzer 24 x 7 and the human expert scoring, as compared with an inter-rater reliability of 77% (Cohen's kappa: 0.68) between two human experts scoring the same dataset. Two Somnolyzer 24 x 7 analyses (including a structured quality control by two human experts) revealed an inter-rater reliability close to 1 (Cohen's kappa: 0.991), which confirmed that the variability induced by the quality control procedure, whereby approximately 1% of the epochs (in 9.5% of the recordings) are changed, can definitely be neglected. Thus, the validation study proved the high reliability and validity of the Somnolyzer 24 x 7 and demonstrated its applicability in clinical routine and sleep studies.
TL;DR: The hypothesis that sleep disturbance is associated with elevated levels of the inflammatory markers IL-6 and sICAM is supported and may be partially the result of disturbances of sleep initiation found in this population of patients with major depressive disorder.
Abstract: OBJECTIVE: This study was conducted to determine whether immune activation occurs in major depression, and to evaluate the associations between disordered sleep and markers of inflammation in patients with major depressive disorder. METHODS: All-night polysomnography was obtained in patients with acute Diagnostic and Statistical Manual of Mental Disorders, 4th edition major depressive disorder (n = 22) and age-, gender-, and body weight-matched comparison controls (n = 18). After the onset of sleep, nocturnal serum levels of interleukin-6 (IL-6), soluble intercellular adhesion molecule (sICAM), monocyte chemotactic protein (MCP-1), and IL-6 soluble receptor (IL-6sR) were sampled. RESULTS: As compared with matched controls, depressed patients showed significant (p or = 0.30). Backward regression analyses indicated that sleep latency (beta = 0.34, p <.05) and REM density (beta = 0.27, p = .09) were better predictors of IL-6 than depressive status. Similarly, sleep latency (beta = 0.27, p = .06) and REM density (beta = 0.32, p = .02) were also better predictors of sICAM. CONCLUSION: These findings support the hypothesis that sleep disturbance is associated with elevated levels of the inflammatory markers IL-6 and sICAM. This relationship was not accounted for by other confounding factors such as age and body weight. These findings suggest that the elevations in inflammatory markers found in depressive subjects may be partially the result of disturbances of sleep initiation found in this population.
TL;DR: The hypothesis that molecular components of the circadian system play a central role in the generation of sleep and wakefulness beyond just the timing of these behavioral vigilance states is strengthened.
Abstract: Study objectives: The finding that deletion or mutation of core circadian clock genes in both mice and flies induce unexpected alterations in sleep amount, sleep architecture and the recovery response to sleep deprivation, has led to new insights into functions of the circadian system that extend beyond its role as a regulator of the timing of the sleep-wake cycle. A key transcription factor in the transcriptional/translational feedback loop of mammalian circadian genes is BMAL1/Mop3, a heterodimeric partner to CLOCK. It was previously shown that mice deficient in the BMAL1/Mop3 gene become immediately arrhythmic in constant darkness and have reduced locomotor activity levels under entrained and constant conditions. In this study, we tested the hypothesis that the mammalian BMAL1/Mop3 gene would have regulatory effects on sleep-wake patterns. Design: In mice with targeted deletion of the BMAL1/Mop3 gene, EEG/EMG sleep-wake patterns were recorded under entrained and freerunning conditions as well as following acute (6-hrs) sleep deprivation. Measurements and results: Mice homozygous for the BMAL1/Mop3 deletion showed an attenuated rhythm of sleep and wakefulness distribution across the 24-hr period. In addition, these mice showed increases in total sleep time, sleep fragmentation and EEG delta power under baseline conditions, and an attenuated compensatory response to acute sleep deprivation. Conclusions: These new data strengthen the hypothesis that molecular components of the circadian system play a central role in the generation of sleep and wakefulness beyond just the timing of these behavioral vigilance states.
TL;DR: Results indicate low brain iron concentration caused by the dysfunction of iron transportation from serum to CNS in patients with idiopathic RLS.
Abstract: The aim of this study is evaluating iron, ferritin, and transferrin in both serum and CSF in patients of restless legs syndrome (RLS), based on the hypothesis that iron deficiency in the central nervous system (CNS) causes the symptoms as a result of the dysfunction of dopaminergic systems. These parameters, polysomnographic sleep measures, and subjective evaluation of the sleep quality were compared in 10 patients of idiopathic RLS (RLS group) and 10 age-matched patients of psychophysiological insomnia without RLS symptoms (non-RLS group). With sleep patterns, sleep latency was longer and sleep efficiency was lower in the RLS group than those in the non-RLS group. Periodic leg movement index in the RLS group was higher than that of the non-RLS group. With serum examination, there were no significant differences for the iron, ferritin, and transferrin values between the both groups. With CSF examination, the iron and ferritin values were lower and the transferrin values were higher in the RLS group than those in the non-RLS group. There was positive correlation between the serum and CSF ferritin levels in the both groups, but the slope of the regression lines for the RLS group was lower than that for the non-RLS group. These results indicate low brain iron concentration caused by the dysfunction of iron transportation from serum to CNS in patients with idiopathic RLS.