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PubMed2003

Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease.

Neither the association between obstructive airways disease (OAD) and sleep apnea-hypopnea (SAH) nor the sleep consequences of each disorder alone and together have been characterized in an adult community setting. Our primary aims were (1) to determine if there is an association between OAD and SAH and (2) identify predictors of oxyhemoglobin desaturation during sleep in persons having OAD with and without SAH. Polysomnography and spirometry results from 5,954 participants in the Sleep Heart Health Study were analyzed. OAD was defined by a FEV1/FVC value less than 70%. Assessment of SAH prevalence in OAD was performed using thresholds of respiratory disturbance index (RDI) greater than 10 and greater than 15. A total of 1,132 participants had OAD that was predominantly mild (FEV1/FVC 63.81 +/- 6.56%, mean +/- SD). SAH was not more prevalent in participants with OAD than in those without OAD (22.32 versus 28.86%, with and without OAD, respectively, at RDI threshold values greater than 10; and 13.97 versus 18.63%, with and without OAD, respectively, at RDI threshold value greater than 15). In the absence of SAH, the adjusted odds ratio for sleep desaturation (> 5% total sleep time with saturation < 90%) was greater than 1.9 when FEV1/FVC was less than 65%. Participants with both OAD and SAH had greater sleep perturbation and desaturation than those with one disorder. Generally mild OAD alone was associated with minimally altered sleep quality. We conclude that (1) there is no association between generally mild OAD and SAH; (2) exclusive of SAH and after adjusting for demographic factors and awake oxyhemoglobin saturation, an FEV1/FVC value less than 65% is associated with increased risk of sleep desaturation; (3) desaturation is greater in persons with both OAD and SAH compared with each of these alone; and (4) individuals with generally mild OAD and without SAH in the community have minimally perturbed sleep.

Aged↗
PubMed1997

Sleep deprivation combined with consecutive sleep phase advance as a fast-acting therapy in depression: an open pilot trial in medicated and unmedicated patients.

OBJECTIVE: The authors' goal was to test the hypothesis that the antidepressant effect of total sleep deprivation can be maintained by initially avoiding sleep during a supposedly "critical" time period in the early morning. METHOD: They studied 33 inpatients with major depression, melancholic type, all of whom responded positively to total sleep deprivation. Twelve of the patients were men and 21 were women; their mean age was 46.7 years (SD = 13.7). After total sleep deprivation, the patients started a sleep schedule from 5:00 p.m. to 12:00 midnight, which then was shifted back by 1 hour each day until a sleep time of 11:00 p.m. to 6:00 a.m. was reached. RESULTS: Twenty (61%) of the 33 patients who responded to total sleep deprivation with an improved state of mood maintained this improvement during sleep phase advance therapy. Drug-free and medicated patients did not differ from each other. CONCLUSIONS: The rapid amelioration of mood observed with total sleep deprivation can be preserved with a succeeding phase shift of the sleep period.

Antidepressive Agents↗
PubMed2005

Sleep-related functioning in euthymic patients with bipolar disorder, patients with insomnia, and subjects without sleep problems.

OBJECTIVE: The authors investigated sleep-related functioning in euthymic patients with bipolar disorder. METHOD: Euthymic patients with bipolar disorder (N=20), patients with insomnia (N=20), and subjects with good sleep (N=20) were compared on data from interviews and questionnaires and on findings from eight consecutive days and nights of sleep diary keeping (subjective sleep estimate) and actigraphy (objective sleep estimate). RESULTS: Seventy percent of the euthymic patients with bipolar disorder exhibited a clinically significant sleep disturbance. Compared with the other groups, the bipolar disorder group exhibited impaired sleep efficiency, higher levels of anxiety and fear about poor sleep, lower daytime activity levels, and a tendency to misperceive sleep. The bipolar disorder group held a level of dysfunctional beliefs about sleep that was comparable to that in the insomnia group and significantly higher than that in the good sleeper group. CONCLUSIONS: Insomnia is a significant problem among euthymic patients with bipolar disorder. Components of cognitive behavior therapy for insomnia, especially stimulus control and cognitive therapy, may be a helpful adjunct to treatment for patients with bipolar disorder.

Adaptation, Psychological↗
PubMed1998

Sleep bruxism is a disorder related to periodic arousals during sleep.

There is evidence that sleep bruxism is an arousal-related phenomenon. In non-REM sleep, transient arousals recur at 20- to 40-second intervals and are organized according to a cyclic alternating pattern. Polysomnographic recordings from six subjects (two females and four males) affected by sleep bruxism (patients) and six healthy age-and gender-matched volunteers without complaints about sleep (controls) were analyzed to: (1) compare the sleep structure of bruxers with that of non-complaining subjects; and (2) investigate the relations between bruxism episodes and transient arousals. Patients and controls showed no significant differences in conventional sleep variables, but bruxers showed a significantly higher number of the transient arousals characterized by EEG desynchronization. Bruxism episodes were equally distributed between non-REM and REM sleep, but were more frequent in stages 1 and 2 (p < 0.0001) than in slow-wave sleep. The great majority of bruxism episodes detected in non-REM sleep (88%) were associated with the cyclic alternating pattern and always occurred during a transient arousal. Heart rate during the bruxism episodes (69.3+/-18.2) was significantly higher (p < 0.0001) than that during the pre-bruxing period (58.1+/-15.9). Almost 80% of all bruxism episodes were associated with jerks at the anterior tibial muscles. The framework of the cyclic alternating pattern offers a unified interpretation for sleep bruxism and arousal-related phenomena.

Adult↗
PubMed1998

Effects of lifestyle, personality, symptoms of anxiety and depression, and genetic predisposition on subjective sleep disturbance and sleep pattern.

The effects on sleep pattern ('short-sleep' versus 'long-sleep') and subjective sleep disturbance of genotype, personality, symptoms of anxiety and depression, and lifestyle, were examined using survey data on a clinically unselected sample of adult Australian twin pairs, aged 17-88 years. When the effects of genotype, personality and symptoms were ignored, lifestyle variables appeared to account for roughly 4% of the variance in sleep disturbance, and 9% of the variance in sleep pattern. Significant genetic effects on sleep disturbance and sleep pattern were found, which were only partly explained by the effects of personality and symptoms of anxiety and depression. Much of the association between sleep disturbance and lifestyle appeared to be explained by separate effects of personality and symptoms of anxiety and depression on sleep and lifestyle ('genotype-risk-factor correlation'). There was little evidence for genetically determined differences in sensitivity to the lifestyle variables ('genotype x risk-factor interaction').

Adolescent↗
PubMed2000

Sleep and breathing disorders: the genesis of obstructive sleep apnea.

Sleep encompasses approximately a third of our lives; however, sleep and the disorders of sleep are not widely understood. Data suggest that sleep plays a restorative role in physiologic mechanisms and that long-term disruption of sleep may contribute to the development of disease. Nearly a third of the adult population is chronically afflicted by sleep disorders, and substantial economic loss is attributable to these disorders in terms of lost time, inefficiency, and accidents. Of the sleep disorders, obstructive sleep apnea (OSA) is one of the more common, clinically affecting up to 5% of the adult population. Obstructive sleep apnea contributes to the development of disease and has an adverse impact on daytime functioning in those affected by the disease. This article reviews basic sleep physiology, how these physiologic mechanisms are disrupted by OSA, and some of the techniques for treating patients with this disorder.

Adult↗
PubMed1975

An attempt to influence by drugs recovery sleep after sleep deprivation.

Rats were deprived of sleep by placing them for 36 hours in a slowly moving drum. After this procedure, during recovery sleep, the latency of onset of the first rhombencephalic - paradoxical sleep period decreased and the proportion of telencephalic/rhombencephalic - slow wave sleep reversed (during the first hour of recovery sleep). Repeated administration during the deprivation period of physostigmine (0,5 mg/kg i. p. in 30 min intervals 20-30 times) inducing in waking animals in EEG pattern close to that of rhombencephalic sleep, or atropine (1 mg/kg i. p. in 60 min intervals 10-15 times) evoking an activity resembling telencephalic sleep, did not change the above measures of recovery sleep. Pharmacologically induced sleep-like patterns did not substitute for the sleep the rats were deprived off.

Animals↗
PubMed1991

Actigraphic home-monitoring sleep-disturbed and control infants and young children: a new method for pediatric assessment of sleep-wake patterns.

Two studies were conducted to evaluate actigraphic home-monitoring for the assessment of infants' and children's sleep patterns. In the first study, 11 children (aged 12 to 48 months) were monitored in the laboratory by traditional polysomnography and by actigraphy for one night. Actigraphic automatic sleep-wake scorings were compared with those of the polysomnograph; total agreement rate was 85.3%. In the second study, sleep patterns of 63 sleep-disturbed and 34 control healthy children (aged 9 to 27 months) were compared. These children were home-monitored by actigraph for a mean of 4.45 nights (total 482 nights). Actigraphic data were analyzed by an automated scoring procedure. Sleep quality of the sleep-disturbed children, measured by actigraphically derived sleep percent and number of longer-than-5-minute wakings, was significantly lower than that of the control subjects (P less than .0001). Sleep measures showed significant night-to-night stability in both groups. The stability of specific measures and their age trends were different between the groups. Actigraphic sleep measures alone could discriminate between sleep-disturbed and control children with a highly correct assignment rate of 79.4% and 91.2%, respectively.

Age Factors↗
PubMed2001

Sleep, sleepiness, sleep disorders and alcohol use and abuse.

The study of ethanol's effects on sleep has a long history dating back to the work of Nathaniel Kleitman. This paper reviews the extensive literature describing ethanol's effects on the sleep of healthy normals and alcoholics and the newer literature that describes its interactive effects on daytime sleepiness, physiological functions during sleep, and sleep disorders. Ethanol initially improves sleep in non-alcoholics at both low and high doses with disturbance in the second half of the night sleep at high doses. Tolerance develops to the initial beneficial effects. In alcoholics sleep is disturbed both while drinking and for months of abstinence and the nature of the abstinent sleep disturbance is predictive of relapse. Ethanol interacts to exacerbate daytime sleepiness and sleep-disordered breathing, even inducing apnea in persons at risk. Ethanol's effects on other physiological functions during sleep and other sleep disorders has yet to be documented. 2001 Harcourt Publishers Ltd

Journal Article↗
PubMed2001

Frontal lobe function, sleep loss and fragmented sleep.

Recent experimental studies involving total sleep loss, sleep reduction and clinically related sleep fragmentation report impaired performance on tasks of frontal lobe or executive function, including measures of verbal fluency, creativity and planning skills. Severity of sleep disturbance in obstructive sleep apnoea syndrome (OSAS) is correlated with level of executive impairment, with some residual impairment despite treatment (continuous positive airway pressure - CPAP). Executive impairment appears to be more closely related to hypoxaemic events rather than daytime sleepiness. Studies of electroencephalographic (EEG) changes throughout the course of sleep and following sleep deprivation as well as functional neuroimaging and psychophysiological changes (event-related potentials - ERPs) following sleep deprivation provide further indication of the relative importance of the frontal regions of the brain to sleep. However, neurocognitive studies present many inconsistencies, task classification is often ambiguous and, in the absence of any unifying explanation at the level of cognitive mechanisms, the overall picture is one of a disparate range of impairment following sleep loss and sleep fragmentation. Poorly defined concepts of frontal lobe function, executive function, memory and attention, using tasks largely developed with more severe deficit levels in mind, create further difficulties in interpreting current findings.

Journal Article↗
PubMed1992

Aging young sleep: a test of the phase advance hypothesis of sleep disturbance in the elderly.

With aging, the phase relationship between sleep and body core temperature is altered such that the temperature minimum occurs substantially earlier in the major nocturnal sleep period. The sleep maintenance difficulties that often accompany normal aging are generally assumed to be associated with this age-related change in the phase angle between sleep and temperature. To test this notion, we used timed exposure to bright light to reproduce in healthy young adults a similar phase relationship between temperature and sleep, to determine if such a manipulation would induce the same fragmented nocturnal sleep commonly observed in individuals over 65 years of age. Seven young adults were exposed to morning bright light for 3 consecutive days following a baseline night. Bright light exposure caused a 97 min phase advance of the fitted temperature minimum when compared with baseline. Significant declines in several measures of sleep quality were associated with the phase advance, including wakefulness after initial sleep onset (WASO), sleep efficiency and number of stage changes. Yet, the severity of sleep disturbance exhibited by these subjects did not approach that exhibited by most elderly subjects. The findings suggest that while chronophysiological changes appear to be strongly associated with the tendency to awaken in the early morning, they cannot account entirely for the severity of sleep disturbance frequently observed in older subjects.

Journal Article↗
PubMed2006

Sleepiness and sleep in patients with both systolic heart failure and obstructive sleep apnea.

BACKGROUND: Adverse effects of obstructive sleep apnea (OSA), including sleep deprivation, can contribute to the progression of heart failure. The usual indication to diagnose and treat sleep apnea is subjective sleepiness. Previous studies suggest that patients with both heart failure and obstructive sleep apnea often do not complain of sleepiness, albeit their sleep time may be reduced. Therefore, we tested the hypothesis that patients with heart failure have less sleepiness and sleep less compared with subjects without heart failure for a given severity of OSA. METHODS: Sleepiness assessed with the Epworth Sleepiness Scale and sleep structure measured with polysomnography were compared among 155 consecutive patients with heart failure and from a random community sample (n = 1139) according to categories of the apnea-hypopnea index (<5, no OSA; 5-14, mild OSA; and > or =15, moderate to severe OSA). RESULTS: Compared with the community sample, for any given severity of OSA, patients with heart failure had lower mean +/- SE Epworth Sleepiness Scale scores (7.1 +/- 0.4 vs 8.3 +/- 0.2 [P = .005]; 6.7 +/- 0.7 vs 9.2 +/- 0.3 [P < .001]; and 7.8 +/- 0.7 vs 9.8 +/- 0.4 [P = .01]), indicating less sleepiness despite sleeping less (total sleep time mean +/- SE [in minutes]: 306 +/- 7 vs 384 +/- 2, 295 +/- 19 vs 384 +/- 5, and 285 +/- 13 vs 359 +/- 7 for no, mild, and moderate to severe OSA, respectively; P < .001 for all comparisons). CONCLUSIONS: Patients with heart failure have less subjective daytime sleepiness compared with individuals from a community sample, despite significantly reduced sleep time, whether or not they have OSA. In patients with heart failure, the absence of subjective sleepiness is not a reliable means of ruling out OSA.

Body Mass Index↗
PubMed2003

Subjective assessment of the effects of CNS-active drugs on sleep by the Leeds sleep evaluation questionnaire: a review.

The Leeds sleep evaluation questionnaire (LSEQ) comprises ten self-rating 100 mm line analogue questions concerned with sleep and early morning behaviour. A literature search identified 83 studies in peer-reviewed journals that reported the use of the LSEQ for psychopharmacological investigations of drug effects on self-reported aspects of sleep. High internal consistency and reliability of the questionnaire have been demonstrated. Findings from studies involving a variety of psychoactive agents indicated that the LSEQ was able to quantify subjective impressions of sleep and waking and the effects of drugs in healthy volunteers, depressed and insomnia patients. In accordance with their known activity profile nocturnal administration of sedative hypnotic agents and antihistamines induced dose-related improvements in self-reported ease of getting to sleep, and quality of sleep but a decrease in alertness and behavioural integrity the following morning. Psychostimulants, on the other hand, impaired subjective ratings of sleep and increased early morning alertness. Antidepressants and certain anxiolytic agents improved both self-reported sleep aspects and early morning alertness. Treatment effects measured by the LSEQ corresponded to those measured for the same drugs by other assessment methods. These data indicate that the LSEQ is a robust and reliable instrument for psychopharmacological evaluations. Self-evaluations of sleep, as obtained by the LSEQ, can therefore provide consistent and meaningful measures for estimating the effectiveness of sleep modulators and sedative-hypnotic drugs.

Central Nervous System Agents↗
PubMed1992

The effects of estazolam on sleep, performance, and memory: a long-term sleep laboratory study of elderly insomniacs.

Insomnia, a common complaint among the elderly, is generally treated with benzodiazepines. Long-acting benzodiazepines (e.g., flurazepam) often produce daytime somnolence and performance deficits, whereas short-acting drugs (e.g., triazolam) have been associated with marked rebound insomnia and anterograde memory loss. The authors designed a pilot study to evaluate the efficacy of an intermediate-acting benzodiazepine, estazolam (e.g., ProSom), as well as its side effects. The parameters studied were sleep, daytime performance, and memory. Ten geriatric patients (greater than 60 years of age) with insomnia participated in the study. They received placebo nightly for 2 weeks (baseline), estazolam 1 mg nightly for the next 4 weeks (treatment phase), and placebo again for 2 weeks (withdrawal period). Sleep was monitored by polysomnography the first two nights of each week in a sleep laboratory. Estazolam significantly decreased sleep latency, nocturnal awakenings, and wake time after sleep onset. Total sleep time increased an average of 63 minutes the first night of treatment. Significant improvements in wake time after sleep onset and total sleep time also were observed in the fourth week of estazolam treatment. Rebound insomnia occurred on the first withdrawal night only for wake time and total sleep time. By the next night, these sleep parameters returned to baseline. Neither day-time performance nor anterograde memory was adversely affected by estazolam treatment or its withdrawal. A 1-mg dose of estazolam appears to be a safe and effective hypnotic for elderly patients with insomnia.

Aged↗
PubMed2005

Sleep and breathing on the first night after adenotonsillectomy for obstructive sleep apnea.

Adenotonsillectomy (T&A) has established effectiveness for the treatment of obstructive sleep apnea (OSA). However, more than 20% of children with OSA have respiratory compromise requiring medical intervention in the postoperative period. The reasons for this complication are not well-defined. We aimed to compare the nature and severity of sleep-disordered breathing in children with mild and severe OSA on the first night following adenotonsillectomy. Ten children were classified into groups of mild and severe OSA, based on preoperative testing. On the first night after T&A, they underwent polysomnography, including electroencephalograph, submental electromyography, bilateral electro-oculograms, monitoring of respiratory movements, heart rate, ECG, and oxygen saturation. Sleep-disordered breathing was assessed by the apnea-hypopnea index, the SaO(2) nadir, and the desaturation index, including dips in saturation below 90% (DI(90)). Sleep quality was assessed by sleep efficiency, time spent in each sleep state, and respiratory arousal index. Obstructive events occurred postoperatively in all children, but were more frequent in those with severe OSA preoperatively: the median (interquartile range) mixed/obstructive apnea/hypopnea indicies were 6.9 (2.2-9.8) events/hr and 21.5 (15.1-112.1) events/hr for the mild OSA group and the severe OSA group, respectively (P = 0.009). Obstructive events were the major cause of desaturation during sleep postoperatively. Sleep quality was severely disrupted in both groups, with reductions in both slow-wave sleep and rapid eye movement sleep. In conclusion, despite removal of obstructing lymphoid tissue, upper airway obstruction occurred on the first postoperative night in children with OSA. This study is the first to demonstrate the mechanism of respiratory compromise after adenotonsillectomy, a common postoperative complication in children with severe OSA.

Adenoids↗
PubMed1987

Sleep and EEG spectra in the Syrian hamster (Mesocricetus auratus) under baseline conditions and following sleep deprivation.

Sleep was studied by continuous 24-h recordings in adult male Syrian hamsters, chronically implanted with EEG and EMG electrodes. Three vigilance states were determined using visual scoring and EEG power spectra (0.25-25 Hz) computed for 4-s episodes. The effects of two methods of total sleep deprivation (SD) were examined on vigilance states and the EEG power spectrum. The animals were subjected to 24 h SD by: (1) forced locomotion in a slowly rotating drum, (2) gentle handling whenever the hamsters attempted a sleeping posture. In addition, the hamsters were subjected to SD by handling during the first 3 h of the L period. Sleep predominated in the L period (78.2% of 12 h) and the D period (51.2%). The power spectra of the 3 vigilance states were similar during the L and D period. In NREM sleep, power density values in the low frequency range (0.25-6.0 Hz) exceeded those of REM sleep and W by a maximum factor of 8.3 and 2.8, respectively. At frequencies above 16 Hz, NREM and REM sleep power density values were significantly lower than during W. A progressive decrease in power density for low EEG frequencies (0.25-7 Hz) during NREM sleep was seen in the course of the L period. Power density values of higher frequencies (8-25 Hz) increased at the end of the L period and remained high during the first hours of the D period. The effect of prolonged SD on vigilance states and EEG spectra was similar by both methods and strikingly small compared to similar results in rats. In contrast, 3 h SD induced a large and more prolonged effect. The similarities and differences of sleep and sleep regulation are summarized for the hamster, rat and man.

Animals↗
PubMed1994

Sleep in depression: the influence of age, gender and diagnostic subtype on baseline sleep and the cholinergic REM induction test with RS 86.

One hundred and eight healthy controls and 178 patients with a major depressive disorder according to DSM-III were investigated in the sleep laboratory after a 7-day drug wash-out period. Subsamples of 36 healthy controls and 56 patients additionally took part in the cholinergic rapid eye movement (REM) sleep induction test with RS 86. Data analysis revealed that age exerted powerful influences on sleep in control subjects and depressed patients. Sleep efficiency and amount of slow wave sleep (SWS) decreased with age, whereas the number of awakenings, early morning awakening, and amounts of wake time and stage 1 increased with age. REM latency was negatively correlated with age only in the group of patients with a major depression. Statistical analysis revealed group differences for almost all parameters of sleep continuity with disturbed indices in the depressed group. Differences in SWS were not detected. REM latency and REM density were altered in depression compared to healthy subjects. Sex differences existed for the amounts of stage 1 and SWS. The cholinergic REM induction test resulted in a significantly more pronounced induction of REM sleep in depressed patients compared with healthy controls, provoking sleep onset REM periods as well in those depressed patients showing baseline REM latencies in the normal range. Depressed patients with or without melancholia (according to DSM-III) did not differ from each other, either concerning baseline sleep or with respect to the results of the cholinergic REM induction test. The results stress the importance of age when comparing sleep patterns of healthy controls with those of depressed patients. Furthermore they underline the usefulness of the cholinergic REM induction test for differentiating depressed patients from healthy controls and support the reciprocal interaction model of nonREM-REM regulation and the cholinergic-aminergic imbalance hypothesis of affective disorders.

Adolescent↗
PubMed1993

ST-segment depression during sleep in obstructive sleep apnea.

It was hypothesized that obstructive sleep apnea may precipitate myocardial ischemia, reflected by ST-segment depression, in some patients during sleep. Overnight sleep studies and simultaneous 3-channel Holter monitoring were performed on 23 consecutive patients with obstructive sleep apnea without a history of coronary artery disease. Each patient was randomly assigned to nasal continuous positive airway pressure for the first half of the night. An episode of significant ST depression was defined as > 1 mm from baseline for > 1 minute. The total duration (minutes) of ST depression was indexed to the total sleep time (minutes per hour of sleep). Seven patients (30%) had ST depression during sleep. In all 7 patients the duration of ST depression decreased during nasal continuous positive airway pressure (30 +/- 18 vs 11 +/- 13 minutes per hour of sleep) in association with a reduction in the apnea-hypopnea index (65 +/- 35 vs 7 +/- 6/hour), arousal index (49 +/- 14 vs 6 +/- 4/hour) and the duration that oxygen saturation was < 90% (44 +/- 27 vs 12 +/- 23% total sleep time). When patients were not on nasal continuous positive airway pressure, the apnea-hypopnea and arousal indexes were higher during periods of ST depression than when ST segments were isoelectric, whereas oxygen saturation was not different. These 7 patients underwent exercise testing, which was positive for inducible myocardial ischemia in 1 patient. It is concluded that ST depression is relatively common in patients with obstructive apnea during sleep and that the duration of ST depression is significantly reduced by nasal continuous positive airway pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗