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PubMedDate not supplied

Purinergic modulation of ethanol-induced sleep time in long-sleep and short-sleep mice.

The long-sleep (LS) and short-sleep (SS) mice were selectively bred for differences in sensitivity to the depressant effects of ethanol. In addition to their differential sensitivity to ethanol, they are also differentially sensitive to purinergic agonists and antagonists. This suggests that there may be differences in the purinergic systems of these lines of mice which may aid in understanding how they differ in ethanol sensitivity. We have investigated whether these drugs are capable of modifying acute ethanol sensitivity as measured by ethanol-induced loss of the righting response (ethanol sleep time), waking blood and brain ethanol concentrations, and blood ethanol elimination rate. The purinergic agonists cyclohexyladenosine (CHA), L-phenylisopropyladenosine (PIA), 2-chloroadenosine (CAD), and N-ethylcarboxamidoadenosine (NEC) increased sleep time in both LS and SS mice, however, LS mice were generally more affected than SS. The LS and SS mice were also differentially sensitive to the purinergic antagonists, theophylline and caffeine. Blood and brain ethanol concentration on awakening suggested that CNS sensitivity to acute ethanol administration was altered by pretreatment with agonists but not antagonists. Two agonists, CHA and NEC, significantly lowered ethanol elimination in both lines of mice while PIA, CAD, and the antagonists theophylline, and caffeine were without affect on elimination rate. These data support previous observations that adenosine-mediated systems may be involved in the modulation of ethanol sensitivity.

2-Chloroadenosine↗
PubMed1986

Effects of temazepam on sleep quality and subsequent mental efficiency under normal sleeping conditions and following delayed sleep onset.

A group of 24 healthy, normal sleepers participated in 2 experiments. The 1st experiment was designed to investigate the effects of 2 nocte doses of temazepam on subjective sleep quality and performance next morning. In contrast to placebo or no-capsule conditions both temazepam 10 and 20 mg improved a number of assessments of sleep quality, although no residual effects on performance were detected. The 2nd experiment was designed to study the effects of temazepam 20 mg on daytime sleeping and subsequent performance following a simulated night shift. Compared to placebo, temazepam had favourable effects on the subjective duration and quality of daytime sleep, but had no overall beneficial or detrimental residual effects on performance.

Adolescent↗
PubMed2001

Examination of accuracy of sleep stages by means of an automatic sleep analysis system 'Sleep Ukiha'.

We examined the differences between the results of an automatic sleep analysis system and inspection decision. Subjects were 10 males (average age 21.6 years). One section consists of 20 s records. The sections that deviated from the algorithm could not be decided. Each sleep stage decided by automatic analysis was compared with the inspection decision. The agreement ratio of stage 3 was 91.6% in the highest, and followed by stage 2, stage 4, stage W and stage 1. The lowest was 62.5% for movement time. The total agreement ratio was 85.8%. The agreement ratios of the apnea index (AI) and the apnea hypopnea index (AHI) were relatively high, but for types of sleep apnea, agreement ratios require improvement.

Adult↗
PubMed1990

Neuroendocrinological investigations during sleep deprivation in depression. II. Longitudinal measurement of thyrotropin, TH, cortisol, prolactin, GH, and LH during sleep and sleep deprivation.

Thyrotropin (TSH), thyroxin (T4), triiodothyronine (T3), free T3 (fT3), cortisol, prolactin, and human growth hormone (HGH) were measured every 2 hr during a night of sleep, the following day, and a night of sleep deprivation (SD) in 14 patients with major depressive disorder. In subgroups fT4 (n = 5), reverse T3 (rT3), and luteinizing hormone (LH) (n = 6) were also investigated. Significant increases in TSH, T4, fT4, T3, fT3, rT3, and cortisol and decreases in prolactin levels occurred during the night of SD, compared to the pattern during the night of sleep. The pre-SD T4 and T3 levels of the responders to SD were already higher than in the nonresponders, and increased less during SD. The cortisol and HGH concentrations of the responders rose higher during SD than those of the nonresponders. Changes in TSH and prolactin were not correlated to clinical response. Analysis of possible neurochemical mechanisms underlying this "pattern" of changes in different endocrine profiles suggests that enhanced noradrenergic activity might play a role in the changes in TSH, cortisol, thyroid hormones, and possibly HGH secretion during SD, and increased dopaminergic tone probably induced the decline in prolactin levels. Additional effects of the serotonergic system cannot be excluded at present. In conclusion, the data suggest that enhanced noradrenergic activity of the locus coeruleus stimulates alpha and/or beta adrenergic receptors in depressed patients during SD. This mechanism could well be involved in the antidepressant effect of this therapy.

Adult↗
PubMed2000

Changing concepts of sudden infant death syndrome: implications for infant sleeping environment and sleep position. American Academy of Pediatrics. Task Force on Infant Sleep Position and Sudden Infant Death Syndrome.

The American Academy of Pediatrics has recommended since 1992 that infants be placed to sleep on their backs to reduce the risk of sudden infant death syndrome (SIDS). Since that time, the frequency of prone sleeping has decreased from >70% to approximately 20% of US infants, and the SIDS rate has decreased by >40%. However, SIDS remains the highest cause of infant death beyond the neonatal period, and there are still several potentially modifiable risk factors. Although some of these factors have been known for many years (eg, maternal smoking), the importance of other hazards, such as soft bedding and covered airways, has been demonstrated only recently. The present statement is intended to review the evidence about prone sleeping and other risk factors and to make recommendations about strategies that may be effective for further reducing the risk of SIDS. This statement is intended to consolidate and supplant previous statements made by this Task Force.

Cause of Death↗
PubMed2003

Clinical significance of pulse rate rise during sleep as a screening marker for the assessment of sleep fragmentation in sleep-disordered breathing.

OBJECTIVE: To assess the clinical utility of the frequencies of transient increases of pulse rate, non-invasively measured with a pulseoximeter, as an indirect indication of the degree of cortical arousal, measured conventionally on an electroencephalogram (EEG), in obstructive sleep apnea-hypopnea syndrome (OSAHS) patients. PATIENTS AND METHODS: Thirty-three consecutive patients referred with suspected OSAHS were studied. Polysomnography (PSG) with determination of esophageal pressure (Pes) and pulseoximetry was monitored to identify breathing-related EEG arousal (B-Ar) associated with apnea, hypopnea or respiratory effort and the frequencies of pulse rate increases. We also assessed the association of B-ArI (defined as the number of B-Ar per hour) with the pulse rate rise index (PRRI)-X(X=4-10) (defined as the number of pulse rate increases per hour). In addition, the sensitivity and specificity of PRRI for the assessment of a B-ArI cutoff point of 30 were calculated. RESULTS: The sensitivity and specificity of pulseoximetry for different thresholds of PRRI-X(X=4-10) demonstrated that the greatest diagnostic accuracy for detecting frequent arousal (B-ArI > or =30) occurs at a cutoff point of 40 PRRI-6 with a sensitivity of 0.88 and specificity of 0.86. This point shows a significant area under the curve of 0.84. In addition, a statistically significant correlation between PRRI-6 and B-ArI (r=0.68, P<0.0001) was observed. CONCLUSIONS: The transient increases in pulse rate measured by pulseoximetry during sleep may be a useful clinical marker for predicting the degree of arousal in OSAHS patients, and may, in addition, prevent cases with frequent respiratory effort related arousals from being overlooked. However, further studies are required to improve the confidence level of the PRRI and to investigate the causes of overestimation of EEG arousals.

Adult↗
PubMed1994

Does the function of REM sleep concern non-REM sleep or waking?

We have hypothesized that REM sleep is functionally and homeostatically related to NREM sleep rather than to waking. In other words, REM sleep rather than to waking. In other words, REM sleep occurs in response to NREM-sleep expression and compensates for some process that takes place during NREM sleep. Under normal conditions, the need for REM sleep does not accrue during waking. The primary basis for this hypothesis is the fact that REM-sleep expression is a function of prior NREM-sleep expression. That is, REM sleep follows NREM sleep within sleep periods, REM-sleep episodes occur at intervals determined by the amount of NREM-sleep time elapsed, and total time spent in REM sleep is consistently about 1/4 of prior NREM-sleep time, regardless of how much time is spent in NREM sleep. Our experimental tests of the hypothesis support it. (1) REM-sleep propensity accumulates quite rapidly during a 2-hr interval spent predominantly in NREM sleep. (2) The timing of individual REM-sleep episodes is controlled homeostatically, by accumulation within NREM sleep of a propensity for REM sleep. The NREM sleep-related model of REM-sleep regulation (Fig. 1) explains a number of phenomena of REM-sleep expression, including the frequent and periodic occurrence of REM-sleep episodes throughout sleep periods, that have been accommodated by the waking-related model but are not functionally accounted for by it. In our opinion, the NREM sleep-related model of REM-sleep regulation recommends itself partly by its simplicity. According to the waking-related model, two independent and competing sleep propensities accumulate during waking and are discharged in two distinct sleep states that perform different waking-related recovery processes. One behaviour, sleep, is thought to perform two independent and competing functions that alternate at regular intervals. In the NREM sleep-related model of REM-sleep regulation, sleep debt simply reflects a need for NREM sleep. That is, the cerebrally less activated state of NREM sleep enables some form of restoration made necessary by the cerebrally activated state of waking. Periodic occurrence of REM-sleep episodes is explained without postulating an oscillatory mechanism to gate expression of NREM sleep versus REM sleep. In assessing the comparative merits of the waking-related and NREM sleep-related models of REM-sleep regulation, one should consider the influence of time-worn habits of thought.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2004

Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan.

OBJECTIVES: The purposes of this study were to identify age-related changes in objectively recorded sleep patterns across the human life span in healthy individuals and to clarify whether sleep latency and percentages of stage 1, stage 2, and rapid eye movement (REM) sleep significantly change with age. DESIGN: Review of literature of articles published between 1960 and 2003 in peer-reviewed journals and meta-analysis. PARTICIPANTS: 65 studies representing 3,577 subjects aged 5 years to 102 years. MEASUREMENT: The research reports included in this meta-analysis met the following criteria: (1) included nonclinical participants aged 5 years or older; (2) included measures of sleep characteristics by "all night" polysomnography or actigraphy on sleep latency, sleep efficiency, total sleep time, stage 1 sleep, stage 2 sleep, slow-wave sleep, REM sleep, REM latency, or minutes awake after sleep onset; (3) included numeric presentation of the data; and (4) were published between 1960 and 2003 in peer-reviewed journals. RESULTS: In children and adolescents, total sleep time decreased with age only in studies performed on school days. Percentage of slow-wave sleep was significantly negatively correlated with age. Percentages of stage 2 and REM sleep significantly changed with age. In adults, total sleep time, sleep efficiency, percentage of slow-wave sleep, percentage of REM sleep, and REM latency all significantly decreased with age, while sleep latency, percentage of stage 1 sleep, percentage of stage 2 sleep, and wake after sleep onset significantly increased with age. However, only sleep efficiency continued to significantly decrease after 60 years of age. The magnitudes of the effect sizes noted changed depending on whether or not studied participants were screened for mental disorders, organic diseases, use of drug or alcohol, obstructive sleep apnea syndrome, or other sleep disorders. CONCLUSIONS: In adults, it appeared that sleep latency, percentages of stage 1 and stage 2 significantly increased with age while percentage of REM sleep decreased. However, effect sizes for the different sleep parameters were greatly modified by the quality of subject screening, diminishing or even masking age associations with different sleep parameters. The number of studies that examined the evolution of sleep parameters with age are scant among school-aged children, adolescents, and middle-aged adults. There are also very few studies that examined the effect of race on polysomnographic sleep parameters.

Adolescent↗
PubMed1996

Nocturia. A rarely recognized symptom of sleep apnea and other occult sleep disorders.

BACKGROUND: Nocturia, awakening from sleep to urinate, is a common symptom in a variety of medical disorders and in the elderly. Awakening from sleep as a result of nocturia is thought to be secondary to a sensation of urinary urgency resulting from an overextended bladder. Nocturia-related awakenings cause significant sleep disruption and fatigue in elderly patients and are correlated with an increased number of falls at night. Sleep disorders such as sleep apnea are also common in the elderly and are frequently the source of awakenings from sleep. The high incidence of both nocturia and sleep disorders in the elderly and other groups of patients suggests that sleep disorders may be the source of some awakenings from sleep usually attributed by patients to nocturia. Nocturia secondary to sleep disorders would be causatively different from nocturia secondary to pressure to urinate in common medical disorders and would require different diagnostic procedures and treatment. OBJECTIVE: To determine the frequency of nocturia as a symptom of primary sleep disorders. METHODS: Eighty consecutive patients, 27 women and 53 men with a mean (+/-SD) age of 58.7+/-14.1 years, undergoing polysomnography (sleep study or PSG) for the evaluation of a suspected sleep disorder and who met the sole criteria of awakening from sleep at least once and urinating voluntarily. Each patient had either a standard PSG recording or a PSG with administration of nasal continuous positive airway pressure. Immediately after each episode of nocturia during the PSG, patients were questioned about the reason they believed they had awakened. The PSG record immediately before awakening from sleep was then reviewed for potential causes of awakening. Patients were also asked on final morning awakening to fill in a questionnaire regarding their awakenings during the prior night. Patient reports were compared with the PSG to determine the accuracy of subjective reports. RESULTS: Patients awakened from sleep and voluntarily urinated a mean (+/- of 1.5+/-0.75 times per night for a total of 121 awakenings for the group. The majority (79.3%) of these awakenings from sleep were found to be directly secondary to sleep apnea, snoring or periodic leg movements in sleep. Patients correctly identified the source of their awakening from sleep on only five(4.9%) occasions and only once was sleep apnea correctly cited by a patient as a source of awakening during the night. CONCLUSION: Most awakenings from sleep attributed by our patients to pressure to urinate were instead a result of sleep disorders, particularly sleep apnea. The fact that patients do urinate once awake likely contributed to faulty post hoc reasoning and might have limited further inquiry by patients and their physicians in clinical settings into the actual sources of awakening from sleep. Even in those patients with well-known medical reasons for noctruria, Sleep disorders were still found to be the source of almost all awakenings from sleep. Patients were extremely poor judges of the reasons they awoke from sleep. The diagnosis of a sleep disorder should be seriously considered whenever a patient reports frequent awakenings from sleep to urinate.

Adult↗
PubMed2005

Sleep patterns and sleep problems among schoolchildren in the United States and China.

OBJECTIVES: Sleep patterns and sleep problems in children are not only influenced by a large number of biological and psychologic factors but also by cultural and social factors. Little is known about similarities and differences in sleep patterns and sleep problems among children across countries. We attempted to compare sleep patterns and sleep problems among schoolchildren from 2 countries with distinctive cultural contexts: the United States and China. METHODS: The data come from 2 cross-sectional surveys in 3 elementary schools of Jinan City, People's Republic of China, and 3 elementary schools from a suburban school district in southeastern New England, United States. The Chinese sample consisted of 517 elementary school children (grades 1 to 5), and the US sample consisted of 494 elementary school children (grades kindergarten through 4). We used the Children's Sleep Habits Questionnaire (CSHQ) to assess children's sleep patterns and sleep problems as reported by parents. Parents of the Chinese sample completed a Chinese version of the CSHQ. RESULTS: For children in both the US and Chinese samples, reported bedtime was delayed and sleep duration decreased with increasing age. Compared with the US children (grades 1-4), Chinese children went to bed approximately half an hour later (9:02 vs 8:27 pm) and woke up half an hour earlier (6:28 vs 6:55 am), resulting in an average sleep duration that was 1 hour less (9.25 vs 10.15 hours). Chinese children were rated significantly higher than the US children on almost all CSHQ scales, indicating more sleep problems in Chinese children. Common sleep problems observed for all children were difficulty falling asleep, having a fear of sleeping in the dark, sleep talking, restless sleep, teeth grinding during sleep, and daytime sleepiness. Shorter daily sleep duration was associated with difficulty falling asleep, struggling at bedtime, and trouble sleeping away for the US children, and with going to bed at different times and having a fear of sleeping alone for Chinese children. Short sleep duration was a main predictor of daytime sleepiness for Chinese children, whereas restless sleep and snoring predicted daytime sleepiness for the US children. CONCLUSIONS: As reported by parents, children in China went to bed later and woke up earlier and their sleep duration was 1 hour shorter than the US children. Chinese children were reported to have more sleep problems than their US counterparts. Daytime sleepiness was determined by sleep duration only for those who slept insufficiently. Unique school schedules and sleep practices may contribute to the differences in the sleep patterns and sleep problems of children from the United States and China.

Adolescent↗
PubMedDate not supplied

Headache and sleep: examination of sleep patterns and complaints in a large clinical sample of migraineurs.

OBJECTIVES: This study characterized sleep parameters and complaints in a large clinical sample of migraineurs and examined sleep complaints in relation to headache frequency and severity. BACKGROUND: The relationship between headache and sleep has been documented at least anecdotally in medical literature for well over a century and clinical texts allude to the importance of sleep as a headache precipitant. A small number of empirical studies have emerged, but the precise nature and magnitude of the headache/sleep association and underlying mechanisms remain poorly understood. METHODS: In this investigation, 1283 migraineurs were drawn from 1480 consecutive headache sufferers presenting for evaluation to a tertiary headache clinic. Patients underwent a physical examination and structured interview assessing a variety of sleep, headache, and demographic variables. Migraine was diagnosed according the IHS criteria (1.1 to 1.6 diagnostic codes). Migraineurs were 84% female, with a mean age of 37.4 years. Groups were formed based on patient's average nocturnal sleep patterns, including short, normal, and long sleep groups, and were compared on headache variables. RESULTS: Sleep complaints were common and associated with headache in a sizeable proportion of patients. Over half of migraineurs reported difficulty initiating and maintaining sleep at least occasionally. Many in this sample reported chronically shortened sleep patterns similar to that observed in persons with insomnia, with 38% of patients sleeping on average 6 hours per night. Migraines were triggered by sleep disturbance in 50% of patients. "Awakening headaches" or headaches awakening them from sleep were reported by 71% of patients. Interestingly, sleep was also a common palliative agent for headache; 85% of migraineurs indicated that they chose to sleep or rest because of headache and 75% were forced to sleep or rest because of headache. Patients with chronic migraine reported shorter nightly sleep times than those with episodic migraine, and were more likely to exhibit trouble falling asleep, staying asleep, sleep triggering headache, and choosing to sleep because of headache. Short sleepers (ie, average sleep period 6 hours) exhibited significantly more frequent and more severe headaches than individuals who slept longer and were more likely to exhibit morning headaches on awakening. CONCLUSIONS: These data support earlier research and anecdotal observations of a substantial sleep/migraine relationship, and implicate sleep disturbance in specific headache patterns and severity. The short sleep group, who routinely slept 6 hours per night, exhibited the more severe headache patterns and more sleep-related headache. Sleep complaints occurred with greater frequency among chronic than episodic migraineurs. Future research may identify possible mediating factors such as primary sleep and mood disorders. Prospective studies are needed to determine if normalizing sleep times in the short sleeps would impact headache threshold.

Adolescent↗
PubMed1995

Physiology of REM sleep, cataplexy, and sleep paralysis.

The main neural structures generating muscle atonia and other phenomena characteristic of REM sleep are present in dorsolateral portions of the pons in the brainstem. Occurrence of REM sleep and the NREM-REM sleep cycle are probably determined by a balance or interaction between the cholinergic and cholinoceptive REM sleep-on neuronal populations and the monoaminergic REM sleep-off neuronal population. Neural activities producing generalized muscle atonia in REM sleep originate mainly in dorsolateral portions of the pontine reticular formation, descend through the medulla and spinal cord, and inhibit the motoneurons in the brainstem and spinal cord, bringing about postural atonia. Cataplexy and sleep paralysis are pathological, dissociated manifestations of the generalized muscle atonia characteristic REM sleep. Cataplexy is triggered by emotional stimuli, probably through activation of the neural structure generating the muscle atonia of REM sleep. During long-lasting cataplectic attacks, narcoleptic humans often experience sleep paralysis and vivid hypnagogic hallucinations in the latter sleep state. Sleep paralysis is caused by the marked dissociation between level of alertness and muscle atonia that often occurs in SOREM sleep episodes. Frequent SOREM sleep episodes in narcoleptic humans and dogs may occur when some of the neural mechanisms producing wakefulness and/or NREM sleep that normally inhibit the occurrence of REM sleep are abnormally weak, or when neural mechanisms facilitating the occurrence of REM sleep are hypersensitive or hyperactive, or both. Both abnormalities may contribute to the occurrence of SOREM sleep episodes and sleep paralysis, and also to the emotional triggering of cataplexy. Frequent occurrence of SOREM sleep episodes seems to be prerequisite but not sufficient for the occurrence of cataplexy. Some additional neural activities induced by emotion also contribute by inhibiting and/or activating the disturbed neural mechanisms related to SOREM sleep episodes. These abnormalities in neural mechanisms probably involve hypersensitivity or hyperactivity of muscarinic cholinergic and/or cholinoceptive neuronal populations in the pontine and suprapontine structures, and/or abnormally decreased activity of noradrenergic or serotonergic neuronal populations in the pons and/or other brainstem structures. This last monoaminergic neuronal population probably has a gating or inhibiting effect upon the cholinergic and cholinoceptive neuronal populations related to the generation of generalized muscle atonia and REM sleep. In spite of many studies and published reports on REM sleep, as well as on cataplexy and sleep paralysis, we are still far from a complete understanding of the physiological mechanisms producing muscle atonia in REM sleep and of the pathophysiological mechanisms of cataplexy and sleep paralysis--though it is apparent that these mechanisms are closely related.

Animals↗
PubMed2002

Cognitive behavioural interventions for sleep problems in adults aged 60+.

BACKGROUND: The prevalence of sleep problems in adulthood increases with age. While not all sleep changes are pathological in later life, severe disturbances may lead to depression, cognitive impairments, deterioration of quality of life, significant stresses for carers and increased healthcare costs. The most common treatment for sleep disorders (particularly insomnia) is pharmacological. The efficacy of non-drug interventions has been suggested to be slower than pharmacological methods, but with no risk of drug-related tolerance or dependency. Cognitive and behavioural treatments for sleep problems aim to improve sleep by changing poor sleep habits, promoting better sleep hygiene practices and by challenging negative thoughts, attitudes and beliefs about sleep. OBJECTIVES: To assess the efficacy of cognitive-behavioural interventions in improving sleep quality, duration and efficiency amongst older adults (aged 60 and above). SEARCH STRATEGY: The following databases were searched: MEDLINE (1966 - October 2001); EMBASE (1980 - January 2002), CINAHL ( 1982 - January 2002; PsychINFO 1887 to 2002; The Cochrane Library (Issue 1, 2002); National Research Register (NRR [2002]). Bibliographies of existing reviews in the area, as well as of all trial reports obtained, were searched. Experts in the field were consulted. SELECTION CRITERIA: Randomised controlled trials of cognitive behavioural treatments for primary insomnia where 80% or more of participants were over 60. Participants must have been screened to exclude those with dementia and/or depression. DATA COLLECTION AND ANALYSIS: Abstracts of studies identified in searches of electronic databases were read and assessed to determine whether they might meet the inclusion criteria. Data were analysed separately depending on whether results had been obtained subjectively or objectively. MAIN RESULTS: Six trials, including 282 participants with insomnia, examined the effectiveness of cognitive-behavioural treatments (CBT) for sleep problems in this population. The final total of participants included in the meta-analysis was 224. The data suggest a mild effect of CBT for sleep problems in older adults, best demonstrated for sleep maintenance insomnia. REVIEWER'S CONCLUSIONS: When the possible side-effects of standard treatment (hypnotics) are considered, there is an argument to be made for clinical use of cognitive-behavioural treatments. Research is needed to establish the likely predictors of success with such treatments. As it may well be the case that the treatment efficacy of cognitive-behavioural therapy itself is not durable, the provision of "top-up" sessions of CBT training to improve durability of effect are worthy of investigation.

Age Factors↗
PubMed2005

Interindividual variation in sleep duration and its association with sleep debt in young adults.

STUDY OBJECTIVE: To determine whether variation in sleep duration reflects variation in sleep need or self-imposed sleep restriction. DESIGN: After habitual bedrest duration of participants was assessed during a 2-week outpatient protocol, volunteers were scheduled to sleep according to this schedule for 1 week prior to and the first night after admission to a general clinical research center. The inpatient protocol included multiple sleep latency testing on the second day and sleep recordings during a bedrest extension protocol that included 16 hours of sleep opportunity (12 hours at night and 4 hours at midday) for 3 consecutive days. SETTING: Outpatient monitoring followed by inpatient assessment of sleep. PARTICIPANTS: Seventeen healthy volunteers (10 women) aged 18-32 years without clinical sleep disorders. INTERVENTIONS: Extension of sleep opportunity. MEASUREMENTS AND RESULTS: The habitual bedrest duration varied from 6.1 to 10.3 hours. Individuals with shorter habitual bedrest duration fell asleep more quickly and frequently during the multiple sleep latency test than did those with longer habitual bedrest duration. On the first day of extended sleep opportunity, the total sleep time of all individuals was greater than their habitual bedrest duration; the average increase in total sleep time was 4.9 hours (P = 0.001). The increase in total sleep time declined across the 3 day bedrest-extension protocol (P = 0.003 for trend). During the third day of increased sleep opportunity, the total sleep time was negatively associated with habitual bedrest duration (P = 0.005); individuals with shorter habitual bedrest duration continued to sleep more than those with longer habitual bedrest duration. CONCLUSION: Those individuals with shorter habitual sleep durations carry a higher sleep debt than do those with longer habitual sleep duration. Interindividual variation in sleep duration may primarily reflect variation in self-selected sleep restriction or wake extension.

Academic Medical Centers↗
PubMed1999

Upper airway resistance syndrome: effect of nasal dilation, sleep stage, and sleep position.

BACKGROUND: The upper airway resistance syndrome (UARS) is one of the mild variants of obstructive sleep disordered breathing. Nasal obstruction is proposed as one of the mechanisms that lowers intrapharyngeal pressure and hence increases airway collapsibility. OBJECTIVE: We evaluated the effect of external nasal dilation and sleep position on sleep in UARS. METHOD: A double blind, randomized, controlled study with a crossover design (using therapeutic and placebo dilators) was conducted in 18 consecutive patients with UARS. Each patient had two overnight sleep studies one to two weeks apart. Cardiorespiratory parameters (AHI, percentage of time that SaO2 was more than 2% below awake [desaturation time] and mean overnight heart rate), sleep architecture (sleep stages, sleep efficiency, and arousal index), and body position were determined. RESULTS: Application of the external nasal dilator resulted in a significant increase in the nasal cross-sectional area (p < 0.001). Treatment reduced stage 1 sleep (as a percent of total sleep time) from 8.6 +/- 0.8% to 7.1 +/- 0.7 (SEM), p = 0.034). Desaturation time was significantly lower with treatment (12.2 +/- 2.2% on placebo versus 9.1 +/- 1.3 on treatment, p = 0.04). There were no additional significant effects on the cardiorespiratory parameters, sleep architecture, or MSLT when the entire night was examined. Controlling for interactions of sleep stage and position and treatment we found that treatment reduced desaturation time (p = 0.03) but not AHI or arousal index. AHI was significantly lower in the lateral position compared to the supine (p = 0.0001) and in NREM sleep compared to REM (p = 0.001). Desaturation time was significantly lower on the lateral compared to the supine position (p = 0.002) and in NREM sleep compared to REM (p = 0.006). Arousal index was highly dependent on sleep stage (p = 0.0001): the index was higher in stage 2 compared to slow wave sleep and REM. Sleep position and treatment had no significant effect on arousals. CONCLUSIONS: External nasal dilation reduced stage 1 sleep, an indirect marker of disrupted sleep, and desaturation time. There were no additional effects on sleep architecture or sleep disordered breathing. Both sleep position and sleep stage had a significant effect on sleep disordered breathing in UARS.

Airway Resistance↗