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PubMed1983

The time course of slow wave sleep and REM sleep in habitual long and short sleepers: effect of prior wakefulness.

Three groups of young good sleepers were selected according to their habitual sleep length as short (SS), regular (RS), or long (LS) sleepers. Their sleep was recorded in three situations: reference nights, a recovery sleep night after 36 h of sleep deprivation, and a sleep night after a morning sleep recovery from sleep deprivation (12 h waking time). Total and cycle-by-cycle amounts of slow wave sleep (SWS) and REM sleep were studied both as a function of experimental conditions and of the group of subjects. In all three conditions, LS had less SWS than other sleepers while the differences in SWS amounts between groups were mainly due to different amounts in the second and third cycles, differences between conditions essentially due to variations of SWS within sleep cycle 1 (SWS1). SWS1 appeared to reflect some physiological process whose level increases during waking and declines during sleep. REM sleep proved to be proportional to sleep length.

Adult↗
PubMed2002

Sleep duration and mortality: The effect of short or long sleep duration on cardiovascular and all-cause mortality in working men and women.

BACKGROUND: There is evidence to suggest that insufficient sleep may have an adverse effect on physical and psychological health. Previous studies have reported that when adjusting for major risk factors for cardiovascular disease and a number of demographic and social variables, sleeping 7-8 h each night is associated with lower mortality. These studies, however, have excluded any consideration of stress, which is known to be related to a number of behavioural risk factors for disease and, like sleep, may influence neurochemical, hormonal and immunological functioning. METHODS: This study revisits the associations between sleep duration, cardiovascular disease risk factors and mortality, taking into account the perceived stress of individuals. The data come from a cohort of working Scottish men and women recruited between 1970 and 1973; approximately half of the cohort was screened for a second time, 4-7 years after the baseline examination. RESULTS: For both men and women, higher self-perceived stress was associated with a reduction in the hours of sleep reported. The pattern of mortality from all causes and the pattern of mortality from cardiovascular disease were consistent for both men and women. When sleep was measured on one occasion only, the risk of dying was reduced for men sleeping more than 8 h in every 24 h compared with those sleeping 7-8 h over the same period. This was after adjustment had been made for age, marital status, social class, cardiovascular risk factors and stress. The risk of dying was increased for women sleeping less than 7 h in every 24 h compared with those sleeping 7-8 h over the same period, after similar adjustments. When the data from the 1st and 2nd screening were considered longitudinally, both men and women who reported that they slept less than 7 h on both occasions that they were questioned, had a greater risk of dying from any cause than those who had reported sleeping 7-8 h at both screenings, after adjusting for age, marital status, social class and stress. CONCLUSIONS: Short sleep over a prolonged period may be associated with an increased risk of mortality: men and women who reported sleeping fewer than 7 h in 24 on two occasions between 4 and 7 years apart, had greater risk of dying from any cause over a 25 year period than those who reported sleeping 7-8 h on both occasions that they were questioned.

Journal Article↗
PubMed2003

Sleep disordered breathing may not be an independent risk factor for diabetes, but diabetes may contribute to the occurrence of periodic breathing in sleep.

OBJECTIVE(S): (a) To determine if self-reported diabetes mellitus is independently associated with sleep-disordered breathing (SDB); (b) to determine if diabetes mellitus is specifically associated with central sleep apnea including periodic breathing (Cheyne-Stokes breathing pattern) during sleep. STUDY POPULATION: The study population reflected participants in the on-going Sleep Heart Health Study (SHHS). Analyses were conducted utilizing data obtained from 4872 SHHS participants without prevalent cardiovascular disease (CVD) and 1002 participants with self-reported CVD, defined as hospitalization for non-fatal coronary heart disease, congestive heart failure, myocardial infarction, coronary artery bypass graft, and stroke. METHODS: SHHS methodologies have been previously reported and include performance of overnight, in-home polysomnography (PSG), which recorded variables reflecting sleep architecture and breathing, permitting identification of obstructive and central apneas, hypopneas, periodic breathing and oxyhemoglobin saturation (SpO(2)). Anthropomorphic metrics as well as systemic blood pressure measurements were obtained at the time of PSG. Other health data were available from questionnaires and the data sets of the parent cohorts from whom SHHS participants were recruited. The investigators assessed and compared breathing parameters, sleep architecture and CVD variables in diabetic and non-diabetic participants. The relationships between diabetes and the various study parameters, independent of potential confounders, were examined by multivariable modeling. Linear regression modeling was employed to examine the relationship between continuously distributed variables such as respiratory disturbance index log (RDI). The relationships between diabetes and dichotomous outcome variables such as central apnea index (CAI), obstructive apnea index (OAI), periodic breathing and the percentage of time spent at various levels below SpO(2) 90% were examined by the logistic regression model. Age, gender, race, BMI and neck circumference were forced into all multivariable analyses since these factors are associated with both diabetes mellitus and SDB. RESULTS: The investigators reported that the prevalence of CVD risk factors including increased BMI, waist circumference, neck circumference, triglycerides, reduced HDL cholesterol and hypertension was greater in diabetic than non-diabetic participants. Native Americans represented a disproportionately high percentage of the diabetic population. Unadjusted data obtained from participants without prevalent CVD indicated that the mean RDI was higher in the diabetic participants. Moreover, there was a greater percentage of diabetic participants in the higher RDI categories (e.g. 23.8% of the 470 diabetics and 15.6% of the 4402 non-diabetics had RDI>15, P<0.001). Similarly, the unadjusted data indicated that a significantly greater proportion of the diabetic participants spent >5% and >10% of sleep time below SpO(2) 90%, compared with the non-diabetic participants. The unadjusted data from participants without prevalent CVD indicated that the diabetic and non-diabetic participants did not differ with regard to distribution by category of OAI severity (e.g. > or =2 events/h, > or =3 events/h, or > or =4 events/h). On the other hand, although the prevalence of central apneas was low, a significantly greater proportion of diabetic participants were in the CAI categories (> or =2 events/h and > or =3 events/h) than non-diabetic subjects. There was no difference between diabetic and non-diabetic individuals with regard to CAI prevalence in the > or =4 events/h category. Of note, a greater percentage of diabetic patients exhibited periodic breathing (3.8% vs. 1.8%, diabetic and non-diabetic participants, respectively, P=0.002). Repeating the above analyses with inclusion of the participants with prevalent CVD did not change these relationships, and in fact, the differences between diabetic and non-diabetic participants with respect to central events and periodic breathing became more evident (the data forre evident (the data for this were not provided in the paper). Linear regression analyses demonstrated that BMI, age and male gender were independently related to increased RDI among participants without prevalent CVD. Furthermore, after adjusting for age, gender, race, BMI and neck circumference, there was no difference in geometric mean RDI between the diabetic and non-diabetic participants. The adjusted odds of having RDI> or =15 and the adjusted odds for spending> or =5% or > or =10% of sleep time with SpO(2) <90% did not differ between the diabetic and non-diabetic individuals. The investigators also examined sleep architecture in the study cohort. There were no differences between the diabetic and non-diabetic groups with regard to the adjusted proportion of time spent in non-REM sleep stages, although the mean percent time spent in REM sleep was 1.1% less in the diabetic individuals. The findings were the same with or without inclusion of participants with known CVD. Even after adjustment for potential confounders, in a sample without or with prevalent CVD, diabetic participants had increased adjusted odds for periodic breathing odds ratio (1.8, 95% confidence interval (CI) with a range of 1.02--3.15 in diabetic participants without prevalent CVD vs. 1.74, 95% CI with a range of 1.16--2.62 in diabetic participants with prevalent CVD). There was a suggestion of increased odds for CAI in diabetic subjects when analyzing populations with and without prevalent CVD. CONCLUSION: The authors concluded that diabetes mellitus is associated with sleep apnea but that this association is largely explained by risk factors in common for both disorders, most notably obesity. After adjusting for confounding factors there was no difference between diabetic and non-diabetic participants with regard to obstructive events. However, even after adjusting for potential confounders, there was a greater prevalence of periodic breathing in diabetic subjects. Although not reaching statistical significance, there was a suggestion of an increased prevalence of central events in the diabetic population, particularly when the sample included participants with known CVD. The investigators believed it unlikely that the findings were attributable to underlying congestive heart failure in as much as the diabetic subjects without prevalent CVD exhibited increased prevalence of periodic breathing and possibly increased central events. The authors proposed that diabetes mellitus might be a cause of SDB, mediated through autonomic neuropathy that may alter ventilatory control mechanisms. In this context, the authors commented that autonomic neuropathy may cause perturbations in ventilatory control by altering chemoreceptor gain or altering cardiovascular function (although the authors discounted underlying congestive heart failure as an explanation for the higher prevalence of periodic breathing in diabetic participants). To reinforce their conclusions, the authors cited the literature indicating increased prevalence of sleep apnea in diabetic patients with autonomic dysfunction, as well as the association between Shy--Drager syndrome, in which autonomic insufficiency is a constitutive element, and central sleep apnea.

Journal Article↗
PubMed1993

Symposium: Normal and abnormal REM sleep regulation: REM sleep in depression-an overview.

Abnormalities of REM sleep, i.e. shortening of REM latency, lengthening of the duration of the first REM period and heightening of REM density, which are frequently observed in patients with a major depressive disorder (MDD), have attracted considerable interest. Initial hopes that these aberrant patterns of sleep constitute specific markers for the primary/endogenous sub-type of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison with other psychopathological groups is challenged as well. Demographic variables like age and sex exert strong influences on sleep physiology and must be controlled when searching for specific markers of depressed sleep. It is still an open question whether abnormalities of sleep are state- or trait-markers of depression. Beyond baseline studies, the cholinergic REM induction test (CRIT) indicated a heightened responsitivity of the REM sleep system to cholinergic challenge in depression compared with healthy controls and other psychopathological groups, with the exception of schizophrenia. A special role for REM sleep in depression is supported by the well-known REM sleep suppressing effect of most antidepressants. The antidepressant effect of selective REM deprivation by awakenings stresses the importance of mechanisms involved in REM sleep regulation for the understanding of the pathophysiology of depressive disorders. The positive effect of total sleep deprivation on depressive mood which can be reversed by daytime naps, furthermore emphasizes relationships between sleep and depression. Experimental evidence as described above instigated several theories like the REM deprivation hypothesis, the 2-process model and the reciprocal interaction model of nonREM-REM sleep regulation to explain the deviant sleep pattern of depression. The different models will be discussed with reference to empirical data gathered in the field.

Journal Article↗
PubMed1994

Renin as a biological marker of the NREM-REM sleep cycle: effect of REM sleep suppression.

We have previously described that, in normal man, the nocturnal oscillations of plasma renin activity (PRA) exactly reflect the rapid eye movement (REM)-non(N)REM sleep cycles, with increasing PRA levels during NREM sleep and decreasing levels during REM sleep. This study was carried out to determine whether REM sleep suppression affects nocturnal renin profiles and to define which sleep stage is essential for renin release. In a first experimental series, REM sleep was suppressed by using clomipramine, a tricyclic antidepressant. Seven healthy young men were studied once during a night when a placebo was given and once during a night following a single dose of 50 mg clomipramine. Blood was collected every 10 min from 23.00 hours to 07.00 hours. PRA was measured by radio-immunoassay and the nocturnal profiles were analysed using the pulse detection program ULTRA. Clomipramine suppressed REM sleep in all subjects but one, but did not affect the number of SWS episodes nor their duration. Similar PRA profiles were observed in both experimental conditions. Neither the mean levels, nor the number and the amplitude of the oscillations were modified and the normal relationship between slow wave sleep and increasing PRA levels was preserved. In a second experimental series, REM sleep was prevented by rapidly awakening the subjects as soon as they fell into REM sleep. The four subjects studied attempted several times to go into REM sleep, but only when PRA levels were decreasing. The interruption of REM sleep by short waking periods did not disturb PRA for which the oscillations remained unaffected. Again, the relationship between SWS and increasing PRA levels was preserved. These results provide evidence that mechanisms increasing slow-wave activity are principally involved in increasing PRA levels and that replacing REM sleep by waking periods and light sleep does not modify nocturnal PRA oscillations.

Journal Article↗
PubMed2026

Wearable Sleep Monitoring in Pediatric Acute Lymphoblastic Leukemia: Associations With Subjective Sleep Ratings and Neurocognitive Functioning.

BACKGROUND: Sleep disturbances are associated with increased fatigue, reduced quality of life, and neurocognitive dysfunction and have emerged as a common complication among pediatric cancer survivors. Sleep disturbances are particularly concerning given their potential to exacerbate existing neurocognitive impacts of cancer treatments. This pilot study examined the feasibility and acceptability of a home-wearable EEG-based sleep device (Sleep ProfilerTM) for acute lymphoblastic leukemia (ALL) survivors as well as associations between specific sleep parameters and neurocognitive functioning. PROCEDURE: Children (ages 8-12; M = 10 years, SD = 1.6; N = 23) >6 months post-treatment for ALL were enrolled at clinical visits and wore the Sleep ProfilerTM for two consecutive nights at home, followed by neurocognitive testing of attention, inhibitory control, working memory, and processing speed. Parents completed subjective measures of child sleep, anxiety, depression, and acceptability. Feasibility reflected the percentage of children wearing the device at least one night and the percentage of nights with good EEG quality data. RESULTS: All participants wore the device both nights, with 84% meeting the threshold for good quality measurement. Few children met recommended quantity and quality sleep thresholds based on objective measurement, including 5 patients with elevated snoring levels; 43.5% of subjective ratings fell above the threshold for sleep disturbance. Greater sleep latency was associated with worse inhibitory control (r = -0.42, p = 0.046), and total sleep time was positively associated with inhibitory control and attention. CONCLUSIONS: Findings confirm the feasibility and acceptability of home EEG sleep monitoring in school-age survivors, and associations of sleep latency and snoring with reduced neurocognitive functioning may offer modifiable risk factors for aspects of neuropsychological dysfunction common in pediatric survivorship. CLINICAL TRIAL REGISTRATION: At the time this study was conducted, we were not required to register the study on ClinicalTrials.gov. It was a single-institution feasibility study without intervention, which was not considered a clinical trial.

Humans↗
PubMed1994

Sleep in a sitting position: effect of triazolam on sleep stages and EEG power spectra.

The effect of triazolam (0.25 mg) and placebo was investigated in healthy, male subjects who slept in a sitting position. After the intake of placebo, sleep efficiency, rapid eye movement (REM) sleep and subjective sleep quality were lower than in the preceding sleep episode in bed, while stage 1 and REM sleep latency were higher. Triazolam did not prevent this impairment of sleep. However, in comparison with the placebo condition, the percentage of slow wave sleep was higher in the first third of the night, and in the morning sleep was rated as more quite. EEG power density in nonREM sleep was reduced in the frequency range of 1.25-10.0 Hz and enhanced in the range of sleep spindles (12.25-13.0 Hz). These changes were still present in the last third of the night. In REM sleep, triazolam reduced spectral activity in some frequency bins between 4.25 and 10.0 Hz. The sitting position itself affected the nonREM sleep spectra, since the placebo level in the 2.25-21.0-Hz range exceeded the baseline level. We conclude that a 0.25 mg dose of triazolam does not effectively counteract a posture-induced sleep disturbance, but induces changes in the EEG spectra which are typical for benzodiazepine receptor agonists.

Adult↗
PubMed1981

Sleep deprivation: effect on sleep stages and EEG power density in man.

Sleep was analysed in 8 young adults subjects during two baseline nights and two recovery nights following 40.5 h sleep deprivation. Sleep stages were scored from the polygraph records according to conventional criteria. In addition, the EEG records of the entire nights were subjected to spectral analysis to compute the frequency distribution of the power density in the 0.25-25 Hz range for 0.5 Hz or 1.0 Hz bins. In the first recovery night, the power density in the delta band was significantly higher than baseline for total sleep time as well as for sleep stages 2, 3 and 4, 4 and REM. These changes were not restricted to the delta band, but extended to higher frequency bands. Minor, but significant, effects of sleep deprivation were seen in the power density distribution of the second recovery night. In the baseline nights, a progressive reduction of power density in the delta/theta range was present for successive non-REM-REM sleep cycles for total sleep time and stages 2, 3 and 4, and 4. The results show that effects of sleep deprivation as well as trends within the sleep periods are readily apparent from spectral analysis, but are inadequately reflected by conventional sleep scoring. When the power density values were integrated over the entire frequency range (0.75-25 Hz) for each non-REM-REM sleep cycle, an exponential decline from cycle 1 to cycle 3 was suggested. The present findings support the hypothesis that the EEG power density in the low frequency range is an indicator of a progressively declining process during sleep whose initial value is determined by the duration of prior waking.

Adult↗
PubMed2005

Sleep quality and more common sleep-related problems in medical students.

BACKGROUND AND PURPOSE: The aim of this paper is to conduct a survey based on a questionnaire that would characterize nighttime and daytime habits in medical students; to estimate how subjective sleep quality is associated with nighttime and daytime habits and sleep problems in students; to estimate how academic progress and workload is associated with subjective sleep quality, nighttime and daytime habits and sleep problems in students; and to estimate the prevalence of self-reported sleep problems in Estonian medical students. PATIENTS AND METHODS: The study group included 413 medical students of the University of Tartu, aged 19-33 years. The self-reported Sleep and Daytime Habits Questionnaire (S&DHQ) covered demographic characteristics (4 questions) and sleep and daytime habits (24 questions). Of the latter, 18 multiple-choice questions provided answers expressed as discontinuous variables on a nominal scale, 4 questions provided answers expressed as continuous variables on an interval scale, and 2 questions provided answers expressed as quality characterization on a five-point scale. The supplement includes information about lifestyle and academic progress on a four-point scale. RESULTS: The S & DHQ could be used to study sleep problems in young medical students. The subjective sleep quality of students was as follows: excellent-29%; good-40%; satisfactory-24%; poor 6%; very poor-1%. Sleep quality is associated with academic progress (R=0.174; P<0.001), leisure activity (R=0.210; P<0.001), and living conditions (R=0.195; P<0.001). Sleep quality is not associated with students' daily (R=0.021; P>0.05) or nightly workload (R=0.0664; P>0.05). Daytime sleepiness poses a significant problem for students and is associated both with sleep disorders and work while studying. CONCLUSIONS: The study demonstrates that complaints about sleep problems are common in young medical students.

Achievement↗
PubMed2006

Sleep habits and risk factors for sleep-disordered breathing in infants and young toddlers in Louisville, Kentucky.

INTRODUCTION: Snoring affects biobehavioral development among preschool and early school-age children. The goals of the present study were to survey the parents of a large community sample of infants and young toddlers to evaluate (a) naturalistic sleep duration and location; (b) snoring prevalence; and (c) demographic measures and sleep behaviors related to the presence of snoring either 2 or >or=3 days/week. METHODS: Questionnaires were completed by parents of children ages 2 weeks to 2 years attending well-baby checkups and were also mailed to the homes of six-month-old infants. RESULTS: Data from 944 children were available for analyses. No age differences were reported for total sleep duration, co-sleeping, or snoring. Average daily sleep duration was 12.5+/-1.8h (standard deviation (SD)), with daytime naps accounting for an increased proportion of total sleep duration among younger infants. Co-sleeping was reported by 15% of families. Snoring 2 days/week was reported in 11.8% and> days/week in 5.3% of participants. Survey items indicating risk for sleep-disordered breathing (SDB) clustered into factors related to the child, their environment, and their family; restless sleep was exclusively related to snoring 2 days/week and ethnicity, sweating during sleep, and noisy breathing exclusive to snoring >or=3 days/week. CONCLUSIONS: Young infants appear to sleep less than currently recommended. Co-sleeping is relatively common and not age-dependent through the first 2 years of life. Items relating to the child's sleep behaviors, environment, and parents' perceptions were predictive of positive report of snoring, with snoring rates consistent with a significant risk for SDB being similar to those reported for older children.

Catchment Area, Health↗
PubMed2001

Sleep and the cholinergic rapid eye movement sleep induction test in patients with primary alcohol dependence.

BACKGROUND: The present study investigated polysomnographically assessed sleep parameters in alcohol-dependent patients after withdrawal and in healthy control subjects during baseline and after a cholinergic stimulation paradigm. The aim of the study was to test whether sleep parameters, especially rapid eye movement (REM) sleep variables, may serve as predictors for relapse in alcohol-dependent patients. METHODS: Forty patients diagnosed with alcohol dependence were admitted to a specialized ward for alcohol withdrawal and were investigated by polysomnography at three time points: 2-3 weeks after withdrawal (T0) and at follow-up investigations 6 (T1) and 12 (T2) months after discharge from the hospital. A subgroup of patients (n = 17) was studied at T0 after challenge with galanthamine, a reversible cholinesterase inhibitor (cholinergic REM induction test, CRIT). Patients were compared with two control groups: a) 30 healthy control subjects (matched for age- and gender-distribution) for comparison at baseline conditions; and b) 17 age- and gender-matched control subjects for comparison with the CRIT. RESULTS: At baseline the patients showed significant disturbances of sleep continuity and sleep architecture (decreased slow-wave sleep, SWS) and exhibited an increase of "REM sleep pressure" (a combined index of REM latency, REM density, and REM sleep percent). Galanthamine provoked significant alterations of sleep continuity, sleep architecture (reduced SWS), and increased most of the components of REM pressure, taking patients and control subjects together. Apart from SWS %SPT (sleep period time) no significant drug-group interactions occurred. Patients who remained abstinent (n = 11) for at least 6 months at follow-up exhibited significantly less abnormalities of REM sleep at T0 compared to the group of patients that relapsed at 6 months follow-up. CONCLUSIONS: It is concluded that increased REM sleep pressure after alcohol withdrawal is a robust predictor of vulnerability to relapse. Thus, a subgroup of alcoholic patients appears to exhibit distinct neurobiological abnormalities assessable by polysomnography that are related to an increased vulnerability for alcoholism and early relapse.

Adult↗
PubMed2001

Sleep quality and blood pressure dipping in obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with poor sleep quality and a high incidence of nondipping. The aim of this study was to determine the association of sleep quality and nocturnal blood pressure (BP) dipping in an OSA population. METHODS: A total of 44 untreated subjects with mild to severe OSA underwent overnight-attended polysomnography and 24-h ambulatory BP monitoring. Subjects were off antihypertensive medication. The percentage of slow wave sleep, percentage of time awake after sleep onset during the sleep period, sleep efficiency, and arousal index were chosen as measurements of sleep quality. Dipping was evaluated using the change in systolic BP, diastolic BP, and mean arterial pressure. Patients were classified as dippers and nondippers based on a nocturnal drop in mean arterial pressure > 10%. Differences between groups were evaluated by independent sample t tests. Pearson correlation and linear regression were used to evaluate the association of sleep quality and dipping. RESULTS: There were no differences between dippers and nondippers with regard to body mass index, age, or respiratory disturbance index. A total of 84% were nondippers. No difference was found between dippers and nondippers in sleep quality. None of the sleep quality measures correlated with the measurements of dipping. In multiple regression analyses, the percentage of slow wave sleep and arousal index each independently predicted only a small percentage of the variance (approximately 10%) of nocturnal DBP dipping. CONCLUSIONS: The prevalence of nondipping was very high in a population of untreated patients with mild to severe OSA. Nonetheless, sleep quality did not appear to be related to BP dipping.

Adult↗
PubMed2000

The usefulness of sleep and sleep deprivation as activating methods in electroencephalographic recording: contribution to a long-standing discussion.

Sedated sleep and sleep deprivation are commonly used methods to increase the diagnostic yield of the electroencephalogram (EEG), especially in the evaluation of people with epilepsy, but the rate of activation achieved by them is controversial, as is the issue of whether it is sleep itself, or sleep deprivation which is responsible for their alleged efficacy. We retrospectively studied the EEGs of epileptic patients, examined in our laboratory, who, after having undergone an inconclusive initial routine recording, had then been examined with a second recording. This was after either: (1) sleep deprivation with evidence of drowsiness in the recordings, (2) sleep deprivation without drowsiness (indicative of the effect which sleep deprivation per se has in eliciting abnormal patterns), or (3) drug-induced sedation. The activation rates found were (1) 22.5%, (2) 24% (22.6% for sleep deprivation collectively, regardless of the presence or not of subsequent drowsiness) and (3) 27% respectively. Only the sleep deprivation rate was statistically different from the 9.6% increased rate of abnormal patterns elicited by the simple repeating of a second routine recording, while the rate of drug-induced sleep was not. Although, sleep deprivation appeared to be more effective as an activating method of EEG compared with sedated sleep, no conclusions could be drawn about which stage of sleep, wakefulness or drowsiness, is primarily responsible for the method's efficacy.

Adolescent↗
PubMed2003

Clinical effects of sleep fragmentation versus sleep deprivation.

Common symptoms associated with sleep fragmentation and sleep deprivation include increased objective sleepiness (as measured by the Multiple Sleep Latency Test); decreased psychomotor performance on a number of tasks including tasks involving short term memory, reaction time, or vigilance; and degraded mood. Differences in degree of sleepiness are more related to the degree of sleep loss or fragmentation rather than to the type of sleep disturbance. Both sleep fragmentation and sleep deprivation can exacerbate sleep pathology by increasing the length and pathophysiology of sleep apnea. The incidence of both fragmenting sleep disorders and chronic partial sleep deprivation is very high in our society, and clinicians must be able to recognize and treat Insufficient Sleep Syndrome even when present with other sleep disorders.

Forced Expiratory Volume↗
PubMed1994

Effect of continuous heat exposure on sleep during partial sleep deprivation.

This study examined the effects of continuous heat exposure on sleep structure during a partial sleep-deprivation regime. The experimental protocol was divided into three periods. After a baseline period (5 days and nights at 20 degrees C), the sleep of the subjects was restricted to the second half of the night (3 a.m.-7 a.m.) for four consecutive nights. The restricted-sleep period was followed by two recovery days and nights. During the deprivation and recovery periods, the ambient temperature was 20 degrees C for six of the 12 subjects and 35 degrees C for the others. Sleep, esophageal and mean skin temperatures were continuously recorded. At 20 degrees C, the expected effect of sleep debt was apparent. There were significant reductions in time spent awake and in latencies for sleep and stage 4 sleep. The duration of stage 4 sleep significantly increased during the four successive restricted-sleep nights, whereas esophageal temperature significantly decreased over the successive days. When heat was added, esophageal temperature decrease was weakened, and the significant increase in stage 4 duration seen at 20 degrees C was not found. The findings suggest that the heat load imposed in our experimental condition has a suppressive effect on sleep stage 4 increase, which is induced by sleep restriction. The hypothesis that an increase in this sleep stage serves as a mechanism for energy conservation should be also considered.

Adult↗
PubMed1999

Effects of method, duration, and sleep stage on rebounds from sleep deprivation in the rat.

Total sleep deprivation (TSD) of rats for 24 hours or less by continually enforced locomotion has consistently produced subsequent rebounds of slow-wave or high-amplitude EEG activity in NREM sleep, which has contributed to the widely held view that this EEG activity reflects particularly "intense" or restorative sleep. These rebounds usually have been accompanied by substantial rebounds of REM sleep. In contrast, chronic TSD (2 weeks or longer) by the disk-over-water (DOW) method has produced only huge, long-lasting rebounds of REM sleep with no rebound of high-amplitude NREM sleep. To evaluate whether the different rebounds result from different methods or from different lengths of deprivation, rats were subjected to 24-hour TSD by the DOW method. Rebounds included increases in high-amplitude and slow-wave activity; i.e., the methods produced similar rebound patterns following short-term TSD. (Chronic TSD by continually enforced locomotion would be strategically difficult and severely confounded with motor fatigue.) Rats subjected to DOW-TSD for 4 days, well before the development of severe TSD symptoms, showed primarily REM sleep rebounds. Rats subjected to 1 day of selective REM sleep deprivation, but not their closely yoked control rats, showed large, significant REM sleep rebounds, which evidently were not induced by the stress of the deprivation method per se. The combined findings prompted reexamination of published evidence relevant to "sleep intensity," including "negative rebounds," rebounds in other species, the effects of stress and fatigue, depth of sleep indicators, and extended sleep. The review points out pitfalls in the designation of any specific pattern as intense sleep.

Animals↗
PubMed2004

Dreaming during non-rapid eye movement sleep in the absence of prior rapid eye movement sleep.

STUDY OBJECTIVES: There is a long-standing controversy surrounding the existence of dream experiences during non-rapid eye movement (NREM) sleep. Previous studies have not answered the question whether this "NREM dream" originates from the NREM sleep mechanism because the subject might simply be recalling experiences from the preceding rapid eye movement (REM) sleep. METHODS: We scheduled 11 healthy men to repeat 20-minute nap trials separated by 40-minute periods of enforced wakefulness across a period of 3 days. At the end of the nap trial, each participant answered questions regarding the formal aspects of his dream experiences during the nap trial, using the structured interviews. RESULTS: We obtained a total of 172 dream reports after naps containing REM sleep (REM naps) and 563 after naps consisting of only NREM sleep (NREM naps). Dream reports from NREM naps were less remarkable in quantity, vividness, and emotion than those from REM naps and were obtained more frequently during the morning hours when the occurrences of REM sleep were highest. CONCLUSIONS: These results suggest that the polysomnographic manifestations of REM sleep are not required for dream experiences but that the mechanisms driving REM sleep alter experiences during NREM sleep in the morning. A subcortical activation similar to REM sleep may occur in human NREM sleep during the morning when REM sleep is most likely to occur, resulting in dream experiences during NREM sleep.

Adult↗
PubMed1995

Sleep and sleep disorders in older adults.

Complaints of sleep disturbance increase with age. Objective sleep assessments using polysomnography reveal sleep impairments (increased wakefulness and arousal from sleep; decreased slow wave sleep) even in healthy seniors. Both polysomnographic sleep and subjective sleep worsen in the presence of health impairments related to drug use, pain, cardiovascular disease, diabetes, depression, or other emotional disorders. In addition to normal aging and chronic disease, sleep complaints can also result from poor sleep habits, specific occult disorders during sleep, or some combination of these factors. Occult disorders include sleep apnea syndrome, periodic leg movements, and restless legs syndrome during sleep. Diagnosis and treatment of these and other sleep disorders is discussed. Both pharmacological and nonpharmacological treatments are considered, with an emphasis on behavioral and educative treatment approaches.

Aged↗