Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SLEEP”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed2001

Effects of pinealectomy on baseline sleep and response to sleep deprivation.

STUDY OBJECTIVES: We have previously reported that older (24 mo.) Fischer rats manifest a diminished post-sleep deprivation increase in NREM and REM sleep. In order to examine whether this decline reflects an age-related change in pineal function, we are now reporting on baseline and recovery sleep parameters in pinealectomized 3-, 12-, and 24-month old rats following 24 hours of sleep deprivation using the disk-over-water method. DESIGN: Three independent age groups; within each group there were sequential measures of sleep under baseline conditions and during recovery from sleep deprivation. SETTING: The Sleep Research Laboratory at the University of Chicago PARTICIPANTS: 56 male Fisher (F344) rats INTERVENTIONS: 24 hours of total sleep deprivation using the disk-over-water method MEASUREMENTS: Sleep staging of EEG and EMG, and power spectral analysis of the EEG RESULTS: Pinealectomized (pinex) rats did not differ from sham-operated (sham) rats in total sleep, REM sleep, super-modal high-amplitude NREM sleep (HS2), a measure of NREM EEG delta power, or circadian rhythm amplitude. In the pinex rats, there was a modest (2.5%) age-independent increase in NREM sleep (p<0.02). The pinex rats of all ages failed to manifest the increase in NREM sleep during recovery seen in the sham-operated animals (p<0.04). CONCLUSIONS: We found no evidence that altered pineal function is responsible for age-related changes in baseline sleep in the rat. These data also suggest that, independent of age, normal pineal function may be relevant to the ability to generate increased NREM sleep in response to prior sleep deprivation.

Animals↗
PubMed2003

Sleep and circadian rhythm disturbances in patients with delayed sleep phase syndrome.

STUDY OBJECTIVES: The objective of this study was to clarify sleep characteristics and pathophysiology in patients with delayed sleep phase syndrome (DSPS), which is a major circadian rhythm sleep disorder subtype. DESIGN: Polysomnography was performed for 2 consecutive nights and core body temperature was sampled for 7 consecutive days, including the polysomnography study period, in all subjects. Findings were compared and statistically analyzed between patients with DSPS and matched controls. SETTING: Sleep disorders unit in National Center Hospital. PARTICIPANTS: 11 DSPS patients and 11 age-matched healthy volunteers. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Sleep latency, total sleep time, wakefulness after sleep-onset, and the amount and percentage of Stage 1 sleep were greater in DSPS patients than in volunteers. Sleep efficiency and the amount and percentage of slow wave sleep were lower in DSPS patients than in volunteers. Compared with the healthy volunteers, DSPS patients showed a decreased number and different temporal distribution of high-voltage and low-frequency delta waves. The time of minimum body temperature appeared earlier in the sleep phase for the patients than for the volunteers. Significant correlation was found between the amount of slow wave sleep and the time from sleep onset to minimum body temperature and between the amount and percentage of slow wave sleep and time from minimum body temperature to sleep offset. CONCLUSIONS: Disturbances were found in the sleep structure of patients with DSPS, and these disturbances were related to the discrepancy between patients and controls in the phase relationship difference between sleep and core body temperature rhythms.

Adult↗
PubMed1986

Effect of sleep position on sleep apnea and parafunctional activity.

Parafunctional activity (toothgrinding, toothclenching and bruxism) is a common problem which may lead to masticatory muscle and temporomandibular joint pain, and may result from sleep arousal or disturbances. Sleep apnea is another common sleep disorder which results in disrupted sleep architecture and frequent arousals. Because sleep apnea leads to sleep arousals, and because sleep arousals are thought to result in increased parafunctional activity, we undertook the present study to determine the relationship between sleep apnea and parafunctional activity. We were also interested in assessing the effects of sleep posture on sleep disordered breathing and parafunctional activity. We prospectively studied 24 patients who were referred to the clinical sleep apnea laboratory for study. They underwent standard nocturnal polysomnographic examination; in addition, masticatory activity was measured with a masseter electromyogram. Patients slept in the supine and lateral decubitus positions. Nocturnal clenching was slightly higher in patients with sleep apnea than those without (12.2 vs 7.6 clenches/hr, p = 0.18), and there was a correlation between the clench index (CI) and apnea plus hypopnea index (A + HI) by linear regression (r = 0.49, p less than 0.05). There were significant falls in both the A + HI (64.4 +/- 28.8 vs 36.5 +/- 36.7, p = 0.02) and CI (12.5 +/- 12.1 vs 7.0 +/- 8.6, p = 0.04) in the lateral decubitus vs supine sleeping positions. We conclude that there is an association between obstructive sleep apnea and parafunctional activity, that sleep position affects the incidence of both sleep disordered breathing and parafunctional activity, and that analysis of apneas and hypopneas in both supine and lateral decubitus sleeping positions may be helpful.

Adolescent↗
PubMed2000

Sleep and periodic limb movement in sleep in juvenile fibromyalgia.

OBJECTIVES: Fibromyalgia has been recently recognized in children and adolescents as juvenile fibromyalgia (JF). In adult fibromyalgia, subjective complaints of nonrestorative sleep and fatigue are supported by altered polysomnographic findings including a primary sleep disorder known as periodic limb movements in sleep (PLMS) in some subjects. Although poor sleep is a diagnostic criterion for JF, few reports in the literature have evaluated specific sleep disturbances. Our objectives were to evaluate in a controlled study the polysomnographic findings of children and adolescents with JF for alterations in sleep architecture as well as possible PLMS not previously noted in this age group. METHODS: Sixteen consecutive children and adolescents (15.0 +/- 2.6 years of age) diagnosed with JF underwent overnight polysomnography. Polysomnography was also performed on 14 controls (14.0 +/- 2.2 years of age) with no history of an underlying medical condition that could impact on sleep architecture. Respiratory variables, sleep stages, and limb movements were measured during sleep in all subjects. RESULTS: JF subjects differed significantly from controls in sleep architecture. JF subjects presented with prolonged sleep latency, shortened total sleep time, decreased sleep efficiency, and increased wakefulness during sleep. In addition, JF subjects exhibited excessive movement activity during sleep. Six of the JF subjects (38%) were noted to have an abnormally elevated PLMS index (>5/hour), indicating PLMS in these subjects. CONCLUSION: Our study demonstrated abnormalities in sleep architecture in children with JF. We also noted PLMS in a significant number of subjects. This has not been reported previously in children with this disorder. We recommend that children who are evaluated for JF undergo polysomnography including PLMS assessment. juvenile fibromyalgia; periodic limb movement in sleep; restless legs syndrome.

Adolescent↗
PubMed1975

[Some indices of the activity of the brain in "rapid" sleep preceeded or not preceeded by delta-sleep].

In order to study the functional interaction between the delta sleep and the REM sleep some psychophysiological features of REM sleep were examined in REM-onset (without any preceding delta sleep--"early REM period") and in the REM period (REMP) terminating the normal sleep cycle (with the preceding delta sleep) of 92 daytime sleep attacks in 10 narcoleptic patients. Under these conditions the significant differences exist in the characteristics of the dream reports and in subjective estimations of sleep quality and duration. Sleep was evaluated as "superficial" and underestimations of sleep duration took place after an early REMP. Correct estimations of sleep duration and evaluations of sleep as "deep" dominated after REMP enging sleep cycles. The results obtained indicate the functional interaction between the delta sleep and REM sleep existing in the sleep cycle and largely determining the psychic content of the brain activity in the REM sleep.

Brain↗
PubMed1977

Selective deprivation of sleep in pycnoleptic children. Effects of deprivation of slow-wave and REM sleep on the frequency and duration of petit mal attacks.

1. Selective deprivation of slow-wave and paradoxical sleep was performed in 10 children with pycnoleptic attacks (8 of them before anticonvulsive treatment, 2 of them while under medication). The frequency and duration of petit mal attacks were intraindividually compared during night sleep and after waking for a 5-h period. 2. After deprivation of slow-wave sleep with reduction of EEG stages 3 and 4 to about one-third of the baseline but normal duration of sleep, petit mal attacks are more frequent and long-lasting than after normal sleep or selective deprivation of REM sleep. 3. Although total sleep time is significantly diminished after selective deprivation of paradoxical sleep the frequency of attacks during the waking state was lower than after normal sleep and deprivation of slow wave sleep. This observation shows a clear i nfluence of the quality of sleep on the frequency of epileptic attacks. 4. During sleep petit mal seizures were mainly found during stages 2 and paradoxical sleep. Single spike and irregular spike were discharges, however, occurred more frequently during slow-wave sleep. Their frequency was not significantly different in the deprivation conditions. 5. In contrast to experimental data in animals, REM deprivation is less provoking to epileptic attacks outside sleep than deprivation of stages 3 and 4 sleep. Therefore a sufficient amount of slow-wave should be preserved for pycnoleptic children.

Child↗
PubMed1984

Effect of sleep deprivation on sleep and EEG power spectra in the rat.

EEG power spectra of the rat were computed for consecutive 4-s epochs of the daily light period and matched with the scores of the vigilance states. Sleep was characterized by a progressive decline of low frequency spectral values (i.e. slow wave activity) in non-rapid eye movement (non-REM) sleep, and a progressive increase in the amount of REM sleep. During recovery from 24-h total sleep deprivation (TSD) the following changes were observed: an increase of slow wave activity in non REM sleep with a persisting declining trend; an enhancement of theta activity (7.25-10.0 Hz) both in REM sleep and waking; a decrease of non-REM sleep and an increase of REM sleep. In addition, a slow wave EEG pattern prevailed in the awake and behaving animal during the initial recovery period. In selective sleep deprivation paradigms, either REM sleep or slow wave activity in non-REM sleep was prevented during a 2-h period following upon 24-h TSD. During both procedures, non-REM sleep spectra in the lowest frequency band showed no increase. There was no evidence for a further enhancement of slow wave activity after its selective deprivation. The results indicate that: (1) slow wave activity in non-REM sleep and theta activity in REM sleep may reflect sleep intensity; and (2) REM sleep and active waking, the two states with dominant theta activity, may be functionally related.

Animals↗
PubMed1986

Clinical aspects of sleep disturbances and sleeping drugs.

Complaints about sleep disturbances are a common every-day problem in the general practitioner's surgery. Only a few patients need a thorough expert examination in a special sleep laboratory. Thanks to EEG, which makes available a continuous record of uninterrupted sleep cycles, knowledge of the physiology of sleep now includes important information about the normal circadian rhythm of waking and sleeping, the alternation of REM and non-REM periods, and the depth of the individual sleep cycles. EEG results are also an important basis for checking the effect of sleeping drugs. Analysis of sleep disturbances is based on the formal distinction between hypersomnia, and hyposomnia and parasomnia. Etiologically, a distinction must be made between exogenic and endogenic sleep disturbances and attention given to the fact that disturbances of night sleep also affect vigilance on the following day. These considerations are also important for the use of sleeping drugs, whose half-life and biological effect allow a useful differentiation between substances giving impulses to sleep, sleep-inducing drugs, and those enabling uninterrupted sleep during night-time. Sleep disturbances combined with certain other symptoms belong to particular syndromes in which it may be necessary to use sleeping drugs, but these should only be used in combination with other drugs, in order to reduce the risk of side effects, tolerance changes, dependence and addiction with long-term treatment. When a combination of different drugs is given, interference through interaction with lipid or protein binding, and induction or enzyme breakdown in the liver should be taken into account.

Circadian Rhythm↗
PubMed1999

Prone infant sleeping despite the "Back to Sleep" campaign.

OBJECTIVES: To determine sleep position variation during the first 6 months of life and to identify risk factors for prone sleeping. DESIGN: Cohort study of healthy term newborns recruited from November 1995 to September 1996 and followed up to age 6 months. Pediatricians were surveyed about sleep position advice. At recruitment, all parents were instructed to avoid prone sleeping. Parents were telephoned at 1 week and then monthly to ensure that they recorded sleep position. Investigators were unaware of sleep position until the infant was 6 months of age, when sleep log data and reasons for sleep position choice were ascertained. SETTING: Practice-based study conducted by the Children's National Medical Center Pediatric Research Network, Washington, DC. PARTICIPANTS: A total of 402 consecutive healthy term newborns followed up by a Pediatric Research Network pediatrician were enrolled. Exclusion criteria were prematurity, a serious medical condition, and absence of a telephone. Of the 402 enrolled newborns, 348 (86.6%) completed the study. RESULTS: Only 34.0% of infants maintained a consistent sleep position. Prone sleeping increased from 12.2% at birth to 32.0% at 6 months. One third of pediatricians discussed sleep position beyond the newborn period. The following were associated (P<.05) with prone sleeping: male sex, lower maternal education level, single marital status, having siblings, and black race. Perceived infant comfort was the main reason for prone sleeping. CONCLUSIONS: Most newborns are placed by parents in nonprone sleep positions. Pediatricians need to consistently reinforce the "Back to Sleep" message when the infants are 2 to 4 months of age because this is the most likely time that they are switched to prone sleeping and the highest risk period of sudden infant death syndrome. Parents should not use prone sleeping as a means of comforting infants.

Cohort Studies↗
PubMed1992

Pontine regulation of REM sleep components in cats: integrity of the pedunculopontine tegmentum (PPT) is important for phasic events but unnecessary for atonia during REM sleep.

Transection, lesion and unit recording studies have localized rapid eye movement (REM) sleep mechanisms to the pons. Recent work has emphasized the role of pontine cholinergic cells, especially those of the pedunculopontine tegmentum (PPT). The present study differentiated REM sleep deficits associated with lesions of the PPT from other pontine regions implicated in REM sleep generation, including those with predominantly cholinergic vs non-cholinergic cells. Twelve hour polygraphic recordings were obtained in 18 cats before and 1-2 weeks after bilateral electrolytic or radio frequency lesions of either: (1) PPT, which contains the dorsolateral pontine cholinergic cell column; (2) laterodorsal tegmental nucleus (LDT), which contains the dorsomedial pontine cholinergic cell column; (3) locus ceruleus (LC), which contains mostly noradrenergic cells; or (4) subceruleus (LC alpha, peri-LC alpha and the lateral tegmental field), which also contains predominantly noncholinergic cells. There were three main findings: (i) Only lesions of PPT and subceruleus significantly affected REM sleep time. These lesions produced comparable reductions in REM sleep time but influenced REM sleep components quite differently: (ii) PPT lesions, estimated to damage 90 +/- 4% of cholinergic cells, reduced the number of REM sleep entrances and phasic events, including ponto-geniculooccipital (PGO) spikes and rapid eye movements (REMs), but did not prevent complete atonia during REM sleep: (iii) Subceruleus lesions eliminated atonia during REM sleep. Mobility appeared to arouse the cat prematurely from REM sleep and may explain the brief duration of REM sleep epochs seen exclusively in this group. Despite the reduced amount of REM sleep, the total number of PGO spikes and REM sleep entrances increased over baseline values. Collectively, the results distinguish pontine loci regulating phasic events vs atonia. PPT lesions reduced phasic events, whereas subceruleus lesions created REM sleep without atonia. Severe REM sleep deficits after large pontine lesions, including PPT and subceruleus, might be explained by simultaneous production of both REM sleep syndromes. However, extensive loss of ACh neurons in the PPT does not disrupt REM sleep atonia.

Animals↗
PubMed1996

Increased basal REM sleep but no difference in dark induction or light suppression of REM sleep in flinders rats with cholinergic supersensitivity.

Increased cholinergic sensitivity in the central nervous system has been postulated to account for some of the neuroendocrine abnormalities and sleep disturbances seen in human depressives. The Flinders Sensitive Line (FSL) rats, which exhibit increased sensitivity to cholinergic agents, have been shown to have REM sleep patterns similar to those seen in depressives, including shorter REM sleep latency and increased daily percentage of REM sleep. We studied the response of FSL and control rats to brief dark pulses administered during the normal light period (which are known to stimulate REM sleep in albino rats) and to brief light pulses during the normal dark period (which suppress REM sleep in albino rats) to determine whether these responses are affected by central cholinergic hypersensitivity. FSL rats showed REM sleep patterns indistinguishable from controls during light or dark pulses, which does not support the primary involvement of cholinergic systems in this mechanism of REM sleep regulation. We also examined REM and non-REM (NREM) sleep patterns in FSL rats and their controls to determine whether they show sleep continuity disturbances or decreased sleep intensity as seen in depression. In agreement with an earlier study, we found that FSL rats had more daily REM sleep and accumulated less NREM sleep between REM bouts than controls. Duration of NREM sleep bouts, total daily NREM sleep time, and EEG amplitude of NREM sleep did not differ between FSL and control rats, suggesting that the cholinergic abnormalities in FSL rats do not produce substantial NREM sleep changes.

Animals↗
PubMed2000

Is narcolepsy a REM sleep disorder? Analysis of sleep abnormalities in narcoleptic Dobermans.

Narcolepsy is a chronic sleep disorder marked by excessive daytime sleepiness, cataplexy, sleep paralysis, and hypnagogic hallucinations. Since the discovery of sleep onset REM periods (SOREMPs) in narcoleptic patients, narcolepsy has often been regarded as a disorder of REM sleep generation: REM sleep intrudes in active wake or at sleep onset, resulting in cataplexy, sleep paralysis, or hypnagogic hallucinations. However, this hypothesis has not been experimentally verified. In the current study, we characterized the sleep abnormalities of genetically narcoleptic-cataplectic Dobermans, a naturally occurring animal model of narcolepsy, in order to verify this concept. Multiple sleep latency tests during the daytime revealed that narcoleptic Dobermans exhibit a shorter sleep latency and a higher frequency of SOREMPs, compared to control Dobermans. The total amount of time spent in wake and sleep during the daytime is not altered in narcoleptic dogs, but their wake and sleep patterns are fragmented, and state transitions into and from wake and other sleep stages are altered. A clear 30 min REM sleep cyclicity exists in both narcoleptic and control dogs, suggesting that generation of the ultradian rhythm of REM sleep is not altered in narcoleptics. In contrast, cataplexy displays no cyclicity and can be elicited in narcoleptic animals anytime with emotional stimulation and displays no cyclicity. Stimulation of a cholinoceptive site in the basal forebrain induces a long-lasting attack of cataplexy in narcoleptic dogs; however, bursts of rapid eye movements during this state still occur with a 30 min cyclicity. Sites and mechanisms for triggering cataplexy may therefore be different from those for REM sleep. Cataplexy and a dysfunction in the maintenance of vigilance states, but not abnormal REM sleep generation, may therefore be central to narcolepsy.

Animals↗
PubMed1987

Effect of 64-hour sleep deprivation on the circadian waveform of thyrotropin (TSH): further evidence of sleep-related inhibition of TSH release.

Half-hourly sampling of plasma TSH was done across 3 days in four normal young men. Sleep was denied for 64 h from 0700 h on awakening from accommodation sleep until polygraphic sleep was resumed at 7100 h of the third day (D3) such that 2 consecutive nights of usual 2300-0700 h sleep were missed. This protocol allowed examination of any modulatory effects on the daily patterns in TSH concentrations during sleep deprivation on D1-2 (1100-3500, 3500-5900 h) or during resumption of usual nightly sleep on D3 (5900-8300) compared to that of a previously studied group of normal young men. The circadian nature of the daily TSH waveform was evidenced by its daily repetition within a subject both basally and during D1-2 sleep deprivation and by its synchronization within the basal, deprived, or resumed sleep days. The peaks in each subject's daily TSH patterns on D1-2 were consistently longer, and the daily maxima and cosine acrophases on D1-2 were consistently later than those on D3 when basal sleep was resumed. About half the daily TSH concentration maxima and daily cosinor amplitudes on D1-2 were greater than those of the respective sleep-resumed TSH patterns of D3. Both the group mean TSH patterns and the cosinor 95% confidence ellipses also indicated the daily peak in the TSH waveform to be significantly longer, later, and larger during D1-2 sleep deprivation than during the basal or D3 periods. These results indicate that significant alteration of the daily TSH waveform can occur in response to absence of sleep and are compatible with the existence of an inhibitory effect in early nightly sleep on TSH release. The TSH patterns during the 1700-2300 h intervals of rising TSH levels were congruent in the basal, deprived, and resumed sleep periods. Prompt reversion to the basal TSH pattern also occurred when sleep was resumed on D3. Both of these observations suggest the alteration in TSH waveform during sleep deprivation to have arisen from an inhibitory effect in sleep rather than from a change in period or phase of a generating oscillator.

Adult↗
PubMed2005

Prevalence of concomitant sleep disorders in patients with obstructive sleep apnea.

We determined the prevalence of concomitant sleep disorders in patients with a primary diagnosis of obstructive sleep apnea (OSA). We retrospectively analyzed 643 patients, aged > or =18, with a primary diagnosis of OSA, evaluated by sleep specialists, in whom clinical and polysomnographic data were derived using standardized techniques by reviewing data from a standardized database and clinical charts. Concomitant sleep disorders were listed according to the International Classification of Sleep Disorders (American Academy of Sleep Medicine, 2000). The mean age was 48.5+/-13.5 years and 55% were male. Racial distributions were African-Americans 51.8% and Caucasian 47%. Indices of disordered breathing were respiratory disturbance index 32.4+/-30.4/h sleep and time <90% O(2) saturation 44.5+/-81.6 min. Thirty-one percent of patients had a concomitant sleep disorder. The most common were inadequate sleep hygiene (14.5%) and periodic limb movement disorder (PLMD, 8.1%). Of patients with other sleep disorders, 66.8% had treatment initiated for these disorders. Predictors of inadequate sleep hygiene (logistic regression) were: age (each decade OR=0.678, P=0.000000), gender (for M, OR=0.536), and the presence of at least one other major system disorder (OR=2.123, P=0.0015). Predictors of PLMD were: age (each decade OR=0.794, P=0.0005), gender (for M, OR=0.433, P=0.004), and total sleep time (for each 10 min, OR=0.972, P=0.0013). We conclude that approximately one third of patients with sleep apnea have another identifiable sleep disorder, usually requiring treatment. This suggests that practitioners evaluating and treating sleep apnea ought to be prepared to deal with other sleep disorders as well.

Female↗
PubMed2000

The relationship between subjective sleep estimation and objective sleep variables in depressed patients.

INTRODUCTION: To our knowledge there is no evidence in the literature about the relationship between subjective sleep estimation and objective sleep variables in depression. It is not known whether the subjective estimation of sleep quality and sleep duration is directly related to any objective sleep variable in depressed patients. METHODS: Thirty patients with major depression and 10 healthy subjects have been investigated in our sleep laboratory during 1 or 2 consecutive nights after 1 night for adaptation. Every subject, after final awakening in the laboratory, answered questions concerning the subjective feelings about sleep duration, number of awakenings and sleep depth. We compared the sleep estimation in both groups and calculated the correlation between objective and subjective sleep variables in depressed patients. RESULTS: The degree of a wrong sleep estimation in depressed patients is larger than in healthy subjects. Slow wave sleep (SWS) in depressed patients correlates positively with the subjective estimation of sleep duration. Eye movement density in REM sleep correlates with the subjective estimation of the number of awakenings. CONCLUSION: SWS in depression has a positive influence on the subjective feeling of sleep duration while phasic REM sleep activity has a negative influence.

Depressive Disorder↗
PubMed1997

Recovery sleep and performance following sleep deprivation with dextroamphetamine.

Twelve subjects were studied to determine the after-effects of using three 10-mg doses of dextroamphetamine to sustain alertness during sleep deprivation. Sleep architecture during recovery sleep was evaluated by comparing post-deprivation sleep after placebo. Performance and mood recovery were assessed by comparing volunteers who received dextroamphetamine first (during sleep deprivation) to those who received placebo first. Stages 1 and 2 sleep, movement time, REM latency, and sleep latency increased on the night after sleep deprivation with dextroamphetamine vs. placebo. Stage 4 was unaffected. Comparisons to baseline revealed more stage 1 during baseline than during either post-deprivation sleep period and more stage 2 during baseline than during sleep following placebo. Stage 4 sleep was lower during baseline and after dextroamphetamine than after placebo. Sleep onset was slowest on the baseline night. Next-day performance and mood were not different as a function of whether subjects received dextroamphetamine or placebo during deprivation. These data suggest dextroamphetamine alters post-deprivation sleep architecture when used to sustain alertness during acute sleep loss, but next-day performance and subjective mood ratings are not substantially affected. A recovery sleep period of only 8 h appears to be adequate to regain baseline performance levels after short-term sleep deprivation.

Adult↗
PubMed2006

Are individuals' nighttime sleep characteristics prior to shift-work exposure predictive for parameters of daytime sleep after commencing shift work?

This study aimed to examine prospectively whether individual nighttime sleep characteristics at baseline (prior to shift-work exposure) are related to parameters of daytime sleep after commencing shift work. A longitudinal field study was carried out with novice police officers of the Dutch Police Force. A total of 26 subjects were examined at baseline before they entered shift work and re-examined during follow-up sessions after four and twelve months of shift-work exposure. Wrist actigraphy and sleep diaries were used to study nocturnal sleep at baseline and daytime sleep after night shifts during follow-up sessions. As outcome variables, estimated total sleep time, sleep efficiency, and subjective sleep quality were analyzed. Daytime total sleep time showed a 66 min decline during the first year of shift-work exposure. Systematic inter-individual differences were observed for daytime total sleep time and subjective sleep quality (explaining 53% and 38% of the variance, respectively), suggesting potential predictability of these sleep parameters. Although no predictors were found for daytime total sleep time, the subjective quality of nighttime sleep before the onset of shift work predicted 40% of the variance in the subjective quality of daytime sleep after commencing shift work. Follow-up studies may reveal whether the subjective quality of baseline nighttime sleep also predicts long-term overall tolerance for shift work.

Adult↗
PubMed1992

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.

Adult↗