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At least 1,117 records · Page 62Linked to original sources
PubMed1987

REM sleep latency during nocturnal sleep in mentally retarded infants.

REM sleep latency observed in 61 mentally retarded infants (4-13 months of age) was studied throughout nocturnal sleep. Mentally retarded infants revealed a J distribution of short (less than 8 min) and long (more than 8 min) REM sleep latencies. This feature of distribution was similar to that obtained by other authors from normal infants under 3 months of age. REM sleep latency did not depend on the duration of prior wakefulness. Long REM sleep latencies were no more often preceded by long episodes of wakefulness than were short REM sleep latencies. No correlation was found between REM sleep latency and age, developmental quotient or daytime clinical EEG abnormalities.

Aging↗
PubMed1991

Variability of normal sleep patterns in 40 consecutive ambulatory sleep-wakefulness records.

Sleep-wakefulness (S-W) patterns were recorded continuously for 40 consecutive 24 h using subcutaneous chronic electrodes and an ambulatory cassette recorder in a healthy 57-year-old volunteer. Variability of sleep patterns was assessed in steady-state conditions and in the course of a scientific journey encompassing flights in both west/east and south/north directions. Data were compared with findings from age-matched laboratory control records. Polysomnographic evaluation of our sleep data shows: (1) Stability of the first 3 sleep cycles and variability of the remaining sleep period with respect to both duration and structure. Vulnerability of REM sleep to environmental interference. (2) Stability of the WASO/drowsiness cluster as an intraindividual biological trait independent of social interactions. The clinical relevance of ambulatory serial recording is stressed. (3) The role of the first sleep cycle structure in the chronobiological adaptation process is documented. Apparently travelling in south/north directions may have similar or even more polygraphic implications than west/east transfer.

Chronobiology Phenomena↗
PubMed1994

Night sleep does not predict day sleep in narcolepsy.

It has been suggested that the increased day sleep in narcolepsy-cataplexy is secondary to the known fragmentation and reduction of night sleep, there being no differences in 24 h sleep totals from normals. Twenty-two untreated patients underwent 24 h sleep wake recordings by ambulatory monitoring. Correlations were assessed by stepwise multiple regression between day sleep and night sleep measures. Almost no significant or near significant correlations emerged. It is concluded that day sleep in narcolepsy is based upon a different mechanism, perhaps a diurnal "subvigilance syndrome" of impaired arousal mechanisms.

Adult↗
PubMed1987

Effect of chronic ethanol consumption on the fine structure of the dentate gyrus in long-sleep and short-sleep mice.

The effect of short- and long-term chronic ethanol consumption on the fine structure of the dentate gyrus was examined in two lines of mice selected for their differential sensitivity to acute ethanol administration. Quantitative electron microscopic analysis of dendritic spines, axon terminals, and synaptic appositions revealed significant differences between the long-sleep and short-sleep mice. In control preparations, long-sleep mice were found to have larger spine areas and perimeters, larger axon terminals, and longer synaptic appositions than short-sleep mice. In addition, the shape of dendritic spines in the long-sleep mice was significantly more complex than those of short-sleep mice. Ethanol tended to increase this complexity in long-sleep mice only. Ethanol had only a limited effect on the other anatomical measures. The results provide evidence for ultrastructural differences between the nervous systems of these lines of mice which may have a role in their differential sensitivity to acute ethanol administration.

Alcoholism↗
PubMed1983

Cerebellar role in the differential ethanol sensitivity of long sleep and short sleep mice.

Two lines of mice have been selectively bred for differential sleep time responses to ethanol. Long sleep (LS) mice sleep over an order of magnitude longer than short sleep (SS) mice. We have found that these behavioral sensitivities are also reflected in the responsiveness of cerebellar Purkinje neurons in those two mouse lines in situ and in intraocular cerebellar brain grafts. The differential sensitivity of Purkinje cells to the depressant effects of ethanol appears to be an intrinsic property of the cerebellum and shows a high genetic correlation with the hypnotic effects of this drug as measured by sleep time. Sleep time studies of neonatally cerebellectomized LS and SS mice indicate that the cerebellum is not the primary determinant of the sensitivity of these mice to the soporific effects of ethanol. The sleep time of SS, but not LS mice, was altered by cerebellectomy suggesting that the cerebellum has different influences on the ethanol-induced loss of righting reflex in these two mouse lines.

Animals↗
PubMed1984

Animal sleep: a review of sleep duration across phylogeny.

Sleep duration and placement within the twenty-four hour day have been primary indices utilized in the examination of sleep function. It is of value, therefore, to evaluate these variables in a wide range of animal species. The present paper examines the literature concerning sleep duration in over 150 animal species, including invertebrates, fish, amphibians, reptiles, birds, and 14 orders of mammals. We first present annotations of almost 200 studies, including number of animals used, photoperiod employed, sleep duration per twenty-four hours and placement of sleep period within the nychthemeron. Both behavioral and electrographic studies are reviewed, as are laboratory and field studies. These data are subsequently presented in a table with representative literature citations for each species. Following the table, a brief discussion is presented concerning some methodological issues which may affect the measurement of sleep duration and some suggestions are made for future examination of sleep duration.

Amphibians↗
PubMed1990

Sleep variables are unaltered by zolantidine in rats: are histamine H2-receptors not involved in sleep regulation?

The effects of the H1-receptor antagonist diphenhydramine and the brain-penetrating H2-receptor antagonist zolantidine were studied in rats implanted for chronic sleep recordings. Diphenhydramine (1.0-4.0 mg/kg) significantly increased slow wave sleep and decreased wakefulness. Zolantidine (0.25-8.0 mg/kg) had no significant effects on any of the sleep parameters examined. One possibility is that zolantidine did not enter the brain in sufficient concentration to produce significant changes on sleep and wakefulness. Another possibility is that blockade of H2-receptor involved parts of the brain other than those implicated in the sleep-wake cycle. The feasibility remains that H2-receptors are not involved in sleep regulation. The absence of selective, brain-penetrating H2-receptor agonists precludes a more detailed analysis of the role of this subtype of receptor in the control of sleep and wakefulness.

Animals↗
PubMed2005

It's practice, with sleep, that makes perfect: implications of sleep-dependent learning and plasticity for skill performance.

Although there is no consensus regarding the functions of sleep, one exciting hypothesis is that sleep contributes importantly to learning and memory. Over the last decade, several studies have provided substantive evidence supporting the role of sleep in memory processing. This article focuses on sleep-dependent learning and brain plasticity in humans, specifically in the development of skill performance that is the foundation of many sports actions. The different forms and stages of human memory are discussed, then evidence of sleep-dependent skill learning and associated sleep-dependent brain plasticity is described. In conclusion, a consideration of the fundamental importance of sleep in real-life skill learning is provided.

Brain↗
PubMed2006

The range and nature of sleep dysfunction in untreated Parkinson's disease (PD). A comparative controlled clinical study using the Parkinson's disease sleep scale and selective polysomnography.

In this study we have explored the nature and range of sleep dysfunction that occurs in untreated Parkinson's disease (PD) comparing data obtained from the use of the Parkinson's disease sleep scale (PDSS) in an untreated PD patient group compared to advanced PD and healthy controls. 25 untreated (drug-naive, DNPD) PD patients (mean age 66.9 years, range 53-80, 18 males) completed the validated Parkinson's disease sleep scale (PDSS), mean duration of PD was 2.1 years (1-10, up to 4 years in all except one patient with tremulous PD reporting tremor duration of 10 years) and mean Hoehn and Yahr score 1.9 (1-3). Data were compared to 34 advanced PD (mean age 70.2 years, range 51-88, 23 male), mean duration of PD 11 years (range 4-22), mean Hoehn and Yahr score 3.4 (3-5) and PDSS data obtained from 131 healthy controls (mean age 66.6 years, range 50-93, 56 males). Total PDSS scores and PDSS sub-items, except PDSS item 2, were highly significantly different (p<0.001) between DNPD, advanced PD and controls. Controls reported higher mean PDSS scores than both groups of patients, and advanced cases reported lower (mean+/-S.D.) PDSS scores (86.95+/-20.78) than drug-naive (105.72+/-21.5) (p<0.001). Logistic regression analysis showed that items PDSS8 (nocturia), PDSS11 (cramps), PDSS12 (dystonia), PDSS13 (tremor), and PDSS15 (daytime somnolence) were significantly impaired in DNPD compared to controls while PDSS7 (nighttime hallucinations) additionally separated advanced PD from DNPD. In a subgroup of 11 advanced PD cases (mean age 62 years, range=49-84 years, mean Hoehn and Yahr score 2.5, range=1-3) with high Epworth Sleepiness Scale (ESS) scores (mean 14.5), low item 15 PDSS score (mean 4.7) and complaints of severe daytime sleepiness, underwent detailed overnight polysomnography (PSG) studies, all showing abnormal sleep patterns. We conclude that nocturia, nighttime cramps, dystonia, tremor and daytime somnolence seem to be the important nocturnal disabilities in DNPD and some of these symptoms may be reminiscent of "off" period related symptoms even though patients are untreated. Furthermore, polysomnography in "sleepy" PD patients may help diagnose unrecognised conditions such as periodic limb movement of sleep (PLMS), obstructive sleep apnoea (OSA) and REM Sleep Behaviour Disorder.

Aged↗
PubMed2004

Disinhibition of ventrolateral preoptic area sleep-active neurons by adenosine: a new mechanism for sleep promotion.

The ventrolateral preoptic area of the hypothalamus (VLPO) contains a population of sleep-active neurons and is hypothesized to be an important part of the somnogenic process. Adenosine (AD) is an endogenous sleep-promoting factor and may play an important role in promoting natural sleep. We hypothesize that AD may promote sleep, in part, by activating the VLPO sleep-active neurons. Although, in the CNS, AD is generally regarded as an inhibitory neuromodulator, it is possible for AD to be directly excitatory via A2 receptors or indirectly via disinhibition. In order to test the hypotheses that AD can excite VLPO neurons we made intracellular recordings from the VLPO in vitro and examined the effects of AD on VLPO neural activity. Whole cell patch-clamp recordings were obtained from rat brain slices and drugs were bath applied. VLPO neurons were electrophysiologically heterogeneous. Depolarizing current steps elicited rhythmic firing (25 of 57), spike frequency adaptation or accommodation (24 of 57), or an unusual burst firing response (eight of 57). Spontaneous synaptic activity was pronounced in most recorded neurons and consisted of either fast excitatory post-synaptic potentials/currents (EPSP/C's) and/or fast inhibitory post-synaptic potentials/currents (IPSP/C's). The IPSC's were fully blocked by 30 microM bicuculline suggesting they are GABA(A)-mediated events, and the EPSC's were blocked by 40 microM DNQX suggesting they are mediated by the AMPA subtype of glutamate receptor (five of five). AD (20-100 microM) reduced the frequency of spontaneous IPSC's in 11 of 17 VLPO neurons (28-100%; mean reduction=63%) without significant effects on resting membrane potential. IPSC was unaffected in five neurons and one neuron displayed increases in spontaneous IPSC's. In contrast, AD decreased EPSC frequency in seven cells (36-73%; mean=59%), increased frequency in five cells (30-236%; mean 83%) and had no effect in six cells. AD application increased the firing rate in two of four cells tested. These data are consistent with the hypothesis that one mechanism which AD may promote sleep is by blocking inhibitory inputs on VLPO sleep-active neurons.

Adenosine↗
PubMed2002

Sleep states and sleep electroencephalographic spectral power in mice lacking the beta 3 subunit of the GABA(A) receptor.

Mice lacking the GABA(A) receptor beta(3) subunit exhibit a profound disruption in thalamic circuitry. We have studied sleep in these mice under baseline conditions and following treatment with the benzodiazepine midazolam. Under baseline conditions, NREM sleep time did not differ between beta(3) subunit knockout mice and wild type mice, while REM sleep time was significantly lower in knockout mice than in wild type mice during the light portion of a 24-h light-dark cycle. In constant dark conditions, circadian rhythmicity remained intact in mutant mice for a period of at least 9 days. EEG delta power (1-4 Hz) was significantly greater in the knockout than in wild type mice during NREM sleep but not during other states. A transient increase in EEG power in the 12-16 Hz range that occurred in wild type mice just prior to the transition from NREM to REM sleep was present but significantly blunted in the knockout. Midazolam decreased NREM delta power and REM time in wild type mice. The former but not the latter response to midazolam was intact in the knockout. These results further support a role for GABAergic transmission in regulating REM sleep and EEG spectral phenomena associated with NREM sleep.

Animals↗
PubMed2000

Dual electroencephalogram markers of human sleep homeostasis: correlation between theta activity in waking and slow-wave activity in sleep.

To investigate the relationship between markers of sleep homeostasis during waking and sleep, the electroencephalogram of eight young males was recorded intermittently during a 40-h waking episode, as well as during baseline and recovery sleep. In the course of extended waking, spectral power of the electroencephalogram in the 5-8Hz band (theta activity) increased. In non-rapid eye movement sleep, power in the 0.75-4.5Hz band (slow-wave activity) was enhanced in the recovery night relative to baseline. Comparison of individual records revealed a positive correlation between the rise rate of theta activity during waking and the increase in slow-wave activity in the first non-rapid eye movement sleep episode. A topographic analysis based on 27 derivations showed that both effects were largest in frontal areas. From these results, we suggest that theta activity in waking and slow-wave activity in sleep are markers of a common homeostatic sleep process.

Adult↗
PubMed2003

Nasal and sleep cycle--possible synchronization during night sleep.

Regular cyclic changes in nostril airflow due to a nasal congestion and decongestion are known in literature as nasal cycle. Registration of breathing from each nostril separately gives possibility to registrate moments of alternative change of airflow of nostrils and periods of nasal cycle. This registration during night sleep shows that the length of these periods are about 1.5h, 3.0 h and 4.5h. The length of these periods are multiple of mean length of sleep cycle--about 1.5h. The alternative change of airflow through nostrils occurs through some of REM stages of the sleep. This shows, that during the night sleep becomes synchronization of nasal and sleep cycles in some of the REM phases of sleep. As a result--length of periods of the nasal cycle are one or more length of sleep cycle.

Activity Cycles↗
PubMed2007

Impact of sleep nasendoscopy on the outcome of mandibular advancement splint therapy in subjects with sleep-related breathing disorders.

AIM: To evaluate the impact of positive sleep nasendoscopy, with simultaneous mandibular advancement, on the outcome of mandibular advancement splint therapy in 120 subjects with sleep-related breathing disorders. METHODOLOGY: Overnight polysomnography and sleep nasendoscopy were performed prior to splint therapy. Follow-up sleep studies, with the appliance in situ, were undertaken for those patients with obstructive sleep apnoea. Subjective outcome measures assessed daytime sleepiness and snoring. RESULTS: One hundred and seven (89 per cent) subjects completed the study. Follow-up sleep studies confirmed the efficacy of treatment, with patients showing a mean reduction in apnoea/hypopnoea index (from 18.9 to 4.9, p<0.001), Epworth sleepiness scale scores (from 11 to seven, p<0.001) and partner-recorded snoring scores (from 14 to eight, p<0.001). CONCLUSION: Sleep nasendoscopy, with concomitant mandibular advancement to mimic the treatment effect, could be of prognostic value in determining successful mandibular advancement splint therapy.

Adult↗
PubMed2003

Sleep depth oscillations: an aspect to consider in automatic sleep analysis.

The automatic sleep analysis aims at providing an accurate description of sleep process. We found that there exist so far poorly known sleep depth oscillations constantly. Quantitative analysis of these oscillations was done in this work via a mean frequency measure and FFT. Overall charasteristics of these oscillations were studied, focusing on the waves with period times of 5-150 s. These sleep depth oscillations have a relatively large amplitude and they should be considered in future sleep analysis systems. The results of this study give directions to automated sleep analysis regarding optimal estimation of sleep depth.

Adult↗
PubMed2001

Lack of changes in serum prolactin, FSH, TSH, and estradiol after melatonin treatment in doses that improve sleep and reduce benzodiazepine consumption in sleep-disturbed, middle-aged, and elderly patients.

An open pilot study on the safety and efficacy of melatonin in the treatment of insomniac patients was conducted in 22 subjects (16 females), mean +/- S.D. age 60.1 +/- 9.5 years. All patients received 3 mg of gelatin melatonin capsules per os daily for 6 months, 30 min before expected sleep time. Twenty of 22 patients were on benzodiazepine treatment and they continued this treatment for part of or for the entire melatonin administration period. Serum concentrations of prolactin, follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), or estradiol were measured by radioimmunoassay (RIA) in morning samples at the beginning and after 6 months of melatonin administration, and standard clinical laboratory tests for blood components were performed. Urinary 6-sulphatoxymelatonin (aMT6s) excretion was measured by RIA before treatment. Serum concentrations of prolactin, FSH, TSH, or estradiol did not exhibit changes after 6 months of melatonin administration, nor were any indications of hematologic or blood biochemistry alteration found. Melatonin augmented significantly the quality and duration of sleep, and decreased sleep latency and the number of awakening episodes, as assessed from sleep logs filled by the patients (first 21 days) and from structured interviews performed by incumbent physicians (up to 6 months). Estimates of next-day function (i.e., alertness in the morning and during the day) also improved significantly during melatonin treatment. The observed effect lasted for the entire period examined (up to 6 months), with 22 out of 22 patients showing improved sleep at the end of treatment. The urinary excretion of aMT6s before starting administration of melatonin correlated negatively and significantly with age, but not with the intensity of sleep the disorder or the outcome of treatment. In 13 of 20 patients taking benzodiazepines together with melatonin, benzodiazepine use could be stopped, and in another four patients, benzodiazepine dose could be decreased to 25-66% of the initial dose. The results of this open, subacute administration trial indicate that melatonin is a safe and useful treatment for sleep disturbances in middle-aged or elderly patients, either by itself or together with benzodiazepines.

Aged↗
PubMed2003

Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: a sleep dose-response study.

Daytime performance changes were examined during chronic sleep restriction or augmentation and following subsequent recovery sleep. Sixty-six normal volunteers spent either 3 (n = 18), 5 (n= 16), 7 (n = 16), or 9 h (n = 16) daily time in bed (TIB) for 7 days (restriction/augmentation) followed by 3 days with 8 h daily TIB (recovery). In the 3-h group, speed (mean and fastest 10% of responses) on the psychomotor vigilance task (PVT) declined, and PVT lapses (reaction times greater than 500 ms) increased steadily across the 7 days of sleep restriction. In the 7- and 5-h groups speed initially declined, then appeared to stabilize at a reduced level; lapses were increased only in the 5-h group. In the 9-h group, speed and lapses remained at baseline levels. During recovery, PVT speed in the 7- and 5-h groups (and lapses in the 5-h group) remained at the stable, but reduced levels seen during the last days of the experimental phase, with no evidence of recovery. Speed and lapses in the 3-h group recovered rapidly following the first night of recovery sleep; however, recovery was incomplete with speed and lapses stabilizing at a level comparable with the 7- and 5-h groups. Performance in the 9-h group remained at baseline levels during the recovery phase. These results suggest that the brain adapts to chronic sleep restriction. In mild to moderate sleep restriction this adaptation is sufficient to stabilize performance, although at a reduced level. These adaptive changes are hypothesized to restrict brain operational capacity and to persist for several days after normal sleep duration is restored, delaying recovery.

Adaptation, Psychological↗
PubMed2003

Effects of sleep loss in men and women with insufficient sleep suffering from chronic disease: a model for supportive nursing care.

This study evaluated self-reported subjective health and effects of sleep loss according to perceived interfering cognitive anxiety related to falling asleep in patients with and without insufficient sleep and gender differences in these aspects 5 years after coronary artery bypass graft and transluminal coronary angioplasty. A total of 145 patients, five years after intervention, responded to a mailed questionnaire. Nearly 60% had severe combined sleep disturbances; 35.9% of these had complained of insufficient sleep and 15% also perceived difficulty falling asleep related to cognitive anxiety. Measurable gender differences were small. A theoretical framework is presented which can increase understanding among nurses, patients and their relatives concerning the quality and quantity of sleep and sleep loss related to quality of life. These results suggest that there are significant relationships between sleep quality, resilience to stress and coping strategy in patients with a chronic disease, indicating the need for more individualised supportive nursing care.

Aged↗