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PubMed2001

Sleep fragmentation: comparison of two definitions of short arousals during sleep in OSAS patients.

The measurement of arousals during sleep is useful to quantify sleep fragmentation. The criteria for electroencephalography (EEG) arousals defined by the American Sleep Disorders Association (ASDA) have recently been criticized because of lack of interobserver agreement. The authors have adopted a scoring method that associates the increase in chin electromyography (EMG) with the occurrence of an alpha-rhythm in all sleep stages (Université Catholique de Louvain (UCL) definition of arousals). The aim of the present study was to compare the two scoring definitions in terms of agreement and repeatability and the time taken for scoring in patients with obstructive sleep apnoea syndrome (OSAS) of varying severity. Two readers using both ASDA and UCL definitions scored twenty polysomnographies (PSGs) each on two occasions. The PSGs were chosen retrospectively to represent a wide range of arousal index (from 6-82) in OSAS patients. There was no difference in the arousal indices between readers and between scoring methods. The mean+/-SD difference between the two definitions (the bias) was 1.1+/-3.76 (95% confidence interval: -0.66-2.86). There was a strong linear relationship between the arousal index scored with the two definitions (r=0.981, p<0.001). Mean+/-SD scoring duration was significantly shorter for UCL than for ASDA definitions (18.5+/-5.4 versus 25.3+/-6.6 min, p<0.001). In conclusion, it has been found that in obstructive sleep apnoea syndrome patients, the American Sleep Disorders Association and Université Catholique de Louvain definitions were comparable in terms of agreement and repeatability.

Adult↗
PubMed1994

Diurnal rhythm of plasma delta-sleep-inducing peptide in humans: evidence for positive correlation with body temperature and negative correlation with rapid eye movement and slow wave sleep.

Since delta-sleep-inducing peptide (DSIP) was isolated in 1977, numerous reports have suggested that this nonapeptide stimulates delta-sleep [slow wave sleep (SWS)]. Although DSIP-like immunoreactivity (DSIP-LI) has been found in the serum of many animals and man, its diurnal rhythm and relation to sleep stages have not been well defined. We hypothesized that circulating levels of this putative sleep hormone would be highest at night and would probably be elevated before or during episodes of SWS. We, therefore, measured plasma DSIP-LI levels every 30 min for 24 h in 12 normal volunteers in whom we obtained simultaneous polygraphic recordings. We found a distinct diurnal rhythm for plasma DSIP-LI levels, with the maximum at 1500 h and the minimum at 0100 h. DSIP-LI levels were substantially lower in rapid eye movement sleep (P < 0.005) and somewhat lower in SWS (P < 0.05) compared to awake values. DSIP-LI levels did not rise before, during, or after a significant percentage of episodes of SWS. We found, however, that the diurnal rhythm of DSIP-LI closely followed that of body temperature with a high degree of correlation (r2 = 0.66; P < 0.0001). We conclude that endogenous elevations of circulating DSIP may be associated with suppression of slow wave and rapid eye movement sleep, and that the circadian rhythm of this peptide is coupled directly or indirectly to that of body temperature.

Adrenocorticotropic Hormone↗
PubMed2003

Sleep-related hypoglycemia-associated autonomic failure in type 1 diabetes: reduced awakening from sleep during hypoglycemia.

Given that iatrogenic hypoglycemia often occurs during the night in people with type 1 diabetes, we tested the hypothesis that physiological, and the resulting behavioral, defenses against developing hypoglycemia-already compromised by absent glucagon and attenuated epinephrine and neurogenic symptom responses-are further compromised during sleep in type 1 diabetes. To do so, we studied eight adult patients with uncomplicated type 1 diabetes and eight matched nondiabetic control subjects with hyperinsulinemic stepped hypoglycemic clamps (glucose steps of approximately 85, 75, 65, 55, and 45 mg/dl) in the morning (0730-1230) while awake and at night (2100-0200) while awake throughout and while asleep from 0000 to 0200 in random sequence. Plasma epinephrine (P = 0.0010), perhaps norepinephrine (P = 0.0838), and pancreatic polypeptide (P = 0.0034) responses to hypoglycemia were reduced during sleep in diabetic subjects (the final awake versus asleep values were 240 +/- 86 and 85 +/- 47, 205 +/- 24 and 148 +/- 17, and 197 +/- 45 and 118 +/- 31 pg/ml, respectively), but not in the control subjects. The diabetic subjects exhibited markedly reduced awakening from sleep during hypoglycemia. Sleep efficiency (percent time asleep) was 77 +/- 18% in the diabetic subjects, but only 26 +/- 8% (P = 0.0109) in the control subjects late in the 45-mg/dl hypoglycemic steps. We conclude that autonomic responses to hypoglycemia are reduced during sleep in type 1 diabetes, and that, probably because of their reduced sympathoadrenal responses, patients with type 1 diabetes are substantially less likely to be awakened by hypoglycemia. Thus both physiological and behavioral defenses are further compromised during sleep. This sleep-related hypoglycemia-associated autonomic failure, in the context of imperfect insulin replacement, likely explains the high frequency of nocturnal hypoglycemia in type 1 diabetes.

Blood Glucose↗
PubMed1998

[The effects of transcutaneous electrical stimulation during sleep on obstructive sleep apnea].

OBJECTIVE: To study the effects of transcutaneous electrical stimulation during sleep on obstructive sleep apnea syndrom (OSAS). METHOD: Sixteen patients with OSAS were studied by polysomnography during all-night sleep with and without submental transcutaneous electrical stimulation (TES) of the genioglossus. RESULT: Fourteen of the 16 patients (87%) who accepted the TES were treated successfully (reduction of Al > 50%). The average apnea index showed a decrease of 29 events per hour when the TES were performed (P < 0.001). The average apnea time decreased from 22 to 7 sec (P < 0.001). The apnea time/TST decreased from 27% +/- 11% to 7% +/- 3%. The lowest SaO2 increased from 71% to 87% (P < 0.001). TES did not cause arousal. The sleep stages of SWS, and REM sleep effect (SE) increased significantly. CONCLUSION: TES is a conservative but effective treatment in patients with obstructive sleep apnea syndrome, although it failed to improve central sleep apnea.

Aged↗
PubMed1999

Frontal predominance of a relative increase in sleep delta and theta EEG activity after sleep loss in humans.

The effect of sleep deprivation (40 h) on topographic and temporal aspects of electroencephalographic (EEG) activity during sleep was investigated by all night spectral analysis in six young volunteers. The sleep-deprivation-induced increase of EEG power density in the delta and theta frequencies (1-7 Hz) during nonREM sleep, assessed along the antero-posterior axis (midline: Fz, Cz, Pz, Oz), was significantly larger in the more frontal derivations (Fz, Cz) than in the more parietal derivations (Pz, Oz). This frequency-specific frontal predominance was already present in the first 30 min of recovery sleep, and dissipated in the course of the 8-h sleep episode. The data demonstrate that the enhancement of slow wave EEG activity during sleep following extended wakefulness is most pronounced in frontal cortical areas.

Adult↗
PubMedDate not supplied

[The role of slow wave sleep in the homeostatic regulation of sleep].

OBJECTIVES: The homeostatic regulation of sleep is based on the model devised by Borb ly in 1982. During the sleep waking cycle there is an interaction between the natural tendency to sleep, which increase as the vigil is prolonged (S process) and the circadian variation (C process). In this study, we aimed to find how slow activity (0.5 4.5 Hz) during sleep (SWA), mainly registered in phases 3 and 4, may be an indicator of process S. PATIENTS AND METHODS: We compared two groups of persons: 10 with chronic sleep deprivation (CSD) (less than 6 hours of sleep/day) as compared with 10 persons who slept more than 6 hours per day, using spectral analysis of their delta activity during sleep. RESULTS: There was a predominance of delta activity in the group of persons with CSD as compared with the control group. CONCLUSIONS: An increase in SWA was accompanied by an increased tendency to sleep and may therefore be considered to be a marker for this. This marker allows conditions associated with hypersomnolence due to alteration of process S to be identified.

Adult↗
PubMed1990

[Effects of delta sleep-inducing peptide on electrophysiological parameters of sleep during alcohol withdrawal in rats].

In rats with the persistent alcohol motivation the electrophysiological sleep pattern was studied during ethanol intake, after 24 and 48 hours of alcohol withdrawal. It was established that during the voluntary ethanol intake rats may be divided into two groups: with comparative deficit (1st group) and comparative abundance (2nd group) of REM sleep. Alcohol withdrawal caused differential alterations of sleep-wakefulness cycle: in the 1st group of rats REM sleep was more suppressed while in the 2nd group--more increased in comparison to those during ethanol intake. In all animals the SWS depression, increase of awakenings, the aggravation of falling asleep and decrease of sleep depth were observed. DSIP (0.1 mg/kg, i.p. 1 hour before sleep recording) was found to regulate sleep disorders caused by ethanol withdrawal. It makes the neuropeptide possible to be recommended for ethanol withdrawal syndrome treatment in clinical practice.

Animals↗
PubMed1990

The multiple sleep latency test in the diagnosis of sleep disorders.

The multiple sleep latency test provides an objective measure of a patient's daytime sleepiness. Sixteen tests were performed at Groote Schuur Hospital in 1987 and 1988 according to a fixed protocol. In 8 patients the test was definitely abnormal (mean sleep latency less than 5 minutes) with 3 subjects diagnosed as having narcolepsy, 1 sleep apnoea syndrome, 1 idiopathic central nervous system hypersomnolence, 2 environment-related hypersomnolence and 1 psychophysiological hypersomnolence. In 2 patients the test results fell in the equivocal range (mean sleep latency 5-10 minutes), while in 5 the test revealed no evidence for a disorder of excessive sleep (mean sleep latency greater than 10 minutes). The test was uninterpretable for technical reasons in only 1 patient. In conclusion, the test--when performed in a standardised manner--is extremely helpful in the elucidation of possible disorders of excessive sleep.

Adult↗
PubMed1985

Sleep function, with particular reference to sleep deprivation.

Human total sleep deprivation (TSD) findings up to the present show that the organ most affected is the brain, which displays psychological and some neurological decriments. The rest of the body seems to cope surprisingly well, indicating little sign of stress or malfunction. Central nervous system (CNS) effects also include some impairment to homeostatic control, particularly thermoregulation, which in humans seem to be minor, but for small mammals the outcome may be more serious. In humans, only a specific part of the lost sleep is made up, suggesting that a certain portion of a night's sleep ("obligatory" sleep) is essential to the brain, and that the remainder ("facultative" sleep) is more dispensable. Contrasting with the nominal TSD effects on the body (excluding the CNS), there are claims that sleep is necessary for general tissue growth and repair. The underlying evidence is examined, but is shown to have alternative interpretations. Anabolism may not rely so much on sleep, but on food intake and rest.

Behavior↗
PubMed1982

Development of sleep-wake patterns and non-rapid eye movement sleep stages during the first six months of life in normal infants.

Thirty-one normal infants were selected for 24-hour polygraphic monitoring at different ages during the first six months of life. The development of sleep-wake distribution patterns during day and night was observed. Qualitative changes in non-rapid eye movement (NREM) sleep as it becomes differentiated in stages 1, 2, and 3-4 were measured. Sustained periods of wake are present by 6 weeks of age. After 3 months of age, wake is predictably distributed in late afternoon and early evening. REM sleep is disproportionately distributed within sleep in 24 hours, presenting a higher percent of total sleep during the night. At 4.5 and 6 months of age, stages 2 and 3-4 NREM are coincident during the nocturnal hours and 3-4 NREM sleep peaks in the early period of the night. The decreasing proportion of REM sleep, particularly in its daytime distribution, suggests a reciprocal relationship to the developing of wakefulness.

Child Development↗
PubMed2000

Familial Aggregation and Segregation Analysis of Snoring and Symptoms of Obstructive Sleep Apnea.

To investigate possible modes of inheritance that would explain familial aggregation in obstructive sleep apnea (OSA), familial correlation and segregation analyses were performed on data derived from 584 pedigrees with 2019 cases enrolled in the Tucson Epidemiologic Study of Obstructive Airways Disease (TESOAD) who were at least 10 years of age and who had information pertaining to snoring and daytime sleepiness. Data were obtained from the 9th (May 1984 to October 1985) and 12th (February 1990 to October 1992) surveys of the TESOAD, which is a random, stratified sample of the non-Hispanic Caucasian population of Tucson, Arizona. A snoring phenotype was considered present if it occurred on at least some nights. A "sleep apnea" phenotype was constructed if participants snored and experienced daytime sleepiness. Familial correlations for snoring showed significant mother-child and sibling correlations but not father-child correlations. For sleep apnea, significant parent-daughter but not parent-son or sibling correlations were observed. Segregation analyses for snoring with regressive familial effects and sibling, age, and obesity covariates showed no evidence for mendelian transmission. However, additional familial effects were present that suggested phenotype aggregation from polygenic or environmental factors, or both. For the sleep apnea phenotype, similar segregation analyses indicated that mendelian dominant or codominant models were possible. However, the analyses also suggested that a nongenetic model fit the data as well. In addition, consistent with the familial correlations, specific maternal- and sibling-related effects remained even after inclusion of age, gender, and obesity covariates. These data support the concept that inheritable or shared environmental factors contribute to the development of OSA and that maternal components may be more important than paternal ones.

Journal Article↗
PubMed2002

Pergolide restores sleep maintenance but impairs sleep EEG synchronization in patients with restless legs syndrome.

BACKGROUND: The treatment with the long-acting dopamine D1/D2 receptor agonist pergolide has been proven as very effective in lowering the frequency of periodic leg movements (PLM) in patients with restless legs syndrome (RLS). To further investigate the influence of this potent dopaminergic drug on the microstructure of rapid eye movement (REM) and non-REM sleep EEG we established a quantitative analysis of the EEG data. METHODS: The study group consisted of 15 patients with primary RLS (mean age 57.1+/-10.1 years) who were a subgroup of patients within a double-blind randomized crossover treatment study with pergolide versus placebo. The polysomnographic recordings were analyzed visually and submitted to a quantitative EEG analysis (fast Fourier transformation). RESULTS: The pergolide treatment induced a significant reduction of the spectral power in the delta range (0.78-3.9 Hz; P<0.05; t-test) during SWS, as well as a significant reduction of PLMs. In addition, we observed a decrease in the sigma EEG activity (12.1-14.8 Hz; P<0.03) during non-REM sleep and stage 2 sleep. The visual sleep scoring revealed a significant increase in stage 2 sleep (P<0.005), whereas wakefulness was markedly diminished (P<0.001). The REM sleep parameters including the EEG power spectrum remained unchanged. CONCLUSIONS: The treatment with pergolide markedly improved the sleep quality in RLS patients but did not restore SWS including the spectral power in the lower frequencies. Our results suggest that the dopamine agonist pergolide interferes with the subcortical mechanisms regulating the process of EEG synchronization during non-REM sleep.

Clinical Trial↗
PubMed1995

Sleep propensity and sleep architecture after bright light exposure at three different times of day.

The aim of this work was to study the effects of bright light-induced circadian phase shifts on sleep propensity and sleep architecture while the timing of the sleep/wake cycle is kept constant. Twenty-three normal subjects underwent an 11-day study including: (i) baseline sleep and vigilance evaluation; (ii) baseline evaluation of the circadian temperature rhythm with a 40-h constant routine; (iii) five hours of bright light exposure on each of three days; (iv) post-treatment sleep and vigilance evaluation; (v) post-treatment circadian rhythm evaluation with a second 40-h constant routine. Subjects were divided into three groups: eight subjects were exposed to bright light in the morning ('Morning group'), eight subjects were exposed in the evening ('Evening group'), and seven subjects were exposed in the afternoon ('Afternoon group'). After light exposure, the Morning group showed an advance of 1.23 h in the phase of the temperature rhythm, the Evening group showed a delay of 1.62 h, and the Afternoon group showed a non-significant advance of 0.5 h. In support of expectations, early-night sleep propensity was decreased by evening bright light, was increased in almost all subjects exposed to morning bright light, and was not changed by afternoon bright light exposure. The phase shift created by bright light exposure did not seem to be large enough to have a systematic effect on sleep consolidation or on REM sleep parameters in any of the three groups, suggesting that these variables are less sensitive to alterations in phase of the circadian oscillator than early-night sleep propensity.

Journal Article↗
PubMed1995

Basic Nordic Sleep Questionnaire (BNSQ): a quantitated measure of subjective sleep complaints.

Sleep-related breathing disturbances, especially obstructive sleep apnoea syndrome (OSAS), are commonly encountered. Epidemiological studies from different countries have shown that poor sleep and complaints about insufficient sleep or poor sleep are often related to poor health. Different studies are, however, difficult to compare with each other. One of the main reasons for this is the frequent methodological differences between questionnaires. There is a need for uniform methods: we need to know the prevalence and incidence of sleep disorders, judged using the same criteria, and also the severity of each problem, i.e. how often a problem or a symptom happens/occurs. In 1988 the Scandinavian Sleep Research Society formed a task group for developing a standardized questionnaire that could be used as a basis for questionnaires used in the Nordic countries. In this article we describe the Basic Nordic Sleep Questionnaire (BNSQ). The main change compared to many previous questionnaires is the five-point scale (scale from 1 to 5) stressing on how many nights/days per week something happens. The basic scale is: 1, 'never or less than once per month'; 2, 'less than once per week'; 3, 'on 1-2 nights per week'; 4, 'on 3-5 nights per week'; and 5, 'every night or almost every night'. For questions about specific rare events the first category may be divided into 'never' and 'less than once per month'. Habitually occurring events such as 'habitual snoring' are defined here as snoring every night or almost every night. The BNSQ has been used widely in a variety of studies performed in Nordic countries during the last years, and it has proven to be a valid tool.

Journal Article↗
PubMed2003

The Safe-T-Sleep device: safety and efficacy in maintaining infant sleeping position.

AIMS: The issue of infant sleeping position has socio-political ramifications. Current recommendations endorse supine sleeping as an aid to reducing the risk of sudden infant death syndrome (SIDS). Persistent sleeping of a newborn infant in the same position may induce plagiocephaly without synostosis (PWS). Parents in our craniofacial clinic, whose children present with PWS, often feel torn between apparently conflicting goals--avoiding SIDS and avoiding PWS. The Safe-T-Sleep device, a form of infant sleep wrap, purportedly allows safe semi-supine positioning, thus ameliorating PWS (by preventing the infant from lying on the cranial 'flat spot') while not increasing the risk of SIDS. Before recommending the device to parents in our plagiocephaly clinics, we designed a prospective, hospital-based trial to assess the safety and efficacy of the device in maintaining selected sleeping positions. This was not a trial of the efficacy of the Safe-T-Sleep device in treating plagiocephaly. METHODS: The devices were trialed on 31 babies, between birth and 11 months of age. A total of 396 hours of observations were recorded. RESULTS: The device maintained the selected body position in 94% of recorded observations and head position in 87%. There were no significant adverse events or complications associated with the use of the Safe-T-Sleep device. CONCLUSIONS: The device appears to be safe and effective. It is now being advocated in our clinic as an aid to active counter-positioning strategies to passively correct incipient or established positional plagiocephaly in younger babies.

Bedding and Linens↗
PubMed1999

Melatonin as a therapy in REM sleep behavior disorder patients: an open-labeled pilot study on the possible influence of melatonin on REM-sleep regulation.

REM sleep behavior disorder (RBD) is clinically impressive by virtue of its vigorous sleep behaviors usually accompanying vivid, striking dreams. The main feature of the disorder, REM sleep without muscle atonia, has been shown in a variety of diseases; therefore, the disorder might possibly be underestimated. In an open-labeled trial, we treated six consecutive RBD patients over a 6-week period with 3 mg melatonin given within 30 minutes before bedtime. There was a dramatic clinical improvement in five of the six patients within a week which extended beyond the end of treatment for weeks or months. A second polysomnogram performed 6 weeks after the beginning of treatment showed a significant tendency toward normalization of the percentage of REM sleep, a significant reduction of 30-second epochs, scored as REM sleep without muscle atonia, a significant reduction of stage-shifts in REM, and a significant reduction in epochs considered as movement time in REM. All other sleep parameters were not changed consistently. We hypothesize that internal desynchrony might be a part of the underlying pathophysiology in RBD. Our data might give first evidence to the hypothesis that exogenous melatonin, administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion, might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.

Adult↗
PubMed1996

Paradoxical sleep deprivation and sleep recording following training in a brightness discrimination avoidance task in Sprague-Dawley rats: paradoxical effects.

Previously, we reported that posttraining paradoxical sleep deprivation (PSD) resulted in an enhancement of the subsequent avoidance performance for rats trained for 15 trials in a Y-maze brightness avoidance discrimination task. A series of experiments were conducted to try to further understand the reasons for results which were contrary to those of the bulk of the sleep-learning literature. Experiment 1 investigated the effectiveness of the PSD technique. Rats (N = 4) were sleep recorded while residing on a "swimming pool" apparatus for 24 h. Compared to their baseline values, all animals showed a very large reduction in paradoxical sleep and spent significantly more time awake. Slow-wave sleep was unchanged. In Experiment 2, proactive motor effects were tested. Rats were deprived of PS for 24 h and then tested in a hole board motor activity task. There was a slight effect of PS deprivation on the day following the PSD and no effect when the rats were retested 1 week later. Experiment 3 investigated possible proactive effects of PSD on avoidance performance. Rats exposed to PSD in the 24 h before training in the Y-maze task did not demonstrate any facilitative effect on the subsequent avoidance performance. Experiment 4 investigated the possibility that the PSD facilitative effect could be due to partial training. Rats were given 75 acquisition trials in the brightness discrimination Y-maze avoidance before being subjected to 24 h of PSD. PS-deprived animals showed superior avoidance scores compared to non-PSD controls when retested 24 h later. In Experiment 5, the same strain of rats (N = 11) were sleep recorded after exposure to a partial acquisition in a Y-maze brightness avoidance discrimination task. They were then continuously monitored for 4 consecutive days. The percent PS for the Trained rats was significantly lower than that for the Control animals. This drop in percent PS was not confined to any particular time period in the 24-h day. None of the other sleep parameters reached significance. Analyses of the present results suggest that PSD exerts its facilitative effects on posttraining consolidation processes. We present arguments suggesting that PSD can have effects opposite to those generally reported, in animals demonstrating poor avoidance abilities, in an avoidance task.

Animals↗
PubMed2000

White blood cells and cortisol after sleep deprivation and recovery sleep in humans.

Sleep deprivation (SD) has enriched our treatment programme for major depression. SD has been demonstrated to modify different host defence activities. There is some evidence that there are reciprocal relationships between immune function and increased hypothalamic-pituitary-adrenocortical (HPA) axis activity in depression. We therefore investigated the number of leukocytes, granulocytes, monocytes, lymphocytes, B cells, T cells, helper T cells, cytotoxic T cells, NK cells and salivary cortisol in 10 healthy men before and after total SD (TSD) as well as after recovery sleep. Blood samples were drawn on 3 consecutive days at 7 am, 1 pm and 7 pm, respectively. Comparison of the 7 am values by contrast analysis yielded significant differences for granulocytes (p = 0.044) and NK cells (p = 0.001) after SD and recovery sleep. NK cells decreased and granulocytes increased after SD and after recovery sleep. Significant differences between single points in time across the day were found for granulocytes (p = 0.022), monocytes (p = 0.031), T cells (p = 0.005), helper T cells (p = 0.004), cytotoxic T cells (p = 0.005) and NK cells (p = 0.017). No significant difference could be detected for leukocytes, lymphocytes and B cells counts. These results favour the thesis that SD and recovery sleep lead to changes in the distribution of peripheral leukocytes, especially in a reduction of NK cells after SD and recovery sleep. The cortisol rhythm was affected neither by SD nor recovery sleep.

Adult↗