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L’identification du sommeil paradoxal a permis l’entree du reve dans le champ des neurosciences. Il est toutefois bien reconnu actuellement que le reve n’est pas l’apanage du sommeil paradoxal uniquement et que des rappels de reves sont obtenus dans les autres phases de sommeil. Les techniques tres pointues d’imagerie ainsi que l’etude du sommeil et du reve dans diverses pathologies neurologiques et du sommeil permettent une meilleure comprehension de l’activite onirique.

OBJECTIVE: The aim of this study was to identify atherosclerotic risk using pulse wave velocity (PWV) in steel workers employed in different shift-work rotations, and to elucidate its relationship to social jetlag and shift schedule details.PARTICIPANTS: Male workers in a steel factory (n=77, 32 fast clockwise (CW), 30 slow counterclockwise (CC), 15 day workers (DW); mean age 42 ± SD 7.6 yrs) with at least 5 years of experience in their current work schedule participated.METHODS: All workers completed questionnaires on demographics, health, psychotropic agents, sleep, social and work life, social jetlag (difference between mid-sleep time on workdays and days off used as a marker of circadian disruption) and chronotype (mid-sleep time on free days corrected for sleep deficit on workdays). In 63 workers we measured PWV, blood pressure (BP), heart rate (HR) between 08:00 and 12:30 h in controlled posture conditions (no caffeine/smoking/exercise).RESULTS: There was no significant difference in PWV (covariates: age, BP) between the different shift-rotations (CW, CC and DW). In all workers combined, HR and social jetlag were significantly positively correlated. Demographic variables did not differ between shift-workers and day workers; shift-workers (CW, CC) reported significantly more stomach upsets, digestion problems, weight fluctuations, and social jetlag. The CW and CC workers did not differ in ratings of how shift-work affected sleep, social and work life.CONCLUSIONS: PWV was not different between the two shift-rotations. This pilot study shows first evidence that HR is related to social jetlag, and therefore warrants more studies in different shift schedules.

Previous studies have shown increased sleepiness and mood changes in shiftworkers, which may be due to sleep deprivation or circadian disruption. Few studies, however, have compared responses of experienced shiftworkers and non-shiftworkers to sleep deprivation in an identical laboratory setting. The aim of this laboratory study, therefore, was to compare long-term shiftworkers and non-shiftworkers and to investigate the effects of one night of total sleep deprivation (30.5 h of continuous wakefulness) and recovery sleep on psychomotor vigilance, self-rated alertness, and mood. Eleven experienced male shiftworkers (shiftwork ≥5 yrs) were matched with 14 non-shiftworkers for age (mean ± SD: 35.7 ± 7.2 and 32.5 ± 6.2 yrs, respectively) and body mass index (BMI) (28.7 ± 3.8 and 26.6 ± 3.4 kg/m(2), respectively). After keeping a 7-d self-selected sleep/wake cycle (7.5/8 h nocturnal sleep), both groups entered a laboratory session consisting of a night of adaptation sleep and a baseline sleep (each 7.5/8 h), a sleep deprivation night, and recovery sleep (4-h nap plus 7.5/8 h nighttime sleep). Subjective alertness and mood were assessed with the Karolinska Sleepiness Scale (KSS) and 9-digit rating scales, and vigilance was measured by the visual psychomotor vigilance test (PVT). A mixed-model regression analysis was carried out on data collected every hour during the sleep deprivation night and on all days (except for the adaptation day), at .25, 4.25, 5.25, 11.5, 12.5, and 13.5 h after habitual wake-up time. Despite similar circadian phase (melatonin onset), demographics, food intake, body posture, and environmental light, shiftworkers felt significantly more alert, more cheerful, more elated, and calmer than non-shiftworkers throughout the laboratory study. In addition, shiftworkers showed a faster median reaction time (RT) compared to non-shiftworkers, although four other PVT parameters did not differ between the groups. As expected, both groups showed a decrease in subjective alertness and PVT performance during and following the sleep deprivation night. Subjective sleepiness and most aspects of PVT performance returned to baseline levels after a nap and recovery sleep. The mechanisms underlying the observed differences between shiftworkers and non-shiftworkers require further study, but may be related to the absence of shiftwork the week prior to and during the laboratory study as well as selection into and out of shiftwork.

In addition to its effects on cognitive function, compelling evidence links sleep loss to alterations in the neuroendocrine, immune and inflammatory systems with potential negative public-health ramifications. The evidence to suggest that shorter sleep is associated with detrimental health outcomes comes from both epidemiological and experimental sleep deprivation studies. This review will focus on the post-sleep deprivation and recovery changes in immune and inflammatory functions in well-controlled sleep restriction laboratory studies. The data obtained indicate non-specific activation of leukocyte populations and a state of low-level systemic inflammation after sleep loss. Furthermore, one night of recovery sleep does not allow full recovery of a number of these systemic immune and inflammatory markers. We will speculate on the mechanism(s) that link(s) sleep loss to these responses and to the progression of cardiovascular disease. The immune and inflammatory responses to chronic sleep restriction suggest that chronic exposure to reduced sleep (

Understanding the interactions between sleep and the immune system may offer insight into why short sleep duration has been linked to negative health outcomes. We, therefore, investigated the effects of napping and extended recovery sleep after sleep restriction on the immune and inflammatory systems and sleepiness. After a baseline night, healthy young men slept for a 2-h night followed by either a standard 8-h recovery night (n=12), a 30-min nap (at 1 p.m.) in addition to an 8-h recovery night (n=10), or a 10-h extended recovery night (n=9). A control group slept 3 consecutive 8-h nights (n=9). Subjects underwent continuous electroencephalogram polysomnography and blood was sampled every day at 7 a.m. Leukocytes, inflammatory and atherogenesis biomarkers (high-sensitivity C-reactive protein, interleukin-8, myeloperoxidase, fibrinogen and apolipoproteins ApoB/ApoA), sleep patterns and sleepiness were investigated. All parameters remained unchanged in the control group. After sleep restriction, leukocyte and - among leukocyte subsets - neutrophil counts were increased, an effect that persisted after the 8-h recovery sleep, but, in subjects who had a nap or a 10-h recovery sleep, these values returned nearly to baseline. Inflammatory and atherogenesis biomarkers were unchanged except for higher myeloperoxidase levels after sleep restriction. The increased sleepiness after sleep restriction was reversed better in the nap and extended sleep recovery conditions. Saliva cortisol decreased immediately after the nap. Our results indicate that additional recovery sleep after sleep restriction provided by a midday nap prior to recovery sleep or a sleep extended night can improve alertness and return leukocyte counts to baseline values.

Resume Notre societe operationnelle 24 heures sur 24 favorise l’eveil au detriment du sommeil. De nombreux individus reduisent leur temps de sommeil volontairement ou par obligation. Si les effets de l’insuffisance de sommeil sur les performances et la vigilance commencent a etre bien documentes, il n’en est pas de meme concernant les effets du manque chronique de sommeil sur la sante et diverses affections dont les maladies cardiovasculaires. Plusieurs etudes ont mis en evidence une relation entre une reduction de la duree de sommeil et les pathologies cardiovasculaires. Les mecanismes impliques dans ces associations ne sont pas elucides a l’heure actuelle. Nous utilisons le modele de la restriction de sommeil afin d’evaluer les relations entre reduction du temps de sommeil et les processus inflammatoires impliques dans les maladies cardiovasculaires. Nos travaux indiquent qu’une restriction de sommeil meme minime est susceptible d’influencer des facteurs de risque cardiovasculaire et ce chez des sujets par ailleurs en bonne sante.

Karim Zouaoui Boudjeltia2, Brice Faraut1,2, Patricia Stenuit1, Maria José Esposito1,2, Michal Dyzma1,2, Dany Brohée2, Jean Ducobu2, Michel Vanhaeverbeek2, Myriam Kerkhofs1,21Sleep Laboratory; 2Laboratory of Experimental Medicine (ULB 222 Unit), CHU de Charleroi Vésale Hospital, Université Libre de Bruxelles, Montigny-le-Tilleul, BelgiumObjectives: This study examines the effects of sleep restricted to four hours for three consecutive nights on blood parameters, known to be associated with cardiovascular risk, in young healthy men.Material and methods: Eight young healthy men (age 24.5 ± 3.3 years) were studied in the sleep restricted group. Nine young healthy men (age 24 ± 2 years) were included in the control group and spent the days and nights in the sleep lab, while sleeping eight hours/night. One baseline night was followed by three nights of sleep restriction to four hours and by one recovery night of eight hours. Blood samplings were performed after the baseline night and after the third night of sleep restriction or without restriction for the control group.Results: A significant increase in white blood cells (WBC) (5.79 ± 1.05 vs. 6.89 ± 1.31 103 cell/µl, p = 0.03), and neutrophils (3.17 ± 0.69 vs 4.24 ± 0.97 103 cell/µl, p = 0.01) was observed after the third night of sleep restriction. Other blood parameters were not affected. No significant variation was observed in the control group.Conclusion: Sleep restriction affected WBC count, mainly neutrophils, considered as risk factor for cardiovascular disease. Stress induced by the short term sleep restriction could be involved in this observation.Keywords: sleep restriction, men, cardiovascular risk, cholesterol, neutrophils

The aim of this pilot study was to explore the risk of metabolic abnormalities in steel workers employed in different shift-work rotations. Male workers in a steel factory [16 employed in a fast clockwise rotation (CW), 18 in slow counterclockwise rotation (CC), 9 day workers (DW); mean age 43.3 ± SD 6.8 years] with at least 5 years experience in their current work schedule participated. All workers provided fasting blood samples between 06:00 and 08:00 h for plasma glucose, insulin, apo-lipoproteins A and B (ApoA, ApoB), high- and low-density lipoproteins (HDL and LDL), total cholesterol (tCH), triglycerides (TG), minimally oxidized (mox) LDL, C-reactive protein (CRP), interleukin-8 (IL-8) and serum 25-hydroxyvitamin D (25(OH)D). HOMA index (homeostatic model assessment) was calculated to evaluate insulin resistance, beta cell function and risk of diabetes. Information on demographics, health, stimulants, sleep, social and work life, chronotype (phase of entrainment) and social jetlag (difference between mid-sleep on workdays and free days) as a surrogate for circadian disruption was collected by questionnaire. Neither chronotype nor social jetlag was associated with any of the metabolic risk blood markers. There were no significant differences in 25(OH)D, ApoA, ApoB, CRP, HDL, IL-8, insulin, LDL, mox-LDL, mox-LDL/ApoB ratio, tCH and TG levels between the three work groups. Although we did observe absolute differences in some of these markers, the small sample size of our study population might prevent these differences being statistically significant. Fasting glucose and HOMA index were significantly lower in CW compared to DW and CC, indicating lower metabolic risk. Reasons for the lower fasting glucose and HOMA index in CW workers remains to be clarified. Future studies of workers in different shift rotations are warranted to understand better the differential effects of shift-work on individual workers and their health indices.

Frederic Bremer was one of the pioneer neurophysiologists who dedicated their career to understanding the neural mechanisms involved in the control of sleep–wake regulation. This paper follows his career and his major achievements. We found that Bremer's interest in sleep resulted from his unexpected observations after transecting the brain at the midcollicular level in the "encephale isole" preparation. The sleep-like behaviour of the animal, accompanied by slow waves in the cortex, convinced him that sleep resulted from cortical deafferentation. He was further convinced that deafferentation was the cause of sleep when he found that transecting the brain at the medullary level did not much affect the sleep–wake cycle. As we show, Bremer's views that sleep is a passive phenomenon imposed on the brain because of deafferentation was shared by most of his contemporaries. Years later Bremer admitted that he interpreted his experimental findings wrongly. He continued to investigate sleep using his preparations and made important contributions to understanding the relationships between the brainstem reticular formation and the basal forebrain hypnogenic centres, as well as the importance of light on these relationships.

The aim of the study was to assess compliance with nasal continuous positive airway pressure (N-CPAP) at home in patients with obstructive sleep apnoea syndrome (OSAS) and to search for predictors of compliance. We studied a cohort of 106 consecutive patients (91 men, 15 women) with a median apnoea hypopnoea index of 62.4 (range 21-132) h(-1), equipped at home with a Rem+ Soft device (Sefam, France), including a pressure monitor and a real-time clock. During the third and fourth months of treatment, the patients used their machine a median of 88% of days (16-100%), with a mean effective use of 5.6 (1.3-11.2) h per effective day. Residual apnoea index on N-CPAP, as recorded by the monitor, was 1.5 (0.3-27.6) h(-1). Mean clock-time for starting with N-CPAP was 23 h 54 min (21 h 34-01 h 42). The mean effective use per effective day correlated negatively with the minimal (and the mean) level of oxyhaemoglobin saturation (r(s) = -0.24, P0.05) while the percentage of days the machine was used correlated negatively with the percentage of slow wave sleep (r(s) = -0.22, P0.05) at baseline polysomnography. In a subset of 30 subjects, earlier start on N-CPAP correlated with longer use of the device in 22 patients (median r--0.48). We conclude that a pressure monitor allows reporting on compliance in terms of regularity (% of days the machine is used) and length of sleep on N-CPAP (effective use per effective day). These compliance variables show modest correlations with baseline polysomnographic features. Late bedtime should be discouraged as it might decrease compliance.

The aim of this study was to delineate the contributions of genetic and environmental factors in the regulation of the 24-h GH secretion. The 24-h profile of plasma GH was obtained at 15-min intervals in 10 pairs of monozygotic and 9 pairs of dizygotic normal male twins, aged 16-34 yr. Sleep was polygraphically monitored. Significant pulses of GH secretion were identified using a modification of the computer algorithm ULTRA. For each significant pulse, the amount of GH secreted was calculated by deconvolution. A procedure specially developed for twin studies was used to partition the variance of investigated parameters into genetic and environmental contributions. A major genetic effect was evidenced on GH secretion during wakefulness (with a heritability estimate of 0.74) and, to a lesser extent, on the 24-h GH secretion. Significant genetic influences were also identified for slow wave sleep and height. These data demonstrate that human GH secretion in young adulthood is markedly dependent on genetic factors.

Background: Previous reports suggest that the clinical dichotomy separating psychotic and nonpsychotic depression corresponds to different neurobiological profiles. The aim of the present study is to further investigate the psychobiological correlates of these two particular depressive subtypes. Methods: Thyroid-stimulating hormone response to thyrotropin-releasing hormone postdexamethasone cortisol levels, and electroencephalgraphic sleep characteristics of 44 psychotic major depressive patients were compared to those of 44 nonpsychotic depressives matched for age, gender, and polarity. Results: Some biological disturbances usually associated with depression (increased wakefulness, diminished rapid eye movement latency, hypercortisolism, blunted thyroid-stimulating hormone response to thyrotropin-releasing hormone stimulation) seemed to be significantly more pronounced in the psychotic depressed group as a reflection of greater illness severity; however, shortened REM latency was not influenced by severity and seemed to be more specifically related to the co-occurrence of psychotic and depressive symptoms. Conclusions: Our data provide further support for the validity of the clinical dichotomy separating psychotic and nonpsychotic major depression independently of severity.

Clinical characteristics and sleep EEG data of 14 unipolar (UPR), 14 bipolar I (BPI) and 14 bipolar II (BPII) patients, matched for age and gender, were investigated during a major depressive episode. We observed a remarkable similarity in the clinical characteristics of the three samples and, concerning sleep EEG data, a trend to a higher percentage of awakening among BP I patients. Pairwise comparisons of the three subgroups showed that only the Newcastle rating scale score reached significant difference between BPI and UPR groups. We observed trends regarding the difference of awakening both between BPI and BPII groups and between BPI and UPR groups, difference of percentage of REM sleep between BPI and BPII groups and difference of Sleep Period Time between BPII and UPR groups. We also observed that the distribution of REM latencies in the BP I subgroup was different from the two others.

To delineate the contributions of genetic and environmental factors in the regulation of human prolactin (PRL) secretion, the 24-h profile of plasma PRL was obtained at 15-min intervals in 10 pairs of monozygotic and 10 pairs of dizygotic twins. Sleep was monitored polygraphically. PRL secretory rates were derived from plasma concentrations by deconvolution. Diurnal (24-h) variations were quantified by a regression curve to define nadir, acrophase, and amplitude. Pulses of PRL secretion were identified using a computerized algorithm. A procedure specifically developed for twin studies was used to partition the variance into genetic and environmental contributions. Significant genetic effects were identified for daytime PRL concentrations, rhythm amplitude, and overall waveshape of the daily PRL profile. In contrast, environmental effects were dominant for mean concentrations during sleep, total secretory output during sleep, overall 24-h concentrations, and total 24-h secretion. However, when interindividual variations in sleep fragmentation were taken into account, the estimates of genetic variance for PRL concentrations and secretion during sleep approached statistical significance. Significant genetic influences were identified for slow-wave sleep (SWS). Because SWS is associated with increased nocturnal PRL secretion, it is possible that genetic effects on PRL secretion during sleep reflect genetic influences on SWS. In conclusion, genetic factors determine partially both the basal daytime concentrations of PRL and the temporal organization of PRL secretion over the 24-h cycle in normal young men.

SummaryObjective Dehydroepiandrosterone (DHEA) administration is widely evocated as a ‘fountain of youth’, but previous studies have provided inconsistent results. We aimed to investigate in healthy postmenopausal women the effects of a 3-week oral DHEA administration on individual steroid levels, multiple 24-h hormonal profiles and sleep architecture. Design Seven healthy nonobese postmenopausal women, off hormone replacement therapy for ≥2 months, were investigated in a randomized, crossover, double-blind, placebo-controlled study. For 3 weeks, subjects took daily at 2300 h a capsule of either 50 mg DHEA or placebo. Sleep was polygraphically recorded during the last two nights, and blood samples were drawn at 15-min intervals during the last 24 h. Results Under DHEA, testosterone and estradiol levels were increased in all individuals. Individual increments were highly variable, not related to each other, and were not related to placebo values. However, the testosterone to estradiol ratio was markedly increased under DHEA. DHEA administration had little, if any, effect on thyroid function, GH secretion, prolactin, ACTH and cortisol profiles. DHEA effects on sleep appeared to be mediated by its conversion to androgens and oestrogens: sleep quality was enhanced by increments in testosterone and dampened by increments in estradiol levels. Conclusion As DHEA-induced elevations in testosterone and estradiol levels varied widely between individuals and were largely unpredictable, DHEA administration might not be the most appropriate approach to compensate for the reduction observed in androgen and oestrogen production in postmenopausal women. DHEA supplementation may result either in sleep stimulation or in inhibition, depending on the ratio between DHEA-induced increments in testosterone vs estradiol.

Study objective To assess the effect of 1 year of therapy for sleep apnea syndrome (SAS) combining domiciliary nasal-continuous positive airway pressure (N-CPAP) and attempted weight loss on the severity of disease and to evaluate the potential for weaning from continuous positive airway pressure (CPAP). Methods and procedures Ninety-five patients having a baseline apnea hypopnea index (AHI) greater than 10/h were prescribed N-CPAP at home. Weight loss was attempted by dietary counseling and by single ring vertical gastroplasty in those patients with a body mass index (BMI) greater than 40 kg/m 2 . Subjects were asked to return after 1 year for a full-night polysomnography (PSG) without CPAP and the results were compared with baseline PSG. Results Thirty-nine patients compliant to CPAP were evaluated. Weight had decreased from 108.3±29.0 to 99.7±17.7 kg as a result of dietary counseling (n=36) or gastroplasty (n=3). A significant improvement was found in AHI (66.5±28.7 → 50.3±38.4/h; p Conclusion In 39 patients with SAS, 1-year domiciliary N-CPAP combined with weight loss resulted in a significant improvement in breathing during sleep and in sleep fragmentation, as judged from PSG without CPAP. Four subjects were successfully weaned, three of whom had in parallel a substantial decrease in weight.

The linear prediction method was applied to obtain a power spectra estimate of sleep EEG in 10 healthy young men. In order to analyze frequency changes of the slow-wave activity (EEG power in the delta band, 0.05-2.88 Hz), the delta mean frequency was computed for each 20-second sleep epoch. A mean delta mean frequency was calculated for each sleep stage in each individual. Our observations indicate that the delta mean frequency decreases during NREM periods and increases mainly at the onset of the REM episodes. This finding, in parallel with the detailed analysis of slow-wave power variations, leads to an additional description of sleep characteristics during transitions between the NREM-REM sleep episodes.

In order to investigate the reliability of the endogenous concept of depressive illness with some sleep EEG parameters, we studied 39 male inpatients suffering from a nonbipolar major depressive episode (15 endogenous (MDDE) and 24 nonendogenous (MDDNE)) and 20 age and sex matched normal controls (C). All patients were diagnosed according to the Research Diagnostic Criteria (RDC) and the endogenous character of the episode was assessed with the Newcastle Endogenous Depression Diagnostic Index. We found significant differences for the following variables between the three groups (MDDE, MDDNE and C): sleep period time (SPT), REM latency, stage II, slow wave sleep (SWS), REM latency expressed as a continuous variable and REM latency expressed as a dichotomizing variable with a threshold of 50 min. These variables were used to compare the endogenous and the nonendogenous depressed patients and also the major depressed patients and the normal controls. Significant differences were observed between all depressed patients and control subjects for amount of SWS and REM latency which were both reduced in endogenous and nonendogenous depressed patients. No significant difference was observed between endogenous and nonendogenous depressed patients, except for the REM latency expressed with a threshold of 50 min (more frequently observed in endogenous depressed patients). Our data support the observation that SWS and REM latency are decreased in major depressive patients. However, in this age and sex controlled study, subtyping nonbipolar major depressive disorder for an endogenous character by the Newcastle Endogenous Depression Diagnostic Index (NEDDI) did not reveal further significant differences for sleep EEG variables, except for the shortening of the REM latency expressed as a dichotomizing variable.

La desadaptation au travail en horaires decales (DTHD) se definit par une insomnie ou une somnolence diurne excessive, associee a une dette de sommeil, en relation avec un travail a horaires irreguliers. Notre outil diagnostique s’appuie sur des echelles d’evaluation validees (score a l’echelle de somnolence d’Epworth, index de severite de l’insomnie, echelle de severite de la fatigue) et sur un calcul de la dette de sommeil en fonction du type de poste. Le but de notre demarche est de detecter les travailleurs souffrant de DTHD et d’evaluer la prevalence de ce trouble du rythme circadien dans une population de travailleurs postes de la siderurgie. Notre population se compose de 2171 travailleurs postes (dont 83,5 % en 3 postes et 25 % de ceux-ci en sens antihoraire). La moyenne d’âge est de 42 ans (DS de 10 ans) et l’anciennete de 16 ans (DS de 11 ans). Nous constatons, parmi les travailleurs postes, que 7,9 % souffrent de somnolence diurne excessive (score > 10), 7,4 % de fatigue pathologique (score > 4), 9 % d’insomnie significative (score > 15), que 38,9 % sont en dette de sommeil significative lors du poste du matin (> 3 h) et 51,9 % en dette de sommeil lors du poste de nuit (> 2 h). En posant le diagnostic de DTHD sur 2 ou plus de 2 mesures pathologiques, nous obtenons une prevalence de 13,8 % de ce trouble extrinseque du rythme circadien dans notre population de travailleurs postes de la siderurgie. Le questionnaire de Berlin est un outil valide, permettant d’identifier les personnes a risque de syndrome des apnees du sommeil (SAS). Au total, 28,3 % de nos travailleurs postes repondaient positivement a ce questionnaire et sur 134 travailleurs enregistres par un systeme de depistage du SAS (Apnealink), 37,3 % presentaient un index d’apnees significatif (moyenne de 11/h). Conclusion Nous presentons une methode diagnostique quantifiee du DTHD qui nous permet de definir un groupe de travailleurs eventuellement intolerants au travail poste dans la siderurgie et d’etudier dans cette population l’influence du chronotype, de l’âge, de l’indice de masse corporelle et d’eventuels troubles intrinseques du sommeil (apnees).

SummarySleep problems are classical complaints in depressed patients. Polygraphie recordings performed in drug free depressed patients during an acute episode of the illness have allowed description of sleep continuity, architecture and REM sleep disturbances. While the specificity of these abnormalities is not fully established, these perturbations appear to be core symptoms of the depressive episode. Antidepressants drugs, whatever their pharmacological profile have been shown to suppress or at least to reduce REM sleep. However, the effects of these drugs on sleep continuity and architecture seem to be related to their specific pharmacological action.

The TSH response to TRH and selected sleep EEG variables were studied in a homogeneous sample of 280 non-bipolar major depressed inpatients (95 males and 185 females). The TSH response to TRH was blunted in 28% of the sample. delta max TSH was correlated negatively with age, Hamilton rating scale, Newcastle scale, percentage of wake, and positively with basal TSH, percentage of stage II, slow wave sleep, REM sleep and REM latency. delta max TSH was also lower in male patients and in patients suffering from an endogenous or a psychotic subtype of major depression. Basal TSH was only correlated negatively with the Newcastle score. In view of intercorrelations between all these variables, and because of the confounding effect of age, gender and severity on both the TSH response to TRH and sleep EEG variables, a multiple regression analysis was performed and demonstrated that basal TSH and gender were the two variables with the highest contribution to the delta max TSH variance, followed by age and the presence of psychotic symptoms. When controlling strictly for these significant effects, correlation with the severity or with the endogenous character of depression, and with sleep EEG parameters disappeared.

To determine whether genetic factors control the expression of human circadian rhythmicity, we analyzed the 24-h profile of plasma cortisol in 11 monozygotic and 10 dizygotic pairs of normal male twins. Blood was sampled every 15 min, and sleep was monitored. Circadian rhythmicity was characterized by measures of amplitude, phase, and overall waveshape. Pulsatility was quantified by pulse frequency, pulse amplitude, and relative contribution of pulsatile vs. circadian variations. Data were analyzed by a procedure specifically developed for twin studies. Genetic control was demonstrated for the timing of the nocturnal nadir and for the proportion of overall temporal variability associated with pulsatility. Environmental effects were detected for the 24-h mean and the timing of the morning acrophase. The timing of the cortisol nadir is a robust marker of human circadian phase and is dependent, under entrained conditions, on the length of the endogenous period. Animal studies have shown that the endogenous period and the pattern of entrainment to exogenous 24-h periodicities are genetically controlled. Our results indicate that, despite the increased impact of social inputs, genetic factors also control human circadian rhythmicity.

In this paper, we present an automatic method for K-complexes detection based on features extraction and the use of fuzzy thresholds. The validity of our process was examined on the basis of two visual K-complexes scorings performed on 5 excerpts of 30 minutes. Results were investigated through all different sleep stages. The algorithm provides global true positive rates of 61.72% and 60.94%, respectively with scorer 1 and scorer 2. The false positive proportions (compared to the total number of visually scored K-complexes) are of 19.62% and 181.25%, while the false positive rates estimated on a one 1 second resolution are only of 0.53% and 1.53%. These results suggest that our approach is completely suitable since its performances are similar to those of the human scorers.

Recurrent brief depression (RBD) has recently been proposed as a new subtype of affective disorder characterized by episodes of major depression which last less than two weeks. The aim of this study was to further evaluate the validity of this putative subtype by means of clinical and biological data. DST, TSH response to TRH and sleep EEG variables were compared in 25 RBD patients sex- and age-matched to 25 major depressed (MD) and 25 healthy subjects. Family history, age at onset, and psychiatric comorbidity did not discriminate RBD from MD. Recurrent unipolar depression was found to be more prevalent in MD. Although less severely depressed during the biological tests, patients with RBD did not significantly differ from those with MDD on basis of DST non-suppression, blunted TSH response and shortening of REM latency. Compared to controls, a greater sleep onset latency was observed both in RBD and MD and a lower total sleep time in MD patients only. These results suggest that RBD could be viewed as a subtype of affective disorder sharing many characteristics with MDD.

Sleep EEG variables were compared in an adolescent population consisting of 11 anorectic girls, 11 young depressed patients and 11 healthy volunteers matched for age and sex. Anorectic patients differed from depressed patients in a greater number and a higher length of awakenings. In comparison with controls, anorectic patients showed less sleep efficiency, a higher length of awakenings and less REM sleep. When anorectic patients were divided in restricting and bulimic subtypes, the bulimic anorectics showed an increase in stage 3 of sleep. These results do not support a direct association between eating disorders and affective disorders. Sleep EEG variables were not significantly correlated to the Body Mass Index.

To delineate possible factors influencing the magnitude of the GH response to GH-releasing hormone (GHRH), eight young healthy men participated in seven 16-h studies involving saline infusions or injections of 0.3 micrograms/kg GHRH at various times of day and stages of sleep. GH responses were quantified by deconvolution, a procedure allowing for secretory rates to be estimated from peripheral levels. While the plasma responses were monophasic, deconvolution revealed that the secretory response to GHRH generally included several distinct bursts in rapid succession. The intersubject variability of GH responses was very wide, but for a given subject, the response was quite reproducible (mean +/- SEM coefficient of variation, 21 +/- 3%). When GHRH was given during the waking period, the magnitude of the response was directly related to the amount of spontaneous GH secretion, negatively correlated with circulating levels of insulin-like growth factor-I (IGF-I) and was not influenced by time of day. When GHRH was given during slow wave sleep, the magnitude of the response was enhanced. When GHRH was given during rapid eye movement sleep, the response was similar to that observed during wake. Awakenings during sleep consistently inhibited the secretory response to GHRH, and resumption of sleep was associated with a reappearance of the secretory process. Thus, in normal men of similar age and body weight, the GH response to GHRH is dependent on the sleep or wake condition, circulating levels of IGF-I, and, possibly, genetic and lifestyle factors.

Neuropeptide Y (NPY), a 36-amino-acid peptide from the pancreatic polypeptide family, is one of the more abundant peptides in the central nervous system. It acts as a neurohormone and as a neuromodulator. NPY is widely distributed in the brain, particularly the hypothalamus, the amygdala, the locus coeruleus and the cerebral cortex. At least six NPY receptors subtypes have been identified. NPY is involved in the regulation of several physiological functions such as food intake, hormonal release, circadian rhythms, cardiovascular disease, thermoregulation, stress response, anxiety and sleep. Sleep promoting effects of NPY as well as wakefulness effects of NPY were found in animals, depending on the site of injection as well as on the functional state of the structure. In humans, NPY was found to have hypnotic properties, possibly acting as a physiological antagonist of corticotropin-releasing hormone (CRH). In conclusion, NPY participates in sleep regulation in humans, particularly in the timing of sleep onset and may as such play a role in the integration of sleep regulation, food intake and metabolism.

In this paper, we present a series of algorithms for dealing with artifacts in electroencephalograms (EEG), electrooculograms (EOG) and electromyograms (EMG). The aim is to apply artifact correction whenever possible in order to lose a minimum of data, and to identify the remaining artifacts so as not take them into account during the sleep stage classification. Nine procedures were implemented to minimize cardiac interference and slow ondulations, and to detect muscle artifacts, failing electrode, 50/60Hz main interference, saturations, highlights abrupt transitions, EOG interferences and artifacts in EOG. Detection methods were developed in the time domain as well as in the frequency domain, using adjustable parameters. A database of 20 excerpts of polysomnographic sleep recordings scored in artifacts by an expert was available for developing (excerpts 1 to 10) and testing (excerpts 11 to 20) the automatic artifact detection algorithms. We obtained a global agreement rate of 96.06%, with sensitivity and specificity of 83.67% and 96.47% respectively.

Alterations of nocturnal sleep have been widely described in affective disorders. However, little is known about putative daytime sleep and to what extent daytime sleep could interfere with nocturnal sleep. The goal of this study was to investigate 24-hr sleep patterns in 12 depressed patients hospitalized for a major depressive disorder and in 10 control subjects studied under the same experimental conditions. Patients and controls were free to sleep whenever they chose, and sleep recordings were performed using the Oxford Medilog System during 60 hr. Daytime sleep episodes were detected in 50% of the patients and in 60% of the controls. Patients took naps at various times of the day, whereas controls napped in the early afternoon, during the well-known "postlunch dip". Thus daytime sleep prevalence was similar in both groups; however, the biphasic distribution of sleep observed in controls disappeared in the patients. Napping did not affect subsequent nocturnal sleep in either group.

Eight WHO research centres from Europe, North America and Asia took part in a WHO study aimed at assessing the reliability and consistency of sleep-EEG abnormalities in major depression. Each centre was asked to include in the study ten depressed patients aged 20–65 years meeting the Research Diagnostic Criteria for a major depressive disorder, and to match them by age and gender with ten controls. There were 67 patients and 66 controls included in the study. Compared with controls, depressed patients showed sleep-continuity disturbances such as increase in sleep-onset latency, and decrease in total sleep time and in sleep efficiency. Stages 2 and 3, as percentages of total sleep time, were reduced in depressed patients, REM latency was shortened and REM density increased. These findings confirm the presence of specific sleep-EEG abnormalities in major depression.

In order to investigate the genetic components of sleep and, in particular, of REM sleep, we performed 3 consecutive all-night EEG recordings in 26 pairs of normal male twins living apart (11 monozygotic and 15 dizygotic). Our results indicate that in man non-genetic rather than genetic influences substantially determine variance in stage REM, in contrast to stages 2, 4 and to delta sleep. In this sample of male twins, waking measures also showed a significant genetic component.

To delineate the physiological effects of aging on basal levels and temporal patterns of neuroendocrine secretions, the 24-h profiles of cortisol, thyroid-stimulating hormone (TSH), melatonin, prolactin, and growth hormone (GH) levels were simultaneously obtained at frequent intervals in eight healthy, active elderly men, age 67-84 yr and in eight young male adults, age 20-27 yr. The study was preceded by an extended period of habituation to laboratory conditions, and sleep was polygraphically recorded. Mean cortisol levels in the elderly were normal, but the amplitude of the circadian rhythm was reduced. Circulating levels of daytime and nighttime levels of both TSH and GH were greatly diminished in old age. In contrast, prolactin and melatonin concentrations were decreased during the nighttime only. The circadian rises of cortisol, TSH, and melatonin occurred 1-1.5 h earlier in elderly subjects, and the distribution of rapid-eye-movement stages during sleep was similarly advanced, suggesting that circadian timekeeping is modified during normal senescence. Despite perturbations of sleep, sleep-related release of GH and prolactin occurred in all elderly men. Age-related decreases in hormonal levels were associated with a decrease in the amplitude, but not the frequency, of secretory pulses. These findings demonstrate that the normal process of aging involves alterations in the central mechanisms controlling the temporal organization of endocrine release in addition to a reduction of secretory outputs.

In this paper, we introduce a new automatic method for electrocardiogram (ECG) artifact elimination from the electroencephalogram (EEG) or the electrooculogram (EOG). It is based on a modification of the independent component analysis (ICA) algorithm which gives promising results while only using a single-channel EEG (or EOG) and the ECG. To check the effectiveness of our approach, we compared its correction rate with those obtained by ensemble average subtraction (EAS) and adaptive filtering (AF). For this purpose, we applied these algorithms to 10 excerpts of polysomnographic sleep recordings containing ECG artifacts and other typical artifacts (e.g. movement, sweat, respiration, etc.). Two hundred successive interference peaks were examined in each excerpt to compute correction rates. We found that our modified ICA was the most robust to various waveforms of cardiac interference and to the presence of others artifacts, with a correction rate of 91.0%, against 83.5% for EAS and 83.1% for AF.

We introduce a new automatic method to eliminate electrocardiogram (ECG) noise in an electroencephalogram (EEG) or electrooculogram (EOG). It is based on a modification of the independent component analysis (ICA) algorithm which gives promising results while using only a single-channel electroencephalogram (or electrooculogram) and the ECG. To check the effectiveness of our approach, we compared it with other methods, that is, ensemble average subtraction (EAS) and adaptive filtering (AF). Tests were carried out on simulated data obtained by addition of a filtered ECG on a visually clean original EEG and on real data made up of 10 excerpts of polysomnographic (PSG) sleep recordings containing ECG artifacts and other typical artifacts (e.g. movement, sweat, respiration, etc.). We found that our modified ICA algorithm had the most promising performance on simulated data since it presented the minimal root mean-squared error. Furthermore, using real data, we noted that this algorithm was the most robust to various waveforms of cardiac interference and to the presence of other artifacts, with a correction rate of 91.0%, against 83.5% for EAS and 83.1% for AF., SCOPUS: ar.j, info:eu-repo/semantics/published

The objective of this study was to investigate the effects of age on women's performance in the psychomotor vigilance task (PVT) during total sleep deprivation (SD). A total of 46 healthy women volunteered. They belonged to two age groups: young (n=34; age range 19-30 years; 12 without, and 22 with oral contraceptives (OC); early phase of the menstrual cycle) and older (n=12; age range 60-68; postmenopausal; without hormone therapy). During a 40-h total SD, the subjects performed the PVT and the Stanford Sleepiness Scale (SSS) at 2-h intervals. At baseline, the reaction speed of the young women was faster as compared to the older women (Mann-Whitney U-test p

Objectives This study examines the effects of sleep restricted to 4 h for three consecutive nights on blood parameters known to be associated with cardiovascular risk in healthy postmenopausal women. Material and methods Ten healthy postmenopausal women aged 55–65 years treated with hormonal replacement therapy (HT) were included in the study. After one baseline night, three nights of sleep restricted to 4 h were performed and were followed by one recovery night of 8 h. Blood samplings were performed after the baseline night and after the third night of sleep restriction. Results A significant increase in white blood cells (WBC), monocytes, neutrophils, total cholesterol, and low density lipoprotein cholesterol (LDL-c) was observed after the third night of sleep restriction. Conclusion Sleep restriction to 4 h of sleep for three consecutive nights affected two factors associated with cardiovascular risk in healthy postmenopausal women treated with HT.

The aim of the present study was to investigate how three nights of sleep restriction affected cognitive functions in young and aged healthy women. Ten young (20-30 years) and ten aged (55-65 years) women participated to the study. After one baseline night (11 pm-07 am), their sleep was restricted to 4h per night (01-05 am) during three nights. A recovery night of 8h (11 pm-07 am) followed the sleep restriction. The neurobehavioural assessment included evaluation of Attention (Stroop, Trail Making test, Tests of Attentional Performance), Memory (Buschke, Logical Memory, PASAT, Brown Peterson), Addition of numbers and Abstraction (Wisconsin). Sleep restriction decreased significantly the speed of execution, particularly in the young women, without affecting the accuracy of the answers. This effect was the most significant on reaction times in simple tests. The more complex tasks (PASAT, Brown Peterson, Logical Memory, Addition of numbers, Wisconsin) were not affected. However, the inhibition of an automatic activity (Stroop test) and the formation of a memory trace (Buschke memory test) were disturbed in both young and older women.

Study Objectives: To investigate how age influences the effects of 3 nights of sleep restriction in healthy women. Design: After a baseline night, sleep was restricted to 4 hours during 3 consecutive nights. One recovery night followed the sleep restriction. Setting: The sleep-restriction experiments were conducted under standardized conditions with continuous electroencephalographic ambulatory recordings. Before entering the study, the subjects underwent a polysomnographic recording for exclusion of sleep disorder and adaptation to the laboratory environment. Participants: Eleven young women (aged 20-30 years) and 10 older women (aged 55-65 years) were included in the study. Intervention: The subjects were admitted to the sleep laboratory for 5 consecutive nights and days. After 1 baseline night, 3 nights of sleep restriction to 4 hours were performed and were followed by 1 recovery night of 8 hours. Continuous ambulatory electroencephalographic recordings were performed, as well as the Maintenance of Wakefulness Test (8:30 AM and 1:30 PM), the Stanford Sleepiness Scale, and the Psychomotor Vigilance Test. Results: Young women were more affected by sleep restriction than were the older women. This was evidenced by more sleep onsets during the Maintenance of Wakefulness Test sessions in the young subjects, who also rated themselves more sleepy than the older women. Conclusions: Age influences the impact of sleep restriction on vigilance in women.

Background: Recent reports have identified the apnoea and hypopnoea index (AHI) as an additional independent risk factor for cardiovascular morbidity and mortality. However, several studies reported contradictory results about the association between the serum C-reactive protein (CRP) level and the severity of apnoea. Objective: The purpose of this work is to study this association in patients referred to the sleep laboratory for clinical suspicion of sleep apnoea and presenting a wide range of AHI. Methods: Forty-nine consecutive patients were included in the study. The SigmaStat® software package (Jandle Scientific) was used. Multilinear regression analysis was tested using a stepwise backward selection of the explicative variables. The clinical characteristics (diabetes, hypertension, smoking habits, gender) were treated as dichotomous variables, while all other data (age, BMI, lipids, white blood cells) were continuous ones; high-sensitivity (hs)-CRP was the dependent variable. Results: In univariate analysis, AHI was correlated to hs-CRP: R = 0.43, p = 0.002. In multivariate analyses, we found an independent association between the AHI, adjusted for classical cardiovascular risk factors, and hs-CRP. Conclusion: In a sample of 49 patients, referred to the sleep laboratory for suspicion of sleep apnoea in routine practice, we observed an independent association between the AHI and hs-CRP.

Several sleep complaints and disturbances have been documented in psychiatric disorders. These modifications of sleep in anxiety disorders, alcoholism, schizophrenia, dementia and eating disorders are reviewed and discussed. At the present time, there is no evidence for any specific sleep pattern in non-affective psychiatric disorders. The co-morbidity of sleep disorders like sleep apnoea, periodic leg movements and parasomnia in psychiatric illness is not very well known at the present time.

Study objectives: Auto-continuous positive airway pressure (CPAP) has been reported to have no more efficacy than constant CPAP in unselected patients with sleep apnea hypopnea syndrome (SAHS). The aim of this study was to evaluate patients judged to be good candidates for auto-CPAP because of a high within-night variability in pressure requirement. Design: Single-blind, randomized, cross-over study (2 8 weeks) to compare auto-CPAP with constant CPAP. Patients: Outpatients with moderate-to-severe SAHS attending the chest clinic. Interventions: Patients were equipped at home in the auto-CPAP mode (model GK418A; Malinckrodt; Nancy, France), using a 4- to 14-cm H2O pressure range. Those individuals having a high within-night variability in pressure requirement, assessed at the end of a 14-day run-in period, were included in the cross-over study. Auto-CPAP was compared with constant CPAP (according to a titration night in the sleep laboratory) in terms of compliance, efficacy on apneas (assessed from the pressure monitor), and sleepiness (assessed on the Epworth sleepiness scale). Measurements and results: Of 90 consecutive patients with SAHS, 27 patients were selected for a within-night variability in pressure requirement exceeding a given threshold. After completion of the cross-over, 24 patients were evaluable. The median percentage of nights the machine was used was 95.5% (range, 45 to 100%) on constant CPAP, and 96.5% (range, 40 to 100%) on auto-CPAP; the median apnea index recorded by the device was 0.40/h (range, 0 to 2.40/h) on constant CPAP, and 0.45/h (range, 0 to 5.80/h) on auto-CPAP (differences not significant). The mean Epworth sleepiness score was significantly (p < 0.01) lower on auto-CPAP (5.1; SD, 2.8) than on constant CPAP (6.1; SD, 2.8). Conclusions: In patients selected for a high within-night variability in pressure requirement, auto-CPAP administered via a GK418A device was equivalent to constant CPAP based on a titration night in the sleep laboratory. Subjective ratings for sleepiness were slightly lower on auto-CPAP. (CHEST 2004; 126:31–37)

A huge amount of knowledge about sleep has accumulated during the last 5 decades following the discovery of rapid eye movement (REM) sleep. Nevertheless, there are numerous areas of considerable ignorance. One of these concerns the particularities of sleep in women. Most basic and clinical studies have been performed in male subjects, and only very recently research groups around the world have addressed women's sleep in health and disease. In this review, we summarize the present knowledge on the influence of oestrogens on the brain and on the distinctive changes of sleep across the menstrual cycle, during pregnancy and menopause. In addition, studies in female rodents are reviewed as well as the knowledge on female peculiarities regarding the interactions between sleep regulation and age-related changes in circadian rhythms. We also address specific aspects of sleep loss and sleep disorders in women. Finally, very recent studies on the sociology of sleep are summarized and future directions in the field are discussed.