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PubMed2002

Sleep and sleep-wake manipulations in bipolar depression.

In the last 30 years, it has been convincingly demonstrated that sleep in major depression is characterized by disturbances of sleep continuity, a reduction of slow wave sleep, a disinhibition of REM sleep including a shortening of REM latency (i.e. the time between sleep onset and the occurrence of the first REM period) and an increase in REM density. Furthermore, manipulations of the sleep-wake cycle like total or partial sleep deprivation or phase advance of the sleep period have been proven to be effective therapeutic strategies for patients with unipolar depression. The database concerning sleep and sleep-wake manipulations in bipolar disorder in comparison is not yet as extensive. Studies investigating sleep in bipolar depression suggest that during the depressed phase sleep shows the same stigmata as in unipolar depression. During the hypomanic or manic phase, sleep is even more curtailed, though subjectively not experienced as disturbing by the patients. REM sleep disinhibition is present as well. An important issue is the question, whether sleep-wake manipulations can also be applied in patients with bipolar depression. Work by others and our own studies indicate that sleep deprivation and a phase advance of the sleep period can be used to treat bipolar patients during the depressed phase. The risk of a switch into hypomania or mania does not seem to be more pronounced than the risk with typical pharmacological antidepressant treatment. For patients with mania, sleep deprivation is not an adequate treatment--in contrast, treatment strategies aiming at stabilizing a regular sleep-wake schedule are indicated.

Animals↗
PubMed2006

Non-rapid eye movement sleep with low muscle tone as a marker of rapid eye movement sleep regulation.

BACKGROUND: It was recently reported that epochs of non-REM sleep (NREMS) with low muscle tone represent a partial correlate of REM sleep (REMS). To further investigate this phenomenon, episodes of restricted night-time sleep (23:00-03.00 h) and subsequent morning sleep (10:00-13:00 h) were analysed. RESULTS: Epochs of NREMS with low muscle tone (NLMT) were identified. Their frequency was higher in morning sleep than in night sleep. At night, the latency to the first occurrence of NLMT showed a bimodal distribution with modes at sleep onset and close to REMS onset. In morning sleep, the distribution was unimodal with the mode at sleep onset. An episode of NLMT at sleep onset occurred in 35.5% of the night sleep episodes and in 60.9% of the morning sleep episodes without sleep onset REMS (SOREMS). Also SOREMS occurred predominantly in morning sleep. REMS episodes were longer and NREMS episodes shorter in morning sleep than in night sleep, whereas cycle duration did not differ. Simulating the time course of slow-wave activity revealed a close correspondence between empirical and computed values for night sleep, and some discrepancies for morning sleep. CONCLUSION: The results provide further evidence that NREMS with low muscle tone is a marker of REMS regulation. NLMT at sleep onset may represent an early manifestation of REMS.

Adult↗
PubMed2004

SLEEP (Sleep Loss Effects On Everyday Performance) Model.

Sleep management affects human productivity, safety, health, and efficiency in the performance of various tasks. Most people seem to be unaware of the value and role of sleep and the various risks that can occur when less than desired amounts of sleep are obtained. People especially seem to be unaware of the dangers associated with the long-term accumulation of reduced sleep. Thus, a need exists to provide tools to enhance sleep education. This paper presents an overview of a sleep simulation and sleep education tool, the SLEEP (Sleep Loss Effects on Everyday Performance) Model. The SLEEP Model includes alcohol and caffeine along with sleep as variables that affect performance. Assumptions and modeling concepts are discussed, and the major mathematical functions are presented as part of this paper. The unique features of the SLEEP Model are: 1) it is based on conservation of REM sleep; 2) it uses a ratio of current day's sleep to sleep need for the day to adjust performance predictors; 3) it is designed for easy input and output of information; and 4) it has a wide range of applications, including sleep, alcohol, and caffeine management. Generally the mathematical functions used in the SLEEP Model fit the calibration data set with an R2 of 0.8 or better and have statistical significance at least at the 0.05 probability level. Several figures of simulated results are presented with a discussion of references that report similar measured results. The SLEEP Model appears to be a practical tool to teach people the value of proper sleep management.

Alcohol Drinking↗
PubMed1980

Distribution of REM sleep in entrained 24 hour and free-running sleep--wake cycles.

One hundred thirty sleep episodes of 6 subjects, living on a natural 24 hr day, were compared with 116 sleep times of the same subjects living isolated from external time cues. The polygraphic sleep recordings were analyzed for the distribution of REM sleep under both conditions. Additionally, the relationship between body temperature and REM sleep was analyzed by comparing sleep episodes in which the temperature minimum occurred early in the sleep episode with those in which there was a late temperature minimum. The results show that there is more REM sleep in the beginning of sleep in sleep episodes of free-running rhythms as compared to sleep episodes of entrained 24 hr rhythms. This higher amount of REM sleep is due to a longer first REM episode and shorter first NREM episodes. The comparison of the sleep episodes that differ in the position of the temperature minimum shows similar differences, i.e., more REM sleep in the beginning of sleep episodes in which the temperature minimum occurs earlier as compared to episodes in which the temperature minimum occurs later. It was hypothesized that the amount of REM sleep depends on the phase relationship between sleep and the circadian temperature cycle. From this point of view, the difference in the distribution of REM sleep in the entrained 24 hr rhythm, on the one hand, and the free-running rhythm, on the other hand, can be explained by the different courses of body temperature during sleep. That only the first REM episode is influenced by circadian parameters may indicate an exceptional role for this REM episode in contrast to the following episodes.

Adult↗
PubMed2000

Critical evaluation of the effect of valerian extract on sleep structure and sleep quality.

A carefully designed study assessed the short-term (single dose) and long-term (14 days with multiple dosage) effects of a valerian extract on both objective and subjective sleep parameters. The investigation was performed as a randomised, double-blind, placebo-controlled, cross-over study. Sixteen patients (4 male, 12 female) with previously established psychophysiological insomnia (ICSD-code 1.A.1.), and with a median age of 49 (range: 22 to 55), were included in the study. The main inclusion criteria were reported primary insomnia according to ICSD criteria, which was confirmed by polysomnographic recording, and the absence of acute diseases. During the study, the patients underwent 8 polysomnographic recordings: i.e., 2 recordings (baseline and study night) at each time point at which the short and long-term effects of placebo and valerian were tested. The target variable of the study was sleep efficiency. Other parameters describing objective sleep structure were the usual features of sleep-stage analysis, based on the rules of Rechtschaffen and Kales (1968), and the arousal index (scored according to ASDA criteria, 1992) as a sleep microstructure parameter. Subjective parameters such as sleep quality, morning feeling, daytime performance, subjectively perceived duration of sleep latency, and sleep period time were assessed by means of questionnaires. After a single dose of valerian, no effects on sleep structure and subjective sleep assessment were observed. After multiple-dose treatment, sleep efficiency showed a significant increase for both the placebo and the valerian condition in comparison with baseline polysomnography. We confirmed significant differences between valerian and placebo for parameters describing slow-wave sleep. In comparison with the placebo, slow-wave sleep latency was reduced after administration of valerian (21.3 vs. 13.5 min respectively, p<0.05). The SWS percentage of time in bed (TIB) was increased after long-term valerian treatment, in comparison to baseline (9.8 vs. 8.1% respectively, p<0.05). At the same time point, a tendency for shorter subjective sleep latency, as well as a higher correlation coefficient between subjective and objective sleep latencies, were observed under valerian treatment. Other improvements in sleep structure - such as an increase in REM percentage and a decrease in NREM1 percentage - took place simultaneously under placebo and valerian treatment. A remarkable finding of the study was the extremely low number of adverse events during the valerian treatment periods (3 vs. 18 in the placebo period). In conclusion, treatment with a herbal extract of radix valerianae demonstrated positive effects on sleep structure and sleep perception of insomnia patients, and can therefore be recommended for the treatment of patients with mild psychophysiological insomnia.

Adult↗
PubMed2001

Sleep and daytime sleepiness in upper airway resistance syndrome compared to obstructive sleep apnoea syndrome.

This study has investigated differences in the nocturnal sleep and daytime sleepiness among patients with obstructive sleep apnoea syndrome (OSAS), upper airway resistance (UARS), sleep hypopnoea syndrome, and normal control subjects, using sleep scoring and spectral activity analysis of the electroencephalogram (EEG). Twelve nonobese males with UARS aged 30-60 yrs were recruited. These subjects were strictly matched for age and body mass index with twelve OSAS patients, 12 sleep hypopnoea syndrome patients, and 12 normal controls, all male. Daytime sleepiness was evaluated using the Epworth Sleepiness Scale (ESS) and the Multiple Sleep Latency Test (MSLT). The macrostructure of sleep was determined using international criteria and spectral analysis of the sleep EEG was obtained from a central lead. The sleep macrostructure of OSAS and UARS patients was significantly different from that of controls. These patients were also sleepier during the daytime than controls. Complaints of tiredness and daytime sleepiness, ESS and MSLT scores were similar in the different patient groups. Mild dysmorphia was present in all three patient groups. However, nocturnal sleep was significantly different among the different groups. OSAS patients had significantly more awake time during sleep than the UARS patients. The spectral activity of the total sleep time of the patient groups also differed significantly from that of controls. When the sleep spectral activity of UARS and OSAS patients were compared, OSAS patients had less slow wave sleep activity than UARS patients. UARS patients had a significantly higher absolute power in the 7-9 Hz bandwidth than OSAS patients. The absolute delta power over the different sleep cycles was also different between controls and patients, and between UARS and OSAS patients. There are clear differences in the macrostructure and spectral activity of sleep between upper airway resistance and obstructive sleep apnoea syndrome patients, demonstrated by differences in the cortical activity recorded in the central lead during sleep. Despite these nocturnal sleep differences, the tests of subjective daytime sleepiness are not significantly different.

Adult↗
PubMed1976

Effect of normal and reversed sleep-wake cycles upon nyctohemeral rhythmicity of plasma thyrotropin: evidence suggestive of an inhibitory influence in sleep.

The relation of nyctohemeral variation in plasma TSH to sleep-wake cycles was examined in 10 normal young men who had their sleep polygraphically monitored and their blood sampled every 20 min for 24,36, or 48 h periods. Studies of normal sleepwake cycles in which sleep was allowed from the usual bedtime to 0630 h totalled 21 nights (night = 1840-0620 h) and their corresponding 16 days. TSH was measured by a sensitive RIA. On 17 nights, the mean nightly TSH significantly exceeded that of the day's and, on 18 nights, clear nyctohemerally maximal peaks in TSH were seen in the 2100-0100 h interval. Greater amplitude, duration and rhythmic repetition over several nights distinguished 2100-0100 h maxima from a background of persistent briefly episodic release. These nyctohemeral peaks were pre-sleep maxima, as rises uniformly began, and on 15 nights, the peaks occurred prior to the onset of sleep. The peaks clustered within the 30 min just before (12 nights) or after (3 nights) entry into sleep. TSH release then declined across sleep. Other evidence suggestive of an inhibitory influence in sleep upon TSH release was that sleep began early on the 3 nights without clear 2100-0100 h TSH maxima and that the mean 2100-0100 h TSH peak was significantly reduced when sleep began prior to the usual 2300-0000 h interval and significantly increased when the onset of sleep was delayed or postponed. After a 24 h baseline, 4 men underwent phase-reversal of their sleep-wake cycles for 48 h, in which sleep was shifted to the 1100-1830 h interval. On the first wakeful night of reversal, the 2100-0100 h peak began normally, but, in the absence of sleep, the enhanced TSH release then simply continued across this night, delaying achievement of the nyctohemeral maxima. On the second wakeful night of reversal, the maximum in mean TSH lay in the same 0400-0600 h interval as that of first reversal night, and the mean 2100-0100 h peak was no longer evident. The TSH of the second 24 h of reversal also was significantly reduced, suggestive of a negative feedback effect of enhanced release of the first reversal day. No shift of basal pre-sleep TSH peaks to the 0900-1300 h interval or of sleep-enhanced TSH release was seen during reversal. Thus, despite the persistence of TSH's nyctohemeral rhythmicity across acute sleep-wake reversal, its pattern changed significantly in relation to shifts in sleep. We currently view these results as consistent with the origin of TSH's nyctohemeral rhythmicity in a circadian mechanism whose expression is subject to modulation by the inhibitory influences of feedback and sleep.

Circadian Rhythm↗
PubMed2003

Outcomes of infant sleep problems: a longitudinal study of sleep, behavior, and maternal well-being.

OBJECTIVES: In a community sample of children aged 3 to 4 years with previous infant sleep problems, we aimed to 1) establish proportions with recurring, persisting, and resolving sleep problems; 2) identify early predictors of later sleep problems; and 3) identify comorbidities of persistent or recurrent sleep problems at age 3 to 4 years. METHODS: A follow-up community survey was conducted of mothers of children aged 3 to 4 years who had, as 8- to 10-month-old infants with identified sleep problems, participated in a community-based, randomized, controlled trial of a brief sleep intervention from 3 middle-class local government areas in Melbourne, Australia. Infant sleep problems (standardized maternal questionnaire), maternal well-being (Edinburgh Postnatal Depression Scale), child behavior problems (Child Behavior Check List for ages 1.5 to 5 years), marital satisfaction (Dyadic Adjustment Scale), and family functioning (General Functioning Scale, McMaster Family Assessment Device) were measured. RESULTS: Seventy-three percent (114 of 156) of mothers responded, 36 (32%) of whom reported a current problem with their child's sleep. Current sleep problems were similar regardless of infant sleep intervention. Twelve percent (14 of 114) reported that their child's sleep problem had persisted, and 19% (21 of 113) reported that it had recurred. Children with current sleep problems were more likely still to be nursed to sleep by an adult and had slightly higher mean scores on Child Behavior Check List subscales for Aggressive Behavior (54 vs 52) and Somatic Problems (55 vs 53). Their mothers had higher Edinburgh Postnatal Depression Scale scores (median: 8 vs 5) and more difficulties with their partner undermining the management of their child. However, early depression did not predict current sleep problems. Families of children with sleep problems were functioning as well as those without sleep problems. CONCLUSIONS: Persistence or recurrence of infant sleep problems in the preschool years is common and is associated with slightly higher child behavior problems and maternal depression scores. Results suggest that depressive symptoms are a result rather than cause of sleep problems. Despite this, families of children with sleep problems are functioning well.

Australia↗
PubMed1994

The subjective meaning of good sleep, an intraindividual approach using the Karolinska Sleep Diary.

The present experiment used an intraindividual design to investigate the meaning and measurement of "good sleep". Each of 16 subjects slept in an isolation unit according to a schedule (15 sleeps) designed to give variable quality of sleep. Self-rated sleep measures (from the Karolinska Sleep Diary) were obtained after each sleep and subjected to intraindividual regression analyses across time. Most subjective sleep measures showed a strong covariation across conditions. Subjective quality of sleep mainly involved variables of sleep continuity, in particular, perceived calmness of sleep and sleep efficiency. "Sleep quality," "calm sleep," "ease of falling asleep," and ability to "sleep throughout" the time allotted strongly covaried and formed an index of sleep quality. Self-rated ease of awakening deviated from the general pattern and was associated with poor sleep quality. So was reported dreaming (related to awakenings). It was concluded that most subjective sleep measures tend to covary across conditions and that "good sleep" is mainly a question of sleep continuity.

Adolescent↗
PubMed1993

Effect of SCN lesions on sleep in squirrel monkeys: evidence for opponent processes in sleep-wake regulation.

Sleep and wakefulness are governed by both the suprachiasmatic nuclei of the hypothalamus (SCN), and a sleep homeostatic process; however, the interaction of these control systems is not well understood. From rodent studies it has been assumed that the SCN promote neither wake nor sleep but gate the homeostatic sleep-promoting process. Yet in humans sleep tendency is lowest during the later waking hours of the day, and sleep duration can be predicted because of the precise circadian timing of waking. Thus in primates, the SCN could assure sleep-wake cycle consolidation by actively promoting or facilitating wakefulness. To evaluate this hypothesis, we examined the sleep-wake and sleep-stage patterns of intact and SCN-lesioned (SCNx) squirrel monkeys maintained in constant light. This diurnal primate has consolidated sleep and wake patterns more similar to man than rodents. Sleep-wake, sleep stages, brain temperature, and drinking circadian rhythms were eliminated, and total sleep time was significantly increased (4.0 hr, P < 0.01) in SCNx monkeys. However, total times in deeper stages of non-rapid eye movement (non-REM; e.g., delta sleep) and REM sleep were not significantly affected by SCN lesions. Increased total sleep time was associated with a reduction in subjective day wake consolidation, as evidenced by substantially shorter wake bout lengths in SCNx monkeys (15 +/- 6 min) as compared to intact monkeys (223 +/- 10 min; P < 0.0001, ANOVA). These findings show that the SCN influence the regulation of daily total wake and sleep times, and implicate an alternative sleep-wake regulatory model in which an SCN-dependent process actively facilitates the initiation and maintenance of wakefulness and opposes homeostatic sleep tendency during the subjective day in diurnal primates.

Analysis of Variance↗
PubMed1993

Dynamics of electroencephalographic sleep spindles and slow wave activity in men: effect of sleep deprivation.

Recent developments in the understanding of the neurophysiological mechanisms underlying electroencephalographic (EEG) slow waves and sleep spindles imply an inverse relationship between these two EEG activities. The interrelationship between slow wave activity (0.75-4.5 Hz) and sleep-spindle activity (12-15 Hz) in electroencephalograms recorded in nine male subjects, during nocturnal baseline sleep and during recovery sleep from 40 h of wakefulness, was analyzed by power spectral analysis based on the fast Fourier transform and by transient patterns detection algorithms. Both techniques revealed that spindle activity was highest in sleep stage 2, increased over consecutive non-rapid-eye-movement sleep (non-REM sleep) episodes and was suppressed during recovery sleep. In contrast, slow wave activity decreased over consecutive non-REM sleep episodes and was enhanced during recovery sleep. Analysis of the dynamics of spindle and slow-wave activity within non-REM sleep episodes demonstrated that in the initial 20% of these episodes both spindle activity and slow wave activity increased, whereafter slow wave activity continued to increase but the average amplitude of spindles and total spindle activity, but not spindle density, decreased. At the end of non-REM sleep episodes the reverse pattern was observed. Sleep deprivation induced a more rapid rise of both spindle and slow wave activity in the very beginning of sleep. These data demonstrate that when averaged per sleep episode or non-REM sleep episode an inverse relationship between SWA and spindle activity exists but that in the initial and final part of non-REM sleep episodes the association between these two activities is positive. This biphasic relationship is discussed with reference to the hypothesis that the transition from sleep spindles to slow waves is dependent on a progressive hyperpolarization of thalamo-cortical neurons.

Adult↗
PubMed2006

Effects of alcohol on sleep and the sleep electroencephalogram in healthy young women.

BACKGROUND: Although the association between sleep and alcohol has been of interest to scientists for decades, the effects of alcohol on sleep and sleep electroencephalogram (EEG) have not been extensively studied in women. Our specific aim was to determine whether sleep stage variables and/or spectral characteristics of the sleep EEG are altered by alcohol administration in women. METHODS: Changes of sleep and the sleep EEG were investigated after administration of a moderate dose of alcohol (0.49 g/kg) in the hour before bedtime compared with placebo in young healthy women. After approximately 2 weeks at home on a fixed 8.5- or 9-hour stabilization sleep schedule, sleep was continuously recorded by polysomnography for 3 consecutive nights [adaptation, placebo, alcohol (mean breath alcohol concentration 0.043 g/% before bedtime)] in the laboratory in 7 women (ages 22-25, mean=23.5, SD=1 year). Sleep stages were scored according to conventional criteria. Electroencephalogram power spectra of the bipolar derivations Fz/Cz (anterior) and Pz/Oz (posterior) were calculated using a fast Fourier transform routine. RESULTS: Only few changes in sleep and the sleep EEG were observed. Across the entire night rapid eye movement (REM) sleep decreased, while minutes of stage 4 sleep were increased in the first 2-hour interval on alcohol nights compared with placebo nights. Spectral analysis of the EEG showed increased power in the alpha range (9-11 Hz) during all-night non-REM (NREM) sleep in anterior derivations after alcohol compared with placebo. Differences in spectral EEG power were also present in 2-hour intervals of NREM sleep; in particular, EEG power was increased on the alcohol night for frequency bins within the alpha range in anterior derivations and within the delta range (3-4 Hz) in posterior derivations during the initial part of the night. CONCLUSIONS: A moderate dose of alcohol just before bedtime resulted in a short-lived increase in sleep intensity. A limitation of the study, however, was that only a single dose of alcohol was used to examine the effects of alcohol on sleep.

Adult↗
PubMed2000

Placebo-controlled sleep laboratory studies on the acute effects of zolpidem on objective and subjective sleep and awakening quality in nonorganic insomnia related to neurotic and stress-related disorder.

UNLABELLED: Recent investigations in our sleep outpatient clinic demonstrated that 30% of patients exhibited organic and 70% nonorganic sleep disorders, with 41% showing as an additional diagnosis neurotic, stress-related, and somatoform disorders, 31% affective disorders and 15% mental and behavioral disorders due to psychoactive substance use. Thus, the aim of the study was to investigate the acute effects of the imidazopyridine zolpidem on objective and subjective sleep and awakening quality in the largest of the above-mentioned groups. In this single-blind, placebo-controlled cross-over study, 15 patients (9 females and 6 males aged 51.1 + 11. 3 years) diagnosed as having nonorganic insomnia (ICD-10: F 51.0) related to neurotic and stress-related disorders (F 1.1:12, F 41.2:2 and F 43.2:1) were included. Objective and subjective sleep and awakening quality measures were investigated in 3 subsequent nights in the sleep laboratory (adaptation, baseline/placebo and zolpidem 10 mg night), utilizing clinical, polysomnographic, psychometric and psychophysiological methods. The drug-free patients were matched according to age and sex with 15 normal healthy controls (age 51.2 + 11.8 years). Statistical analysis of polysomnographic variables demonstrated a significant lengthening of the total sleep period (TSP) and total sleep time (TST), an improvement in sleep efficiency and a shortening of sleep latencies after zolpidem as compared with placebo. These changes were opposite to the differences between patients and controls. Concerning sleep architecture, zolpidem increased the length of S4 and S3 + S4 as compared with placebo. Subjective sleep and awakening quality and the thymopsychic variables drive, mood, affectivity and wakefulness in the morning showed no significant changes, as a significant improvement had already occurred from the adaptation to the baseline/placebo night. Noopsychic variables (attention, concentration, attention variability, numerical memory, fine motor activity, reaction time measures) showed similar findings. Moreover, subjective sleep and awakening quality, thymopsychic and noopsychic measures during baseline/placebo recordings did not differ significantly from normative data (except for fine motor activity). Psychophysiological measures did not show any significant alterations either, except for a decrease in systolic blood pressure in the evening. CONCLUSION: As compared with placebo, zolpidem induced a significant improvement in objective sleep quality, mainly by increasing TSP, TST and sleep efficiency and shortening sleep latencies, thereby normalizing the disorder of initiating and maintaining sleep. Deep sleep stages S3 + S4 increased (although at baseline/placebo these stages did not differ from controls), while S1, S2 and SREM did not change significantly. Subjective sleep and awakening quality as well as thymopsychic and noopsychic performance in the morning mainly showed a placebo and 'first- night effect' phenomenon in these patients. Thus, the changes induced by zolpidem were somewhat different from those after classical benzodiazepines.

Cross-Over Studies↗
PubMed2000

Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentrations of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin. In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography. Sleep onset was associated with an increase in serum levels of IL-6 (P < 0.05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1-2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melatonin showed no concordance with sleep. Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning. Alternatively, given the association between sleep stages and IL-6 levels, depressed or aged populations who show increased amounts of REM sleep and a relative loss of slow wave sleep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.

Adult↗
PubMed1998

Differences in self-reported sleep complaints in elderly persons living in the community who do or do not take sleep medication.

BACKGROUND: Sleep disorders and the use of sleep medication are major health issues. Since complaints about sleep disturbances are subjective phenomena, the aim of the present study was to investigate which sleep complaints and self-reported disturbances of sleep behavior are connected with the utilization of sleep medication. METHOD: In the Berlin Aging Study, a random sample of 516 persons aged 70 to over 100 underwent extensive psychiatric and medical examinations including several medication assessments and a special interview on sleep complaints and sleep behavior. RESULTS: 19.1% of the elderly were taking some form of sleep medication. Univariate and discriminant analyses showed that neither self-reported duration of sleep time nor difficulties with sleeping through the night but complaints about difficulties initiating sleep and global complaints about disturbed sleep differentiated between those who do or do not take sleep medication. CONCLUSION: Persons taking sleep medication nevertheless have a higher rate of sleep-related complaints than those who take no medication. Waking up in the night per se does not discriminate between drug users and controls. Instead, it is the inability to fall asleep or fall back into sleep after waking and global discontent with subjective sleep quality that make a difference.

Age Distribution↗
PubMed2005

Night sleep EEG and daytime sleep propensity in adult hypopituitary patients with growth hormone deficiency before and after six months of growth hormone replacement.

BACKGROUND: Hypopituitary patients with growth hormone deficiency (GHD) complain of reduced vitality, general fatigue, lack of concentration, irritability and reduced alertness during daytime. It is unclear whether these symptoms are primarily due to GH-deficiency and/or secondary to GHD related sleep impairments. Bi-directional interactions between the somatotropic system and human sleep patterns are well established. However, data on the effect of GH either in subjects without GHD or in patients with GHD under GH replacement therapy on the sleep electroencephalogram (EEG) are controversial. No reports exist about objective measures of daytime sleepiness in GH deficient patients before and during GH-therapy. OBJECTIVE: To assess the effects of GH on nocturnal and daytime sleep in adult patients with GHD before and during recombinant human GH (rhGH, Somatropin) replacement therapy. METHODS: Eighteen adult patients with GHD (4 women and 14 men) participated in the study. Mean age at the beginning of the study was 48.5 years (range 27-64 years). Ten patients were recruited from a double-blind, randomized placebo controlled trial over 6 months, followed by an open treatment period of 6 additional months (Group I). In all patients from this group, only the effects of the first 6 months of GH treatment were assessed. Eight additional patients were treated in an open study design for 6 months (Group II). Nocturnal sleep recordings and daytime sleep EEGs with a multiple sleep latency test were performed at baseline and after 6 months of additional GH replacement therapy. RESULTS: One patient dropped out due to side effects and was not included in sleep analysis. IGF-1 levels were increased in all patients, partially in a supraphysiologic range. Side effects were mainly mild but in one patient (from group II), general muscle pain led to interruption of the study. Therefore sleep analysis was only done in 17 patients. Sleep parameters were comparable to healthy control groups from the literature. GH substitution over 6 months did neither affect total sleep time nor times spent in different sleep stages. REM sleep density was also not changed. Daytime sleep propensity as measured by the multiple sleep latency test was not influenced by GH treatment. CONCLUSIONS: GH replacement does neither affect night sleep nor daytime sleep propensity in GH deficient hypopituitary adults. GH substitution has no sleep disturbing effect.

Adenoma↗
PubMed2002

Sleep deprivation as a probe of homeostatic sleep regulation in primary alcoholics.

BACKGROUND: Alcoholic patients show prominent disturbances of sleep electroencephalograms (EEGs) with a marked loss of slow wave sleep that is even more profound in African American alcoholics as compared to European Americans. Using partial sleep deprivation, this study examined the extent to which abnormal sleep is reversible in alcoholic subjects. METHODS: In a sample stratified on ethnicity, polysomnographic and spectral sleep EEG measures were compared in male primary alcoholic in patients (n=46) and age-matched comparison controls (n=32) at baseline-and recovery sleep following a night of partial sleep deprivation. RESULTS: As compared to controls, alcoholic patients showed a loss of slow wave sleep and more spectral power in beta frequencies. Following sleep deprivation, slow wave sleep and delta power differentially changed between the groups. European American controls showed increases of slow wave sleep that were more robust than responses found in African American controls, whereas both alcoholic groups failed to show increases of slow wave sleep from baseline to recovery. Spectral EEG analyses revealed similar results; sleep deprivation induced significant increases of delta power during NREM-1 in the controls, but not in the alcoholics. CONCLUSIONS: Alcohol dependence compromises the augmentation of slow wave sleep and delta power seen in healthy adults following sleep deprivation. The differential effect of alcoholism on sleep stage physiology suggests a defect in the regulation or plasticity of slow wave sleep with implications for theories linking sleep depth to morbidity and outcome in alcoholics.

Adult↗
PubMed2004

Age-related sleep change: Gender and estrogen effects on the subjective-objective sleep quality relationships of healthy, noncomplaining older men and women.

OBJECTIVE: The sleep of a large group of healthy older men and women was studied in an effort to better understand the relationship between self-reported subjective and objectively measured sleep quality. METHODS: We examined the baseline subjective and objective sleep quality of 150 healthy older (67.5+/-0.5) men (n=55) and women (n=95). Subjects were carefully screened to exclude sleep disorders and did not complain of significant sleep disturbance. RESULTS: Despite their noncomplaining status, significant proportions of both women (33%) and men (16%) endorsed Pittsburgh Sleep Quality Index (PSQI) scores of >5, a criterion indicative of significant sleep disturbance. When examined as a function of this criterion, objective sleep was significantly impaired with longer sleep latency, less total sleep time, and lower sleep efficiency, for the high-PSQI (H-PSQI) men compared to low-PSQI (L-PSQI) men. These L-PSQI versus H-PSQI differences were much weaker for women and disappeared completely in women on estrogen replacement therapy. CONCLUSIONS: This large group of healthy, noncomplaining older adults manifested significantly disturbed sleep relative to healthy younger subjects, indicating that while aging results in significant changes in sleep, it does not of necessity result in complaints of insomnia and that many healthy older individuals apparently adapt their perception of what is "acceptable" sleep. A considerable correspondence between subjective and objective sleep quality was observed for men but not for women, despite women more frequently endorsing the presence of significant sleep disturbance. This finding is provocative and suggests that what we consider objective measures of good-quality sleep may be appropriate for older men but that older women may be evaluating their sleep quality using other criteria.

Aged↗