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The Pittsburgh study of normal sleep in young adults: focus on the relationship between waking and sleeping EEG spectral patterns.

The effects of age and gender on spectral characteristics of the waking EEG were investigated in a large sample of young adult men and women. In addition, relationships between spectral characteristics of the waking and sleeping EEG within an individual were explored. The sample included 28 females and 33 males in two age groups: 20-29 years (n = 32), and 30-40 years (n = 29). Spectral analysis was used to quantify EEG frequency characteristics for waking EEG just prior to sleep onset, as well as for the entire sleep recording. Significant effects of age were seen in the waking EEG but only in the delta frequency range (0.5-4.5 Hz) with lower delta activity in the older group (F = 11.6, P = 0.001). No significant gender effects were found in the waking EEG. Independent of age and gender, spectral profiles in the delta, theta, alpha and beta frequency bands of a subject's waking EEG were found to be highly correlated with their sleep EEG. In addition, subjects with high voltage alpha profiles during waking were found to sleep significantly longer and deeper than those with low voltage records. Significant correlations between waking and sleep EEG suggest that the spectral signature of an individual's EEG may be found across sleep/wake states.

Adult↗

Effects of REM sleep awakenings and related wakening paradigms on the ultradian sleep cycle and the symptoms in depression.

In 1975 Vogel and coworkers published their classical study where they compared selective rapid eye movement (REM) sleep deprivation by brief awakenings to a control intervention paradigm in depressed patients. The superior antidepressive impact of the first procedure was attributed to the REM pressure accumulating during the treatment period. The laborious procedure and the considerable effort necessary to evaluate the sleep profiles in real time have prevented similar experiments so far. Based on artificial neural networks we developed a software for the real time detection of REM sleep. In combination with an alarm system the algorithm allowed us to wake up subjects automatically and to reduce REM sleep by about 50%. The procedure was then compared to a modified nonREM intervention paradigm for a treatment period of ten consecutive nights in depressed patients (n(1)=14, n(2)=13). These simultaneously received moderate dosages of Trimipramine. We found a strong and robust but not significantly different reduction of the average Hamilton rating scores (33 and 41% of baseline levels). While the REM sleep awakenings shortened the sleep cycle duration considerably, our nonREM intervention paradigm lengthened the ultradian alternations. Both effects might be interpreted as a challenge imposed on the nonREM-REM alternating mechanism possibly responsible for the antidepressive impact. A different timing of the control interventions might have caused the discrepancy between our findings and those of Vogel and coworkers.

Adult↗

Sleep and memory. I: The influence of different sleep stages on memory.

A new approach to the sleep stages role in memory is discussed in the context of the two opposite patterns of behavior-search activity and renunciation of search. Search activity is activity designed to change the situation (or the subjects attitudes to it) in the absence of a definite forecast of the results of such activity, but with the constant consideration of these results at all stages of activity. Search activity increases general adaptability and body resistance while renunciation of search decreases adaptability and requires REM sleep for its compensation. Unprepared learning, which is often accompanied by failures on the first steps of learning, is suggested to produce renunciation of search, which decreases learning ability, suppress retention, and increase REM sleep requirement. A prolonged REM sleep deprivation before training causes learned helplessness and disturbs the learning process, while short REM sleep deprivation cause the "rebound" of the compensatory search activity that interferes with passive avoidance. REM sleep deprivation performed after a training session can increase distress caused by a training procedure, with the subsequent negative outcome on retention.

Animals↗

The effect of sleep fragmentation on sleep and performance in younger and older subjects.

Groups of 12 normal 55-70-year-old and young adult subjects had their sleep experimentally disturbed at a rate of approximately 14 times per hour to determine the residual effects of moderate sleep disturbance and to determine any differential impact as a function of age. Normal age-related changes in sleep were seen on baseline and recovery nights. In the second night of sleep disturbance, the older subjects had a smaller increase in total awakenings than young adults. Older subjects had a slower increase in auditory arousal threshold as sleep disturbance progressed. The older subjects also tended to have less performance deterioration on morning testing than did young adults, and this difference was significant for numbers of correctly completed addition problems. These evidences led to the conclusion that, while both age groups were sensitive to moderate sleep disturbance, the older individuals appeared somewhat less sensitive than the young adults.

Adaptation, Physiological↗

Sleep and sleep homeostasis in mice lacking the 5-HT2c receptor.

Studies in humans and rats indicate that serotonin (5-hydroxytryptamine, 5-HT) receptors are involved in mammalian sleep expression. We investigated the contribution of the 5-HT2c receptor to sleep expression by examining sleep patterns in mice bearing a targeted null mutation of this receptor. 5-HT2c receptor knock-out mice had more wakefulness, several abnormalities in rapid eye movement sleep expression and an enhanced response to sleep deprivation compared with wild-type control mice. These findings suggest that 5HT2c receptors may mediate several effects on sleep that have been ascribed to serotonin.

Animals↗

Limbic activity in slow wave sleep in a healthy subject with alpha-delta sleep.

All-night electroencephalographic (EEG) activity was recorded in a healthy subject with known alpha-delta sleep. Recordings were made from all 19 of the 10/20 system electrode sites, and low resolution electromagnetic tomography (LORETA) was used to estimate intracerebral current densities. Sleep stages were compared within classical frequency bands by statistical parametric mapping (SPM). With the onset of sleep, occipital alpha abated. With increasing depth of sleep, alpha power increased in a region comprising the left frontal lobe, the anterior and parietal cingulum, and the anterior and medial right front lobe. In slow wave sleep (SWS), frontal alpha power was much greater than in wakefulness. The maximum of frontal alpha power of SWS was localised symmetrically in the left and right anterior cingulum. The observed alpha activity was different from the occipital alpha characteristic of wakefulness; it was a distinct activity of separate origin. The anterior limbic lobes seemed to play an active part in SWS in this healthy volunteer with an alpha-delta sleep pattern.

Adult↗

Cognitive flexibility across the sleep-wake cycle: REM-sleep enhancement of anagram problem solving.

Flexible or 'fluid' cognitive processes are regarded as fundamental to problem solving and creative ability, requiring a specific neurophysiological milieu. REM-sleep dreaming is associated with creative processes and abstract reasoning with increased strength of weak associations in cognitive networks. REM sleep is also mediated by a distinctive neurophysiological profile, different to that of wake and NREM sleep. This study compared the performance of 16 subjects on a test of cognitive flexibility using anagram word puzzles following REM and NREM awakenings across the night, and waking performances during the day. REM awakenings provided a significant 32% advantage in the number of anagrams solved compared with NREM awakenings and was equal to that of wake time trials. Correlations of individual performance profiles suggest that REM sleep may offer a different mode of problem solving compared with wake and NREM. When early and late REM and NREM awakening data were separated, a dissociation was evident, with NREM task performance becoming more REM-like later in the night, while REM performance remained constant. These data suggest that the neurophysiology of REM sleep represents a brain state more amenable to flexible cognitive processing than NREM and different from that in wake, and may offer insights into the neurocognitive properties of REM-sleep dreaming.

Adolescent↗

Topographical changes in N1-P2 amplitude upon awakening from recovery sleep after slow-wave sleep deprivation.

OBJECTIVES: To assess auditory evoked potentials (AEPs) before sleep and upon 3 awakenings during an undisturbed baseline night and to compare them to AEPs during a night characterized by a recuperative increase in the amount of slow-wave sleep (SWS) as a consequence of two consecutive nights of selective SWS deprivation. METHODS: Ten male subjects slept in the laboratory for 6 consecutive nights. The first 2 nights were undisturbed. The 3rd night was considered as baseline. During the 4th and 5th nights, selective SWS deprivation was obtained by means of acoustic stimulation. The 6th night was a recovery. The data reported here were collected during the baseline and the recovery night. Subjects were awakened 3 times: after 2 h, 5 h (nocturnal awakenings) and 7.5 h (final morning awakening) of sleep, respectively. All the awakenings were carried out from stage 2. The AEP recordings were carried out in bed, while subjects were performing a simple auditory reaction time task. RESULTS: The amplitude of the N1-P2 complex decreased upon the first awakening of the baseline night as compared to pre-sleep wakefulness levels; during the recovery night, the decrease of N1-P2 amplitude was present also upon the second and final awakening. N1 latency increased upon the two nocturnal awakenings regardless of the night, while P2 latency was not affected. Moreover, the N1-P2 amplitude increased during recovery at the frontal midline derivation as compared to baseline, while it decreased at Pz and Oz. CONCLUSIONS: The N1-P2 amplitude and, to a lesser extent, the N1 latency, are sensitive in showing a state of brain deactivation during the sleep-wake transition. The decrease of N1-P2 amplitude at the parieto-occipital locations during recovery is coherent with the hypothesis of a functional link between SWS amount and cortical hypoarousal upon awakening. The unexpected increase of the same variable at Fz can be interpreted as the effect of a compensatory effort of the frontal areas for the increased homeostatic drive for sleep during the recovery night.

Adult↗

Human sleep spindle characteristics after sleep deprivation.

OBJECTIVE: Sleep spindles (12-15 Hz oscillations) are one of the hallmarks of the electroencephalogram (EEG) during human non-rapid eye movement (non-REM) sleep. The effect of a 40 h sleep deprivation (SD) on spindle characteristics along the antero-posterior axis was investigated. METHODS: EEGs during non-REM sleep in healthy young volunteers were analyzed with a new method for instantaneous spectral analysis, based on the fast time frequency transform (FTFT), which yields high-resolution spindle parameters in the combined time and frequency domain. RESULTS: FTFT revealed that after SD, mean spindle amplitude was enhanced, while spindle density was reduced. The reduction in spindle density was most prominent in the frontal derivation (Fz), while spindle amplitude was increased in all derivations except in Fz. Mean spindle frequency and its variability within a spindle were reduced after SD. When analyzed per 0.25 Hz frequency bin, amplitude was increased in the lower spindle frequency range (12-13.75 Hz), whereas density was reduced in the high spindle frequency range (13.5-14.75 Hz). CONCLUSIONS: The observed reduction in spindle density after SD confirms the inverse homeostatic relationship between sleep spindles and slow waves whereas the increase in spindle amplitude and the reduction in intra-spindle frequency variability support the hypothesis of a higher level of synchronization in thalamocortical cells when homeostatic sleep pressure is enhanced.

Adult↗

Human circadian melatonin rhythm phase delay during a fixed sleep-wake schedule interspersed with nights of sleep deprivation.

The human circadian pacemaker, with an intrinsic period between 23.9 and 24.5 hr, can be reset by low levels of light. Biomathematical models of the human clock predict that light-dark cycles consisting of only approximately 3.5 lux during 16 hr of wakefulness and 0 lux during 8 hr of sleep should entrain approximately 45% of the population. However, under real-life conditions, sleep-wake schedules and the associated light-dark exposures are often irregular. It remains unclear whether the phase of the pacemaker would remain stable under such conditions. We investigated the stability of the circadian phase in dim light by assessing the plasma melatonin rhythm during nine consecutive circadian cycles. Ten subjects were scheduled to sleep for 8 hr (0.03 lux) and to be awake for 16 hr (5-13 lux) during all days except on days 4 and 8, during which the subjects were sleep deprived for 40 hr (5-13 lux), either in a sitting/standing or supine body posture. In all subjects, the phase of the melatonin rhythm occurred at a later clock time on day 9 than on day 2 (average delay: 1.4 hr). Largest delays in the melatonin onset were observed in subjects with low amplitude melatonin rhythms. The area under the curve during active melatonin secretion was significantly reduced when subjects were sleep deprived in the 40-hr supine body posture condition compared with either the 40-hr sitting/standing sleep deprivation (SD) or the ambulatory condition under non-SD conditions. Posture differences did not significantly affect the relative phase position of the melatonin profiles. The data indicate that under conditions of reduced zeitgeber strength, the phase of the human circadian pacemaker, using plasma melatonin as a marker, can be phase delayed by one night of SD and the associated dim light exposure.

Biological Clocks↗

Information processing during sleep onset and sleep.

This Special Section examines the extent of information processing during sleep onset and sleep itself. It is generally agreed that, stimulus input is markedly inhibited during sleep, thus preventing conscious awareness of the external environment. Overt behavioural responses are rarely made within sleep. Two neurophysiological measures are therefore often used. The electrical activity of the brain (the EEG) can be employed to distinguish waking (conscious) from sleeping (unconscious) states. It is also possible to quantify the EEG prior to and following a detection (or a failure of a detection) of a stimulus. Such measures can thus be used to predict conscious awareness. A second measure that frequently has been employed is the brain's response to an external stimulus (the evoked potential). Different components of the evoked potential can be used to trace the extent of information processing during the different states of consciousness. Some are associated with a preconscious detection while others are associated with conscious awareness. Other evoked potentials may be unique to sleep.

Consciousness↗

Validity of sleep log compared with actigraphic sleep-wake state II.

Twenty-five young people (Y group), three elderly people and seven people with various sleep disorders (SD group) kept a sleep log for 2-7 days, and their wrist-activity was monitored simultaneously. The sensitivity and specificity of the sleep log, and the ratio of agreement between the sleep log and actigraphic sleep-wake state were calculated. The sensitivity and specificity in Y group were 87.93+/-6.49% and 96.51+/-2.37%, respectively. The sensitivity in SD group was significantly lower than in Y group. Even in Y group one-hour agreement ratios dropped during the sleep onset period.

Adult↗

Sleep architectures of obstructive sleep apnea syndrome in the young child.

The sleep architectures of obstructive sleep apnea syndrome (OSAS) in the young child (child-OSAS, n = 17; mean age: 5.9+/-2.7 years; male:female 14:3) were compared with that of OSAS in the adult (n = 19; mean age: 44.7+/-10.7 years; male:female 18:1) and that of primary snoring in the child (n = 5; mean age: 7.0+/-2.4 years; male:female 5:0). Child-OSAS and OSAS in the adult had the same severity in oxygen desaturation. Child-OSAS showed lower Apnea-Hypopnea Index compared with OSAS in the adult. Sleep continuity in child-OSAS was not impaired compared with OSAS in the adult. Sleep fragmentation in child-OSAS was not so remarkable. The quantity of slow wave sleep in child-OSAS was similar to that of primary snoring in the child. Both profiles of sleep architectures showed nearly the same pattern.

Cerebral Cortex↗

Subjective sleep quality and sleep problems in the general Japanese adult population.

To dimensionally describe subjective sleep quality using the Pittsburgh Sleep Quality Index (PSQI) and estimate the prevalence rate of sleep problems (PSQI global score > 5) in the general Japanese adult population, 1871 subjects randomly selected from the 1995 Census were examined. The PSQI component scores (mean +/- SD) widely ranged (e.g. 0.04 +/- 0.31 in hypnotic medication use for males aged 20-29 years, 0.03 +/- 0.18 in hypnotic medication use for females aged 20-29 years, 1.10 +/- 0.94 in sleep latency for males aged 80 or older, 1.52 +/- 1.03 in sleep latency for females aged 80 or older). Statistical significance was found in each component score among age groups by gender. The PSQI global scores (mean +/- SD) by age groups ranged from 4.00 +/- 2.59 to 5.02 +/- 3.89 for males (P < 0.39) and 4.30 +/- 2.34 to 6.75 +/- 4.10 for females (P < 0.001). The respective prevalence rates of sleep problems were 26.4% (95% CI = 23.6, 29.3) for males and 31.1% (95% CI = 28.1, 33.9) for females.

Adult↗

[The influence of sulpirid on sleep. Results of polygraphic night sleep recordings (author's transl)].

Short and long term effects of sulpirid on the sleep EEG in humans were investigated in 8 patients aged 20-68 years (average 40.4) suffering from autonomic instability. In each patient seven polygraphic night sleep recording were performed. After an adaption night and two nights without medication each subject got 200-400 mg sulpirid i.m. for two days and then 300-600 mg orally for a three-week period. In both groups the short-term application of sulpirid caused a reduction of waking periods and a slight decrease of stage 3, while stage 2 was increased. In psychotic patients the long-term orally administered substance was followed by an increase of deep synchronous sleep (stage 4). As this alteration of sleep couldn't be revealed in the control group, we consider this finding as a result of the improvement of psychosis. In the patient group the amount of REM sleep was augmented during the short-term application as well as during the long-term application, where, as in the control group the amount of REM sleep decreased when sulpirid was given orally for three weeks. This result is discussed in comparison with the properties of the tricyclic antidepressant drugs and monoamine oxidase inhibitors and the clinical effects of sulpiride.

Administration, Oral↗

[The relationship between sleep position and therapeutic effect of the Esmarch-Scheine appliance in sleep apnea syndromes].

Recently an oral appliance is being used increasingly for the treatment of sleep apnea syndrome. But the success rate of oral appliance therapy shows large interindividual difference, and which factors influence its efficiency remain uncertain. To elucidate the influence of the sleep posture on the therapeutic effect of the Esmarch device, 58 patients with sleep apnea syndrome were investigated polysomnographically before and after insertion of the device. The sleep position during each apnea was classified into three types; supine, lateral and prone. The mean apnea index (25.6 +/- 18.7) decreased significantly (p < 0.0001) after insertion of the device (11.5 +/- 12.6). The number of apneas (in the supine and prone) positions was significantly reduced from 18.0 +/- 16.7 and 2.0 +/- 3.6 to 5.0 +/- 11.2, p < 0.001, and 0.3 +/- 0.4, p < 0.005, respectively, but that in the lateral position was slightly increased from 5.6 +/- 9.4 and 6.2 +/- 8.9. The percent of apneas was 70.3% for supine, 21.9% for lateral, and 7.8% for prone before therapy and 43.5%, 53.9% and 2.6%, respectively after therapy. The results indicated that the effectiveness of oral appliance therapy can differ greatly with the sleep posture. The sleep posture recorded polysomnography may be important for choice of oral appliance therapy and its prognosis.

Female↗

Renin-angiotensin-aldosterone system, HPA-axis and sleep-EEG changes in unmedicated patients with depression after total sleep deprivation.

BACKGROUND: Changes in the activity of the renin-angiontensin-aldosterone system (RAAS) in depression have recently been reported. Renin and aldosterone secretion are coupled to sleep in healthy subjects. As total sleep deprivation (TSD) leads to a rapid mood improvement in patients with depression, it is of interest to investigate its effect on the response of the RAAS in the recovery night in this population as a possible probe for the neurobiological effects of TSD and potentially other rapid acting antidepressive interventions. Additionally we explored the HPA-system and the sleep-EEG-changes. METHODS: We compared the sleep related activity of the RAAS before and after TSD in seven depressed patients. After an accommodation night, a polysomnographic examination was performed between 23.00 h and 7.00 h. This was followed by 40 h of TSD and a second polysomnography. During the examination blood samples were taken in the night every 20 min for analysis of renin, aldosterone, ACTH and cortisol. RESULTS: During recovery-sleep renin was significantly increased (p < 0.05). Aldosterone showed no change. ACTH and cortisol were decreased by trend in the first half of the night. REM-density and intermittent wakefulness was significantly decreased (p < 0.05), whereas slow wave sleep increased by trend in the first half of the night. CONCLUSION: TSD in patients with depression leads to an increase in renin secretion and a concomitant trend for a decrease in HPA axis activity in the recovery night. These changes could be a "fingerprint" of a rapidly antidepressive treatment.

Adrenocorticotropic Hormone↗

Genetic basis for sleep regulation and sleep disorders.

Sleep disorders arise by an interaction between the environment and the genetic makeup of the individual but the relative contribution of nature and nurture varies with diseases. At one extreme are the disorders with simple Mendelian patterns of inheritance such as familial advanced sleep phase syndrome, and at the other extreme are diseases such as insomnia, which can be associated with a multitude of medical and psychiatric conditions. In this article, we review data on the relative contribution of genetic and environmental factors in the pathogenesis of various sleep disorders. The understanding of many of these disorders has been advanced by the study of sleep and circadian rhythms in model laboratory organisms. We summarize this model system research and how it relates to human sleep disorders. The current challenge in this field is the identification of susceptibility genetic loci for complex diseases such as obstructive sleep apnea. We anticipate such identification will increase our ability to assess risk for disease before symptom onset and by doing so will shift the focus from treatment to prevention of disease.

Circadian Rhythm↗