Showing papers in "Journal of Sleep Research in 1992"
TL;DR: It was revealed that prior wakefulness within a range of 0–18 h significantly reduced alertness and performance and that the circadian rhythm of core body temperature paralleled the circadian Rhythm of alerts and performance.
Abstract: Circadian and sleep/wake dependent processes underlying variations in subjective alertness and cognitive performance were assessed in a constant routine protocol and in a protocol in which the sleep/wake cycle was uncoupled from the output of the endogenous circadian pacemaker In the latter protocol, the contribution of a sleep/wake dependent process and a circadian process to alertness and performance were separated by folding the data at either the period of the sleep/wake cycle or at the period of the endogenous circadian body temperature rhythm This analysis revealed that prior wakefulness within a range of 0-18 h significantly reduced alertness and performance and that the circadian rhythm of core body temperature paralleled the circadian rhythm of alertness and performance During the first 16 h of the constant routine protocol, which coincided with the subjects' habitual period of wakefulness, alertness and performance remained at a stable level The latter finding was explained by assuming that during our usual waking day the circadian system counteracts the detrimental effects of increasing duration of prior wakefulness
582 citations
TL;DR: Contrary to earlier findings, it is reported here that the circadian rhythm of short‐term memory varies in parallel with the circadian rhythms of subjective alertness, calculation performance, and core body temperature under both these experimental conditions.
Abstract: Previous studies have led to the beliefs: (1) that short-term memory is best during the night when the body temperature is at its nadir, and (2) that the circadian rhythms of short-term memory and subjective alertness are driven by oscillators independent from each other and from the body temperature cycle. Unfortunately, these conclusions, which would have major implications for understanding the organization of the human circadian timing system, are largely based on field and laboratory studies, which in many cases sampled data infrequently and/or limited data collection to normal waking hours. In order to investigate these points further, we have monitored behavioural variables in two different protocols under controlled laboratory conditions: (1) during a period of 36-60 h of sustained wakefulness; and (2) during forced desynchrony between the body temperature and sleep/wake cycles, allowing testing of non-sleep-deprived subjects at all circadian phases. Contrary to earlier findings, we report here that the circadian rhythm of short-term memory varies in parallel with the circadian rhythms of subjective alertness, calculation performance, and core body temperature under both these experimental conditions. These results challenge the notion that short-term memory is inversely linked to the body temperature cycle and suggest that the human circadian pacemaker, which drives the body temperature cycle, is the primary determinant of endogenous circadian variations in subjective alertness and calculation performance as well as in the immediate recall of meaningful material.
239 citations
TL;DR: Close links have emerged between the processes postulated by the various models and specific brain mechanisms, and the modelling approach has become one of the potent research strategies in sleep science.
Abstract: Various mathematical models have been proposed to account for circadian, ultradian and homeostatic aspects of sleep regulation. Most circadian models assume that multiple oscillators underlie the differences in period and entrainment properties of the sleep/wake cycle and other rhythms (e.g. body temperature). Interactions of the oscillators have been postulated to account for multimodal sleep/wake patterns. The ultradian models simulate the cyclic alternation of nonREM sleep and REM sleep by assuming a reciprocal interaction of two cell groups. The homeostatic models propose that a sleep/wake dependent process (Process S) underlies the rise in sleep pressure during waking and its decay during sleep. The time course of this process has been derived from EEG slow-wave activity, an indicator of nonREM sleep intensity. The predictions of homeostatic models have been most extensively tested in experiments. The interaction of Process S with a single circadian process can account for multimodal sleep/wake patterns, internal desynchronization and the time course of daytime sleepiness. Close links have emerged between the processes postulated by the various models and specific brain mechanisms. Due to its recent quantitative elaboration and experimental validation, the modelling approach has become one of the potent research strategies in sleep science.
228 citations
TL;DR: Results support the hypothesis that sleep serves a function of cognitive restitution, particularly in the maintenance of attentional mechanisms, and suggest that cognitive measures following sleep deprivation have not been adequately explored.
Abstract: SUMMARY Twelve male undergraduate students were deprived of sleep for one night and were tested with a series of cognitive tasks. Their performance was compared to the performance of thirteen control subjects. Two hourly tasks and three occasional tasks were administered in order to examine cognitive performance following sleep loss. In an attempt to replicate the findings of Horne (1988a), the figural form of the Torrance Tests of Creative Thinking was administered. To explore the effects of short-term sleep deprivation on attention, the following tasks were also administered: a working memory task, a trail-making task, a vowel/consonant discrimination task, and a letter recognition task. Results of the Torrance test, trail-making task and letter recognition task revealed decreases in cognitive abilities following sleep loss, although all tasks required less than 10 minutes to administer. The results of this study suggest that cognitive measures following sleep deprivation have not been adequately explored. Results support the hypothesis that sleep serves a function of cognitive restitution, particularly in the maintenance of attentional mechanisms.
155 citations
TL;DR: The epidemiology of self‐reported snoring, sleep apnoea and OSAS, and their relationships with various symptoms, were evaluated in 1504 randomly selected males and females, aged 30, 40, 50 and 60 years.
Abstract: SUMMARY Several epidemiological studies have estimated the prevalence of obstructive sleep apnoea syndrome (OSAS). As many of those suffering from sleep apnoea may be asymptomatic, the occurrence of sleep apnoea may be underestimated. The epidemiology of self-reported snoring, sleep apnoea and OSAS, and their relationships with various symptoms, were evaluated in 1504 randomly selected males and females, aged 30, 40, 50 and 60 years. Nocturnal respiration was determined in 748 participants using inductive plethysmography.
Habitual snoring was reported by 19.1% (9.2–24.2%, age 30–60 years) of the males and 7.9% (3.8–11.7%, age 30–60 years) of the females. Respiratory Distress Index (RDI) was calculated as the number of apnoeas and hypopnoeas per hour lasting longer than 10s. RDI≥5 per hour was found in 10.9% (7.1–18.3%, age 30–60 years) of the males and in 6.3% (5.3–7.6%, age 30–60 years) of the females. Hypersomnia increased with the severity of sleep apnoea (P< 0.005) and was reported by 15.9% of those with RDI≥5.
The prevalence of OSAS (hypersomnia and RDI ≥5) was 0.9% in the females, 1.9% in the males, and in total 1.4% of all aged 30–60 years. The sensitivity was 70.8% and the specificity was 47.7% for self-reported snoring predicting RDI ≥5.
The following factors were associated with RDI ≥5: age (P<0.05), gender (P< 0.0001), BMI (P< 0.0001), tobacco (P<0.02) and alcohol (P<0.05) consumption. Snoring correlated with age (P<0.02), gender (P<0.001), BMI (P<0.0001) and alcohol consumption (P<0.05).
We conclude that sleep apnoea is common and many of those with sleep apnoea are asymptomatic. Self-reported hypersomnia and snoring are not sensitive enough alone to identify those with sleep apnoea. Sufficient control of the questionnaire is thus essential in studies on snoring and the risk of cardiovascular diseases.
152 citations
TL;DR: It was concluded that sleepiness is not an unidimensional construct and further studies are necessary to elucidate the nature of its components.
Abstract: SUMMARY Two assumptions underlying the Stanford Sleepiness Scale (SSS) were evaluated: that the descriptors defining each level of the scale are equivalent ways of characterizing a particular level of sleepiness; and that sleepiness, thus measured, is an unidimensional construct. Twenty-four True/False items were derived from the descriptors at each level of the SSS. This revised scale was administered to 340 undergraduates in a questionnaire which also included: the SSS; four visual analogue scales; items identifying the subject's age, sex, and circadian type; and the time of administration. Analyses of the responses indicated that endorsement of items on the revised scale was not consistent with the SSS level endorsed, indicating that the descriptors at each scale level are not equivalent. A principal components analysis revealed two components, tentatively identified as activation and sleepiness, accounting, respectively, for 24.2 and 20.6% of the variance. It was concluded that sleepiness is not an unidimensional construct. Further studies are necessary to elucidate the nature of its components.
150 citations
TL;DR: In the recovery sleep, following unihemispheric sleep deprivation, there was a rebound of delta sleep only in the deprived hemisphere, and the animals exhibited an increase in delta sleep in both hemispheres.
Abstract: SUMMARY Unihemispheric and bihemispheric sleep deprivation were performed in bottlenose dolphins. One brain hemisphere was capable of being deprived of delta (0.5-3.0 Hz) sleep in the former condition. Here, an increase in sleep pressure was observed during sleep deprivation in the deprived hemisphere. In the recovery sleep, following unihemispheric sleep deprivation, there was a rebound of delta sleep only in the deprived hemisphere. Following bihemispheric sleep deprivation the animals exhibited an increase in delta sleep in both hemispheres.
120 citations
TL;DR: New data show cortical slow‐wave activity is controlled by thalamocortical neurons' membrane potential level, which is strongly controlled during sleep by brainstem cholinergic input arising from REM‐on neurons, which leads to a neurobiologi‐cally justified integration of the LCRIM and of the two‐process model of sleep control.
Abstract: SUMMARY New data bearing on the neurobiological basis of REM sleep and on mechanisms of EEG synchronization/desynchronization are presented. The revision of the limit cycle reciprocal interaction model (LCRIM) of REM cycle control incorporates new information on monoamine inhibition of mesopontine cholinergic neurons and of cholinergic mechanisms promoting REM sleep. New data also show cortical slow-wave activity is controlled by thalamocortical neurons' membrane potential level, which, in turn, is strongly controlled during sleep by brainstem cholinergic input arising from REM-on neurons. This new knowledge leads to a neurobiologi-cally justified integration of the LCRIM and of the two-process model of sleep control.
109 citations
TL;DR: Results of a photoperiod experiment show that human sleep can be unconsolidated and polyphasic, like the sleep of other animals.
Abstract: Results of a photoperiod experiment show that human sleep can be unconsolidated and polyphasic, like the sleep of other animals. When normal individuals were transferred from a conventional 16-h photoperiod to an experimental 10-h photo-period, their sleep episodes expanded and usually divided into two symmetrical bouts, several hours in duration, with a 1-3 h waking interval between them. The durations of nocturnal melatonin secretion and of the nocturnal phase of rising sleepiness (measured in a constant routine protocol) also expanded, indicating that the timing of internal processes that control sleep and melatonin, such as circadian rhythms, had been modified by the change in photoperiod. Previous work suggests that the experimental results could be simulated with dual-oscillators, entrained separately to dawn and dusk, or with a two-process model, having a lowered threshold for sleep-onset during the scotoperiod.
96 citations
TL;DR: Investigation of whether sleep‐like states occur in the cockroach, Blaberus giganteus, by applying the methods formerly used for another cockroach species, Leucophaea maderae and the scorpions, Heterometrus and Pandinus found a nocturnal behaviour exhibiting a bout of locomotion at dark onset which lasted several hours, and a preference for rest in the light period.
Abstract: SUMMARY Our objective was to investigate whether sleep-like states occur in the cockroach, Blaberus giganteus by applying the methods formerly used for another cockroach species, Leucophaea maderae and the scorpions, Heterometrus and Pandinus. The behaviour of isolated animals (n= 10) kept under LD 12:12 h was recorded by time-lapse video for three consecutive 24-h periods. Nine behavioural states were scored for 1-min real-time epochs. Rest was subdivided into 4 sub-states on the basis of body posture and the position of the antennae. The cockroaches showed a nocturnal behaviour exhibiting a bout of locomotion at dark onset which lasted several hours, and a preference for rest in the light period. Immobility with both the body and the antennae touching the substrate (state 1) was the predominating state in the light period.
In order to establish whether the sub-states of rest represented different levels of vigilance the arousal threshold was measured by determining the latency of a behavioural response to a vibration stimulus. The levels of arousal differed significantly in four behavioural states in the light period but not in the dark period. In state 1 the animals exhibited the lowest arousal whereas in the activity states arousal was the highest. The state with the highest arousal threshold occurred in the beginning of the light period. Thereafter, arousal progressively increased and remained relatively high during the dark period.
The effect of 6-h deprivation of rest by the gentle shaking of the cages whenever the animals were immobile, resulted in a reduced latency to state 1, a small increase of state 1 and a more prominent initial increase of activity during recovery.
In conclusion, this study provides evidence for the existence of a 24-h variation of vigilance in the cockroach. It further indicates that a ‘rest deficit’ gives rise to a compensatory response. The data support the notion that sleep-like states are present in these insects.
92 citations
TL;DR: An extended model is now proposed which combines the ultraradian REM regulation modelled by the LCRIM with the homeostatic regulation of slow‐wave activity modelling by the Two‐Process Models of Borbély, Achermann and Beersma.
Abstract: The Limit Cycle Reciprocal Interaction Model (LCRIM) describes the stable interaction of REM-promoting and REM-antagonizing neurons which generates the periodic Occurrence of REM sleep. The cycling of this physiological oscillator is subject to perturbation from excitatory input, referred to as E, which derives from other parts of the nervous system. An extended model is now proposed which combines the ultraradian REM regulation modelled by the LCRIM with the homeostatic regulation of slow-wave activity modelled by the Two-Process Models of Borbely, Achermann and Beersma. In addition, this integrated model extends the E construct to relate explicitly to both the REM and slow-wave sleep control systems, and to have stochastic dynamics. Overall, the model generates qualitatively realistic SWA, REM and wake-up patterns. However, its performance awaits quantitative validation.
TL;DR: Sleep and wakefulness were studied in rats following administration of a selective 5‐HT1A agonist (8‐OH‐DPAT), a non‐selective 5‐ HT1A antagonist [(‐) pindolol] and a combination of 8‐OH-DPAT and (—) pINDolol.
Abstract: SUMMARY Sleep and wakefulness were studied in rats following administration of a selective 5-HT1A agonist (8-OH-DPAT), a non-selective 5-HT1A antagonist [(-) pindolol] and a combination of 8-OH-DPAT and (—) pindolol.
8-OH-DPAT (1.0–4.0 μg) injected into the dorsal raphe nucleus increased slow-wave sleep and decreased wakefulness. Administration of the 5-HT1A agonist by subcutaneous route induced biphasic effects such that low doses (0.010 mg kg-1) decreased wakefulness and increased slow-wave sleep while higher doses (0.375 mg kg-1) induced opposite effects. REM sleep was suppressed and REM latency was increased, what could be tentatively ascribed to a non-specific effect (hypothermia). (-) Pindolol (1.0–4.0 mg kg-1) induced an initial increase of wakefulness and a decrease of NREM sleep and REM sleep. Thereafter, NREM sleep showed a marked increase while REM sleep remained depressed. Pretreat-ment with (—) pindolol reversed the effects of both small and large doses of 8-OH-DPAT on slow-wave sleep and wakefulness.
The opposite effects, observed on the waking EEG after activation of either serotonin autoreceptors or postsynaptic 5-HT1A receptors with adequate doses of 8-OH-DPAT, tend to indicate an active role for the 5-HT1A receptor in the control of the waking state.
TL;DR: It is shown that the different models proposed to account for processes underlying the regulation of sleep and alertness are not mutually exclusive but that they can be integrated as ‘modules’ in a combined model.
Abstract: Different models have been proposed to account for processes underlying the regulation of sleep and alertness. Specific models have addressed sleep homeostasis, the nonREM-REM sleep cycle, the circadian sleep/wake rhythm, and changes of daytime alertness. We show that the different models are not mutually exclusive but that they can be integrated as 'modules' in a combined model.
TL;DR: The method uses non-metabolizable analogues of an understanding of brain blood flow and metabolism would glucose: bring about anUnderstanding of the functions of sleep.
Abstract: Students of sleep have always been fascinated by the centration of glucose, which is the normal substrate of problem of brain circulatory and metabolic changes during cerebral energy metabolism (see Sokoloff 1984, for a rethe sleep/wake cycle. It was clear from the first studies that view). The method uses non-metabolizable analogues of an understanding of brain blood flow and metabolism would glucose: bring about an understanding of the functions of sleep. For (i) 2-deoxy-D-glucose (DG, b-emitter; for autoradio-
TL;DR: In this article, a 10-min blood sampling was performed in 24 young healthy subjects during normal sleep and six of the subjects then underwent a partial sleep deprivation experiment, sleep was permitted from 03.00 hours to 07.30 hours.
Abstract: SUMMARY The thyrotropin (TSH) nycthemeral pattern is known to be strongly influenced by sleep, but previous studies have failed to demonstrate any link between sleep structure and TSH variations. Using 10-min blood sampling, nocturnal TSH profiles were analysed in 24 young healthy subjects during normal sleep. Six of the subjects then underwent a partial sleep deprivation experiment, sleep was permitted from 03.00 hours to 07.00 hours. Descending slopes of TSH values were observed for the first 20 minutes of SWS episodes, whereas no significant trend was found for other sleep stages. During the period of sleep deprivation, nocturnal TSH levels increased and then declined immediately after sleep onset; however, the association between SWS and descending TSH slopes persisted. This temporal concordance suggests that some particular mechanisms associated with SWS may modulate TSH release, or conversely that increasing TSH levels prevent the occurrence of SWS.
TL;DR: While chronophysiological changes appear to be strongly associated with the tendency to awaken in the early morning, they cannot account entirely for the severity of sleep disturbance frequently observed in older subjects.
Abstract: SUMMARY With aging, the phase relationship between sleep and body core temperature is altered such that the temperature minimum occurs substantially earlier in the major nocturnal sleep period. The sleep maintenance difficulties that often accompany normal aging are generally assumed to be associated with this age-related change in the phase angle between sleep and temperature. To test this notion, we used timed exposure to bright light to reproduce in healthy young adults a similar phase relationship between temperature and sleep, to determine if such a manipulation would induce the same fragmented nocturnal sleep commonly observed in individuals over 65 years of age. Seven young adults were exposed to morning bright light for 3 consecutive days following a baseline night. Bright light exposure caused a 97 min phase advance of the fitted temperature minimum when compared with baseline. Significant declines in several measures of sleep quality were associated with the phase advance, including wakefulness after initial sleep onset (WASO), sleep efficiency and number of stage changes. Yet, the severity of sleep disturbance exhibited by these subjects did not approach that exhibited by most elderly subjects. The findings suggest that while chronophysiological changes appear to be strongly associated with the tendency to awaken in the early morning, they cannot account entirely for the severity of sleep disturbance frequently observed in older subjects.
TL;DR: It appears that 5‐HT could be released throughout the sleep/wake cycle according to two different modalities: by the axonal nerve endings during the waking state (W) and by the dendrites and/or the soma during sleep.
Abstract: SUMMARY SUMMARY That serotonin (5-HT) plays a determinant role in sleep was first suggested by the well-known PCPA-5HTP (p.chlorophenylalanine-5-hydroxytryptophan) paradigm. This involvement, however, is paradoxical since localized cooling of the nucleus raphe dorsalis (n.RD) is sleep inducing, and unitary activity of 5-HT neurons decreases during slow wave sleep (SWS) and paradoxical sleep (PS). Furthermore, on the basis of voltammetric 5-hydroxyindole (5-OHlcs) measurements, it appears that 5-HT could be released throughout the sleep/wake cycle according to two different modalities: by the axonal nerve endings during the waking state (W) and by the dendrites and/or the soma during sleep. The axonal release of 5-HT might participate in sleep preparation by stimulating the synthesis of hypnogenic factors within target structures like the basal hypothalamus (BH). When such a release is increased by an immobilization stress (IS) or electrical stimulation of the n.RD, a sleep rebound is induced. The somato-dendritic release of 5-HT might be primarily responsible through an auto-inhibitory process for the decrease and abolition of the 5-HT neuronal unitary activity as well as for the reduction of the axonal release of 5-HT; both phenomena being constantly observed during sleep. Finally, the hypnogenic factors might initiate and maintain sleep by influencing the n.RD sleep gating mechanisms either through the somato-dendritic release of 5-HT, or directly.
TL;DR: It was concluded that the decline of SWA across time may deviate from an exponential shape under real life conditions.
Abstract: SUMMARY The aim of the present study was to estimate the time course of slow wave activity (SWA) in naturally occurring long sleep episodes (ad lib). Sixteen male shift workers were subjected to 24 h ambulatory polysomnography in connection with an afternoon shift. The EEG was subjected to spectral analysis (FFT) as well as to traditional sleep stage scoring. SWA (0.5-4.5 Hz band, both nonREM and REM sleep) declined exponentially and reached an asymptote by the fifth or sixth sleep cycle. However, half the subjects showed a reduced SWA in the first cycle, with a subsequent recovery in the second cycle. The SWA reduction of the first cycle was associated with a reduced REM-latency and it was suggested that uncontrolled external influences of the real life settings may have affected SWA in the first cycle. It was concluded that the decline of SWA across time may deviate from an exponential shape under real life conditions.
TL;DR: It is concluded that the concept of sleep homeostasis that has been elaborated and formalized in the two‐process model for human sleep, can also be applied to simulate sleep in other mammals.
Abstract: A brief overview of models on the regulation of sleep/waking or rest/activity is provided. Applications of the two-process model are illustrated in two species: The homeostatic facet of the model (Process S) was used to quantitatively simulate sleep in the rat and guinea pig. The model parameters were estimated for rat sleep by an optimization procedure. A close correspondence between the time course of slow-wave activity and Process S was obtained for both species under baseline conditions. Whereas in the rat a close fit was obtained also for the recovery period from sleep deprivation, some discrepancies were present in the guinea pig. It is concluded that the concept of sleep homeostasis that has been elaborated and formalized in the two-process model for human sleep, can also be applied to simulate sleep in other mammals.
TL;DR: Questions remain with regard to the physiological significance of the 5‐HT2 receptor‐mediated deep SWS regulation, the anatomical site(s) of 5‐ HT2 receptors involved in this regulation and the mechanism underlying diurnal fluctuations in the functional activity of 5-HT2 receptors.
Abstract: SUMMARY In the light of recent pharmacological investigations using agonists and antagonists that have potent actions on 5-hydroxytryptamine-2 (5-HT2) receptors, the possible functional role of 5-HT2 receptors in the modulation of the sleep/wakefulness states was examined. Data obtained from animals and from clinical studies suggest that serotonin may exert an inhibitory control on deep slow-wave sleep (SWS) through 5-HT2 receptors. In further investigations, the existence of a diurnal variation in the functional activity of 5-HT2 receptors, that depends on the day/night cycle and/or the melatonin rhythm, was revealed. Questions remain with regard to the physiological significance of the 5-HT2 receptor-mediated deep SWS regulation, the anatomical site(s) of 5-HT2 receptors involved in this regulation and the mechanism underlying diurnal fluctuations in the functional activity of 5-HT2 receptors.
TL;DR: The identification of a P3‐like potential during sleep suggests that the P3 potential is not solely a marker of active cognitive processes, but contains a small component which reflects automatic, pre‐attentive evaluation of deviant stimuli.
Abstract: SUMMARY Event-related potential (ERP) recordings were used to investigate the nature of auditory stimulus evaluation during stage 2 sleep. Frequent and rare stimuli, differing in intensity and frequency, were presented to six adult subjects while awake and asleep. The latency and voltage distribution of one of the long-latency components evoked during sleep resembled the P3 component evoked while awake. However, it was attenuated in voltage and superimposed on N3, a large late negative component, most probably the slow potential of the K complex. The identification of a P3-like potential during sleep suggests that the P3 potential is not solely a marker of active cognitive processes, but contains a small component which reflects automatic, pre-attentive evaluation of deviant stimuli.
TL;DR: Auditory stimuli applied in sleep induced a burst of MSA followed by a transient increase of arterial blood pressure only when they elicited an arousal response in the EEG, such as a K‐complex, transient EEG desynchronization, or a short train of alpha waves.
Abstract: SUMMARY Muscle nerve sympathetic activity (MSA) was recorded from the peroneal nerve during wakefulness and in different sleep states in healthy young adults. The burst rate (BR) of MSA significantly decreased in NREM, but not in REM sleep, compared with that during wakefulness. Transient increases of MSA frequently appeared in association with rapid eye movements during REM sleep. K-complexes in Stage 2 were almost always accompanied by a burst of MSA, and were followed by a transient elevation of arterial blood pressure. Auditory stimuli applied in sleep induced a burst of MSA followed by a transient increase of arterial blood pressure, only when they elicited an arousal response in the EEG, such as a K-complex, transient EEG desynchronization, or a short train of alpha waves. The same stimuli applied during wakefulness did not induce such changes in MSA and in arterial blood pressure. KEYWORDS arousal response, K-complex microneurography
TL;DR: The enhanced low‐frequency power and delayed REM sleep after bright light exposure could represent a circadian phase‐shift and/or the effect of an elevated rectal temperature, possibly mediated by the suppression of melatonin.
Abstract: Five male subjects were exposed to a single 2-h period of bright (2500 lux) or dim (<100 lux) light prior to sleep on two consecutive nights. The two conditions were repeated the following week in opposite order. Bright light significantly suppressed salivary melatonin and raised rectal temperature 0.3 degrees C (which remained elevated during the first 1.5 h of sleep), without affecting tympanic temperature. Bright light also increased REM latency, NREM period length, EEG spectral power in low frequency, 0.75-8 Hz and sigma, 12-14 Hz (sleep spindle) bandwidths during the first hour of sleep, and power of all frequency bands (0.5-32 Hz) within the first NREMP. Potentiation of EEG slow wave activity (0.5-4.0 Hz) by bright light persisted through the end of the second NREMP. The enhanced low-frequency power and delayed REM sleep after bright light exposure could represent a circadian phase-shift and/or the effect of an elevated rectal temperature, possibly mediated by the suppression of melatonin.
TL;DR: Sleep architecture was studied in four subjects with agenesis of the corpus callosum and four control subjects matched for age, gender, and hand preference and found that the former is essential for normal human sleep.
Abstract: SUMMARY Whether the corpus callosum is essential for normal human sleep cannot be decided from current knowledge. We thus studied sleep architecture in four subjects with agenesis of the corpus callosum (ACC) and four control subjects matched for age, gender, and hand preference. All-night EEG, EOG, and EMG activity were monitored in the laboratory for one adaptation night and one data acquisition night. Standard sleep variables were calculated for the second night.
Agenesis subjects were found to have a greater percentage of stage 3 + 4 sleep and a lower percentage of stage 2 sleep than control subjects. Agenesis subjects also tended to have more REM sleep periods and a shorter REM cycle length than controls.
The pattern of results is similar to that produced by partial callosotomy. It is also relevant to two hypotheses about the function of the corpus callosum in sleep. First, the corpus callosum may facilitate synchronization of activity between homologous regions in the two hemispheres but interfere with synchronization of neuronal populations within each hemisphere. Its absence may thus explain both an augmentation of slow-wave activity (and thus more slow-wave sleep) and a decrease in interhemispheric EEG coherence. Secondly, the corpus callosum may play a role in the regulation of the ultradian rhythm which underlies timing and duration of REM sleep.
TL;DR: In this paper, the authors present broad guidelines that stress the main important physiological events and their consequences that need to be assessed, and then interpreted in conjunction with the patient's symptoms.
Abstract: Our understanding of sleep-related breathing disorders is still in a period of rapid change. Considerable uncertainty exists in several major areas of patient assessment. Although early definitions of sleep apnoea enshrined the concept of rigid guidelines, such an approach is no longer helpful, and may constrain potential advances. The recognition of the basic pathophysiological events in obstructive sleep apnoea (OSA) has evolved from purely apnoeas, to include hypopnoeas, and now to increased upper airway resistance alone. Our view as to the significant consequences of such respiratory events has also evolved from alterations to the classic sleep architecture, to hypoxic events, and now to micro-arousals and cardio-vascular events. The exact nature of a significant arousal is also far from clear, with the suggestion that perhaps even EEG based approaches to their measurement may not be telling us the whole story. Finally, the frequency of such respiratory events and their consequences, that lead to significant symptoms and long-term damage, is not known either. Thus, given this situation, the best we can achieve is broad guidelines that stress the main important physiological events and their consequences that need to be assessed, and then interpreted in conjunction with the patient's symptoms. This will not necessarily be the same for all patients and this report offers some general guidance, based on the experience of several centres throughout Europe.
TL;DR: It is argued that TSD sets off a psychological disinhibition process on the basis of cerebral fatigue; in particular the prefrontal (orbital?) areas of the cerebral cortex may be implicated, possibly in relation to a dampening down of subcortical arousal systems.
Abstract: In view of the opposing theories regarding the arousing or de-arousing action of total sleep deprivation (TSD) in producing antidepressant effects, 23 patients with a major depressive disorder were deprived of a night’s sleep twice weekly for two weeks, and self-rated their condition 38 times using von Zerssen’s scale for depression and, concurrently, Thayer’s Activation Deactivation Adjective Check List (AD ACL). Transient relief of depression after TSD, indicated by eight patients, was mimicked by their AD ACL scores, which revealed the same underlying factors as were found in Thayer’s studies. TSD appears to be simultaneously arousing (giving more energy) and de-arousing (leading to less tension), while this response takes place against a background of increased tiredness/sleepiness. It is argued that TSD sets off a psychological disinhibition process on the basis of cerebral fatigue; in particular the prefrontal (orbital?) areas of the cerebral cortex may be implicated, possibly in relation to a dampening down of subcortical arousal systems.
TL;DR: A modelling approach is briefly outlined which emphasizes the maintenance of the phase and amplitude characteristics of the circadian rhythm of body (and brain) temperature and predicts the circasemidian phenomena.
Abstract: SUMMARY Evidence for circasemidian sleep/wake regulation is briefly reviewed with respect to protocols used to quantify sleep propensity. Existing models of sleep/wake regulation are examined in view of their ability to accommodate data which demonstrate an afternoon sleep period. Finally, a modelling approach is briefly outlined which emphasizes the maintenance of the phase and amplitude characteristics of the circadian rhythm of body (and brain) temperature and predicts the circasemidian phenomena.
TL;DR: The relationship between REM sleep latency and nocturnal cortisol concentration in 12 outpatients with major depression showed a significant inverse correlation, raising the possibility that these biological disruptions may have a common neurochemical basis.
Abstract: Due to conflicting reports on the possible association between shortening of rapid eye movement (REM) latency and increased cortisol secretion in patients with severe depression, this study examined the relationship between REM sleep latency and nocturnal cortisol concentration in 12 outpatients with major depression. The results showed a significant inverse correlation (r = -0.71, P < 0.01) between REM sleep latency and mean (23.00 hours-03.00 hours) plasma cortisol concentration. Age and severity of depression did not contribute to the inverse relationship. REM activity and density during the first REM period showed no significant correlations with the cortisol measures. A review of the literature suggests that this relationship might be unique to subjects with major depression, and again raises the possibility that these biological disruptions may have a common neurochemical basis.
TL;DR: It was concluded that the occurrence of SOREMs is primarily due to the residual somnolence in narcoleptic subjects, however, their occurrence during the MSLT is largely independent of the prior history of sleep and waking.
Abstract: Thirty-two narcoleptic subjects with excessive daytime sleepiness and cataplexy were recorded for 33 continuous hours. The continuous polysomnographic recording (CPSG) was followed by a standard MSLT at 2-h intervals. There were 64 sleep onset REM episodes (SOREMs) vs 64 sleep onset nonREM episodes (SONREMs) during the CPSG, and 102 SOREMs vs 50 SONREMS during the MSLT. Both sleep onset types peaked at 13-15 h during the CPSG while sleep onsets were evenly distributed during the MSLT. In the latter procedure, the mean sleep latency was significantly shorter with SOREMs occurrence than with SONREMs occurrence. Two factors were extracted in each procedure by means of a Varimax Rotated Factor Analysis. During the CPSG, SOREMs were related to the preceding nocturnal sleep parameters in the first factor, and to the daytime total sleep time and the total number of sleep onsets in the second factor. During the MSLT, SOREMs were related only to the mean sleep latency and the total number of sleep onsets. It was concluded that the occurrence of SOREMs is primarily due to the residual somnolence in narcoleptic subjects. However, their occurrence during the MSLT is largely independent of the prior history of sleep and waking. Thus, we propose a nonREM-REM sleep dysregulation hypothesis to account for the appearance of SOREMs in narcolepsy.
TL;DR: Night sleep in sedentary African subjects living in the sahelian zone lasts from 7 h to 8 h, with high amounts of slow‐wave sleep (SWS) and paradoxical sleep (PS), SWS being present in each sleep cycle.
Abstract: Night sleep in sedentary African subjects living in the sahelian zone lasts from 7 h to 8 h, with high amounts of slow-wave sleep (SWS) and paradoxical sleep (PS), SWS being present in each sleep cycle. We report here on sleep patterns in 6 healthy male European expatriates (aged 32-39 years) living in the same tropical climate. Polysomnography was taken for 3 consecutive nights in February (mean ambient temperature, Ta: 29.5 degrees C), March (Ta: 31.6 degrees C) and May (Ta: 33.3 degrees C). Comparisons between seasons were made with an analysis of variance, with P >/= 0.05. Because of a first night effect, the first nocturnal recording was discarded. Total sleep time (TST) increased in May vs February and March (P < 0.05). Stage 2 was shorter in March than in February (P < 0.001) and its proportion decreased from February to March (P < 0.02) and from March to May (P < 0.05). Conversely, SWS increased from February to March and March to May (duration, P < 0.001; proportion, P < 0.05), due to an augmentation in stage 4 with more numerous and longer stage 4 phases. Stage 3 was also increased in May vs March. The latency to SWS was shorter in March. SWS was present in each sleep cycle. PS was high, but did not vary. The sleep pattern changes were directly correlated with Ta. In conclusion, Caucasians living in the tropics slept similarly to Africans. The seasonal sleep variations favour the hypothesis that SWS is increased when thermoregulatory processes are triggered, either through passive climatic heating or exercise-induced hyperthermia.