Showing papers on "Non-rapid eye movement sleep published in 1995"
TL;DR: Analyses of the (nonadditive) interaction of the circadian and sleep-dependent components of sleep propensity and sleep structure revealed that the phase relation between the sleep-wake cycle and the circadian pacemaker during entrainment promotes the consolidation of sleep and wakefulness and facilitates the transitions between these vigilance states.
Abstract: The role of the endogenous circadian pacemaker in the timing of the sleep-wake cycle and the regulation of the internal structure of sleep, including REM sleep, EEG slow-wave (0.75-4.5 Hz) and sleep spindle activity (12.75-15.0 Hz) was investigated. Eight men lived in an environment free of time cues for 33-36 d and were scheduled to a 28 hr rest-activity cycle so that sleep episodes (9.33 hr each) occurred at all phases of the endogenous circadian cycle and variations in wakefulness preceding sleep were minimized. The crest of the robust circadian rhythm of REM sleep, which was observed throughout the sleep episode, was positioned shortly after the minimum of the core body temperature rhythm. Furthermore, a sleep-dependent increase of REM sleep was present, which, interacting with the circadian modulation, resulted in highest values of REM sleep when the end of scheduled sleep episodes coincided with habitual wake-time. Slow-wave activity decreased and sleep spindle activity increased in the course of all sleep episodes. Slow-wave activity in non-REM sleep exhibited a low amplitude circadian modulation which did not parallel the circadian rhythm of sleep propensity. Sleep spindle activity showed a marked endogenous circadian rhythm; its crest coincident with the beginning of the habitual sleep episode. Analyses of the (nonadditive) interaction of the circadian and sleep-dependent components of sleep propensity and sleep structure revealed that the phase relation between the sleep-wake cycle and the circadian pacemaker during entrainment promotes the consolidation of sleep and wakefulness and facilitates the transitions between these vigilance states.
1,241 citations
TL;DR: Data show that significant sleep loss exists in one-third or more of normal adults, that the effects are large and replicable and that similar effects can be produced in just 1 night in the laboratory.
Abstract: Summary: Data from recent laboratory studies indicate that nocturnal sleep periods reduced by as little as 1.3 to 1.5 hours for 1 night result in reduction of daytime alertness by as much as 32% as measured by the Multiple Sleep Latency Test (MSLT). Other data document that 1) 170/0--57% of normal young adults have MSLT latencies of ::;5.5 minutes, whereas ::;50% have MSLT values of ~ 10 minutes and 2) 28°/0--29% of young adults reported normally sleeping ::;6.5 hours on each weeknight. More extensive reduction of daily sleep amount is seen in night shift workers. A minimum of 2%-4% of middle-aged adults have hypersomnolence associated with sleep apnea. Together, these data show that significant sleep loss exists in one-third or more of normal adults, that the effects are large and replicable and that similar effects can be produced in just I night in the laboratory. In light of the magnitude of this sleep debt, it is not surprising that fatigue is a factor in 57% of accidents leading to the death of a truck driver and in 10% of fatal car accidents and results in costs of up to 56 billion dollars per year. A recent sleep extension study suggests that the average underlying sleep tendency in young adults is about 8.5 hours per night. By comparison, the average reported sleep length of 7.2-7.4 hours is deficient, and common sleep lengths of ::;6.5 hours can be disastrous. We must recognize the alertness function of sleep and the increasing consequences of sleepiness with the same vigor that we have come to recognize the societal impact of alcohol. Key Words: Sleep deprivation-Sleepiness-Sleep disorders- Work schedule tolerance. Weare in the midst of a golden age of discovery of the intricate interrelationship between our nocturnal sleep process and our level of daytime function. Fueled by the discovery of the tremendous incidence of sleep apnea and periodic leg movements in the population, the relationship between fragmented sleep and residual sleepiness, as well as the increased ability to measure the level of objective sleepiness with an objective test [the Multiple Sleep Latency Test (MSLT)] and in am bulatory environments, the pervasive role of excessive sleepiness in our society is becoming apparent. Much literature documents the negative effects of sleep deprivation on a wide range of psychomotor per formance tasks and mood variables. For the sake of simplicity, the primary outcome measure reported in this paper will be MSL T. However, the MSL T findings reported are consistent with similar changes in a broad range of abilities, including reaction time, short-term memory, vigilance and mood (1). Many empirical and applied studies have provided evidence for our national sleep debt. The degree of our
483 citations
TL;DR: In animals, there is continuing evidence of relatively small, vulnerable paradoxical sleep windows (PSWs) following successful acquisition, which appear to exhibit shorter latencies to onset when the amount of material presented during acquisition is increased.
452 citations
TL;DR: Exposure to light early or late in the subjective night has been used therapeutically to produce corrective phase delays or advances in both the sleep pattern and circadian rhythms.
Abstract: Advanced and delayed sleep phase disorders, and the hypersomnia that can accompany winter depression, have been treated successfully by appropriately timed artificial bright light exposure. Under entrainment to the 24-h day-night cycle, the sleep-wake pattern may assume various phase relationships to the circadian pacemaker, as indexed, for example, by abnormally long or short intervals between the onset of melatonin production or the core body temperature minimum and wake-up time. Advanced and delayed sleep phase syndromes and non-24-h sleep-wake syndrome have been variously ascribed to abnormal intrinsic circadian periodicity, deficiency of the entrainment mechanism, or--most simply--patterns of daily light exposure insufficient for adequate phase resetting. The timing of sleep is influenced by underlying circadian phase, but psychosocial constraints also play a major role. Exposure to light early or late in the subjective night has been used therapeutically to produce corrective phase delays or advances, respectively, in both the sleep pattern and circadian rhythms. Supplemental light exposure in fall and winter can reduce the hypersomnia of winter depression, although the therapeutic effect may be less dependent on timing.
233 citations
TL;DR: The data indicate that a saliva level of caffeine as low as 3 mumol/l directly affects sleep propensity or, alternatively, that the presence of caffeine in the central nervous system during the waking episode reduces the progressive increase of sleep propensity associated with wakefulness.
191 citations
TL;DR: It is concluded that triazolam increases the arousal threshold to airway occlusion, but that this results in only modest prolongation of event duration and increased desaturation at a dose of 0.25 mg in a group of large sleep apnea patients.
Abstract: The purpose of this study was to assess the effect of triazolam (0.25 mg) on apnea duration and the arousal response to airway occlusion during sleep in patients with severe obstructive sleep apnea (OSA). Twelve male subjects with a mean (+/- SD) age of 46.6 +/- 14.1 yr and body weight of 260.8 +/- 55.9 lb were studied on two nights separated by a nonstudy night. They ingested triazolam (0.25 mg) or placebo 0.5 h before bedtime in a randomized double-blind crossover manner. In non-rapid-eye-movement (NREM) sleep, the mean (+/- SEM) duration of apnea/hypopnea was slightly increased (26.8 +/- 1.7 versus 23.8 +/- 1.2 s, p < 0.02) and the mean nadir in arterial oxygen saturation lower (80.1 +/- 1.9 versus 84.2 +/- 1.4%, p < 0.001) on triazolam nights. In NREM sleep, the deflections in esophageal pressure prior to apnea termination were higher on triazolam nights (53.3 +/- 5.4 versus 44.5 +/- 4.8 cm H2O, p < 0.001). However, the rate of increase in inspiratory effort (esophageal pressure deflections) during obstructive events was not decreased by triazolam. We conclude that triazolam increases the arousal threshold to airway occlusion, but that this results in only modest prolongation of event duration and increased desaturation at a dose of 0.25 mg in a group of large sleep apnea patients.
173 citations
TL;DR: The comparison of mammalian species has revealed striking similarities in the way sleep is regulated which indicates common underlying mechanisms.
170 citations
TL;DR: An increase in sleep instability and in arousal oscillation seems to be a typical microstructural feature of delta sleep-related parasomnias and probably plays a role in triggering abnormal motor episodes during sleep in patients with motor and behavioral phenomena during sleep.
Abstract: Some non-rapid eye movement (NREM) parasomnias, such as sleep-walking (SW), sleep terror (ST) and, in some aspects, sleep enuresis (SE), are considered "arousal disorders" without significant polysomnographic changes in classic sleep macrostructure. The aim of our study was to evaluate sleep microstructure and oscillations of arousal level by cyclic alternating pattern (CAP) scoring in some NREM parasomnias. Nocturnal polysomnography and videotape recording was used to study 21 patients with motor and behavioral phenomena during sleep: 13 in Group A (seven SW, six ST) with delta sleep-related episodes, eight in Group B with other parasomnias (six sleep bruxism and two SE), and six healthy controls. Classic sleep macrostructural parameters were no different in the parasomniacs and controls. Compared with the controls, our patients' sleep microstructure, scored by CAP analysis, showed increases in CAP rate (a measure of NREM instability with high level of arousal oscillation), in number of the CAP cycles, and in arousals with EEG synchronization, the increases being more significant in Group A than in Group B. An increase in sleep instability and in arousal oscillation seems to be a typical microstructural feature of delta sleep-related parasomnias and probably plays a role in triggering abnormal motor episodes during sleep in these patients.
170 citations
TL;DR: Patients with obstructive sleep apnea in early Stage 2 sleep were studied and obstructive apneic events with and without typical EEG arousals were analyzed, defining an arousal as a frequency shift to waking alpha rhythm of 1 s or longer.
Abstract: Patients with obstructive sleep apnea (OSA) experience severe sleep disruption and consequent daytime sleepiness. Current arousal scoring criteria show that some obstructive apneic events do not end in a recognizable cortical electroencephalographic (EEG) arousal. It is not known whether events that end in an obvious EEG arousal differ from those that do not, in terms of EEG frequency changes during the apneic event, the respiratory effort developed prior to apnea termination, the degree of the postapneic increase in blood pressure, or changes in CO2 tensions. We studied 15 patients with OSA in early Stage 2 sleep and analyzed obstructive apneic events with and without typical EEG arousals, defining an arousal as a frequency shift to waking alpha rhythm of 1 s or longer. EEG signals were digitized and analyzed by fast Fourier transform during and immediately after each apnea. The median EEG frequency and mean pleural pressure of the first and second halves of the apneic episode were compared with that of ...
148 citations
TL;DR: The alpha NREM sleep anomaly is present in only a small proportion of patients with fibromyalgia and does not correlate with disease severity nor is it affected by treatment with amitriptyline.
Abstract: Objective. To determine the prevalence and clinical correlations of an anomaly consisting of electroencephalographic (EEG) waves within the alpha frequency band during non–rapid eye movement (NREM) sleep in patients with fibromyalgia, and to evaluate the alpha NREM sleep anomaly as a predictor of response to amitriptyline.
Methods. Twenty-two patients with fibromyalgia were studied in a 2-month, double-blind, crossover trial of amitriptyline (25 mg/day) versus placebo. Nocturnal EEGs were conducted on 2 consecutive nights at baseline and at the end of each 2-month treatment period.
Results. Six patients (27%) had a clinical response to amitriptyline, while none responded to placebo (P = 0.02). Treatment with amitriptyline or placebo did not result in any changes in the alpha ratings during NREM sleep. Only 8 patients (36%) exhibited the alpha NREM sleep anomaly at baseline. Those patients reported more sleep difficulty, but otherwise were clinically indistinguishable from those without this EEG sleep anomaly. Lower baseline alpha NREM sleep ratings were seen in responders to amitriptyline than in nonresponders, but these differences did not reach statistical significance.
Conclusion. The alpha NREM sleep anomaly is present in only a small proportion of patients with fibromyalgia. It does not correlate with disease severity nor is it affected by treatment with amitriptyline. A larger sample size will be needed to adequately assess the value of this sleep anomaly in predicting the response to amitriptyline.
148 citations
Journal Article•
TL;DR: The main neural structures generating muscle atonia and other phenomena characteristic of REM sleep are present in dorsolateral portions of the pons in the brainstem, and this last monoaminergic neuronal population probably has a gating or inhibiting effect upon the cholinergic and cholinoceptive neuronal populations related to the generation of generalized Muscle atonia in REM sleep.
Abstract: The main neural structures generating muscle atonia and other phenomena characteristic of REM sleep are present in dorsolateral portions of the pons in the brainstem. Occurrence of REM sleep and the NREM-REM sleep cycle are probably determined by a balance or interaction between the cholinergic and cholinoceptive REM sleep-on neuronal populations and the monoaminergic REM sleep-off neuronal population. Neural activities producing generalized muscle atonia in REM sleep originate mainly in dorsolateral portions of the pontine reticular formation, descend through the medulla and spinal cord, and inhibit the motoneurons in the brainstem and spinal cord, bringing about postural atonia. Cataplexy and sleep paralysis are pathological, dissociated manifestations of the generalized muscle atonia characteristic REM sleep. Cataplexy is triggered by emotional stimuli, probably through activation of the neural structure generating the muscle atonia of REM sleep. During long-lasting cataplectic attacks, narcoleptic humans often experience sleep paralysis and vivid hypnagogic hallucinations in the latter sleep state. Sleep paralysis is caused by the marked dissociation between level of alertness and muscle atonia that often occurs in SOREM sleep episodes. Frequent SOREM sleep episodes in narcoleptic humans and dogs may occur when some of the neural mechanisms producing wakefulness and/or NREM sleep that normally inhibit the occurrence of REM sleep are abnormally weak, or when neural mechanisms facilitating the occurrence of REM sleep are hypersensitive or hyperactive, or both. Both abnormalities may contribute to the occurrence of SOREM sleep episodes and sleep paralysis, and also to the emotional triggering of cataplexy. Frequent occurrence of SOREM sleep episodes seems to be prerequisite but not sufficient for the occurrence of cataplexy. Some additional neural activities induced by emotion also contribute by inhibiting and/or activating the disturbed neural mechanisms related to SOREM sleep episodes. These abnormalities in neural mechanisms probably involve hypersensitivity or hyperactivity of muscarinic cholinergic and/or cholinoceptive neuronal populations in the pontine and suprapontine structures, and/or abnormally decreased activity of noradrenergic or serotonergic neuronal populations in the pons and/or other brainstem structures. This last monoaminergic neuronal population probably has a gating or inhibiting effect upon the cholinergic and cholinoceptive neuronal populations related to the generation of generalized muscle atonia and REM sleep. In spite of many studies and published reports on REM sleep, as well as on cataplexy and sleep paralysis, we are still far from a complete understanding of the physiological mechanisms producing muscle atonia in REM sleep and of the pathophysiological mechanisms of cataplexy and sleep paralysis--though it is apparent that these mechanisms are closely related.
TL;DR: The notion that gender-related anatomical differences have a general effect on EEG amplitude, including during slow-wave sleep, supports the notion that aging affects the neurophysiologicalSlow-wave-generating mechanism.
Abstract: Low-frequency EEG was analyzed quantitatively during 2 nights in 40 females and 34 males aged 26 to 101 years. Analyses were based on Rechtschaffen and Kales NREM sleep stages, on absolute low-frequency amplitude (i.e. power in the range of 0.2-2.0 Hz) and on low-frequency continuity. The latter parameter describes how much (0-100%) of the current slow-wave activity is continued in the near-future EEG. Such continuation can occur through closed loops in the underlying neuronal network and cells. These loops are slow, thus corresponding to slow-wave frequencies, and can consist of electrophysiological, chemical and/or other pathways. The continuity percentage then monitors the relative activity of these loops. It does not depend directly on absolute EEG amplitudes. All analyzed parameters, including amplitude-independent continuity, decreased substantially and significantly with increasing age. The amplitudes of low-frequency EEG in females were significantly and substantially (40%) larger than those in males. However, the amplitude-independent continuity percentage did not differ between the genders. These findings support the notion that gender-related anatomical differences have a general effect on EEG amplitude, including during slow-wave sleep. Aging, however, specifically affects the neurophysiological slow-wave-generating mechanism.
TL;DR: The first field tests of a home-based sleep monitoring system, the Nightcap, which uses eyelid and body movement sensors to discriminate wake, NREM, and REM sleep automatically are described, suggesting that this new device is sensitive to clinically relevant changes in the quality of sleep.
Abstract: In this paper, we describe the first field tests of a home-based sleep monitoring system, the Nightcap, which uses eyelid and body movement sensors to discriminate wake, NREM, and REM sleep automatically. Ten normal young adults were studied in the sleep laboratory and at home to allow comparison of Nightcap-derived measures with those obtained by traditional polysomnography. The agreement between the two techniques was 87% based on 1-min epochs--93% for NREM, 80% for REM, and 72% for wake. When the values for sleep latency, REM latency, wake time, NREM time, and REM time calculated from polysomnograph records were compared with the values calculated from Nightcap data, no significant differences were seen. In cases of extremely poor sleep, objective sleep efficiency estimates correlated well with subjective reports, suggesting that the Nightcap is sensitive to clinically relevant changes in the quality of sleep. This new device should prove useful to researchers wishing to study the psychophysiology and pathophysiology of sleep in more naturalistic and cost-effective paradigms than possible in the traditional sleep laboratory.
TL;DR: Changes in the EEG are to some extent similar to those induced by benzodiazepine hypnotics and to the contribution of the endogenous circadian pacemaker to the spectral composition of the sleep EEG when sleep occurs at night.
TL;DR: Results are consistent with a hypothesis that the activation of sleep-related warm-sensitive neurons and the deactivation of wake-related cold-sensitive neuron may play a key role in the onset and regulation of NREM sleep.
Abstract: Thermosensitive neurons of the preoptic/anterior hypothalamic area (POAH) have been implicated in the regulation of non-rapid eye movement (NREM) sleep. We attempted to identify those medial POAH thermosensitive neurons that may be involved in NREM sleep regulation. The thermosensitivity of medial POAH neurons was studied in five freely moving adult cats by local cooling or warming of the medial POAH with a water-perfused thermode. Of 308 neurons, 65 (21%) were classified as thermosensitive, including 31 (10%) warm-sensitive and 34 (11%) cold-sensitive neurons. The spontaneous discharge rates of 28 warm-sensitive, 34 cold-sensitive, and 115 randomly selected thermoinsensitive neurons were recorded through one to three sleep-waking cycles. Patterns of spontaneous activity for warm- and cold-sensitive neurons were different. Of 28 warm-sensitive neurons, 18 (64%) exhibited increased discharge rate during NREM sleep compared with waking (NREM/wake, > or = 1.2). This subpopulation of warm-sensitive neurons also exhibited significantly increased thermosensitivity when tested during NREM sleep. Of 34 cold-sensitive neurons, 25 (74%) discharged more slowly during NREM sleep compared with waking (NREM/wake, < or = 0.8). This subpopulation of cold-sensitive neurons exhibited decreased thermosensitivity during NREM sleep. These results are consistent with a hypothesis that the activation of sleep-related warm-sensitive neurons and the deactivation of wake-related cold-sensitive neurons may play a key role in the onset and regulation of NREM sleep.
01 Jan 1995
TL;DR: In this article, low-frequency EEG was analyzed quantitatively during two nights in 40 females and 34 males aged 26 to 101 years, and the amplitude-independent continuity percentage did not differ significantly with increasing age.
Abstract: Summary: Low-frequency EEG was analyzed quantitatively during 2 nights in 40 females and 34 males aged 26 to 101 years. Analyses were based on Rechtschaffen and Kales NREM sleep stages, on absolute low-frequency amplitude (i.e. power in the range of 0.2-2.0 Hz) and on low-frequency continuity. The latter parameter describes how much (0-100%) of the current slow-wave activity is continued in the near-future EEG. Such continuation can occur through closed loops in the underlying neuronal network and cells. These loops are slow, thus corresponding to slow-wave frequencies, and can consist of electro physiological, chemical and/or other pathways. The continuity percentage then monitors the relative activity of these loops. It does not depend directly on absolute EEG amplitudes. All analyzed parameters, including amplitude-independent continuity, decreased substantially and significantly with increasing age. The amplitudes of low-frequency EEG in females were significantly and substantially (40%) larger than those in males. However, the amplitude-independent continuity percentage did not differ between the genders.
TL;DR: In this paper, the effects of sleep loss on the ability to ignore distracting irrelevant stimuli were measured using a finding embedded figures test (FEFT), which was shown to be significantly sensitive to one night's sleep deprivation.
Abstract: In four sleep loss experiments we aimed, first, to compare performance during long-term sleep reduction with performance during short-term total sleep deprivation, and second, to measure the effects of both methods of sleep loss on ability to ignore distracting irrelevant stimuli, using a finding embedded figures test (FEFT). Logical reasoning, auditory vigilance and finding embedded figures tasks were shown to be significantly sensitive to one night's sleep deprivation. However, in one sleep reduction study subjects reduced to a mean of 5.2 hours sleep per night for 4 weeks showed no performance deficits on logical reasoning. In a second sleep reduction study subjects reduced to a mean of 4.3 hours sleep per night for 4 nights, and subjects reduced to a mean of 5.3 hours sleep per night for 18 nights, showed no performance deficits on logical reasoning or auditory vigilance, despite their reports of severe increases in subjective sleepiness and reduced concentration. Both these sleep reduction groups, though, did show decrements on the FEFT, which we interpret in terms of dearousal increasing distractibility, which the sleep-reduced subjects could not overcome with effort, as they did with the other tests.
TL;DR: The hypothesis is put forward that rapid eye movement (REM) sleep in early life serves as an indicator for the degree of brain maturation and the promoter of further brain development.
TL;DR: The effects of rapid-eye movement (REM) sleep on various mechanisms involved in cardiorespiratory control are of particular significance during the postnatal period since newborns spend much of their time in this sleep state.
Abstract: The cardiorespiratory control system undergoes functional maturation after birth. Until this process is completed, the cardiorespiratory system is unstable, placing infants at risk for cardiorespiratory disturbances, especially during sleep. The profound influence of states of alertness on respiratory and cardiac control has been the focus of intense scrutiny during the last decade. The effects of rapid-eye movement (REM) sleep on various mechanisms involved in cardiorespiratory control are of particular significance during the postnatal period since newborns spend much of their time in this sleep state. In fullterm newborns, REM sleep occupies more than 50% of total sleep time, and this percentage is even greater in preterm newborns. From term to six months of age, the proportion of REM sleep decreases. Since respiratory and cardiac disturbances are known to occur selectively during REM sleep, the predominance of REM sleep may be a risk factor for abnormal sleep-related events during early infancy. Awareness of these developmental changes in sleep patterns is important for clinicians dealing with problems such as apparent life-threatening events (ALTE), sudden infant death syndrome (SIDS), and/or cardiorespiratory responses to respiratory disorders. Our current understanding of respiratory and cardiac control rests mainly on studies conducted during the first months of life. There is a paucity of data on late infancy and early childhood. The present paper will review available data on how sleep affects 1) ventilatory mechanics, in particular of the upper airways and the chest wall; ventilation and apnea; gas exchange; chemoreceptor function; and arousal responses; 2) changes in heart rate and heart rate variability, and the occurrence and mechanisms of bradycardia.
TL;DR: To investigate the time course of sleep inertia, self-ratings of alertness and reaction time in a memory task were repeatedly assessed after nighttime and daytime sleep episodes in healthy young men to demonstrate that sleep inertia is a robust, quantifiable process that can be incorporated in models of sleep and vigilance.
Abstract: Sleep inertia refers to the period of reduced vigilance following upon awakening from sleep To investigate the time course of sleep inertia, self-ratings of alertness and reaction time in a memory task were repeatedly assessed after nighttime and daytime sleep episodes in healthy young men Alertness gradually increased and reaction time gradually decreased within the first hour after awakening Their time course could be described by exponential functions with time constants of 045 h and 03 h, respectively The data demonstrate that sleep inertia is a robust, quantifiable process that can be incorporated in models of sleep and vigilance
Journal Article•
TL;DR: In patients with muscle weakness, nocturnal oxygenation correlates with diaphragmatic strength, and loss of this "accessory inspiratory" effect may contribute to "central" hypopnoea.
Abstract: Patients with respiratory muscle weakness show nocturnal hypoventilation, with oxygen desaturation particularly during rapid eye movement (REM) sleep, but evidence in individuals with isolated bilateral diaphragmatic paresis (BDP) is conflicting. The effect of sleep on relative activity of the different respiratory muscles of such patients and, consequently, the precise mechanisms causing desaturation have not been clarified. We have studied eight patients, four with generalized muscle weakness and four with isolated BDP during nocturnal sleep with measurements including oxygen saturation and surface electromyographic (EMG) activity of various respiratory muscle groups. Nocturnal oxygenation correlated inversely with postural fall in vital capacity, an index of diaphragmatic strength. During REM sleep, hypopnoea and desaturation occurred particularly during periods of rapid eye movements (phasic REM sleep). In most subjects, such events were "central" in type and associated with marked suppression of intercostal muscle activity, but two subjects had recurrent desaturation due to "obstructive" hypopnoea and/or apnoea. Expiratory activity of the external oblique muscle was present whilst awake and during non-rapid eye movement (NREM) sleep in seven of the eight subjects in the semirecumbent posture. This probably represents an "accessory inspiratory" effect, which aids passive caudal diaphragmatic motion as the abdominal muscles relax at the onset of inspiration. Expiratory abdominal muscle activity was suppressed in phasic REM sleep, suggesting that loss of this "accessory inspiratory" effect may contribute to "central" hypopnoea. We conclude that, in patients with muscle weakness, nocturnal oxygenation correlates with diaphragmatic strength.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The precise regulation of slow-wave and spindle activity as a function of the duration and intensity of prior sleep and wakefulness demonstrates that these EEG oscillations are accurate indicators of non-REM-sleep homeostasis and suggests that they are fundamental to the sleeping brain.
TL;DR: Comparing sleep quality and daytime sleepiness in patients with congestive heart failure who develop Cheyne-Stokes respiration during sleep and patients without CSR found that patients with CHF who develop CSR experience excessive daytime sleepness due to sleep disruption.
TL;DR: The results suggest that the major determinant of vivid visual imagery and enhanced cognitive activity during sleep is a pattern of subcortical and cortical activation that is common to both the REM phase of the REM-NREM cycle and the activated phase ofThe 24-h diurnal wake-sleep cycle.
TL;DR: The existence of alpha activity which differs in generation site (thalamus), scalp distribution (frontal‐central), and behavioural correlates (e.g. enhancement to stimulation during wakefulness, concentration in the first‐half of the night during sleep, and absence of sleep disturbance) from occipital alpha activity is suggested.
Abstract: SUMMARY Alpha activity occurring during sleep is generally considered to reflect arousal processes and a shift toward wakefulness. This long-standing interpretation is based on physiological and behavioural arousal correlates of alpha activity presumed to have an occipital focus. In addition to the application of this interpretation to sleep/wake state determinations, there have been reports of nonrefreshing or nonrestorative sleep in clinical populations exhibiting dramatic amounts of alpha intrusion during sleep in the absence of awakening. Reports of the presence of alpha activity during sleep in normal subjects without sleep disruption or complaints of daytime sleepiness call into question the interpretation that this activity is associated with arousal. A re-examination of this literature, incorporating the results from recent investigations employing multi-site EEG recordings, electronic processing and source diple analyses of this activity, suggests the existence of alpha activity which differs in generation site (thalamus), scalp distribution (frontal-central), and behavioural correlates (e.g. enhancement to stimulation during wakefulness, concentration in the first-half of the night during sleep, and absence of sleep disturbance) from occipital alpha activity. Such marked differences in defining characteristics imply different functional correlates for these activities. In this context, it is proposed that this fronto-central alpha activity is associated with sleep-maintaining processes which may be enhanced in response to sleep-disturbing events.
TL;DR: The decreased power in the low-frequency range might reflect a disorder in homoeostatic and circadian mechanisms during sleep and may contribute to daytime symptoms in patients with fibromyalgia.
Abstract: Alpha electroencephalography (EEG) predominance has been described during sleep in patients suffering from the fibromyalgia syndrome (FMS). However, EEG power density in the lower frequency bands probably better reflects the restorative functions of sleep. This study was conducted to describe the energy in all frequency bands in the sleep EEG. Ambulatory sleep recordings were performed on 12 women with FMS and 14 control women. Epochs were classified according to standard criteria. Moreover, all 2-s segments (n = 287 355) of the EEG in non-rapid-eye-movement (NREM) 2-4 sleep were subjected to frequency analysis using autoregressive modelling. Frequency bands were : delta (0.5-3.5 Hz), theta (3.5-8 Hz), alpha (8-12 Hz), sigma (12-14.5 Hz) and beta (14.5-25 Hz). In patients with FMS, there was a predominance of EEG power in the higher frequency bands [two-way analysis of variance (ANOVA), alpha : P = 0.043 ; sigma : P = 0.004] at the expense of the lower frequencies (ANOVA, delta : P = 0.005 ; theta : P = 0.008). The same trends were obtained for the individual sleep cycles. The calculations of total delta power in the time domain showed an exponentially declining curve in healthy subjects, but a flatter decline in FMS. The decreased power in the low-frequency range might reflect a disorder in homoeostatic and circadian mechanisms during sleep and may contribute to daytime symptoms in patients with fibromyalgia.
TL;DR: It is hypothesized that sleep-related violent behavior associated with parasomnias occurs as the result of a diathesis and is precipitated by stressors and mediated by disturbed nonrapid eye movement (NREM) sleep physiology.
Abstract: We hypothesized that sleep-related violent behavior associated with parasomnias occurs as the result of a diathesis and is precipitated by stressors and mediated by disturbed nonrapid eye movement (NREM) sleep physiology. Sixty-four consecutive adult patients (mean age 30 years) who were investigated for sleepwalking or sleep terrors were categorized according to clinical history into three groups: serious violence during sleep to other people or to property or self (n = 26); harmful, but not destructive behavior (n = 12); and nonviolent behavior (n = 26). Log linear analysis showed that a diathesis (childhood parasomnia and/or family history of parasomnia) and a stressor (psychologic distress, substance abuse and sleep schedule disorder) predicted the presence of sleepwalking or night terror. Serious violent acts were more likely to occur with males (p < 0.004) who showed sleep schedule disorder (p < 0.03). Both harmful and serious violent sleep behavior occurred with drug abuse (p < 0.009). In comparison to all other groups, those who were violent to other people were males who experienced more stressors (p < 0.02), drank excessive caffeinated beverages, abused drugs (p < 0.03) and showed less stage 4 sleep (p < 0.02) and less alpha (7.5-11 Hz) electroencephalogram NREM sleep (p < 0.02) on polysomnography. Being male and having < 2% stage 4 sleep provided 89% sensitivity, 80% specificity and 81% diagnostic accuracy for individuals who were violent to others. The forensic implications of these findings are discussed.
TL;DR: In both groups, the frequency of nocturnal wandering increased with an increase in daytime stressors, and Pharmacological and psychiatric treatment approaches were beneficial in both groups.
Abstract: Forty-one subjects between 12 and 63 years of age with a complaint of nocturnal wandering were reviewed retrospectively, and a prospective investigation of their compliance to treatment was performed Twenty-nine of 41 subjects committed violence against themselves or others ("violent group") Clinical investigation of their problem involved polysomnography, wake and sleep EEGs and ambulatory EEG recording in the home environment The nocturnal wandering may have started from NREM sleep or REM sleep, and violence was observed in both of these sleep states Arousal from sleep may have been triggered by sleep-disordered breathing or may have been related to temporal lobe abnormalities, and, in some cases, no abnormal polygraphic features were noted Violence was always preceded by many instances of nocturnal wandering that had received little clinical attention Temporal lobe abnormalities, a rare cause of nocturnal wandering, were present only in the "violent" group This group also had a higher percentage of men than the "nonviolent" group In both groups, the frequency of nocturnal wandering increased with an increase in daytime stressors Pharmacological and psychiatric treatment approaches were beneficial in both groups Language: en
TL;DR: The recovery of sleep quantity was accomplished by increased sleep during the dark hours, resulting in a long-lasting disruption of normal circadian sleep patterning.
TL;DR: Interestingly, REM was characterized by higher incidence and amplitude delta than those found in stage 1 sleep, which suggests that period analysis provides a detailed description of EEG frequency characteristics during sleep but does not reveal dramatic gender differences.
Abstract: Period-analyzed electroencephalographic (EEG) activity was evaluated in 11 men and 11 women to explore the distribution of EEG frequencies during sleep and potential gender differences. Significant stage-of-sleep main effects were noted for both incidence and amplitude measures. Power measures seemed to best differentiate between non-rapid eye movement (NREM) stages, although incidence measures showed roughly the same distributions across sleep stages. Beta incidence and amplitude was highest in stage 1 sleep followed in descending order by rapid eye movement (REM), stage 2, and slow-wave sleep (SWS). Delta incidence and amplitude were highest in SWS, with slightly lower values in stage 2. Interestingly, REM was characterized by higher incidence and amplitude delta than those found in stage 1 sleep. EEG variables did not show striking sex differences in any sleep stage, although a global measure of delta power in NREM sleep was higher among women. Hemispheric asymmetries were small throughout REM and NREM stages. These findings suggest that period analysis provides a detailed description of EEG frequency characteristics during sleep but does not reveal dramatic gender differences.