Showing papers on "Non-rapid eye movement sleep published in 1997"
TL;DR: The experiments for the first time dissociate specific effects of early and late sleep on two principal types of memory, declarative and procedural, in humans, and the benefit from sleep on recall depended on the phase of sleep and on the type of memory.
Abstract: Recall of paired-associate lists (declarative memory) and mirror-tracing skills (procedural memory) was assessed after retention intervals defined over early and late nocturnal sleep. In addition, effects of sleep on recall were compared with those of early and late retention intervals filled with wakefulness. Twenty healthy men served as subjects. Saliva cortisol concentrations were determined before and after the retention intervals to determine pituitary-adrenal secretory activity. Sleep was determined somnopolygraphically. Sleep generally enhanced recall when compared with the effects of corresponding retention intervals of wakefulness. The benefit from sleep on recall depended on the phase of sleep and on the type of memory: Recall of paired-associate lists improved more during early sleep, and recall of mirror-tracing skills improved more during late sleep. The effects may reflect different influences of slow wave sleep (SWS) and rapid eye movement (REM) sleep since time in SWS was 5 times longer during the early than late sleep retention interval, and time in REM sleep was twice as long during late than early sleep (p < 0.005). Changes in cortisol concentrations, which independently of sleep and wakefulness were lower during early retention intervals than late ones, cannot account for the effects of sleep on memory. The experiments for the first time dissociate specific effects of early and late sleep on two principal types of memory, declarative and procedural, in humans.
942 citations
TL;DR: The arousal data along with Stage 2 sleep transition data support the contention that increases in central nervous system sympathetic activity precede and possibly play a role in the initiation of REM sleep and arousals during sleep.
413 citations
TL;DR: Age and morningness were both important predictors of the habitual sleep patterns and polysomnographic sleep characteristics of people in the middle years of life (20‐59 y).
Abstract: The following four issues were assessed in a group of 110 adults between the age of 20 and 59y: (1) the effect of age (regarded as a continuous variable) on polysomnographic sleep characteristics, habitual sleep-diary patterns, and subjective sleep quality; (2) the effects of age on morningness-eveningness; (3) the effects of morningness-eveningness on sleep, after controlling for the effects of age; and (4) the role of morningness-eveningness as a mediator of the age and sleep relationship. Increasing age was related to earlier habitual waketime, earlier bedtime, less time in bed and better mood and alertness at waketime. In the laboratory, increasing age was associated with less time asleep, increased number of awakenings, decreased sleep efficiency, lower percentages of slow-wave sleep (SWS) and rapid eye movement (REM) sleep, higher percentages of Stage 1 and 2, shorter REM latency and reduced REM activity and density. Increasing age was also associated with higher morningness scores. After controlling for the effects of age, morningness was associated with earlier waketime, earlier bedtime, less time in bed, better alertness at waketime, less time spent asleep, more wake in the last 2 h of sleep, decreased REM activity, less stage REM (min and percentage), more Stage 1 (min and percentage) and fewer minutes of Stage 2. For one set of variables (night time in bed, waketime, total sleep time, wake in the last 2 h of sleep and minutes of REM and REM activity), morningness-eveningness accounted for about half of the relationship between age and sleep. For another set of variables (bedtime, alertness at waketime, percentages of REM and Stage 1), morningness-eveningness accounted for the entire relationship between age and sleep. In conclusion, age and morningness were both important predictors of the habitual sleep patterns and polysomnographic sleep characteristics of people in the middle years of life (20-59 y).
290 citations
TL;DR: It is suggested that PrP plays a role in promoting sleep continuity by comparing baseline recordings and the effects of sleep deprivation in PrP knockout mice and wild-type controls, which are the mice used for most gene targeting experiments and whose behavior is not well characterized.
Abstract: Mice are the preferred mammalian species for genetic investigations of the role of proteins. The normal function of the prion protein (PrP) is unknown, although it plays a major role in the prion diseases, including fatal familial insomnia. We investigated its role in sleep and sleep regulation by comparing baseline recordings and the effects of sleep deprivation in PrP knockout mice (129/SV) and wild-type controls (129/SV x C57BL/6), which are the mice used for most gene targeting experiments and whose behavior is not well characterized. Although no difference was evident in the amount of vigilance states, the null mice exhibited a larger degree of sleep fragmentation than the wild-type with almost double the amount of short waking episodes. As in other rodents, cortical temperature closely reflected the time course of waking. The increase of slow-wave activity (SWA; mean EEG power density in the 0.25-4.0 Hz range) at waking to nonrapid eye movement (NREM) sleep transitions was faster and reached a lower level in the null mice than in the wild-type. The contribution of the lower frequencies (0.25-5.0 Hz) to the spectrum was smaller than in other rodents in all three vigilance states, and the distinction between NREM sleep and REM sleep was most marked in the theta band. After the sleep deprivation, SWA was increased, but the changes in EEG power density and SWA were more prominent and lasted longer in the PrP-null mice. Our results suggest that PrP plays a role in promoting sleep continuity.
287 citations
TL;DR: Improvements in methods to detect and quantitate changes in the cortical electroencephalogram (EEG) may better define the relationship between arousal and apnea termination, and result in improved criteria for identifying EEG changes of clinical significance.
Abstract: The mechanisms by which respiratory stimuli induce arousal from sleep and the clinical significance of these arousals have been explored by numerous studies in the last two decades. Evidence to date suggests that the arousal stimulus in nonrapid eye movement sleep (NREM) is related to the level of inspiratory effort rather than the individual stimuli that contribute to ventilatory drive. A component of the arousal stimulus proportional to the level of inspiratory effort may originate in mechanoreceptors either in the upper airway or respiratory pump. Medullary centers responsible for ventilatory drive may also send a signal proportionate to the level of drive to higher centers in the brain which are responsible for arousal. Thus, the arousal stimulus may consist of multiple components, each increasing as inspiratory effort increases. The level of effort triggering arousal is an index of the arousability of the brain (arousal threshold). A deeper stage of sleep, central nervous system depressants, prior sleep fragmentation, and the presence of obstructive sleep apnea (OSA) have been observed to increase the arousal threshold to airway occlusion. Less information is available concerning the mechanisms of arousal from rapid eye movement (REM) sleep. While REM sleep is associated with the longest obstructive apneas in patients with OSA, normal human subjects appear to have a similar or lower arousal threshold to respiratory stimuli in REM compared to NREM sleep. Recent studies have challenged the assumption that the termination of all obstructive apnea is dependent on arousal from sleep. Improvements in methods to detect and quantitate changes in the cortical electroencephalogram (EEG) may better define the relationship between arousal and apnea termination. This may result in improved criteria for identifying EEG changes of clinical significance. While little is known concerning the mechanisms of arousal in central sleep apnea, arousal may play an important role in inducing this type of apnea in some patients.
277 citations
TL;DR: The regional differences in sleep EEG spectra indicate that sleep is not only a global phenomenon but also a local brain process with a different regional involvement of neuronal populations.
Abstract: The brain topography of power spectra along the antero-posterior (A-P) axis was studied in the all-night human sleep EEG. Spectra (0.25 - 25.0 Hz) were computed for an anterior (A; F3-C3), a middle (M; C3-P3) and a posterior (P; P3-O1) bipolar derivation, and the spectral gradients between two adjacent derivations were expressed by power ratios (A/M and M/P). At NREM-REM sleep transitions a power shift from A to M was present over almost the entire frequency range, while the direction of shifts between M and P differed between frequency bands. Within NREM sleep, frequency specific power gradients were present: In the low delta band power in both A (0.25 Hz bin) and P (0.25-1.0 Hz bins) was higher than in M. In the 4-9 Hz range the relation was A > M > P, and in the 15 - 25 Hz range power was largest in M. Power in the spindle frequency range was highest at 11.75 Hz in M, and at 13.5 - 13.75 Hz in A. Topographical differences were seen also in the temporal changes of power across and within NREM sleep episodes. Whereas NREM sleep power in the 2-Hz bin was higher in A than in M in the first episode, this difference vanished in the course of the night. This result points to a specific involvement of frontal parts of the cortex in sleep homeostasis. The regional differences in sleep EEG spectra indicate that sleep is not only a global phenomenon but also a local brain process with a different regional involvement of neuronal populations.
251 citations
TL;DR: Data indicate that the circadian pacemaker induces changes in EEG activity during REM and non‐REM sleep, which are dissimilar from the spectral changes induced by sleep deprivation and exhibit a close temporal association with the melatonin rhythm and the endogenous circadian phase of sleep consolidation.
Abstract: 1. The circadian pacemaker regulates the timing, structure and consolidation of human sleep. The extent to which this pacemaker affects electroencephalographic (EEG) activity during sleep remains unclear. 2. To investigate this, a total of 1.22 million power spectra were computed from EEGs recorded in seven men (total, 146 sleep episodes; 9 h 20 min each) who participated in a one-month-long protocol in which the sleep-wake cycle was desynchronized from the rhythm of plasma melatonin, which is driven by the circadian pacemaker. 3. In rapid eye movement (REM) sleep a small circadian variation in EEG activity was observed. The nadir of the circadian rhythm of alpha activity (8.25-10.5 Hz) coincided with the end of the interval during which plasma melatonin values were high, i.e. close to the crest of the REM sleep rhythm. 4. In non-REM sleep, variation in EEG activity between 0.25 and 11.5 Hz was primarily dependent on prior sleep time and only slightly affected by circadian phase, such that the lowest values coincided with the phase of melatonin secretion. 5. In the frequency range of sleep spindles, high-amplitude circadian rhythms with opposite phase positions relative to the melatonin rhythm were observed. Low-frequency sleep spindle activity (12.25-13.0 Hz) reached its crest and high-frequency sleep spindle activity (14.25-15.5 Hz) reached its nadir when sleep coincided with the phase of melatonin secretion. 6. These data indicate that the circadian pacemaker induces changes in EEG activity during REM and non-REM sleep. The changes in non-REM sleep EEG spectra are dissimilar from the spectral changes induced by sleep deprivation and exhibit a close temporal association with the melatonin rhythm and the endogenous circadian phase of sleep consolidation.
246 citations
TL;DR: It is demonstrated that melatonin exerts effects on the main characteristics of human sleep, that is, latency to sleep onset, sleep consolidation, slow waves, sleep spindles, an M sleep.
Abstract: The endogenous circadian rhythm of melatonin, driven by the suprachiasmatic nucleus, exhibits a close association with the endogenous circadian component of the sleep propensity rhythm and the endogenous circadian component of the variation in electroencephalogram (EEG) oscillations such as sleep spindles and slow waves. This association is maintained even when the sleep-wake cycle is desynchronized from the endogenous circadian rhythm of melatonin. Administration of melatonin during the day increases daytime sleep propensity as indexed by both the latency to sleep onset and sleep consolidation. The EEG during daytime sleep after melatonin administration exhibits characteristics reminiscent of the nocturnal sleep EEG, that is, increased sleep spindle activity and reduced slow-wave sleep and slow-wave activity, as detected by quantitative EEG analysis. Administration of higher doses of melatonin (5 mg or more) prior to nocturnal sleep results in an increase in rapid eye movement (REM) sleep. These data demonstrate that melatonin exerts effects on the main characteristics of human sleep, that is, latency to sleep onset, sleep consolidation, slow waves, sleep spindles, and REM sleep. There is a need for further studies using physiological doses and delivery systems that generate physiological plasma melatonin profiles to firmly establish the role of the endogenous circadian rhythm of melatonin in the circadian regulation of sleep.
228 citations
TL;DR: Sleep architecture, particularly the rapid eye movement (REM) component, was mapped in rats following exposure to chronic mild stress, and changes in REM sleep included increases in the duration of and transitions into REM sleep over the sleep part of the sleep-wake cycle, and a reduced latency to the onset of the first REM period.
172 citations
TL;DR: The results indicate that the duration of wakefulness prior to sleep and the timing of sleep determine its physiological expression, which in turn determines its subjective impression.
Abstract: SUMMARY The present study used short sleep episodes to explore the relation between subjective sleep quality, timing and physiological content of sleep. Eight subjects participated in 18 4-h sleep episodes to provide 4, 8, and 12 h of prior time awake before bedtimes at six different times of day in a sleep laboratory insulated from environmental disturbances. The results were analysed by ANOVAs and multiple regression techniques. Subjective sleep quality, calmness of sleep, ease of falling asleep, ability to ‘sleep through’, number of awakenings, and sleep latency showed a significant pattern of ‘better’ sleep with increasing prior time awake and with closeness to the circadian minimum (nadir) of rectal temperature (morning hours). ‘Ease of awakening’ in contrast, ‘decreased’ with increasing time awake and with closeness to the nadir/ morning hours. Multiple regression analysis showed that subjective sleep quality was predicted by subjective calmness of sleep and ease of falling asleep, among the subjective measures, and by total sleep time (TST) and slow-wave sleep (SWS – stages 3 +4) among the physiological sleep measures. The subjective ease of awakening was predicted by slow-wave sleep (negatively) and the circadian maximum of rectal temperature. The results indicate that the duration of wakefulness prior to sleep and the timing of sleep determine its physiological expression, which in turn determines its subjective impression.
166 citations
TL;DR: Rates of protein synthesis are increased in many regions of the brain during deep sleep compared with light sleep, and correlations between ICPSleu, and percent time in deep sleep were positive in all regions and were statistically significant in 35 of the regions.
Abstract: Local rates of cerebral protein synthesis (ICPSleu) were determined with the autoradiographic L-[1-14C]leucine method in seven awake and seven asleep, adult rhesus monkeys conditioned to sleep in a restraining chair in a darkened, ventilated chamber while EEG, EOG, and EMG were monitored. Prior to the period of measurement all animals slept for 1-4 h. Controls were awakened after at least one period of rapid-eye-movement (REM) sleep. Experimental animals were allowed to remain asleep, and they exhibited non-REM sleep for 71-99% of the experimental period. Statistically significant differences in ICPSleu between control and experimental animals were found in four of the 57 regions of brain examined, but these effects may have occurred by chance. In the sleeping animals, however, correlations between ICPSleu and percent time in deep sleep were positive in all regions and were statistically significant (P < or = 0.05) in 35 of the regions. When time in deep sleep was weighted for the integrated specific activity of leucine in grey matter, positive correlations were statistically significant (P < or = 0.05) in 18 regions in the experimental animals. These results suggest that rates of protein synthesis are increased in many regions of the brain during deep sleep compared with light sleep.
TL;DR: The strong increase in EEG slow-wave activity (SWA) after social defeat indicates that sleep may function to offset the mental loads imposed on the nervous system during wakefulness.
TL;DR: It is concluded that patients with CHD and obstructive sleep apnea are endangered by apnea-associated ischemia and that these ischemic episodes lead to activation of the CNS and additional fragmentation of sleep.
TL;DR: Data imply that GABAA agonists promote deep NREM sleep, without suppressing REM sleep, which is opposite to those induced by agonistic modulators ofGABAA receptors such as benzodiazepines and at variance with established mechanisms according to which GAB AA agonists and modulatory agonists would have similar effects.
Abstract: Recent studies in the rat demonstrated that systemic administration of muscimol and THIP, both selective GABAA receptor agonists, elevates slow wave activity in the EEG during non-rapid eye movement (NREM) sleep. In this placebo-controlled study, we assessed the influence of an oral dose of 20 mg THIP on nocturnal sleep in young healthy humans. Compared to placebo, THIP increased slow wave sleep by about 25 min. Spectral analysis of the EEG within NREM sleep revealed significant elevations in the lower frequencies (< 8 Hz) and reductions in the spindle frequency range (approximately 10-16 Hz). In accordance with previous findings in the rat, these data imply that GABAA agonists promote deep NREM sleep, without suppressing REM sleep. These effects are opposite to those induced by agonistic modulators of GABAA receptors such as benzodiazepines and are at variance with established mechanisms according to which GABAA agonists and modulatory agonists would have similar effects. The sleep response to GABAA agonists is highly similar to that evoked by sustained wakefulness, suggesting that GABAA receptors may be implicated in the homeostatic regulation of sleep.
TL;DR: Differences in sleep patterns cannot reliably distinguish patients with depression from those with other psychiatric disorders, but sleep changes may provide a window on neurobiologieal abnormalities in depression.
TL;DR: This study provides three new interesting results related to the maturation of sleep mechanisms and functions: the high stability of the percentage of slow-wave sleep along these 2 years, the presence (from 12 months of age) of a stage 2/REM sleep ratio equal to one, and a sleep change occuring earlier, during the diurnal rather than the nocturnal part of the nycthemere.
Abstract: The sleep organization of 15 normal infants (seven boys, eight girls) was studied at their homes during six 24-hour periods, i.e. at 3, 6, 9, 12, 18, and 24 months of age, using the Oxford Medical System. Sleep states and stages were scored visually at 30-second intervals, according to Rechtschaffen and Kales' criteria, adapted for children by Guilleminault. All sleep parameters were analyzed for the entire 24-hour period, i.e. during both the nocturnal and the diurnal part of the nycthemere. The results showed a continuous decrease in total sleep time, rapid eye movement (REM) sleep, and indeterminate sleep, and also an increase in waking time, quiet sleep, and stages 1 and 2 sleep. Except for slow-wave sleep, which remained very stable for the different ages, analysis of variance applied to the data showed clear age and day-night effects on sleep ontogenesis. Modifications with age were more precocious and more pronounced for the diurnal part of the nycthemere, especially as regards REM sleep. For the nocturnal part, there was a significant increase in sleep efficiency and in the length of the REM period after 12 months of age, while total sleep duration and number of awakenings decreased. In addition to normative data for clinical use, this study provides three new interesting results related to the maturation of sleep mechanisms and functions: 1) the high stability of the percentage of slow-wave sleep along these 2 years, 2) the presence (from 12 months of age) of a stage 2/REM sleep ratio equal to one, and a sleep change occuring earlier, during the diurnal rather than the nocturnal part of the nycthemere. The first two points could be regarded as indexes of sleep maturation reflecting developmental and neurophysiological changes in central nervous system structures. The third point underlines the importance of the circadian rhythm and the concept of "experience" in the maturation of sleep.
TL;DR: This work suggests that neonatal QS is not an immature form of SWS and that AS is best considered as an undifferentiated behavioral state from which bothSWS and REM sleep develop.
Abstract: Active sleep (AS) in the neonate has been considered to be an immature form of rapid eye movement (REM) sleep. Quiet sleep (QS) has been thought to represent an immature form of slow wave sleep (SWS). To determine the relationship between the behaviorally determined states of AS and QS and electrographically determined REM sleep and SWS, we examined sleep ontogeny in the developing rat using an experimental routine that permitted long-term recordings and minimized the effects of maternal separation. Under these conditions, a transient state that included electroencephalographic slow wave activity and phasic motor activity was eventually replaced with the mature SWS pattern. Our work suggests that neonatal QS is not an immature form of SWS and that AS is best considered as an undifferentiated behavioral state from which both SWS and REM sleep develop.
TL;DR: Since this polygraphic finding may be present in subjects without any sleep complaint and in patients with initial neurological impairment, diagnosis of the sleep disorders might be allowed only when the polygraphic characteristic of persistent tonus and complex motor behavior are recorded.
TL;DR: The sleep of 15 adult subjects who reported heightened generalized anxiety in the absence of other psychiatric syndromes and a 15-adult contrast group were studied, indicating disrupted sleep depth and continuity similar to that documented in clinical anxiety disorder patients and distinct from that of depressed patients.
Abstract: The sleep of 15 adult subjects who reported heightened generalized anxiety in the absence of other psychiatric syndromes and a 15-adult contrast group were studied by means of nocturnal polysomnography. Analysis of polysomnography variables revealed a significant discriminant function that accounted for 79% of the variance between groups, indicating that high-anxiety/worry subjects took longer to fall asleep, had a smaller percentage of deep (slow-wave) sleep, and more frequent transitions into light sleep [stage 1 nonrapid eye movement (NREM)]. Additional analyses indicated that high-anxiety/worry subjects had a greater percentage of light sleep, more early microarousals, a lower rapid eye movement (REM) density relative to low-anxiety subjects. These subjects also showed more electrodermal storming when slow-wave sleep and REM sleep variables were covaried. Results indicated disrupted sleep depth and continuity similar to that documented in clinical anxiety disorder patients and distinct from that of depressed patients. These results indicate that generalized anxiety and worry in otherwise healthy individuals may act to produce a clinically significant sleep disturbance in the absence of other psychiatric symptoms.
TL;DR: It is speculated that the greater increase in UAR in healthy young men may represent a gender-related susceptibility to sleep-disordered breathing that, in conjunction with other predisposing factors, may contribute to the development of obstructive sleep apnea.
Abstract: Trinder, John, Amanda Kay, Jan Kleiman, and Judith Dunai.Gender differences in airway resistance during sleep.J. Appl. Physiol. 83(6): 1986–1997, 1997.—At the onset of non-rapid-eye-movement (NREM)...
TL;DR: It is demonstrated that maxillomandibular advancement is successful in a high percentage of patients carefully selected by cephalometric and polysomnographic investigation, and postoperative success has proved to be stable over a period of 2 yrs.
Abstract: Obstructive sleep apnoea (OSA) is a common disorder with potentially serious consequences. If maxillary and mandibular deficiency, often in combination with a narrow posterior airway space is present, therapy of OSA by maxillomandibular osteotomy is possible. However, long-term follow-up of patients undergoing these procedures is lacking. We present the results of 15 OSA patients (1 female and 14 males), who underwent maxillomandibular advancement surgery with a follow-up of at least 2 yrs. Polysomnography was performed before surgery, after 6-12 weeks, and 1 and 2 yrs postoperatively. Mean apnoea/hypopnoea index (AHI) decreased from 51.4 events.h-1 before therapy to 5.0 events.h-1 6 weeks postoperatively, and was 8.5 events.h-1 after 2 yrs. Oxygen saturation significantly increased following surgery. After 2 yrs, the AHI was < 10 events.h-1 in 12 out of 15 subjects. No significant changes were found comparing the 6-12 weeks versus the 2 year follow-up data. The significant increase in stage 3/4 non-rapid eye movement (NREM) sleep and decrease in stage 1 NREM sleep, indicative of the restoration of normal physiological sleep structure, persisted in 14 of the 15 subjects 2 yrs postoperatively. Three patients, however, did not show satisfactory improvement 2 yrs postoperatively; two showed obstructive and one central respiratory events. This study demonstrates that maxillomandibular advancement is successful in a high percentage of patients carefully selected by cephalometric and polysomnographic investigation. Postoperative success has proved to be stable over a period of 2 yrs. Further preoperative evaluation seems necessary in patients with predominantly mixed or central apnoeas.
TL;DR: Patients with major depression who suffered a recurrence of depression had less delta EEG activity at baseline and remission, particularly in the lowest delta frequency band of 0.5-1.0 Hz.
TL;DR: It is concluded that noninvasive positive pressure ventilation improves sleep-related hypoxaemia and hypercapnia in severe cystic fibrosis patients without affecting sleep.
Abstract: Progressive deterioration of lung function in cystic fibrosis (CF) patients may lead to significant hypoxaemia and hypercapnia, especially during sleep. The effects of bi-level noninvasive positive pressure nasal mask ventilation (NIPPV) on respiration and sleep were compared to those of low-flow oxygen therapy in six CF patients (mean +/- SD age 22.3 +/- 4.7 yrs, with severe lung disease (forced expiratory volume in one second (FEV1) 29.4 +/- 3.4% predicted). Compared to the control night, NIPPV and oxygen therapy significantly improved overall night-time oxygen saturation during both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep stages. However, significant increases in transcutaneous CO2 tension occurred during oxygen therapy, while NIPPV markedly improved alveolar ventilation during all sleep states. Sleep architecture and arousals remained unchanged during NIPPV and oxygen therapy treatment nights. We conclude that noninvasive positive pressure ventilation improves sleep-related hypoxaemia and hypercapnia in severe cystic fibrosis patients without affecting sleep. The long-term compliance and benefits of noninvasive positive pressure ventilation remain unclear.
TL;DR: It was concluded that early morning work causes a reduction of sleep time and an increase in apprehension stress.
Abstract: The aim of the present study is to investigate how early morning work affects sleep and alertness. Twenty-two females, employed as airline cabin crew members, participated in the study. The design included two sleep conditions (work day and free day) for an early group and for a control group. The results show that early morning work reduced sleep to 5 hours and 12 minutes and that the reduction of sleep consisted of less stage 2 and rapid eye movement (REM) sleep. However, when the analysis was restricted to the first 5 hours, no differences in sleep stages, arousals, or sleep continuity were obtained between groups or conditions. Analysis of electroencephalogram (EEG) power density for the 0.5-16.5 Hz bands across nonREM periods showed no differences. With respect to the subjective ratings, early morning work was associated with more apprehension of difficulties in awakening and insufficient sleep. Daytime alertness and ease of awakening did not differ between groups, but the early group had significantly more sleepiness and complained more of unrefreshing sleep in connection with the work day compared to the free day. Ratings of insufficient sleep and high daytime sleepiness were mainly predicted (multiple regression analyses) by short total sleep time (TST), whereas apprehension of an unpleasant awakening was predicted by an early wake-up time. It was concluded that early morning work causes a reduction of sleep time and an increase in apprehension stress.
TL;DR: This observation shows that sleep does not develop simultaneously in all cortical areas but may affect some areas earlier than others, and in particular conditions, local sleep of certain areas may be a stable and long-lasting phenomenon.
Abstract: We have recorded from extrastriate area V4 in monkeys performing a visual search task When animals became tired or drowsy, responses to visual stimulation were often reduced or even completely blocked, and background activity changed to the burst-pause pattern typically seen in sleep In spite of such neuronal sleep observed in V4, animals continued to perform the visual task, indicating that at least the primary visual cortex was still working This observation shows that sleep does not develop simultaneously in all cortical areas but may affect some areas earlier than others In particular conditions, local sleep of certain areas may be a stable and long-lasting phenomenon
TL;DR: It is suggested that periodic leg movements in sleep are common in people with essential hypertension, although they do not seem to be associated with any particular sleep disorder.
Abstract: The presence of periodic leg movements in sleep (PLMS) was assessed in 91 subjects diagnosed with essential hypertension. More than 18 per cent of the sample had PLMS, which is considerably higher than in normal controls. Also, the prevalence was significantly correlated with the severity of hypertension, as well as with age. Periodic leg movements in sleep were more frequent in the first few hours of the sleep period and during sleep stages 1 and 2. The arousing effect of PLMS was minimal, with only 17 per cent of all events related to an EEG arousal. Our results suggest that PLMS are common in people with essential hypertension, although they do not seem to be associated with any particular sleep disorder.
TL;DR: It is suggested that, as a minor alarm response to endogenous/exogenous stimuli, arousal develops and is often followed by motor activation, such as a burst of bruxing, with, as in any situation when motor activity suddenly increases, a secondary increase of heart activity.
Abstract: We studied 24 bruxers (23-67 years old). They often complained of orofacial and bodily pain and presented autonomic symptoms (sweating 23%, palpitations at night 62%, decreased libido 50%); 19% had increased blood pressure requiring treatment, and 65% reported frequent headaches in the morning. Deep sleep and rapid eye movement (REM) were delayed. An average of 167 orofacial episodes developed during the night. The mean number of masseter bursts strictly defined as bruxism was 79, the mean delay for the first occurrence after sleep onset 18 minutes. The majority of bruxism occurred in stage 2 sleep and REM sleep. The mean number of shifts of sleep stages was 70, one-third occurring within the first minute following a bruxing episode, and 15% of bruxing episodes developed after a shift in sleep stage. Electroencephalogram showed alpha-delta pattern in 15% of the subjects. Short-lasting alpha activity was often encountered during the 10 seconds preceding the development of a bruxing episode. Tachycardia developed at its onset, persisting for 10 seconds. We suggest that, as a minor alarm response to endogenous/exogenous stimuli, arousal develops and is often followed by motor activation, such as a burst of bruxing, with, as in any situation when motor activity suddenly increases, a secondary increase of heart activity.
TL;DR: The results indicate that the commonly reported SWS and REM sleep changes in schizophrenia reflect the remnant of prior neuroleptic treatment rather than the pathophysiology of the disorder itself.
TL;DR: Impaired attention is found in the electrodermal-orienting response, a measure of attentional shift or capture, which indicates decreased attentional allocation to stimuli, and the third revealing more rapid loss of attention to repeated stimuli.
Abstract: Ever increasing societal demands for uninterrupted work are causing unparalleled amounts of sleep deprivation among workers. Sleep deprivation has been linked to safety problems ranging from medical misdiagnosis to industrial and vehicular accidents. Microsleeps (very brief intrusions of sleep into wakefulness) are usually cited as the cause of the performance decrements during sleep deprivation. Changes in a more basic physiological phenomenon, attentional shift, were hypothesized to be additional factors in performance declines. The current study examined the effects of 36 hours of sleep deprivation on the electrodermal-orienting response (OR), a measure of attentional shift or capture. Subjects were 71 male undergraduate students, who were divided into sleep deprivation and control (non-sleep deprivation) groups. The expected negative effects of sleep deprivation on performance were noted in increased reaction times and increased variability in the sleep-deprived group on attention-demanding cognitive tasks. OR latency was found to be significantly delayed after sleep deprivation, OR amplitude was significantly decreased, and habituation of the OR was significantly faster during sleep deprivation. These findings indicate impaired attention, the first revealing slowed shift of attention to novel stimuli, the second indicating decreased attentional allocation to stimuli, and the third revealing more rapid loss of attention to repeated stimuli. These phenomena may be factors in the impaired cognitive performance seen during sleep deprivation.
TL;DR: In this paper, the effects of CRF alone, and co-administered with NPY, on spontaneous brain activity as well as on auditory processing were evaluated using electrophysiological measures.
Abstract: Neuropeptide Y (NPY) has neuromodulatory actions on multiple brain functions including endocrine, behavioral, and circadian processes and has been implicated in the pathophysiology of both anxiety and depression. Behavioral studies suggest that NPY is a potent anxiolytic, whereas CRF is anxiogenic, thus it seems that a balance of these two peptides may exert important influences on behavioral state regulation. However, little is known about how the NPY/CRF balance affects general arousal, attention, and/or sleep states. The present study evaluated the effects of CRF alone, and co-administered with NPY, on spontaneous brain activity as well as on auditory processing using electrophysiological measures. Electroencephalographic (EEG) and event-related potentials (ERPs) were obtained in rats following intracerebroventricular administration of CRF (0.5 μg) and CRF (0.5 μg)/NPY (5.0 or 15 μg). Auditory processing, as assessed by ERPs, was affected most significantly in the frontal cortex where CRF produced increases in the N1 and P3 components of the ERP, and NPY/CRF co-administration produced significant decreases. These data are consistent with a role for CRF in hyperarousal, and further suggest that NPY may be capable of reversing such states. Administration of CRF also produced a significant increase in the time to sleep onset and a decrease in the amount of time spent in non-rapid eye movement (NREM) sleep as quantified by scoring the EEG paper records. Co-administration of NPY with CRF reversed the effects of CRF on sleep duration and sleep onset in a dose-dependent fashion. Spectral analysis revealed that CRF produced quantitative changes in the EEG that were similar to what has previously been reported. CRF-induced increases in fast frequency activity were found to be reversed by co-administration of NPY. Taken together these data suggest that “dysregulation” of sleep and arousal states in depression and anxiety may be consistent with an upset of the balance between hypothalamic neuropeptide systems. Depression and Anxiety 6:1–9, 1997. © 1997 Wiley-Liss, Inc.