Showing papers on "Non-rapid eye movement sleep published in 2002"

Learning-dependent increases in sleep spindle density.

Abstract: Declarative memory consolidation is enhanced by sleep. In the investigation of underlying mechanisms, mainly rapid eye movement (REM) sleep and slow-wave sleep have been considered. More recently, sleep stage 2 with sleep spindles as a most prominent feature has received increasing attention. Specifically, in rats hippocampal ripples were found to occur in temporal proximity to cortical sleep spindles, indicating an information transfer between the hippocampus and neocortex, which is supposed to underlie the consolidation of declarative memories during sleep. This study in humans looks at the changes in EEG activity during nocturnal sleep after extensive training on a declarative learning task, as compared with a nonlearning control task of equal visual stimulation and subjectively rated cognitive strain. Time spent in each sleep stage, spindle density, and EEG power spectra for 28 electrode locations were determined. During sleep after training, the density of sleep spindles was significantly higher after the learning task as compared with the nonlearning control task. This effect was largest during the first 90 min of sleep ( p < 0.01). Additionally, spindle density was correlated to recall performance both before and after sleep ( r = 0.56; p < 0.05). Power spectra and time spent in sleep stages did not differ between learning and nonlearning conditions. Results indicate that spindle activity during non-REM sleep is sensitive to previous learning experience.

The cognitive neuroscience of sleep: neuronal systems, consciousness and learning

Abstract: Sleep can be addressed across the entire hierarchy of biological organization. We discuss neuronal-network and regional forebrain activity during sleep, and its consequences for consciousness and cognition. Complex interactions in thalamocortical circuits maintain the electroencephalographic oscillations of non-rapid eye movement (NREM) sleep. Functional neuroimaging affords views of the human brain in both NREM and REM sleep, and has informed new concepts of the neural basis of dreaming during REM sleep — a state that is characterized by illogic, hallucinosis and emotionality compared with waking. Replay of waking neuronal activity during sleep in the rodent hippocampus and in functional images of human brains indicates possible roles for sleep in neuroplasticity. Different forms and stages of learning and memory might benefit from different stages of sleep and be subserved by different forebrain regions.

Sleep deprivation in the rat: X. Integration and discussion of the findings.

Abstract: The results of a series of studies on total and selective sleep deprivation in the rat are integrated and discussed. These studies showed that total sleep deprivation, paradoxical sleep deprivation, and disruption and/or deprivation of non-rapid eye movement (NREM) sleep produced a reliable syndrome that included death, debilitated appearance, skin lesions, increased food intake, weight loss, increased energy expenditure, decreased body temperature during the late stages of deprivation, increased plasma norepinephrine, and decreased plasma thyroxine. The significance of this syndrome for the function of sleep is not entirely clear, but several changes suggested that sleep may be necessary for effective thermoregulation.

REM Sleep and the Early Development of Posttraumatic Stress Disorder

Abstract: Objective: The potential for chronicity and treatment resistance once posttraumatic stress disorder (PTSD) has become established has stimulated interest in understanding the early pathogenesis of the disorder. Arousal regulation and memory consolidation appear to be important in determining the development of PTSD; both are functions of sleep. Sleep findings from patients with chronic PTSD are complex and somewhat contradictory, and data from the acute phase are quite limited. The aim of the present study was to obtain polysomnographic recordings during an acute period after life-threatening experiences and injury and to relate measures of sleep duration and maintenance and the timing, intensity, and continuity of REM sleep to the early development of PTSD. Method: Twenty-one injured subjects meeting study criteria received at least one polysomnographic recording close to the time of medical/surgical stabilization and within a month of injury. PTSD symptoms were assessed concurrently and 6 weeks later. Sleep measures were compared among injured subjects with and without significant PTSD symptoms at follow-up and 10 noninjured comparison subjects and were also correlated with PTSD severity. Results: There was more wake time after the onset of sleep in injured, trauma-exposed patients than in noninjured comparison subjects. Development of PTSD symptoms was associated with shorter average duration of REM sleep before a stage change and more periods of REM sleep. Conclusions: The development of PTSD symptoms after traumatic injury is associated with a more fragmented pattern of REM sleep.

NREM sleep EEG frequency spectral correlates of sleep complaints in primary insomnia subtypes.

Abstract: Design: We compared EEG frequency spectra from REM and NREM sleep in PPI subjects subtyped as subjective insomnia sufferers (those with relatively long total sleep time and relative underestimation of sleep time compared with PSG), and objective insomnia sufferers (those with relatively short PSG total sleep time) with EEG frequency spectra in normals. We also studied the correlation between these indices and the degree of underestimation of sleep. Further, we determined the degree to which sleep EEG indexes related to sleep complaints. Setting: Duke University Medical Center Sleep Laboratory. Participants: Normal (N=20), subjective insomnia (N=12), and objective insomnia (N=18) subjects. Interventions: N/A Measurements and Results: Lower delta and greater alpha, sigma, and beta NREM EEG activity were found in the patients with subjective insomnia but not those with objective insomnia, compared with the normal subjects. These results were robust to changes in the subtyping criteria. No effects were found for REM spectral indexes. Less delta non- REM EEG activity predicted greater deviation between subjective and PSG estimates of sleep time across all subjects. For the subjective insomnia subjects, diminished low-frequency and elevated higher frequency non- REM EEG activity was associated with their sleep complaints. Conclusions: NREM EEG frequency spectral indexes appear to be physiologic correlates of sleep complaints in patients with subjective insomnia and may reflect heightened arousal during sleep.

Selective Activation of the Extended Ventrolateral Preoptic Nucleus during Rapid Eye Movement Sleep

Abstract: We found previously that damage to a cluster of sleep-active neurons (Fos-positive during sleep) in the ventrolateral preoptic nucleus (VLPO) decreases non-rapid eye movement (NREM) sleep in rats, whereas injury to the sleep-active cells extending dorsally and medially from the VLPO cluster (the extended VLPO) diminishes REM sleep. These results led us to examine whether neurons in the extended VLPO are activated during REM sleep and the connectivity of these neurons with pontine sites implicated in producing REM sleep: the laterodorsal tegmental nucleus (LDT), dorsal raphe nucleus (DRN), and locus ceruleus (LC). After periods of dark exposure that triggered enrichment of REM sleep, the number of Fos-positive cells in the extended VLPO was highly correlated with REM but not NREM sleep. In contrast, the number of Fos-positive cells in the VLPO cluster was correlated with NREM but not REM sleep. Sixty percent of sleep-active cells in the extended VLPO and 90% of sleep-active cells in the VLPO cluster in dark-treated animals contained galanin mRNA. Retrograde tracing from the LDT, DRN, and LC demonstrated more labeled cells in the extended VLPO than the VLPO cluster, and 50% of these in the extended VLPO were sleep-active. Anterograde tracing showed that projections from the extended VLPO and VLPO cluster targeted the cell bodies and dendrites of DRN serotoninergic neurons and LC noradrenergic neurons but were not apposed to cholinergic neurons in the LDT. The connections and physiological activity of the extended VLPO suggest a specialized role in the regulation of REM sleep.

Human regional cerebral glucose metabolism during non-rapid eye movement sleep in relation to waking

Abstract: Sleep is an essential human function. Although the function of sleep has generally been regarded to be restorative, recent data indicate that it also plays an important role in cognition. The neurobiology of human sleep is most effectively analysed with functional imaging, and PET studies have contributed substantially to our understanding of both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. In this study, PET was used to determine patterns of regional glucose metabolism in NREM sleep compared with waking. We hypothesized that brain structures related to waking cognitive function would show a persistence of function into the NREM sleep state. Fourteen healthy subjects (age range 21-49 years; 10 women, 4 men) underwent concurrent EEG sleep studies and [(18)F]fluoro-2-deoxy-D-glucose PET scans during waking and NREM sleep. Whole-brain glucose metabolism declined significantly from waking to NREM sleep. Relative decreases in regional metabolism from waking to NREM sleep occurred in wide areas of frontal, parietal, temporal and occipital association cortex, primary visual cortex, and in anterior/dorsomedial thalamus. After controlling for the whole-brain declines in absolute metabolism, relative increases in regional metabolism from waking to NREM were found bilaterally in the dorsal pontine tegmentum, hypothalamus, basal forebrain, ventral striatum, anterior cingulate cortex and extensive regions of the mesial temporal lobe, including the amygdala and hippocampus, and in the right dorsal parietal association cortex and primary somatosensory and motor cortices. The reductions in relative metabolism in NREM sleep compared with waking are consistent with prior findings from blood flow studies. The relative increases in glucose utilization in the basal forebrain, hypothalamus, ventral striatum, amygdala, hippocampus and pontine reticular formation are new observations that are in accordance with the view that NREM sleep is important to brain plasticity in homeostatic regulation and mnemonic processing.

Nighttime sleep-wake patterns and self-soothing from birth to one year of age: a longitudinal intervention study.

Abstract: For infants who sleep independently, the ability to self-soothe when falling asleep at the beginning of the night and following nighttime awakenings appears to be a key ingredient for the development of healthy sleep-wake patterns. Although a number of studies have described the development of sleep-wake patterns during infancy, relatively few have examined factors related to the emergence of self-soothing behavior. Theoretically, self-soothing refers to an infant’s ability to regulate states of arousal; for example, calming from crying to quiet wakefulness without parental assistance. In this study, self-soothing refers to an infant’s ability to settle to sleep at the beginning of the night and to put herself back to sleep upon awakening during the night. The purpose of the current study was to objectively monitor infant sleep-wake patterns and other variables thought to relate to the development of self-soothing across the first year of life. The development of sleep-wake patterns follows a somewhat prescribed path during infancy. First, the 24-hour distribution of sleep changes across the first year. Newborns tend to sleep for 16–17 hours in 3–4 hour increments dispersed throughout the 24-hour day (Parmelee, Shulz, & Disbrow, 1961). By 1 year of age, the bulk of sleep shifts to the nighttime hours and sleep periods lengthen (consolidate), but the total amount of sleep per 24 hours decreases relatively little (Anders & Keener, 1985; Kleitman & Engelmann, 1953). Second, the proportions of sleep states change with age, such that rapid eye movement (REM) or active sleep decreases and non-rapid eye movement (NREM) or quiet sleep increases over the first year (Anders & Keener, 1985; Fagioli & Salzarulo, 1982). Although these basic patterns have been confirmed by numerous studies over the past 40 years, few large-scale longitudinal investigations have examined factors associated with the development of nighttime self-soothing. The few investigations that have examined falling asleep and self-soothing after nighttime awakenings during the first year of life have shown that this ability develops in some infants, but not others, by the end of the first year (Anders, Halpern, & Hua, 1992; Keener, Zeanah, & Anders, 1988; Goodlin-Jones, Burnham, Gaylor, & Anders, 2001; Goodlin-Jones, Eiben, & Anders, 1997). During the first months of life, infants most often fall asleep during or immediately after a feeding both at the beginning and during the middle of the night; self-soothing is observed only occasionally. By 4 to 6 months of age, however, self-soothing behaviors at sleep onset and following nighttime awakenings begin to appear in some infants and tend to increase in frequency to the first birthday (Goodlin-Jones et al., 2001). Infants who self-soothe are generally considered by parents to be better sleepers than infants who consistently need assistance to make the wake-sleep transition. Infant sleep disturbances are often brought to the attention of pediatricians during well-child visits due to the sleep disruption imposed on families (Lozoff, Wolf, & Davis, 1985). Indeed, France and Blampied (1999) define a sleep-disturbed infant as ‘one who is unable to settle back to sleep without the parents being aware of the awakening’. More precisely, awakenings are most disturbing to parents when the child cannot return to sleep on her own and requires parental intervention. For the purposes of the current investigation, these infants are considered ‘non-self-soothers’. Clearly, infants who do not develop the ability to self-soothe can create turmoil in some families. A simple linear model that describes the emergence of self-soothing is not sufficient. A transactional model embraces the complexities of interacting systems or domains across a developmental time span (Sameroff & Fiese, 2000). A transactional perspective to self-soothing might include infant characteristics, parental characteristics, and interactions between infants and parents. Figure 1 displays a tentative model of potential domains associated with self-soothing (Anders, 1994; Goodlin-Jones, Burnham, & Anders, 2000). Variables in the four domains are thought to relate to each other and, ultimately, to whether the child is or is not able to self-soothe to sleep from the waking state. The model reflects the notion that self-regulation of wake to sleep transitions results from a dynamic, interactive process between the infant and a number of proximal and distal influences, mediated mostly through interactions with caregivers. This model is a work in progress. Thus far, partial support for the transactional model comes from small-scale and/or cross-sectional investigations (e.g., Goodlin-Jones et al., 2001). There have been no longitudinal studies specifically designed to investigate the hypothesized links. Figure 1 A transactional model for the development of self-soothing behaviors related to wake-to-sleep state transitions. The model, derived from empirical and clinical experience, provides a framework to guide investigation. More research is required to assess ... Within the infant domain, the variable receiving most research attention in relation to infant sleep has been temperament. Infant temperament has been consistently, albeit moderately, related to the quality of nighttime sleep (Halpern, Anders, Garcia Coll, & Hua, 1994; Minde, Popiel, Leos, Falkner et al., 1993; Scher, Tirosh, & Lavie, 1998; Van Tassel, 1985). An association between temperament and middle-of-the-night self-soothing also has been reported (Keener et al., 1988). Fathers were found to rate non-self-soothing infants as more temperamentally difficult than self-soothing infants; however, a similar relationship did not hold for mothers’ ratings of temperament. Minde and colleagues (1993) reported an association between difficult temperament and problem sleep. In their study, problem sleepers were unable to return to sleep without a parental intervention (i.e., they were non-self-soothers). Parental factors also have been associated with infant sleep disruption. Seifer and colleagues (Seifer, Sameroff, Dickstein, Hayden, & Schiller, 1996) reported an association between both higher levels of maternal mental illness and lower levels of overall family functioning and bedtime problems in toddlers. Benoit, Zeanah, Boucher, and Minde (1992) found that all of the sleep-disturbed toddlers in their sample had mothers with insecure attachment styles. Another study, however, failed to find a relation between maternal psychological well-being and infants’ tendency to self-soothe during the night. This null finding may have been due to the non-clinical range of maternal depression scores reported in this study (Goodlin-Jones et al., 2001). Associations between the sleep context and sleep-wake domains and self-soothing have been illustrated most clearly to date. Infants who are placed into their cribs awake at the beginning of the night and who use a sleep aid are more likely to self-soothe than their counterparts (Anders et al., 1992; Goodlin-Jones et al., 1997). In addition, self-soothing infants have longer continuous sleep periods and longer total sleep times at night (Anders et al., 1992; Goodlin-Jones et al., 2001). There is clearly some evidence in support of the relationships between each of the model domains and nighttime self-soothing. A more detailed review of these associations has been published recently (France & Blampied, 1999). The current study had three goals. As the first relatively large-scale longitudinal study to objectively investigate infant sleep, the first goal was to replicate previous work on the basic patterns of sleep-wake development across the first year of life. The second goal was to test a double blind, random assignment intervention trial to enhance self-soothing at night. The third goal was to identify potential factors leading to the development of self-soothing at 12 months of age.

Sleep-waking discharge patterns of median preoptic nucleus neurons in rats

Abstract: Several lines of evidence show that the preoptic area (POA) of the hypothalamus is critically implicated in the regulation of sleep. Functionally heterogeneous cell groups with sleep-related discharge patterns are located both in the medial and lateral POA. Recently a cluster of neurons showing sleep-related c-Fos immunoreactivity was found in the median preoptic nucleus (MnPN). To determine the specificity of the state-related behaviour of MnPN neurons we have undertaken the first study of their discharge patterns across the sleep-waking cycle. Nearly 76% of recorded cells exhibited elevated discharge rates during sleep. Sleep-related units showed several distinct types of activity changes across sleep stages. Two populations included cells displaying selective activation during either non-rapid eye movement (NREM) sleep (10%) or REM sleep (8%). Neurons belonging to the predominant population (58%) exhibited activation during both phases of sleep compared to wakefulness. Most of these cells showed a gradual increase in their firing rates prior to sleep onset, elevated discharge during NREM sleep and a further increase during REM sleep. This specific sleep-waking discharge profile is opposite to that demonstrated by wake-promoting monoaminergic cell groups and was previously found in cells localized in the ventrolateral preoptic area (vlPOA). We hypothesize that these vlPOA and MnPN neuronal populations act as parts of a GABAergic/galaninergic sleep-promoting (‘anti-waking’) network which exercises inhibitory control over waking-promoting systems. MnPN neurons that progressively increase activity during sustained waking and decrease activity during sustained sleep states may be involved in homeostatic regulation of sleep.

Effect of sleep on epilepsy.

Abstract: There is an extremely intimate relationship between sleep and epilepsy. In this manuscript I will review the influence that sleep has on epilepsy. Sleep is a potent activator of interictal epileptiform discharges. Sharp waves are infrequent during wakefulness in benign focal epilepsy of childhood, but may occur in runs of several discharges per page in sleep. The interictal discharges become almost continuous in non-REM sleep in the syndrome of encephalopathy with electrical status epilepticus during slow wave sleep. In some patients with West syndrome a hypsarrhythmia pattern may only appear in sleep whereas in others there may be an increase in discharges in a semiperiodic fashion resulting in a burst-suppression like pattern. Seizures appear to have a very close relationship with sleep in certain epilepsy syndromes. In benign focal epilepsy of childhood the seizures occur almost exclusively in sleep, while supplementary sensorimototor area seizures tend to occur in clusters during sleep. Juvenile myoclonic epilepsy has a close relationship with the sleep-wake cycle with seizures tending to occur predominantly on awakening. I also discuss the role of sleep and sleep deprivation in the EEG evaluation of epilepsy.

Relationship of epileptic seizures to sleep stage and sleep depth.

Abstract: Study objectives Interictal epileptiform discharges (IEDs) are facilitated by NREM stages 3 and 4 sleep and as sleep is deepening. To determine whether sleep influences seizures in a similar way to IEDs, we examined seizure rates in various stages of sleep in epilepsy patients undergoing overnight video-EEG-polysomnography (VPSG). Design Cross-sectional study. Setting Neurology Department. PATIENTS, MEASUREMENTS, AND INTERVENTIONS: We reviewed VPSGs from our Sleep and Epilepsy Laboratories to identify patients with recorded seizures during sleep. A total of 55 patients having 117 seizures were identified. Results Ninety-five percent of seizures occurred in NREM sleep (61% in stage 2, 20% in stage 1, 14% in stages 3 and 4 combined), and 5% in REM sleep. Adjusting for time spent in each stage of sleep, patients had 0.34 seizures per hour in stage 1, 0.38 seizures per hour in stage 2, 0.29 seizures/hr in stage 3 and 4 combined, and 0.09 seizures per hour in REM sleep. Seizures/hour was higher in NREM sleep (0.35 for NREM and 0.09 for REM; p=0.0001). For single seizures occurring in 1 night, seizure rate was significantly higher in NREM stages 1 and 2 as compared to NREM stages 3 and 4 sleep. A significant increase in log delta power, an automated measure of sleep depth, was observed in the 10 minutes prior to seizures. Conclusions Both seizures and IEDs are facilitated by NREM sleep. While deeper stages of NREM sleep activate IEDs, lighter stages of NREM sleep promote seizures, at least for single seizures occurring in 1 night.

Rapid eye movement sleep behavior disorder in children with autism.

Abstract: We performed nocturnal polysomnography on 11 children with autism who had symptoms of disrupted sleep and nocturnal awakenings. We identified rapid eye movement (REM) sleep behavior disorder in 5 of these 11 patients. Since REM sleep behavior disorder typically affects elderly males with neurodegenerative diseases, the identification of this phenomenon in autistic children could have profound implications for our understanding of the neurochemical and neurophysiologic bases of autism. Further, accurate diagnosis of REM sleep behavior disorder would enable specific treatment with clonazepam and help the family and the child consolidate sleep and improve daytime performance.

Sleep and breathing in neuromuscular disease

Abstract: Respiratory muscle weakness in neuromuscular disease causes significant morbidity and mortality. The published data on respiratory muscle activity and breathing during sleep in normal subjects, the impact of respiratory muscle weakness on sleep and breathing and the relations to daytime respiratory function in neuromuscular disease are reviewed here. In normal subjects during sleep upper airway resistance increases, chemosensitivity is reduced and the wakefulness drive to breathe is lost, resulting in a fall in ventilation. During rapid eye movement (REM) sleep, ribcage and accessory breathing muscles are suppressed, particularly during bursts of eye movements, and breathing is more irregular, rapid and shallow, with a further fall in ventilation. In subjects with respiratory muscle weakness sleep is fragmented, with shorter total sleep time, frequent arousals, an increase in stage 1 sleep and a reduction in, or complete suppression of, REM sleep. Sleep-disordered breathing and nocturnal desaturation are common and most severe during REM sleep. Correlations between daytime respiratory function and nocturnal desaturation are moderate or weak, but daytime respiratory function has greater prognostic value than nocturnal measurements. Noninvasive ventilation improves sleep quality and breathing in subjects with respiratory muscle weakness. However, the optimal criteria for initiation of ventilation and its role in rapidly progressive neuromuscular diseases are unclear.

Changes in emotional responses to aversive pictures across periods rich in slow-wave sleep versus rapid eye movement sleep.

Abstract: OBJECTIVE Since Freud's "Interpretation of Dreams," sleep has been related to emotional functions, where dreams were assumed to play a cathartic role. In psychophysiological research, this role was attributed mainly to rapid eye movement (REM) sleep. The present study compared processing pictures with negative emotional impact over intervals covering either early sleep dominated by slow-wave sleep (SWS) or late REM sleep-dominated sleep. METHOD Emotional reactions were assessed by a nonverbal rating procedure along the two emotional dimensions valence (positive vs. negative) and arousal (low vs. high). Two groups of healthy men were tested across 3-hour periods of early and late nocturnal sleep (sleep group) or corresponding intervals filled with wakefulness (wake group). After the intervals, subjects rated new pictures together with old pictures already presented before the interval. Sleep was recorded polysomnographically. RESULTS As expected, the amount of REM sleep was about three times greater during late than early nocturnal sleep, whereas a reversed distribution was observed for SWS (p<.001). Valence ratings indicated a shift toward enhanced negative ratings after late sleep (p<.05), contrasting with a trend toward more positive ratings after early sleep (p<.10). Arousal habituated slightly to repeated presentation of the same stimuli, but sleep generally enhanced subsequent arousal ratings (p<.05). Effects of sleep did not depend on whether pictures had low or high emotional impact. CONCLUSIONS Indicating a priming-like enhancement of emotional reactivity after periods rich in REM sleep, results do not confirm a cathartic function of REM sleep or sleep in general.

The value of sleep deprivation as a diagnostic tool in adult sleepwalkers

Abstract: Objective: Adult somnambulism can result in injury to the sleeper and to others. Attempts to induce sleepwalking episodes in the sleep laboratory have yielded mixed results. 1,2 Having shown that sleepwalkers have lower slow-wave activity power than control subjects, 3 the authors hypothesized that an enhanced pressure of the homeostatic process underlying sleep regulation could affect the disorder’s characteristics even further. Therefore, the effects of 38 hours of sleep deprivation in adult sleepwalkers and control subjects were investigated. Methods: Ten adult somnambulistic patients and 10 sex- and age-matched control subjects were studied in the sleep laboratory. After a screening night, participants were monitored during 1) one night of baseline recording, and 2) one recovery night in which subjects slept ad libitum immediately after the sleep deprivation protocol. Behavioral manifestations were assessed for frequency and complexity using a 3-point scale of increasing complexity. Results: None of the control subjects had any behavioral manifestations on either of the two nights. Conversely, sleepwalkers showed a significant increase in the frequency and complexity of the somnambulistic episodes during the recovery night compared with baseline. Somnambulistic patients had a greater number of awakenings from slow-wave sleep than control subjects on both nights, but there was no significant increase during the recovery night. Conclusion: Sleep deprivation can be an effective tool for inducing somnambulistic episodes in the laboratory, thereby facilitating the diagnosis of sleepwalking.

Incidence of RBD and hallucination in patients affected by Parkinson's disease: 8-year follow-up.

Abstract: We describe the 8-years follow-up of 80 patients affected by idiopathic, L-dopa-responsive Parkinson's disease. All patients were evaluated at baseline and during the follow-up with visual evoked potential, P300 event related potentials and polysomnography. The patients and their relatives compiled sleep and hallucination questionnaires. Statistical analysis was performed to evaluate if visual abnormalities, abnormal P300 recordings or sleep disturbances were linked to the development and hallucinations. Our results show that abnormal vision and abnormal P300 did not correlate with the incidence of hallucinations. However, the presence of REM sleep behavioral disorder (RBD) was significantly related to the development of hallucinations,independently of age, gender or duration of disease but dependent on the amount of dopaminoagonist treatment.

The association between daytime sleepiness and sleep-disordered breathing in NREM and REM sleep.

Abstract: SLEEP-DISORDERED BREATHING IS CHARACTERIZEDBY REPETITIVE EPISODES OF PARTIAL OR COMPLETECOLLAPSE OF THE UPPER AIRWAY DURING SLEEP. Theresulting decrease or cessation in airflow is often associated withoxyhemoglobin desaturation and/or an arousal from sleep. Inpatients with sleep-disordered breathing, respiratory events mayoccur throughout non-rapid eye movement (NREM) and rapideye movement (REM) sleep. The typical finding is that respira-tory events during REM sleep are longer and are associated witha greater degree of hypoxemia than events that occur duringNREM sleep. These characteristics may be related to the markeddifferences in arousal responses to respiratory stimuli (i.e.,hypoxemia and hypercapnia) between REM and NREM sleep.In general, greater stimulus intensities are required to elicit anarousal from REM than NREM sleep.

Does sleep fragmentation impact recuperation? A review and reanalysis.

Abstract: SUMMARY Studies have shown that next-day performance and alertness are impaired by sleep fragmentation procedures even when total sleep time (TST) is unaffected. Based on these studies it has been hypothesized that both the duration and continuity of sleep determine its recuperative value. This review of the literature suggests that when sleep fragmentation procedures increase the relative amount of stage 1 sleep, next-day performance and alertness are impaired. Other studies suggest that stage 1 sleep has little or no recuperative value. Total sleep time, however, is typically defined as the sum of time spent in sleep stages 1, 2, 3, 4, and REM. In the present paper it is shown that when stage 1 sleep is excluded from TST, a stronger relationship between TST and subsequent alertness and performance emerges - and the need to invoke 'sleep continuity' as a variable that contributes independently to recuperative sleep processes is obviated. In the same way that partial or total sleep deprivation impairs alertness and performance, it is proposed that sleep disruption also impairs alertness and performance by reducing true recuperative sleep time.

Sleep deprivation in prion protein deficient mice sleep deprivation in prion protein deficient mice and control mice: genotype dependent regional rebound.

Abstract: We have previously reported a larger and more prolonged increase of slow wave activity (SWA) in NREM sleep after sleep deprivation (SD) in prion protein deficient mice (PrP) compared to wild-type mice. Regional differences in the SWA increase were investigated by comparing the effect of 6 h SD on a frontal and occipital derivation in PrP deficient mice and wild-type mice. The larger increase of SWA after SD in PrP deficient mice was restricted to the occipital derivation. The difference appeared after the waking-NREM sleep transitions, making it unlikely that PrP is involved in the mechanisms enabling the transition to sleep. Our findings may reflect differences between the genotypes in the need for recovery in this particular brain region.

Lactation is associated with an increase in slow-wave sleep in women

Abstract: Major physiological changes occur following parturition and the onset of lactation, including the withdrawal of oestrogen and progesterone, with a consequent increase in circulating prolactin (PRL). Changes in other circulating hormones are well known to alter sleep architecture in other circumstances. We therefore aimed to assess whether sleep architecture is altered in fully lactating women as a result of hormonal changes associated with lactation. A descriptive comparison study was undertaken on 12 fully breastfeeding women (B/F), 12 age-matched control women (CTRL), and seven postnatal women who had chosen to bottle-feed their infants (BOTTLE). Maternal age, infant age and body mass index (BMI) were similar between all three groups. We performed overnight polysomnography utilizing the Portable Compumedics P-series. The total sleep time (TST) and rapid eye movement (REM) sleep time were similar in the three groups of women. However, B/F women demonstrated a marked increase in slow wave sleep (SWS), 182 +/- 41 min compared with CTRL (86 +/- 22 min, P < 0.001 compared with B/F) and BOTTLE subjects (63 +/- 29 min, P < 0.001 compared with B/F). There was a compensatory reduction in light non-rapid eye movement (NREM) sleep in B/F when compared with CTRL and BOTTLE. The most likely explanation for the altered sleep architecture noted to occur in women who are fully breastfeeding their infants is an increase in circulating PRL, which occurs in lactating women. Enhanced SWS may be another important factor to support breastfeeding in the postnatal period.

Prostaglandin D2 in Sleep-Wake Regulation: Recent Progress and Perspectives:

Abstract: Prostaglandin (PG) D2 is one of the most active endogenous sleep-promoting substances, which induces physiological sleep in rodents, primates, and most probably in humans as well. In this update article, we review recent experimental results concerning the molecular mechanisms underlying sleep-wake regulation by PGD2, the link between the humoral regulation by the PGD2 system, and the neural network involved in the promotion of non-rapid eye movement (NREM) sleep and the abnormality of NREM sleep regulation found in gene-manipulated mice for PGD synthase.

Genioglossus Muscle Responsiveness to Chemical and Mechanical Stimuli during Non–Rapid Eye Movement Sleep

Abstract: Previous studies have suggested that during non-rapid eye movement (NREM) sleep, neither large short-duration resistive loads nor sustained normoxic hypercapnia alone leads to increased genioglossus muscle activation. However, in normal individuals during stable NREM sleep, genioglossus activity rises above baseline as PCO2 rises and airway resistance increases. We therefore hypothesized that combinations of chemical (PCO2, PO2) and mechanical stimuli during NREM sleep would lead to increased genioglossal activation. We studied 15 normal subjects (9 males, 6 females) during stable NREM sleep, measuring genioglossus electromyogram, epiglottic/choanal pressure, and airflow under six conditions: (1) baseline, (2) inspiratory resistive loading (-5 to -15 cm H2O/ L/second), (3) increased PCO2 (5-10 mm Hg above baseline), (4) combined resistive loading and increased PCO2, (5 ) hypoxia (SaO2 80-85%), and (6 ) combined hypoxia/inspiratory resistive loading. Only the combined condition of hypercapnia and resistive loading led to significantly increased genioglossal activation, 3.91 +/- 0.77% to 9.64 +/- 1.96% of maximum. These data suggest that the genioglossus muscle is less responsive to either chemical stimuli (hypercapnia, hypoxia) or inspiratory resistive loading alone during NREM sleep at the degrees tested. When hypercapnia is combined with resistive loading, the muscle does respond. However, the possibility that higher levels of PCO2 or greater resistive loading alone could activate the muscle cannot be excluded.

Hypothalamic gray matter changes in narcoleptic patients.

Abstract: globally activate the stress response (data not shown), although the Lewy body–like inclusions immunolabel for Hsp70 (ref. 5). As 3 μg/ml prevents dopaminergic cell loss due to α-synuclein toxicity, it is possible that only a modest change in or redistribution of molecular chaperones is sufficient for neuroprotection. Current anti-PD agents, including levodopa, dopamine receptor agonists (such as bromocriptine), and monoamine oxidase B inhibitors (such as deprenyl), are designed to relieve the symptoms of PD by restoring dopamine levels in the basal ganglia. Our studies define a potential drug class that promotes the survival of dopaminergic neurons. Although we suggest that geldanamycin is acting by upregulating or otherwise modulating molecular chaperone activity, the drug may also be modulating other pathways regulated by Hsp90. Regardless, these studies have revealed a drug that can fully protect against the toxicity of α-synuclein to dopaminergic neurons in Drosophila. Geldanamycin and its derivatives warrant further exploration as cytoprotective agents for the treatment of neurodegenerative diseases involving α-synuclein toxicity, including PD.

Ultradian oscillations of insulin secretion in humans.

Abstract: Ultradian rhythmicity appears to be characteristic of several endocrine systems. As described for other hormones, insulin release is a multioscillatory process with rapid pulses of about 10 min and slower ultradian oscillations (50--120 min). The mechanisms underlying the ultradian circhoral oscillations of insulin secretion rate (ISR), which arise in part from a rhythmic amplification of the rapid pulses, are not fully understood. In humans, included in the same period range is the alternation of rapid eye movement (REM) and non-REM (NREM) sleep cycles and the associated opposite oscillations in sympathovagal balance. During sleep, the glucose and ISR oscillations were amplified by about 150%, but the REM-NREM sleep cycles did not entrain the glucose and ISR ultradian oscillations. Also, the latter were not related to either the ultradian oscillations in sympathoagal balance, as inferred from spectral analysis of cardiac R-R intervals, or the plasma fluctuations of glucagon-like peptide-1 (GLP-1), an incretin hormone known to potentiate glucose-stimulated insulin. Other rhythmic physiological processes are currently being examined in relation to ultradian insulin release.