Sleep Architecture (sleep + architecture)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol Withdrawal

ALCOHOLISM, Issue 7 2006
Lynn M. Veatch
Background: Insomnia and other sleep difficulties are perhaps the most common and enduring symptoms reported by alcoholics undergoing detoxification, especially those alcoholics with a history of multiple detoxifications. While some studies have reported sleep disruptions in animal models after chronic ethanol exposure, the reports are inconsistent and few address sleep architecture across repeated ethanol exposures and withdrawals. The present study evaluated sleep time and architecture in a well-characterized mouse model of repeated chronic ethanol exposure and withdrawal. Methods: C57BL6/J mice were fitted with electrodes in frontal cortex, hippocampus, and nuchal muscle for collection of continuous electroencephalogram (EEG)/electromyogram (EMG) data. Baseline data were collected, after which mice received 4 cycles of 16-hour exposure to alcohol (ethanol: EtOH) vapor separated by 8-hour periods of withdrawal or similar handling in the absence of EtOH vapor. Ethanol-exposed mice attained a blood ethanol concentration of 165 mg%. Upon completion of vapor exposure, EEG/EMG data were again collected across 4 days of acute withdrawal. Data were subjected to automated analyses classifying 10-second epochs into wake, non,rapid eye movement (REM) sleep, or REM sleep states. Results: Mice in withdrawal after chronic EtOH exposure showed profound disruptions in the total time asleep, across the acute withdrawal period. Sleep architecture, the composition of sleep, was also disrupted with a reduction in non-REM sleep concomitant with a profound increase in REM sleep. While altered sleep time and non-REM sleep loss resolved by the fourth day of withdrawal, the increase in REM sleep ("REM rebound") persisted. Conclusions: These results mirror those reported for the human alcoholic and demonstrate that EtOH withdrawal,induced sleep disruptions are evident in this mouse model of alcohol withdrawal,induced sensitization. This mouse model may provide mechanisms to investigate fully the high correlation between unremitting sleep problems and increased risk of relapse documented clinically. [source]


Sleep staging and respiratory events in refractory epilepsy patients: Is there a first night effect?

EPILEPSIA, Issue 12 2008
Linda M. Selwa
Summary Purpose:, We performed this analysis of possible first night effects (FNEs) on sleep and respiratory parameters in order to evaluate the need for two serial night polysomnograms (PSGs) to diagnose obstructive sleep apnea (OSA) in epilepsy patients. Methods:, As part of a pilot multicenter clinical trial investigating the effects of treating sleep apnea in epilepsy, two nights of PSG recording were performed for 40 patients with refractory epilepsy and OSA symptoms. Sleep architecture was examined in detail, along with respiratory parameters including apnea/hypopnea index (AHI) and minimum oxygen saturation. Analysis included two-tailed t -tests, Wilcox sign rank analysis, and Bland Altman measures of agreement. Results:, Total sleep time differed between the two nights (night 1,363.8 min + 59.4 vs. 386.3 min + 68.6, p = 0.05). Rapid eye movement (REM) sleep and percentage of REM sleep were increased during night two (night 1: 12.3% + 5.9 vs. night 2: 15.5% + 6.2, p = 0.007), and the total minutes of slow-wave sleep (SWS) were increased (night 1: 35.6 + 60.7 vs. night 2: 46.4 + 68.1, p = 0.01). No other sleep or respiratory variables differed between the two nights. Given an AHI inclusion criterion of five apneas per hour, the first PSG identified all but one patient with OSA. Discussion:, Respiratory parameters showed little variability between the first and second nights. Sleep architecture was mildly different between the first and second PSG night. Performing two consecutive baseline PSGs to diagnose OSA may not be routinely necessary in this population. [source]


Sleep architecture in children with adenoidal hypertrophy

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 10 2006
Xiao-Wen Zhang
Aim: Adenoidal hypertrophy (AH) in children is associated with obstructive manifestations like mouth breathing, snoring. Unfortunately, little is known regarding sleep architecture of AH in children. The purpose of this study was therefore undertaken to investigate the polysomnographic variables in children with AH. Method: 47 children with AH and 11 controls underwent nocturnal polysomnography. Sleep was scored manually according to the standard set by Rechtschaffen. Results: In AH, stage 1 sleep percentage and rapid eye movement (REM) latency were increased significantly, while the sleep percentage of stage 2 and REM was decreased remarkably compared with that of controls. Arousal index in AH was much more higher than that in controls. Arousal index in REM sleep was higher than that in non-rapid eye movement (NREM) sleep in AH, but the number of arousals in REM sleep was lower than that in NREM sleep. Hypopnea events were the most common type of respiratory events, followed by obstructive events in AH and controls. Apnea/hypopnea index in AH was higher in comparison to controls. No significant difference was found between the children with AH and controls in SaO2 nadir (%) and base mean SaO2 (%). Apnea/hypopnea index was related to hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep. Conclusion: AH is predominantly characterised by a hypopnea with little obstruction in children. Our results clearly and for the first time demonstrated that sleep architecture was abnormal in children with AH. We therefore speculate that hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep may play an important role in the course of respiratory disturbance. [source]


Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol Withdrawal

ALCOHOLISM, Issue 7 2006
Lynn M. Veatch
Background: Insomnia and other sleep difficulties are perhaps the most common and enduring symptoms reported by alcoholics undergoing detoxification, especially those alcoholics with a history of multiple detoxifications. While some studies have reported sleep disruptions in animal models after chronic ethanol exposure, the reports are inconsistent and few address sleep architecture across repeated ethanol exposures and withdrawals. The present study evaluated sleep time and architecture in a well-characterized mouse model of repeated chronic ethanol exposure and withdrawal. Methods: C57BL6/J mice were fitted with electrodes in frontal cortex, hippocampus, and nuchal muscle for collection of continuous electroencephalogram (EEG)/electromyogram (EMG) data. Baseline data were collected, after which mice received 4 cycles of 16-hour exposure to alcohol (ethanol: EtOH) vapor separated by 8-hour periods of withdrawal or similar handling in the absence of EtOH vapor. Ethanol-exposed mice attained a blood ethanol concentration of 165 mg%. Upon completion of vapor exposure, EEG/EMG data were again collected across 4 days of acute withdrawal. Data were subjected to automated analyses classifying 10-second epochs into wake, non,rapid eye movement (REM) sleep, or REM sleep states. Results: Mice in withdrawal after chronic EtOH exposure showed profound disruptions in the total time asleep, across the acute withdrawal period. Sleep architecture, the composition of sleep, was also disrupted with a reduction in non-REM sleep concomitant with a profound increase in REM sleep. While altered sleep time and non-REM sleep loss resolved by the fourth day of withdrawal, the increase in REM sleep ("REM rebound") persisted. Conclusions: These results mirror those reported for the human alcoholic and demonstrate that EtOH withdrawal,induced sleep disruptions are evident in this mouse model of alcohol withdrawal,induced sensitization. This mouse model may provide mechanisms to investigate fully the high correlation between unremitting sleep problems and increased risk of relapse documented clinically. [source]


Pulsed radio-frequency electromagnetic fields: dose-dependent effects on sleep, the sleep EEG and cognitive performance

JOURNAL OF SLEEP RESEARCH, Issue 3 2007
SABINE J. REGEL
Summary To establish a dose,response relationship between the strength of electromagnetic fields (EMF) and previously reported effects on the brain, we investigated the influence of EMF exposure by varying the signal intensity in three experimental sessions. The head of 15 healthy male subjects was unilaterally exposed for 30 min prior to sleep to a pulse-modulated EMF (GSM handset like signal) with a 10 g-averaged peak spatial specific absorption rate of (1) 0.2 W kg,1, (2) 5 W kg,1, or (3) sham exposed in a double-blind, crossover design. During exposure, subjects performed two series of three computerized cognitive tasks, each presented in a fixed order [simple reaction time task, two-choice reaction time task (CRT), 1-, 2-, 3-back task]. Immediately after exposure, night-time sleep was polysomnographically recorded for 8 h. Sleep architecture was not affected by EMF exposure. Analysis of the sleep electroencephalogram (EEG) revealed a dose-dependent increase of power in the spindle frequency range in non-REM sleep. Reaction speed decelerated with increasing field intensity in the 1-back task, while accuracy in the CRT and N-back task were not affected in a dose-dependent manner. In summary, this study reveals first indications of a dose,response relationship between EMF field intensity and its effects on brain physiology as demonstrated by changes in the sleep EEG and in cognitive performance. [source]


Radiofrequency Tongue Reduction Through a Cervical Approach: A Pilot Study,

THE LARYNGOSCOPE, Issue 10 2006
Marc B. Blumen MD
Abstract Objective/Hypothesis: The objective of this prospective cohort study was to determine the feasibility, safety, and efficacy of radiofrequency tongue base reduction through a cervical approach in patients with obstructive sleep apnea syndrome (OSAS). Methods: Patients with moderate to severe OSAS and predominant tongue base obstruction by physical examination were included at our institution from 1999 to 2003. A sonogram was obtained to identify the lingual arteries, and an electrode was inserted through the neck and into the tongue under fluoroscopic guidance. Adverse events were recorded as well as efficacy on snoring (visual analog scale), daytime sleepiness (Epworth score), and polysomnography. Results: The 10 patients received a mean of 14,288 ± 3,251 J per session. No cases of tongue palsy or infection occurred. During the first 7 days, mean pain score (0,10 scale) was 1.3 ± 1.5. Snoring volume (0,10 scale) decreased from 6.2 ± 2.3 to 3.9 ± 2.6 (P = .017) and sleepiness (0,24 scale) from 8.7 ± 5.6 to 4.7 ± 3.3 (P = .011). The respiratory disturbance index (events/hour) decreased from 52.0 ± 19.6 to 33.6 ± 24.4 (P = .016). Mean minimal oxygen saturation (%) increased from 64.2 ± 13.0 to 75.8 ± 10.3 (P = .003). Sleep architecture improved although not significantly. Conclusion: Radiofrequency tongue base reduction through a cervical approach proved feasible and safe despite the large energy doses used. Fluoroscopic guidance enables to place the electrode at the desired site of treatment. Although OSAS improved in nine of 10 patients, greater efficacy might be achieved in patients with less severe OSAS at baseline. Studies are needed to correlate objective clinical efficacy with the dose per lesion site and the number of lesion sites per session. [source]


Effects of Vigabatrin on Sleep,Wakefulness Cycle in Amygdala-Kindled Rats

EPILEPSIA, Issue 2 2000
Y. H. Raol
Summary: Purpose: Our aim was to study the effect of prolonged administration of vigabatrin (VGB) on sleep-wakefulness cycle in kindled seizure-induced rats. Methods: Adult male Wistar rats were implanted stereotaxically with electrodes for kindling and polysomnography. The rats were divided into two groups, kindled and VGB-treated kindled rats. VGB was administered intraperitonially every day for 21 days, and polysomnographic recordings were taken after doses 1, 7, 14, and 21. The drug effects were evaluated by comparing the records of kindled and drug-treated kindled rats. Results: The VGB-administered kindled rats showed an increase in total sleep time (TST) due to an increase in total non-rapid eye movement (NREM) and light slow-wave sleep stage I (SI) with a decrease in wakefulness. The number of episodes and REM onset latencies were found to be decreased after drug treatment. Conclusions: It can therefore be concluded that VGB has a somnolence-inducing effect and that it might mediate its anti-convulsant effect by altering sleep architecture through sleep-regulating areas. [source]


Sensory gating in primary insomnia

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2010
Ilana S. Hairston
Abstract Although previous research indicates that sleep architecture is largely intact in primary insomnia (PI), the spectral content of the sleeping electroencephalographic trace and measures of brain metabolism suggest that individuals with PI are physiologically more aroused than good sleepers. Such observations imply that individuals with PI may not experience the full deactivation of sensory and cognitive processing, resulting in reduced filtering of external sensory information during sleep. To test this hypothesis, gating of sensory information during sleep was tested in participants with primary insomnia (n = 18) and good sleepers (n = 20). Sensory gating was operationally defined as (i) the difference in magnitude of evoked response potentials elicited by pairs of clicks presented during Wake and Stage II sleep, and (ii) the number of K complexes evoked by the same auditory stimulus. During wake the groups did not differ in magnitude of sensory gating. During sleep, sensory gating of the N350 component was attenuated and completely diminished in participants with insomnia. P450, which occurred only during sleep, was strongly gated in good sleepers, and less so in participants with insomnia. Additionally, participants with insomnia showed no stimulus-related increase in K complexes. Thus, PI is potentially associated with impaired capacity to filter out external sensory information, especially during sleep. The potential of using stimulus-evoked K complexes as a biomarker for primary insomnia is discussed. [source]


PER2 controls circadian periods through nuclear localization in the suprachiasmatic nucleus

GENES TO CELLS, Issue 11 2007
Koyomi Miyazaki
Molecular circadian clock regulation engages a negative feedback loop comprising components of the negative limb, PERs and CRYs. In addition to the rhythmic transcriptional regulation of clock genes, controlled subcellular localization might contribute to the molecular mechanism of the mammalian circadian clock. To address this issue, we generated transgenic (TG) mice lines harboring either rat PER2 (rPER2) with a deleted nuclear localizing domain [NLD(,)] or intact PER2. In comparison with wild-type (WT) control, the period of the circadian locomotor rhythm in TG mice over-expressing NLD(,) PER2 was longer, while that in TG mice over-expressing intact PER2 was shorter. The nuclear entry of endogenous PER2, CRY1 and CRY2 was delayed in the suprachiasmatic nucleus (SCN) of NLD(,) PER2 TG mice under constant darkness, whereas that of mouse PER2 (mPER2) is accelerated in the SCN of intact PER2 TG mice. Under constant light, the locomotor activity of NLD(,) PER2 TG mice became arrhythmic, whereas WT animals remained rhythmic. These data indicate that PER2 controls circadian periods through nuclear localization in the SCN. In addition, sleep architecture was also affected in intact PER2 TG mice, suggesting PER2 can modulate a sleep molecular mechanism. [source]


Impact of the novel antidepressant agomelatine on disturbed sleep,wake cycles in depressed patients,

HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2010
Maria-Antonia Quera-Salva
Abstract Background Disturbance of sleep,wake cycles is common in major depressive disorder (MDD), usually as insomnia, but also as hypersomnia or reduced daytime alertness. Agomelatine, an MT1 and MT2 receptor agonist and 5-HT2C receptor antagonist, represents a novel approach in MDD, with proven antidepressant efficacy and a positive impact on the sleep,wake cycle. We review the effects of agomelatine 25/50,mg/day on objective and subjective measures of the sleep,wake cycle in MDD. Subjective measures Agomelatine improved all aspects of the sleep,wake cycle from as early as 1 week in randomized trials versus selective serotonin reuptake inhibitors and venlafaxine, particularly getting off to sleep and quality of sleep, with an improvement in daytime alertness. Objective measures Agomelatine's effect on sleep architecture in MDD has been measured by polysomnography (PSG). There were significant improvements in sleep efficiency, slow-wave sleep (SWS), and the distribution of delta activity throughout the night, but no change in amount or latency of rapid eye movement (REM) sleep. Furthermore, the slow-wave sleep was resynchronized to the first sleep cycle of the night. Conclusion Agomelatine, a novel antidepressant, improves disturbed sleep,wake cycles in MDD. The improvement of both nighttime sleep and daytime functioning with agomelatine are promising features of this antidepressant regarding the management of MDD. Copyright © 2010 John Wiley & Sons, Ltd. [source]


New insights into the pathophysiology of postoperative cognitive dysfunction

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2010
L. KRENK
There is evidence that postoperative cognitive dysfunction (POCD) is a significant problem after major surgery, but the pathophysiology has not been fully elucidated. The interpretation of available studies is difficult due to differences in neuropsychological test batteries as well as the lack of appropriate controls. Furthermore, there are no internationally accepted criteria for defining POCD. This article aims to provide an update of current knowledge of the pathogenesis of POCD with a focus on perioperative pathophysiology and possible benefits achieved from an enhanced postoperative recovery using a fast-track methodology. It is concluded that the pathogenesis of POCD is multifactorial and future studies should focus on evaluating the role of postoperative sleep disturbances, inflammatory stress responses, pain and environmental factors. Potential prophylactic intervention may include minimal invasive surgery, multi-modal non-opioid pain management and pharmacological manipulation of the inflammatory response and sleep architecture. [source]


Exploratory Analysis of Cerebral Oxygen Reserves During Sleep Onset in Older and Younger Adults

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2008
Barbara W. Carlson RN
OBJECTIVES: To explore differences in cerebral oxygen reserves during sleep in old and young adults. DESIGN: Descriptive cross-sectional study. SETTING: General clinical research center. PARTICIPANTS: Nine old (aged 65,84) and 10 young (aged 21,39) adults. MEASUREMENTS: Subjects were monitored during the first nightly sleep cycle using standard polysomnography, including measures of arterial oxyhemoglobin saturation (SaO2). Changes in regional cerebral oxyhemoglobin saturation (rcSO2) were used to estimate cerebral oxygen reserves. General linear models were used to test group differences in the change in SaO2 and rcSO2 during sleep. RESULTS: Older subjects had lower SaO2 than young subjects before sleep (baseline) (F(1,18)=5.1, P=.04) and during sleep (F(1,18)=10.7, P=.01). During sleep, half of the older subjects and none of the younger ones had SaO2 values below 95%. In addition, the older subjects had more periods of oxygen desaturation (drops in SaO2,4%) (chi-square=24.3, P=.01) and lower SaO2 levels during desaturation (F(1,18)=11.1, P<.01). Although baseline values were similar, rcSO2 decreased during sleep 2.1% in older subjects (F(1,8)=3.8, P=.05) but increased 2.1% during sleep in younger subjects (F(1,9)=4.6, P=.04). When the older subjects awakened from sleep, rcSO2, but not SaO2, returned to baseline; both returned to baseline in younger subjects. CONCLUSION: This exploratory analysis generated the hypothesis that lower SaO2, combined with declines in regional blood flow, contributes to decline in cerebral oxygen reserves during sleep in older subjects. Further study will assess the effects of factors (e.g., medical conditions, subclinical disorders, and sleep architecture) that might account for these differences. [source]


Sleep architecture in children with adenoidal hypertrophy

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 10 2006
Xiao-Wen Zhang
Aim: Adenoidal hypertrophy (AH) in children is associated with obstructive manifestations like mouth breathing, snoring. Unfortunately, little is known regarding sleep architecture of AH in children. The purpose of this study was therefore undertaken to investigate the polysomnographic variables in children with AH. Method: 47 children with AH and 11 controls underwent nocturnal polysomnography. Sleep was scored manually according to the standard set by Rechtschaffen. Results: In AH, stage 1 sleep percentage and rapid eye movement (REM) latency were increased significantly, while the sleep percentage of stage 2 and REM was decreased remarkably compared with that of controls. Arousal index in AH was much more higher than that in controls. Arousal index in REM sleep was higher than that in non-rapid eye movement (NREM) sleep in AH, but the number of arousals in REM sleep was lower than that in NREM sleep. Hypopnea events were the most common type of respiratory events, followed by obstructive events in AH and controls. Apnea/hypopnea index in AH was higher in comparison to controls. No significant difference was found between the children with AH and controls in SaO2 nadir (%) and base mean SaO2 (%). Apnea/hypopnea index was related to hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep. Conclusion: AH is predominantly characterised by a hypopnea with little obstruction in children. Our results clearly and for the first time demonstrated that sleep architecture was abnormal in children with AH. We therefore speculate that hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep may play an important role in the course of respiratory disturbance. [source]


Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol Withdrawal

ALCOHOLISM, Issue 7 2006
Lynn M. Veatch
Background: Insomnia and other sleep difficulties are perhaps the most common and enduring symptoms reported by alcoholics undergoing detoxification, especially those alcoholics with a history of multiple detoxifications. While some studies have reported sleep disruptions in animal models after chronic ethanol exposure, the reports are inconsistent and few address sleep architecture across repeated ethanol exposures and withdrawals. The present study evaluated sleep time and architecture in a well-characterized mouse model of repeated chronic ethanol exposure and withdrawal. Methods: C57BL6/J mice were fitted with electrodes in frontal cortex, hippocampus, and nuchal muscle for collection of continuous electroencephalogram (EEG)/electromyogram (EMG) data. Baseline data were collected, after which mice received 4 cycles of 16-hour exposure to alcohol (ethanol: EtOH) vapor separated by 8-hour periods of withdrawal or similar handling in the absence of EtOH vapor. Ethanol-exposed mice attained a blood ethanol concentration of 165 mg%. Upon completion of vapor exposure, EEG/EMG data were again collected across 4 days of acute withdrawal. Data were subjected to automated analyses classifying 10-second epochs into wake, non,rapid eye movement (REM) sleep, or REM sleep states. Results: Mice in withdrawal after chronic EtOH exposure showed profound disruptions in the total time asleep, across the acute withdrawal period. Sleep architecture, the composition of sleep, was also disrupted with a reduction in non-REM sleep concomitant with a profound increase in REM sleep. While altered sleep time and non-REM sleep loss resolved by the fourth day of withdrawal, the increase in REM sleep ("REM rebound") persisted. Conclusions: These results mirror those reported for the human alcoholic and demonstrate that EtOH withdrawal,induced sleep disruptions are evident in this mouse model of alcohol withdrawal,induced sensitization. This mouse model may provide mechanisms to investigate fully the high correlation between unremitting sleep problems and increased risk of relapse documented clinically. [source]


Changes in dreaming induced by CPAP in severe obstructive sleep apnea syndrome patients

JOURNAL OF SLEEP RESEARCH, Issue 4 2006
EVA CARRASCO
Summary To study dream content in patients with severe obstructive sleep apnea syndrome (OSAS) and its modification with Continuous Positive Airway Pressure (CPAP) therapy. We assessed twenty consecutive patients with severe OSAS and 17 healthy controls. Polysomnograms were recorded at baseline in patients and controls and during the CPAP titration night, 3 months after effective treatment and 2 years later in patients. Subjects were awakened 5,10 min after the beginning of the first and last rapid eye movement (REM) sleep periods and we measured percentage of dream recall, emotional content of the dream, word count, thematic units, sleep architecture and REM density. Dream recall in REM sleep was similar in patients at baseline and controls (51.5% versus 44.4% respectively; P = .421), decreased to 20% and 24.3% the first and third month CPAP nights, and increased to 39% 2 years later (P = 0.004). Violent/highly anxious dreams were only seen in patients at baseline. Word count was higher in patients than in controls. REM density was highest the first CPAP night. Severe OSAS patients recall dreams in REM sleep as often as controls, but their dreams have an increased emotional tone and are longer. Despite an increase in REM density, dream recall decreased the first months of CPAP and recovered 2 years later. Violent/highly anxious dreams disappeared with treatment. A dream recall decrease with CPAP is associated with normalization of sleep in OSAS patients. [source]


Long-term vs. short-term processes regulating REM sleep

JOURNAL OF SLEEP RESEARCH, Issue 1 2002
PAUL FRANKEN
In cats, rats, and mice, the amount of rapid eye movement sleep (REMS) lost during a sleep deprivation (SD) predicts the subsequent REMS rebound during recovery sleep. This suggests that REMS is homeostatically regulated and that a need or pressure for REMS accumulates in its absence, i.e. during both wakefulness and non-rapid eye movement sleep (NREMS). Conversely, it has been proposed that REMS pressure accumulates exclusively during NREMS [Benington and Heller, Am. J. Physiol. 266 (1994) R1992; Prog. Neurobiol. 44 (1994b) 433]. This hypothesis is based on the analysis of the duration of successive NREMS and REMS episodes and of electroencephalogram (EEG) events preceding REMS. Pre-REMS events (PREs) do not always result in sustained REMS and can thus be regarded as REMS attempts that increase as NREMS progresses. It is assumed that two processes regulating REMS can resolve the apparent contradiction between these two concepts: a `long-term' process that homeostatically regulates the daily REMS amount and a `short-term' process that regulates the NREM,REMS cycle. These issues were addressed in two SD experiments in rats. The two SDs varied in length (12 and 24 h) and resulted in very similar compensatory changes in NREMS but evoked very different changes for all REMS parameters studied. The large REMS increase observed after 24-h SD was accompanied by a reduction in unsuccessful PREs and an increase in sustained REMS episodes, together resulting in a threefold increase in the success-rate to enter REMS. Changes in success-rate matched those of a theoretically derived long-term REMS pressure. The SD induced changes in sleep architecture could be reproduced by assuming that the increased long-term REMS pressure interacts with the short-term process by increasing the probability to enter and remain in REMS. [source]


Inflammation and Sleep Disordered Breathing in Children: A State-of-the-Art Review,

PEDIATRIC PULMONOLOGY, Issue 12 2008
Aviv D. Goldbart MD
Abstract Sleep disordered breathing (SDB) represents a spectrum of breathing disorders, ranging from snoring to obstructive sleep apnea syndrome (OSAS), that disrupt nocturnal respiration and sleep architecture. OSAS is a common disorder in children, with a prevalence of 2,3%. It is associated with neurobehavioral, cognitive, and cardiovascular morbidities. In children, adenotonsillectomy is the first choice for treatment and is reserved for moderate to severe OSAS, as defined by an overnight polysomnography. In adults, OSAS is the result of mechanical dysfunction of the upper airway, manifesting as severity-dependent nasal, oropharyngeal, and systemic inflammation that decrease after continuous positive airway pressure therapy. Inflammatory changes have been reported in upper airway samples from children with OSAS, and systemic inflammation, as indicated by high-sensitivity C-reactive protein (hsCRP) levels, has been shown to decrease in children with OSAS after adenotonsillectomy. Anti-inflammatory treatments for children with mild OSAS are associated with major improvements in symptoms, polysomnographic respiratory values, and radiologic measures of adenoid size. Inflammation is correlated to some extent with OSAS-related neurocognitive morbidity, but the role of inflammatory markers in the diagnosis and management of OSAS, and the role of anti-inflammatory treatments, remains to be clarified. This review examines the role of inflammation in the pathophysiology of sleep-disordered breathing in pediatric patients and the potential therapeutic implications. Pediatr. Pulmonol. 2008; 43:1151,1160. © 2008 Wiley-Liss, Inc. [source]


Are there ethnic differences in sleep architecture?

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 3 2002
Judi Profant
The possibility of ethnic differences in sleep architecture was initially examined in conjunction with studies of sleep apnea (study 1). This possibility was then examined in another cohort of patients to determine whether the results might generalize (study 2). Polysomnography was obtained in both cohorts as part of larger protocols investigating sympathetic nervous system activity, blood pressure, and sleep. Sleep monitoring took place in an inpatient clinical research center of a university hospital. Study 1 focused on sleep apnea physiology and involved volunteers with sleep apnea who were otherwise healthy. Study 2 focused on differences in stress reactivity between American Black and White subjects and involved hypertensive and normotensive volunteers who were otherwise healthy. Analyses include 61 participants from study 1 and 35 participants from study 2. Ethnicity in both cohorts was determined by self-report. Participants in both studies were monitored during sleep with traditional polysomnography including electroencephalography (EEG), electromyography (EMG), electrooculography (EOG), and oximetry. In Study 1, Blacks had longer TST (P < 0.01), more REM sleep (P < 0.05), and less WASO (P < 0.05) than Whites. After controling for RDI, Blacks had longer TST and spent a smaller percentage of time in deep sleep (P < 0.05). In study 2, Blacks had longer TST and REM sleep, lower percent deep sleep, and lower percent deep sleep controling for RDI (P < 0.05). In two separate studies, Blacks had longer TST, more minutes of REM, and lower percentage deep sleep. These findings suggest possible ethnic differences in sleep architecture. Am. J. Hum. Biol. 14:321,326, 2002. © 2002 Wiley-Liss, Inc. [source]


Effects of desmopressin on the sleep of children suffering from enuresis

ACTA PAEDIATRICA, Issue 7 2010
C Rahm
Abstract Aim:, To evaluate the effect of 1-desamino-8-D-Arginine Vasopressin (DDAVP) on sleep architecture and arousal reactions in children with primary monosymptomatic nocturnal enuresis (PME). Methods:, A prospective, placebo-controlled, randomized, double-blind, cross-over study was performed on children suffering from bed-wetting. Placebo and DDAVP were given for 7 days each after which an unattended home polysomnography (PSG) was recorded. After lifting the blinding, the PSGs were compared. Results:, A total of 20 children with PME, aged 6,15 years, were enrolled in the study. The number of wet nights decreased significantly with DDAVP treatment. Delta power, distribution of sleep stages, number of arousals, arousal index and the effect of arousals on sleep stages did not differ significantly. Bed-wetting occurred within each sleep stage and did not follow any particular pattern. In most cases, it was preceded by an arousal reaction, but no awakening occurred. Conclusion:, DDAVP has no effect on the sleep architecture of children with PME when analysed by classical PSG, which is determined by collecting the electric activity of cortical neurons. Taking recent research findings into account, this supports the thesis that the disturbances causing PME occur at brain stem level and do not reach consciousness. [source]