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Sleep Cycle (sleep + cycle)
Selected AbstractsLate-life insomnia: A reviewGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 3 2009Arne Fetveit Aging is associated with substantial changes in sleep patterns, which are almost always negative in nature. Typical findings in the elderly include a reduction in the deeper stages of sleep and a profound increase in the fragmentation of nighttime sleep by periods of wakefulness. The prevalence of specific sleep disorders increases with age, such as a phase advance in the normal circadian sleep cycle, restless legs syndrome, and obstructive sleep apnea, which is increasingly seen among older individuals and is significantly associated with cardio- and cerebrovascular disease as well as cognitive impairment. Elderly patients with sleep disturbances are often considered difficult to treat; yet, they are among the groups with the greatest need of treatment. Management of sleep disturbances begins with recognition and adequate assessment. Hypnotic drugs have clearly been shown to improve subjective and objective sleep measures in short-term situations, but their role in chronic insomnia still remains to be further defined by research evidence. Non-pharmacological treatments, particularly stimulus control and sleep restriction, are effective for conditioned aspects of insomnia and are associated with a stable, long-term improvement in sleep. This review delineates the common causes of disordered sleep in older individuals, and effective diagnostic approaches and treatments for these conditions. [source] Impact of the novel antidepressant agomelatine on disturbed sleep,wake cycles in depressed patients,HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2010Maria-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] Exploratory Analysis of Cerebral Oxygen Reserves During Sleep Onset in Older and Younger AdultsJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2008Barbara 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 electroencephalogram in children with a parental history of alcohol abuse/dependenceJOURNAL OF SLEEP RESEARCH, Issue 1p2 2010LEILA TAROKH Summary We examined the sleep electroencephalogram (EEG) in 9- and 10-year-old children with (PH+) and without (PH,) a parental history of alcohol abuse/dependence to determine whether sleep disturbances associated with alcohol precede the onset of alcohol use. Participants slept on a fixed sleep schedule that ensured at least a 10-h time in bed for 1 week before an adaptation and baseline night. Data were collected in a four-bed sleep research laboratory. Thirty healthy boys and girls aged 9 or 10 years were classified as either PH+ or PH, based on DSM-IV criteria applied to structured parental interviews. All-night polysomnography was performed, sleep data were scored visually in 30-s epochs, and EEG power spectra were calculated for each epoch. All-night EEG spectra were calculated for rapid eye movement (REM) and non-REM (NREM) sleep, and cycle-by-cycle spectra were calculated for NREM sleep. The two groups did not differ on any sleep stage variable. All-night analyses revealed normalized power in the delta band and spindle range were lower in PH+ children. Within NREM sleep cycles PH+ children exhibited less normalized power in the delta band and spindle range compared with PH, children. This effect occurred in the first four cycles and was most pronounced in the first sleep cycle of the night. We found no signs of sleep disruption in sleep stages for PH+ children. Sleep EEG spectral differences, however, suggest that certain circuits responsible for ,protecting' sleep may be impaired in PH+ children, which may lead to disrupted sleep later in life. [source] Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the ratJOURNAL OF SLEEP RESEARCH, Issue 1 2002ADRIÁN OCAMPO-GARCÉS An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light,dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle. [source] Does Alzheimer's disease begin in the brainstem?NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 6 2009G. Simic Although substantial evidence indicates that the progression of pathological changes of the neuronal cytoskeleton is crucial in determining the severity of dementia in Alzheimer's disease (AD), the exact causes and evolution of these changes, the initial site at which they begin, and the neuronal susceptibility levels for their development are poorly understood. The current clinical criteria for diagnosis of AD are focused mostly on cognitive deficits produced by dysfunction of hippocampal and high-order neocortical areas, whereas noncognitive, behavioural and psychological symptoms of dementia such as disturbances in mood, emotion, appetite, and wake,sleep cycle, confusion, agitation and depression have been less considered. The early occurrence of these symptoms suggests brainstem involvement, and more specifically of the serotonergic nuclei. In spite of the fact that the Braak and Braak staging system and National Institutes of Aging , Reagan Institute (NIA-RI) criteria do not include their evaluation, several recent reports drew attention to the possibility of selective and early involvement of raphe nuclei, particularly the dorsal raphe nucleus (DRN), in the pathogenesis of AD. Based on these findings of differential susceptibility and anatomical connectivity, a novel pathogenetic scheme of AD progression was proposed. Although the precise mechanisms of neurofibrillary degeneration still await elucidation, we speculated that cumulative oxidative damage may be the main cause of DRN alterations, as the age is the main risk factor for sporadic AD. Within such a framework, ,-amyloid production is considered only as one of the factors (although a significant one in familial cases) that promotes molecular series of events underlying AD-related neuropathological changes. [source] Sinusoidal heart rate pattern: Reappraisal of its definition and clinical significanceJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 3 2004Houchang D. Modanlou Abstract Objectives: To address the clinical significance of sinusoidal heart rate (SHR) pattern and review its occurrence, define its characteristics, and explain its physiopathology. Background: In 1972, Manseau et al. and Kubli et al. described an undulating wave form alternating with a flat or smooth baseline fetal heart rate (FHR) in severely affected, Rh-sensitized and dying fetuses. This FHR pattern was called ,sinusoidal' because of its sine waveform. Subsequently, Modanlou et al. described SHR pattern associated with fetal to maternal hemorrhage causing severe fetal anemia and hydrops fetalis. Both Manseau et al. and Kubli et al. stated that this particular FHR pattern, whatever its pathogenesis, was an extremely significant finding that implied severe fetal jeopardy and impending fetal death. Undulating FHR pattern: Undulating FHR pattern may be due to the following: (1) true SHR pattern; (2) drugs; (3) pre-mortem FHR pattern; (4) pseudo-SHR pattern; and (5) equivocal FHR patterns. Fetal conditions associated with SHR pattern: SHR pattern has been reported with the following fetal conditions: (1) severe fetal anemia of several etiologies; (2) effects of drugs, particularly narcotics; (3) fetal asphyxia/hypoxia; (4) fetal infection; (5) fetal cardiac anomalies; (6) fetal sleep cycles; and (7) sucking and rhythmic movements of fetal mouth. Definition of true SHR pattern: Modanlou and Freeman proposed the following definition for the interpretation of true SHR pattern: (a) stable baseline FHR of 120,160 bpm; (b) amplitude of 5,15 bpm, rarely greater; (c) frequency of 2,5 cycles per minute; (d) fixed or flat short-term variability; (e) oscillation of the sinusoidal wave from above and below a baseline; and (f) no areas of normal FHR variability or reactivity. Physiopathology: Since its early recognition, the physiopathology of SHR became a matter of debate. Murata et al. noted a rise of arginine vasopressin levels in the blood of posthemorrhagic/anemic fetal lamb. Further works by the same authors revealed that with chemical or surgical vagotomy, arginine vasopressin infusion produced SHR pattern, thus providing the role of autonomic nervous system dysfunction combined with the increase in arginine vasopressin as the etiology. Conclusion: SHR is a rare occurrence. A true SHR is an ominous sign of fetal jeopardy needing immediate intervention. The correct diagnosis of true SHR pattern should also include fetal biophysical profile and the absence of drugs such as narcotics. [source] | ||||||||||