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Showing papers on "Rapid eye movement sleep published in 2011"


Journal ArticleDOI
TL;DR: 5-HT(2A) and 5- HT(2C) receptor knock-out mice show a significant increase of W and a reduction of slow wave sleep (SWS) which has been ascribed to the increase of catecholaminergic neurotransmission involving mainly the noradrenergic and dopaminergic systems.

417 citations


Journal ArticleDOI
TL;DR: It is proposed that in particular, sleep SWA represents a good marker for structural changes in neuronal networks reflecting cortical maturation during adolescence, which supports the notion that adolescence represents a sensitive period for cortex maturation.
Abstract: Deep (slow wave) sleep shows extensive maturational changes from childhood through adolescence, which is reflected in a decrease of sleep depth measured as the activity of electroencephalographic (EEG) slow waves. This decrease in sleep depth is paralleled by massive synaptic remodeling during adolescence as observed in anatomical studies, which supports the notion that adolescence represents a sensitive period for cortical maturation. To assess the relationship between slow-wave activity (SWA) and cortical maturation, we acquired sleep EEG and magnetic resonance imaging data in children and adolescents between 8 and 19 years. We observed a tight relationship between sleep SWA and a variety of indexes of cortical maturation derived from magnetic resonance (MR) images. Specifically, gray matter volumes in regions correlating positively with the activity of slow waves largely overlapped with brain areas exhibiting an age-dependent decrease in gray matter. The positive relationship between SWA and cortical gray matter was present also for power in other frequency ranges (theta, alpha, sigma, and beta) and other vigilance states (theta during rapid eye movement sleep). Our findings indicate a strong relationship between sleep EEG activity and cortical maturation. We propose that in particular, sleep SWA represents a good marker for structural changes in neuronal networks reflecting cortical maturation during adolescence.

223 citations


Journal ArticleDOI
TL;DR: In this paper, diffusion tensor imaging (DTI) and statistical parametric mapping (SPM) were applied to objectively identify focal changes of MRI parameters throughout the entire brain volume.
Abstract: Objective We applied diffusion-tensor imaging (DTI) including measurements of mean diffusivity (MD), a parameter of brain tissue integrity, fractional anisotropy (FA), a parameter of neuronal fiber integrity, as well as voxel-based morphometry (VBM), a measure of gray and white matter volume, to detect brain tissue changes in patients with idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). Methods Magnetic resonance imaging (MRI) was performed in 26 patients with iRBD (mean disease duration, 9.2 ± 6.4 years) and 14 age-matched healthy control subjects. Statistical parametric mapping (SPM) was applied to objectively identify focal changes of MRI parameters throughout the entire brain volume. Results SPM localized significant decreases of FA in the tegmentum of the midbrain and rostral pons and increases of MD within the pontine reticular formation overlapping with a cluster of decreased FA in the midbrain (p < 0.001). VBM revealed increases of gray matter densities in both hippocampi of iRBD patients (p < 0.001). Interpretation The observed changes in the pontomesencephalic brainstem localized 2 areas harboring key neuronal circuits believed to be involved in the regulation of REM sleep and overlap with areas of structural brainstem damage causing symptomatic RBD in humans. Bilateral increases in gray matter density of the hippocampus suggest functional neuronal reorganization in this brain area in iRBD. This study indicates that DTI detects distinct structural brainstem tissue abnormalities in iRBD in the regions where REM is modulated. Further studies should explore the relationship between MRI pathology and the risk of patients with iRBD of developing alpha-synuclein–related neurodegenerative diseases like Parkinson disease. Ann Neurol 2011.

188 citations


Journal ArticleDOI
TL;DR: It is found that SDB, regardless of the severity, was associated with increased BP during sleep and wake compared with nonsnoring control children, and the importance of considering the cardiovascular effects of SDB of any severity in children is highlighted.
Abstract: Sleep-disordered breathing (SDB) in adults has been as- sociated with elevated blood pressure (BP); however, the effects of severity of SDB on BP in children are uncertain. We addressed this issue by measuring BP noninvasively and continuously during sleep in children with a range of severities of SDB and in a group of nonsnoring control children. METHODS: A total of 105 children referred for assessment of SDB and 36 nonsnoring controls were studied. Routine polysomnography (PSG) was performed with continuous BP monitoring. Children were as- signed to groups according to obstructive apnea/hypopnea index (OAHI). BP data were categorized as quiet awake (recorded before sleep onset), non-rapid eye movement sleep 1 and 2 combined, slow- wave sleep, and rapid eye movement sleep. RESULTS: BP during awake before sleep onset and during overnight sleep was elevated by 10 to 15 mm Hg in the 3 SDB groups compared with the control group; this finding was independent of SDB severity. BP during stable sleep (with respiratory events and movements excluded) was also elevated in the children with OSA compared with the control group. BP was elevated in rapid eye movement sleep compared with the non-rapid eye movement sleep, and heart rate was higher during wake state than in all sleep states. CONCLUSIONS: We recorded BP continuously overnight and found that SDB, regardless of the severity, was associated with increased BP during sleep and wake compared with nonsnoring control children. These findings highlight the importance of considering the cardiovas- cular effects of SDB of any severity in children, and the need to review current clinical management that focuses primarily on more severe SDB. Pediatrics 2011;128:e85-e92

139 citations


Journal ArticleDOI
01 Nov 2011-Brain
TL;DR: Using a comprehensive assessment of the clinical, demographic and ophthalmological correlates of visual hallucinations in Parkinson's disease, the combined data support the hypothesized model of impaired visual processing, sleep-wake dysregulation and brainstem dysfunction, and cognitive, particularly frontal, impairment all independently contributing to the pathogenesis of visual hallucination.
Abstract: The exact pathogenesis of visual hallucinations in Parkinson's disease is not known but an integrated model has been proposed that includes impaired visual input and central visual processing, impaired brainstem regulation of sleep–wake cycle with fluctuating vigilance, intrusion of rapid eye movement dream imagery into wakefulness and emergence of internally generated imagery, cognitive dysfunction and influence of dopaminergic drugs. In a clinical study, we assessed motor and non-motor function, including sleep, mood, autonomic and global, frontal and visuoperceptive cognitive function in patients with and without visual hallucinations. A subgroup of patients underwent detailed ophthalmological assessment. In a separate pathological study, histological specimens were obtained from cases of pathologically proven Parkinson's disease and a retrospective case notes review was made for reporting of persistent formed visual hallucinations. An assessment of Lewy body and Lewy neurite pathology was carried out in five cortical regions as recommended by diagnostic criteria for dementia with Lewy Bodies and in brainstem nuclei. Ninety-four patients (mean age 67.5 ± 9.5 years) participated in the clinical study of whom 32% experienced visual hallucinations. When corrected for multiple comparisons, patients with visual hallucinations had significantly greater disease duration, treatment duration, motor severity and complications, sleep disturbances, in particular excessive daytime somnolence and rapid eye movement sleep behavioural disorder, disorders of mood, autonomic dysfunction and global, frontal and visuoperceptive cognitive dysfunction. Of the 94 patients, 50 (53%) underwent ophthalmological assessment. There were no differences in ocular pathology between the visual hallucination and non-visual hallucination groups. In a logistic regression model the four independent determinants of visual hallucinations were rapid eye movement sleep behavioural disorder (P = 0.026), autonomic function (P = 0.004), frontal cognitive function (P = 0.020) and a test of visuoperceptive function (object decision; P = 0.031). In a separate study, post-mortem analysis was performed in 91 subjects (mean age at death 75.5 ± 8.0 years) and persistent visual hallucinations were documented in 63%. Patients in the visual hallucinations group had similar disease duration but had significantly higher Lewy body densities in the middle frontal (P = 0.002) and middle temporal gyri (P = 0.033) and transentorhinal (P = 0.005) and anterior cingulate (P = 0.020) cortices but not parietal cortex (P = 0.22). Using a comprehensive assessment of the clinical, demographic and ophthalmological correlates of visual hallucinations in Parkinson's disease, the combined data support the hypothesized model of impaired visual processing, sleep–wake dysregulation and brainstem dysfunction, and cognitive, particularly frontal, impairment all independently contributing to the pathogenesis of visual hallucinations in Parkinson's disease. These clinical data are supported by the pathological study, in which higher overall cortical Lewy body counts, and in particular areas implicated in visuoperception and executive function, were associated with visual hallucinations.

130 citations


Journal ArticleDOI
01 Aug 2011-Brain
TL;DR: It is suggested that the study of sleep and homoeostatic regulation of slow wave activity may provide a complementary tool for the assessment of brain function in minimally conscious state and vegetative state patients.
Abstract: The existence of normal sleep in patients in a vegetative state is still a matter of debate. Previous electrophysiological sleep studies in patients with disorders of consciousness did not differentiate patients in a vegetative state from patients in a minimally conscious state. Using high-density electroencephalographic sleep recordings, 11 patients with disorders of consciousness (six in a minimally conscious state, five in a vegetative state) were studied to correlate the electrophysiological changes associated with sleep to behavioural changes in vigilance (sustained eye closure and muscle inactivity). All minimally conscious patients showed clear electroencephalographic changes associated with decreases in behavioural vigilance. In the five minimally conscious patients showing sustained behavioural sleep periods, we identified several electrophysiological characteristics typical of normal sleep. In particular, all minimally conscious patients showed an alternating non-rapid eye movement/rapid eye movement sleep pattern and a homoeostatic decline of electroencephalographic slow wave activity through the night. In contrast, for most patients in a vegetative state, while preserved behavioural sleep was observed, the electroencephalographic patterns remained virtually unchanged during periods with the eyes closed compared to periods of behavioural wakefulness (eyes open and muscle activity). No slow wave sleep or rapid eye movement sleep stages could be identified and no homoeostatic regulation of sleep-related slow wave activity was observed over the night-time period. In conclusion, we observed behavioural, but no electrophysiological, sleep wake patterns in patients in a vegetative state, while there were near-to-normal patterns of sleep in patients in a minimally conscious state. These results shed light on the relationship between sleep electrophysiology and the level of consciousness in severely brain-damaged patients. We suggest that the study of sleep and homoeostatic regulation of slow wave activity may provide a complementary tool for the assessment of brain function in minimally conscious state and vegetative state patients.

128 citations


Journal ArticleDOI
TL;DR: This work shows that mice with impaired glycine and GABAA receptor function exhibit REM motor behaviors, non-REM muscle twitches, sleep disruption, and EEG slowing—the defining disease features of rapid eye movement (REM) sleep behavior disorder.
Abstract: Rapid eye movement (REM) sleep behavior disorder (RBD) is a neurological disease characterized by loss of normal REM motor inhibition and subsequent dream enactment. RBD is clinically relevant because it predicts neurodegenerative disease onset (e.g., Parkinson's disease) and is clinically problematic because it disrupts sleep and results in patient injuries and hospitalization. Even though the cause of RBD is unknown, multiple lines of evidence indicate that abnormal inhibitory transmission underlies the disorder. Here, we show that transgenic mice with deficient glycine and GABA transmission have a behavioral, motor, and sleep phenotype that recapitulates the cardinal features of RBD. Specifically, we show that mice with impaired glycine and GABA(A) receptor function exhibit REM motor behaviors, non-REM muscle twitches, sleep disruption, and EEG slowing--the defining disease features. Importantly, the RBD phenotype is rescued by drugs (e.g., clonazepam and melatonin) that are routinely used to treat human disease symptoms. Our findings are the first to identify a potential mechanism for RBD--we show that deficits in glycine- and GABA(A)-mediated inhibition trigger the full spectrum of RBD symptoms. We propose that these mice are a useful resource for investigating in vivo disease mechanisms and developing potential therapeutics for RBD.

111 citations


Journal ArticleDOI
TL;DR: Avian sleep does not appear to be involved in transferring hippocampal memories to other brain regions, and the slow‐oscillation, the defining feature of mammalian and avian SWS, may serve a more general function independent of that related to coordinating the transfer of information from the hippocampus to the PFC in mammals.
Abstract: The transition from wakefulness to sleep is marked by pronounced changes in brain activity. The brain rhythms that characterize the two main types of mammalian sleep, slow-wave sleep (SWS) and rapid eye movement (REM) sleep, are thought to be involved in the functions of sleep. In particular, recent theories suggest that the synchronous slow-oscillation of neocortical neuronal membrane potentials, the defining feature of SWS, is involved in processing information acquired during wakefulness. According to the Standard Model of memory consolidation, during wakefulness the hippocampus receives input from neocortical regions involved in the initial encoding of an experience and binds this information into a coherent memory trace that is then transferred to the neocortex during SWS where it is stored and integrated within preexisting memory traces. Evidence suggests that this process selectively involves direct connections from the hippocampus to the prefrontal cortex (PFC), a multimodal, high-order association region implicated in coordinating the storage and recall of remote memories in the neocortex. The slow-oscillation is thought to orchestrate the transfer of information from the hippocampus by temporally coupling hippocampal sharp-wave/ripples (SWRs) and thalamocortical spindles. SWRs are synchronous bursts of hippocampal activity, during which waking neuronal firing patterns are reactivated in the hippocampus and neocortex in a coordinated manner. Thalamocortical spindles are brief 7–14 Hz oscillations that may facilitate the encoding of information reactivated during SWRs. By temporally coupling the readout of information from the hippocampus with conditions conducive to encoding in the neocortex, the slow-oscillation is thought to mediate the transfer of information from the hippocampus to the neocortex. Although several lines of evidence are consistent with this function for mammalian SWS, it is unclear whether SWS serves a similar function in birds, the only taxonomic group other than mammals to exhibit SWS and REM sleep. Based on our review of research on avian sleep, neuroanatomy, and memory, although involved in some forms of memory consolidation, avian sleep does not appear to be involved in transferring hippocampal memories to other brain regions. Despite exhibiting the slow-oscillation, SWRs and spindles have not been found in birds. Moreover, although birds independently evolved a brain region—the caudolateral nidopallium (NCL)—involved in performing high-order cognitive functions similar to those performed by the PFC, direct connections between the NCL and hippocampus have not been found in birds, and evidence for the transfer of information from the hippocampus to the NCL or other extra-hippocampal regions is lacking. Although based on the absence of evidence for various traits, collectively, these findings suggest that unlike mammalian SWS, avian SWS may not be involved in transferring memories from the hippocampus. Furthermore, it suggests that the slow-oscillation, the defining feature of mammalian and avian SWS, may serve a more general function independent of that related to coordinating the transfer of information from the hippocampus to the PFC in mammals. Given that SWS is homeostatically regulated (a process intimately related to the slow-oscillation) in mammals and birds, functional hypotheses linked to this process may apply to both taxonomic groups.

108 citations


Journal ArticleDOI
TL;DR: There is evidence thatintensive care patients' sleep is significantly disrupted and alternative methods of quantifying sleep for intensive care patients may be required.

95 citations


Journal ArticleDOI
TL;DR: Alcohol intoxication increases subjective sleepiness and disrupts sleep objectively more in healthy women than in men, with no differences evident by family history of alcoholism status.
Abstract: Background: This study evaluated sex and family history of alcoholism as moderators of subjective ratings of sleepiness/sleep quality and polysomnography (PSG) following alcohol intoxication in healthy, young adults. Methods: Ninety-three healthy adults [mean age 24.4 ± 2.7 years, 59 women, 29 subjects with a positive family history of alcoholism (FH+)] were recruited. After screening PSG, participants consumed alcohol (sex/weight adjusted dosing) to intoxication [peak breath alcohol concentration (BrAC) of 0.11 ± 0.01 g% for men and women] or matching placebo between 20:30 and 22:00 hours. Sleep was monitored using PSG between 23:00 and 07:00 hours. Participants completed the Stanford Sleepiness Scale and Karolinska Sleepiness Scale at bedtime and on awakening and a validated post-sleep questionnaire. Results: Following alcohol, total sleep time, sleep efficiency, nighttime awakenings, and wake after sleep onset were more disrupted in women than men, with no differences by family history status. Alcohol reduced sleep onset latency, sleep efficiency, and rapid eye movement sleep while increasing wakefulness and slow wave sleep across the entire night compared with placebo. Alcohol also generally increased sleep consolidation in the first half of the night, but decreased it during the second half. Sleepiness ratings were higher following alcohol, particularly in women at bedtime. Morning sleep quality ratings were lower following alcohol than placebo. Conclusions: Alcohol intoxication increases subjective sleepiness and disrupts sleep objectively more in healthy women than in men, with no differences evident by family history of alcoholism status. Evaluating moderators of alcohol effects on sleep may provide insight into the role of sleep in problem drinking.

84 citations


Journal ArticleDOI
TL;DR: In this paper, the authors reported a cascade of homeostatic events, wherein sleep deprivation induces the production of inducible nitric oxide synthase (iNOS)-dependent NO in BF, leading to enhanced release of extracellular adenosine.
Abstract: Both adenosine and nitric oxide (NO) are known for their role in sleep homeostasis, with the basal forebrain (BF) wakefulness center as an important site of action. Previously, we reported a cascade of homeostatic events, wherein sleep deprivation (SD) induces the production of inducible nitric oxide synthase (iNOS)-dependent NO in BF, leading to enhanced release of extracellular adenosine. In turn, increased BF adenosine leads to enhanced sleep intensity, as measured by increased non-rapid eye movement sleep EEG delta activity. However, the presence and time course of similar events in cortex has not been studied, although a frontal cortical role for the increase in non-rapid eye movement recovery sleep EEG delta power is known. Accordingly, we performed simultaneous hourly microdialysis sample collection from BF and frontal cortex (FC) during 11 h SD. We observed that both areas showed sequential increases in iNOS and NO, followed by increases in adenosine. BF increases began at 1 h SD, whereas FC increases began at 5 h SD. iNOS and Fos-double labeling indicated that iNOS induction occurred in BF and FC wake-active neurons. These data support the role of BF adenosine and NO in sleep homeostasis and indicate the temporal and spatial sequence of sleep homeostatic cascade for NO and adenosine.

Journal ArticleDOI
TL;DR: The results show that poor sleep quality and greater severity of SAS were associated with impaired language function reflecting frontal-subcortical pathology in patients with MCI, suggesting that vulnerability to a specific brain damage associated with SAS could increase the risk for dementia.
Abstract: Objectives Sleep apnea syndrome (SAS) is considered a risk factor for cognitive decline in the elderly. The specific neurocognitive decline has been suggested as a predictive factor for dementia in patients with mild cognitive impairment (MCI). The authors aim to illustrate the sleep characteristics related to the specific neurocognitive decline in the community-dwelling elderly including patients with MCI. Design Cross-sectional. Settings Center for sleep and chronobiology in Kangwon National University Hospital. Participants Thirty patients with MCI and 30 age- and sex-matched normal elderly subjects were selected. Measurements The authors administered seven tests in the Korean version of the Consortium to Establish A Registry of Alzheimer's Disease Neuropsychological battery and conducted nocturnal polysomnography. A p value below 0.05 was considered a statistical significance. Results There was no significant difference in sleep parameters between the MCI and normal comparison (NC) groups. Sleep efficiency was positively correlated with Constructional Recall (CR) scores in both NC and MCI groups (r = 0.393 and 0.391, respectively). The amount of slow wave sleep (SWS) was also positively correlated with Boston naming test (BNT) scores in both groups (r = 0.392, 0.470, respectively). Stepwise multiple regression models showed that SWS and the apnea index were significant independent variables associated with the BNT score (Δβ = 0.43 and −0.34, respectively; adjusted R 2 = 0.298) in the MCI group, and the amount of rapid eye movement sleep was a significant independent variable associated with the CR score (Δβ = 0.49; adjusted R 2 = 0.217) in the NC group. Conclusions Our results show that poor sleep quality and greater severity of SAS were associated with impaired language function reflecting frontal-subcortical pathology in patients with MCI. This suggests that vulnerability to a specific brain damage associated with SAS could increase the risk for dementia.

Journal ArticleDOI
TL;DR: Evidence is provided of regional cerebral blood flow abnormalities in rapid eye movement sleep behavior disorder that are similar to those seen in Parkinson's disease and Lewy body dementia and a relationship between loss of olfactory discrimination and regional cerebral flow reduction in the bilateral anterior parahippocampal gyrus was found.
Abstract: Potential early markers of neurodegeneration such as subtle motor signs, reduced color discrimination, olfactory impairment, and brain perfusion abnormalities have been reported in idiopathic rapid eye movement sleep behavior disorder, a risk factor for Parkinson's disease and Lewy body dementia. The aim of this study was to reproduce observations of regional cerebral blood flow abnormalities in a larger independent sample of patients and to explore correlations between regional cerebral blood flow and markers of neurodegeneration. Twenty patients with idiopathic rapid eye movement sleep behavior disorder and 20 healthy controls were studied by single-photon emission computerized tomography. Motor examination, color discrimination, and olfactory identification were examined. Patients with rapid eye movement sleep behavior disorder showed decreased regional cerebral blood flow in the frontal cortex and in medial parietal areas and increased regional cerebral blood flow in subcortical regions including the bilateral pons, putamen, and hippocampus. In rapid eye movement sleep behavior disorder, brain perfusion in the frontal cortex and occipital areas was associated with poorer performance in the color discrimination test. Moreover, a relationship between loss of olfactory discrimination and regional cerebral blood flow reduction in the bilateral anterior parahippocampal gyrus, a region known to be involved in olfactory functions, was found. This study provides further evidence of regional cerebral blood flow abnormalities in rapid eye movement sleep behavior disorder that are similar to those seen in Parkinson's disease and Lewy body dementia. Moreover, regional cerebral blood flow anomalies were associated with markers of neurodegeneration.

Journal ArticleDOI
TL;DR: The relationship between rapid eye movement sleep behavior disorder and autonomic dysfunction in Parkinson's disease as measured by cardiac beat‐to‐beat variability is examined.
Abstract: Background: Recent studies have suggested a close connection between autonomic dysfunction and rapid eye movement sleep behavior disorder, which differs in nature from other early-stage markers of Parkinson's disease. In this study we examined the relationship between rapid eye movement sleep behavior disorder and autonomic dysfunction in Parkinson's disease as measured by cardiac beat-to-beat variability. Methods: In 53 patients with Parkinson's disease and 36 controls, electrocardiographic trace from a polysomnogram was assessed for measures of beat-to-beat RR variability including RR-standard deviation and frequency domains (low- and high-frequency components). Results were compared between patients with Parkinson's disease and controls, and between patients with Parkinson's disease with and without rapid eye movement sleep behavior disorder. Results: On numerous cardiac autonomic measures, patients with Parkinson's disease showed clear abnormalities compared with controls. However, these abnormalities were confined only to those patients with associated rapid eye movement sleep behavior; those without were not different than controls. Conclusions: As with other clinical autonomic variables, cardiac autonomic denervation is predominantly associated not with Parkinson's disease itself, but with the presence of rapid eye movement sleep behavior disorder. © 2011 Movement Disorder Society

Journal ArticleDOI
TL;DR: Results indicate that increases in stimulated monocyte production of IL-6 may be associated with decreases in slow wave sleep and increases in REM sleep duration, which may be one pathway through which cellular inflammation leads to daytime fatigue.
Abstract: Individuals with underlying inflammation present with a high prevalence of non-specific co-morbid symptoms including sleep disturbance and fatigue. However, the association between cellular expression of proinflammatory cytokines, alterations of sleep depth and daytime fatigue has not been concurrently examined. In healthy adults (24 – 61 years old), evening levels of monocyte intracellular proinflammatory cytokine production were assessed prior to evaluation of polysomonographic sleep and measures of fatigue the following day. Stimulated monocyte production of interleukin-6 (IL-6), but not tumor necrosis factor α (TNF- α), was negatively associated with slow wave sleep (ΔR2 =.17, p=.029). In contrast, stimulated monocyte production of IL-6 was positively associated with rapid-eye movement (REM) sleep duration during the first sleep cycle (ΔR2 = .26, p<.01). Moreover, evening stimulated production of IL-6 was associated with fatigue the following day (ΔR2 = .17, p=.05). Mediation analyses showed that slow wave sleep, but not REM sleep duration, mediated the relationship between evening levels of IL-6 production and daytime fatigue. These results indicate that increases in stimulated monocyte production of IL6 may be associated with changes in sleep architecture with decreases in slow wave sleep and increases in REM sleep duration. Relative loss of slow wave sleep may be one pathway through which cellular inflammation leads to daytime fatigue.

Journal ArticleDOI
TL;DR: Evidence from in vivo and in vitro studies showing REMS deprivation increases noradrenaline level in the brain, which stimulates neuronal Na-K ATPase, the key factor for maintaining neuronal excitability, the fundamental property of a neuron for executing brain functions is presented.

Journal ArticleDOI
26 Oct 2011-PLOS ONE
TL;DR: Results provide evidence for a 7-day sleep-dependent non-linear memory consolidation process that is specific to REM sleep, and accord with proposals for the importance of REM sleep to emotional memory consolidation.
Abstract: This study investigates evidence, from dream reports, for memory consolidation during sleep. It is well-known that events and memories from waking life can be incorporated into dreams. These incorporations can be a literal replication of what occurred in waking life, or, more often, they can be partial or indirect. Two types of temporal relationship have been found to characterize the time of occurrence of a daytime event and the reappearance or incorporation of its features in a dream. These temporal relationships are referred to as the day-residue or immediate incorporation effect, where there is the reappearance of features from events occurring on the immediately preceding day, and the dream-lag effect, where there is the reappearance of features from events occurring 5–7 days prior to the dream. Previous work on the dream-lag effect has used spontaneous home recalled dream reports, which can be from Rapid Eye Movement Sleep (REM) and from non-Rapid Eye Movement Sleep (NREM). This study addresses whether the dream-lag effect occurs only for REM sleep dreams, or for both REM and NREM stage 2 (N2) dreams. 20 participants kept a daily diary for over a week before sleeping in the sleep laboratory for 2 nights. REM and N2 dreams collected in the laboratory were transcribed and each participant rated the level of correspondence between every dream report and every diary record. The dream-lag effect was found for REM but not N2 dreams. Further analysis indicated that this result was not due to N2 dream reports being shorter, in terms of number of words, than the REM dream reports. These results provide evidence for a 7-day sleep-dependent non-linear memory consolidation process that is specific to REM sleep, and accord with proposals for the importance of REM sleep to emotional memory consolidation.

Journal ArticleDOI
TL;DR: Several recent lines of evidence suggest a strong link between rapid eye movement sleep behavior disorder and the risk of neurodegenerative diseases such as PD.
Abstract: Sleep disturbances are common problems affecting the quality life of Parkinson's disease (PD) patients and are often underestimated. The causes of sleep disturbances are multifactorial and include nocturnal motor disturbances, nocturia, depressive symptoms, and medication use. Comorbidity of PD with sleep apnea syndrome, restless legs syndrome, rapid eye movement sleep behavior disorder, or circadian cycle disruption also results in impaired sleep. In addition, the involvement of serotoninergic, noradrenergic, and cholinergic neurons in the brainstem as a disease-related change contributes to impaired sleep structures. Excessive daytime sleepiness is not only secondary to nocturnal disturbances or dopaminergic medication but may also be due to independent mechanisms related to impairments in ascending arousal system and the orexin system. Notably, several recent lines of evidence suggest a strong link between rapid eye movement sleep behavior disorder and the risk of neurodegenerative diseases such as PD. In the present paper, we review the current literature concerning sleep disorders in PD.

Journal ArticleDOI
TL;DR: Post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities, and post-learning treatment of normal rats with nicotine for 24h enhanced long-term memory.

Journal ArticleDOI
TL;DR: The data indicate that specific EEG frequency- and topography changes underlie differences between dream recall and no recall after both NREM and REM sleep awakening, which holds strong implications for the mechanistic understanding of this complex ongoing cognitive process.

Journal ArticleDOI
TL;DR: Interestingly, the results revealed that both short and long naps resulted in similar delayed performance gains, which might suggest that the presence of slow wave and rapid eye movement sleep does not provide additional benefits for the sleep-dependent motor skill consolidation following MI practice.
Abstract: Sleep is known to contribute to motor memory consolidation. Recent studies have provided evidence that a night of sleep plays a similar functional role following motor imagery (MI), while the simple passage of time does not result in performance gains. Here, we examined the benefits of a daytime nap on motor memory consolidation after MI practice. Participants were trained by MI on an explicitly known sequence of finger movements at 11:00. Half of the participants were then subjected (at 14:00) to either a short nap (10 min of stage 2 sleep) or a long nap (60-90 min, including slow wave sleep and rapid eye movement sleep). We also collected data from both quiet and active rest control groups. All participants remained in the lab until being retested at 16:00. The data revealed that a daytime nap after imagery practice improved motor performance and, therefore, facilitated motor memory consolidation, as compared with spending a similar time interval in the wake state. Interestingly, the results revealed that both short and long naps resulted in similar delayed performance gains. The data might also suggest that the presence of slow wave and rapid eye movement sleep does not provide additional benefits for the sleep-dependent motor skill consolidation following MI practice.

Journal ArticleDOI
TL;DR: The hypothesis that arousal is a defensive mechanism that may preserve cognitive function by counteracting the respiratory events, at the expense of sleep maintenance and NREM sleep instability, is supported.

Journal ArticleDOI
01 Mar 2011-Brain
TL;DR: It is concluded that parkinsonism also disappears during rapid eye movement sleep behaviour disorder in patients with multiple system atrophy, but this improvement is not due to enhanced dopamine transmission because these patients are not levodopa-sensitive.
Abstract: Multiple system atrophy is an atypical parkinsonism characterized by severe motor disabilities that are poorly levodopa responsive. Most patients develop rapid eye movement sleep behaviour disorder. Because parkinsonism is absent during rapid eye movement sleep behaviour disorder in patients with Parkinson's disease, we studied the movements of patients with multiple system atrophy during rapid eye movement sleep. Forty-nine non-demented patients with multiple system atrophy and 49 patients with idiopathic Parkinson's disease were interviewed along with their 98 bed partners using a structured questionnaire. They rated the quality of movements, vocal and facial expressions during rapid eye movement sleep behaviour disorder as better than, equal to or worse than the same activities in an awake state. Sleep and movements were monitored using video-polysomnography in 22/49 patients with multiple system atrophy and in 19/49 patients with Parkinson's disease. These recordings were analysed for the presence of parkinsonism and cerebellar syndrome during rapid eye movement sleep movements. Clinical rapid eye movement sleep behaviour disorder was observed in 43/49 (88%) patients with multiple system atrophy. Reports from the 31/43 bed partners who were able to evaluate movements during sleep indicate that 81% of the patients showed some form of improvement during rapid eye movement sleep behaviour disorder. These included improved movement (73% of patients: faster, 67%; stronger, 52%; and smoother, 26%), improved speech (59% of patients: louder, 55%; more intelligible, 17%; and better articulated, 36%) and normalized facial expression (50% of patients). The rate of improvement was higher in Parkinson's disease than in multiple system atrophy, but no further difference was observed between the two forms of multiple system atrophy (predominant parkinsonism versus cerebellar syndrome). Video-monitored movements during rapid eye movement sleep in patients with multiple system atrophy revealed more expressive faces, and movements that were faster and more ample in comparison with facial expression and movements during wakefulness. These movements were still somewhat jerky but lacked any visible parkinsonism. Cerebellar signs were not assessable. We conclude that parkinsonism also disappears during rapid eye movement sleep behaviour disorder in patients with multiple system atrophy, but this improvement is not due to enhanced dopamine transmission because these patients are not levodopa-sensitive. These data suggest that these movements are not influenced by extrapyramidal regions; however, the influence of abnormal cerebellar control remains unclear. The transient disappearance of parkinsonism here is all the more surprising since no treatment (even dopaminergic) provides a real benefit in this disabling disease.

Journal ArticleDOI
TL;DR: Donepezil can increase the amount of time that children with an ASD spend in the REM sleep state and a double-blind, placebo-controlled trial is needed to assess the association between REM sleep augmentation and learning, cognition, and behavior in such children.
Abstract: Background: Rapid eye movement (REM) sleep is greatest in the developing brain, is driven by acetylcholine, and may represent a protected time for neuroplasticity. Recently published data from our lab observed that children with autism spent significantly less time in this state during a single night recording than did typically developing children and those with developmental delay without autism. The objective of this study was to determine whether or not donepezil can increase the REM % in children with diagnosed autism spectrum disorder (ASD) found to have REM % values of at least two standard deviations below expected for age. Methods: Five subjects found to have an ASD (ages 2.5–6.9 years) and demonstrated deficits in REM sleep compared with within-lab controls were enrolled in a dose finding study of donepezil. Each subject was examined by polysomnography for REM sleep augmentation after drug administration. Results: REM sleep as a percentage of Total Sleep Time was increased significantly...

Journal ArticleDOI
TL;DR: REM sleep rebound after exposure to volatile anesthetics suggests that these volatileAnesthetics do not fully substitute for natural sleep, compared with the published actions of propofol for which no REM sleep rebound occurred.
Abstract: BACKGROUND General anesthesia has been likened to a state in which anesthetized subjects are locked out of access to both rapid eye movement (REM) sleep and wakefulness. Were this true for all anesthetics, a significant REM rebound after anesthetic exposure might be expected. However, for the intravenous anesthetic propofol, studies demonstrate that no sleep debt accrues. Moreover, preexisting sleep debts dissipate during propofol anesthesia. To determine whether these effects are specific to propofol or are typical of volatile anesthetics, the authors tested the hypothesis that REM sleep debt would accrue in rodents anesthetized with volatile anesthetics. METHODS Electroencephalographic and electromyographic electrodes were implanted in 10 mice. After 9-11 days of recovery and habituation to a 12 h:12 h light-dark cycle, baseline states of wakefulness, nonrapid eye movement sleep, and REM sleep were recorded in mice exposed to 6 h of an oxygen control and on separate days to 6 h of isoflurane, sevoflurane, or halothane in oxygen. All exposures were conducted at the onset of light. RESULTS Mice in all three anesthetized groups exhibited a significant doubling of REM sleep during the first 6 h of the dark phase of the circadian schedule, whereas only mice exposed to halothane displayed a significant increase in nonrapid eye movement sleep that peaked at 152% of baseline. CONCLUSION REM sleep rebound after exposure to volatile anesthetics suggests that these volatile anesthetics do not fully substitute for natural sleep. This result contrasts with the published actions of propofol for which no REM sleep rebound occurred.

Journal ArticleDOI
TL;DR: Supporting functional and behavioral roles for SIRT1 in wake–active neurons, transgenic whole animal, and conditional loss of brain Sirt1 in the adult mouse impart selective impairments in wakefulness, without disrupting non-rapid eye movement or rapid eye movement sleep.
Abstract: Wake neurons in the basal forebrain and brainstem provide critical inputs to optimize alertness and attention. These neurons, however, evidence heightened vulnerability to a diverse array of metabolic challenges, including aging. SIRT1 is an nicotinamide adenine dinucleotide responsive deacetylase serving diverse adaptive responses to metabolic challenges, yet this metabolic rheostat may be downregulated under conditions of significant oxidative stress. We hypothesized that SIRT1 might serve as a critical neuroprotectant for wake neurons in young animals but that this protectant would be lost upon aging, rendering the neurons more vulnerable to metabolic insults. In this collection of studies, we first established the presence of nuclear SIRT1 in wake neurons throughout the forebrain and brainstem. Supporting functional and behavioral roles for SIRT1 in wake-active neurons, transgenic whole animal, and conditional loss of brain SIRT1 in the adult mouse impart selective impairments in wakefulness, without disrupting non-rapid eye movement or rapid eye movement sleep. Populations of wake neurons, including the orexinergic, locus ceruleus, mesopontine cholinergic, and dopaminergic wake neurons, evidence loss of dendrites and neurotransmitter synthesis enzymes and develop accelerated accumulation of lipofuscin, consistent with a senescence-like phenotype in wake neurons. Normal aging results in a progressive loss of SIRT1 in wake-active neurons, temporally coinciding with lipofuscin accumulation. SIRT1 is a critical age-sensitive neuroprotectant for wake neurons, and its deficiency results in impaired wakefulness.

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TL;DR: Data confirm the previous hypothesis that inhalational agents do not satisfy the homeostatic need for REM sleep, and that the relationship between sleep and anesthesia is likely to be agent and state specific.
Abstract: Background Prolonged propofol administration does not result in signs of sleep deprivation, and propofol anesthesia appears to satisfy the homeostatic need for both rapid eye movement (REM) and non-REM (NREM) sleep. In the current study, the effects of sevoflurane on recovery from total sleep deprivation were investigated. Methods Ten male rats were instrumented for electrophysiologic recordings under three conditions: (1) 36-h ad libitum sleep; (2) 12-h sleep deprivation followed by 24-h ad libitum sleep; and (3) 12-h sleep deprivation, followed by 6-h sevoflurane exposure, followed by 18-h ad libitum sleep. The percentage of waking, NREM sleep, and REM sleep, as well as NREM sleep δ power, were calculated and compared for all three conditions. Results Total sleep deprivation resulted in significantly increased NREM and REM sleep for 12-h postdeprivation. Sevoflurane exposure after deprivation eliminated the homeostatic increase in NREM sleep and produced a significant decrease in the NREM sleep δ power during the postanesthetic period, indicating a complete recovery from the effects of deprivation. However, sevoflurane did not affect the time course of REM sleep recovery, which required 12 h after deprivation and anesthetic exposure. Conclusion Unlike propofol, sevoflurane anesthesia has differential effects on NREM and REM sleep homeostasis. These data confirm the previous hypothesis that inhalational agents do not satisfy the homeostatic need for REM sleep, and that the relationship between sleep and anesthesia is likely to be agent and state specific.

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TL;DR: It is indicated that a “trait-like” aspect can be detected in the sleep EEG across adolescent development despite considerable neurodevelopmental changes, indicating that the brain oscillators responsible for generating theSleep EEG signal remain relatively stable across adolescentDevelopment.
Abstract: Waking and sleep data in adults show high heritability and trait-like characteristics in EEG spectra. This phenomenon has not been examined in children and adolescents where brain development influences the EEG. The present study examines whether a trait-like sleep EEG pattern is detectable across adolescent development. Two consecutive nights of standard sleep recordings were performed in 19 9–10-year-old children and 26 15–16-year-old teens, and were repeated 1.5–3 years later. EEG spectra averaged across the night for non-rapid eye movement and rapid eye movement sleep separately were classified using hierarchical cluster analysis, which showed that all 4 nights of a participant clustered together for a majority of participants. Intraclass correlation coefficients were also very high (>0.7) across nights separated by several years, indicating a trait-like feature of the sleep EEG. In summary, our results, using two measures of stability, indicate that a “trait-like” aspect can be detected in the sleep EEG across adolescent development despite considerable neurodevelopmental changes. This finding indicates that the brain oscillators responsible for generating the sleep EEG signal remain relatively stable across adolescent development.

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TL;DR: The inverse relationship between changes in PRF levels of GABA and ACh during REM sleep indicates that low GABAergic tone combined with high cholinergic tone in the PRF contributes to the generation of REM sleep.
Abstract: Studies using drugs that increase or decrease GABAergic transmission suggest that GABA in the pontine reticular formation (PRF) promotes wakefulness and inhibits rapid eye movement (REM) sleep. Cholinergic transmission in the PRF promotes REM sleep, and levels of endogenous acetylcholine (ACh) in the PRF are significantly greater during REM sleep than during wakefulness or non-REM (NREM) sleep. No previous studies have determined whether levels of endogenous GABA in the PRF vary as a function of sleep and wakefulness. This study tested the hypothesis that GABA levels in cat PRF are greatest during wakefulness and lowest during REM sleep. Extracellular GABA levels were measured during wakefulness, NREM sleep, REM sleep, and the REM sleep-like state (REMNeo) caused by microinjecting neostigmine into the PRF. GABA levels varied significantly as a function of sleep and wakefulness, and decreased significantly below waking levels during REM sleep (−42%) and REMNeo (−63%). The decrease in GABA levels during NREM sleep (22% below waking levels) was not statistically significant. Compared with NREM sleep, GABA levels decreased significantly during REM sleep (−27%) and REMNeo (−52%). Comparisons of REM sleep and REMNeo revealed no differences in GABA levels or cortical EEG power. GABA levels did not vary significantly as a function of dialysis site within the PRF. The inverse relationship between changes in PRF levels of GABA and ACh during REM sleep indicates that low GABAergic tone combined with high cholinergic tone in the PRF contributes to the generation of REM sleep.

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TL;DR: Results suggest that the MBH is required for the essential task of integrating sleep-wake and feeding rhythms, a function that allows animals to accommodate changeable patterns of food availability.
Abstract: Sleep and feeding rhythms are highly coordinated across the circadian cycle, but the brain sites responsible for this coordination are unknown. We examined the role of neuropeptide Y (NPY) receptor-expressing neurons in the mediobasal hypothalamus (MBH) in this process by injecting the targeted toxin, NPY-saporin (NPY-SAP), into the arcuate nucleus (Arc). NPY-SAP-lesioned rats were initially hyperphagic, became obese, exhibited sustained disruption of circadian feeding patterns, and had abnormal circadian distribution of sleep-wake patterns. Total amounts of rapid eye movement sleep (REMS) and non-REMS (NREMS) were not altered by NPY-SAP lesions, but a peak amount of REMS was permanently displaced to the dark period, and circadian variation in NREMS was eliminated. The phase reversal of REMS to the dark period by the lesion suggests that REMS timing is independently linked to the function of MBH NPY receptor-expressing neurons and is not dependent on NREMS pattern, which was altered but not phase reversed by the lesion. Sleep-wake patterns were altered in controls by restricting feeding to the light period, but were not altered in NPY-SAP rats by restricting feeding to either the light or dark period, indicating that disturbed sleep-wake patterns in lesioned rats were not secondary to changes in food intake. Sleep abnormalities persisted even after hyperphagia abated during the static phase of the lesion. Results suggest that the MBH is required for the essential task of integrating sleep-wake and feeding rhythms, a function that allows animals to accommodate changeable patterns of food availability. NPY receptor-expressing neurons are key components of this integrative function.