Showing papers on "Rapid eye movement sleep published in 2016"
TL;DR: It is demonstrated that MSGABA neuronal activity specifically during REMS is required for normal memory consolidation, and optogenetically silenced medial septum γ-aminobutyric acid–releasing (MSGABA) neurons selectively during a REMS critical window after learning erased subsequent novel object place recognition and impaired fear-conditioned contextual memory.
Abstract: Rapid eye movement sleep (REMS) has been linked with spatial and emotional memory consolidation. However, establishing direct causality between neural activity during REMS and memory consolidation has proven difficult because of the transient nature of REMS and significant caveats associated with REMS deprivation techniques. In mice, we optogenetically silenced medial septum γ-aminobutyric acid-releasing (MS(GABA)) neurons, allowing for temporally precise attenuation of the memory-associated theta rhythm during REMS without disturbing sleeping behavior. REMS-specific optogenetic silencing of MS(GABA) neurons selectively during a REMS critical window after learning erased subsequent novel object place recognition and impaired fear-conditioned contextual memory. Silencing MS(GABA) neurons for similar durations outside REMS episodes had no effect on memory. These results demonstrate that MS(GABA) neuronal activity specifically during REMS is required for normal memory consolidation.
474 citations
TL;DR: Studies provide some evidence for a role of certain dietary patterns and foods in the promotion of high-quality sleep, but more studies are necessary to confirm those preliminary findings.
306 citations
TL;DR: Physicians should be aware of the full clinical expression of IRBD, a sleep disturbance that represents a neurodegenerative disease and highlight frequent features that were not reported or not sufficiently emphasized in previous publications.
Abstract: Objective To describe the clinical phenotype of idiopathic rapid eye movement (REM) sleep behavior disorder (IRBD) at presentation in a sleep center. Methods Clinical history review of 203 consecutive patients with IRBD identified between 1990 and 2014. IRBD was diagnosed by clinical history plus video-polysomnographic demonstration of REM sleep with increased electromyographic activity linked to abnormal behaviors. Results Patients were 80% men with median age at IRBD diagnosis of 68 y (range, 50-85 y). In addition to the already known clinical picture of IRBD, other important features were apparent: 44% of the patients were not aware of their dream-enactment behaviors and 70% reported good sleep quality. In most of these cases bed partners were essential to convince patients to seek medical help. In 11% IRBD was elicited only after specific questioning when patients consulted for other reasons. Seven percent did not recall unpleasant dreams. Leaving the bed occurred occasionally in 24% of subjects in whom dementia with Lewy bodies often developed eventually. For the correct diagnosis of IRBD, video-polysomnography had to be repeated in 16% because of insufficient REM sleep or electromyographic artifacts from coexistent apneas. Some subjects with comorbid obstructive sleep apnea reported partial improvement of RBD symptoms following continuous positive airway pressure therapy. Lack of therapy with clonazepam resulted in an increased risk of sleep related injuries. Synucleinopathy was frequently diagnosed, even in patients with mild severity or uncommon IRBD presentations (e.g., patients who reported sleeping well, onset triggered by a life event, nocturnal ambulation) indicating that the development of a neurodegenerative disease is independent of the clinical presentation of IRBD. Conclusions We report the largest IRBD cohort observed in a single center to date and highlight frequent features that were not reported or not sufficiently emphasized in previous publications. Physicians should be aware of the full clinical expression of IRBD, a sleep disturbance that represents a neurodegenerative disease. Commentary A commentary on this article appears in this issue on page 7.
160 citations
TL;DR: Neuromelanin-sensitive imaging provides an early marker of non-dopaminergic alpha-synucleinopathy that can be detected on an individual basis in patients with idiopathic rapid eye movement sleep behaviour.
Abstract: Idiopathic rapid eye movement sleep behaviour disorder is characterized by nocturnal violence, increased muscle tone during rapid eye movement sleep and the lack of any other neurological disease. However, idiopathic rapid eye movement sleep behaviour disorder can precede parkinsonism and dementia by several years. Using 3 T magnetic resonance imaging and neuromelanin-sensitive sequences, we previously found that the signal intensity was reduced in the locus coeruleus/subcoeruleus area of patients with Parkinson’s disease and rapid eye movement sleep behaviour disorder. Here, we studied the integrity of the locus coeruleus/subcoeruleus complex with neuromelanin-sensitive imaging in 21 patients with idiopathic rapid eye movement sleep behaviour disorder and compared the results with those from 21 age- and gender-matched healthy volunteers. All subjects underwent a clinical examination, motor, cognitive, autonomous, psychological, olfactory and colour vision tests, and rapid eye movement sleep characterization using video-polysomnography and 3 T magnetic resonance imaging. The patients more frequently had preclinical markers of alpha-synucleinopathies, including constipation, olfactory deficits, orthostatic hypotension, and subtle motor impairment. Using neuromelanin-sensitive imaging, reduced signal intensity was identified in the locus coeruleus/subcoeruleus complex of the patients with idiopathic rapid eye movement sleep behaviour. The mean sensitivity of the visual analyses of the signal performed by neuroradiologists who were blind to the clinical diagnoses was 82.5%, and the specificity was 81% for the identification of idiopathic rapid eye movement sleep behaviour. The results confirm that this complex is affected in idiopathic rapid eye movement sleep behaviour (to the same degree as it is affected in Parkinson’s disease). Neuromelanin-sensitive imaging provides an early marker of non-dopaminergic alpha-synucleinopathy that can be detected on an individual basis.
137 citations
TL;DR: It is demonstrated that RBD is associated with a prominent loss of volume in the pontomesencephalic tegmentum, where cholinergic, GABAergic and glutamatergic neurons are located and implicated in the promotion of REM sleep and muscle atonia.
Abstract: Characterized by dream-enactment motor manifestations arising from rapid eye movement (REM) sleep, REM sleep behavior disorder (RBD) is frequently encountered in Parkinson’s disease (PD). Yet the specific neurostructural changes associated with RBD in PD patients remain to be revealed by neuroimaging. Here we identified such neurostructural alterations by comparing large samples of magnetic resonance imaging (MRI) scans in 69 PD patients with probable RBD, 240 patients without RBD and 138 healthy controls, using deformation-based morphometry (p < 0.05 corrected for multiple comparisons). All data were extracted from the Parkinson’s Progression Markers Initiative. PD patients with probable RBD showed smaller volumes than patients without RBD and than healthy controls in the pontomesencephalic tegmentum, medullary reticular formation, hypothalamus, thalamus, putamen, amygdala and anterior cingulate cortex. These results demonstrate that RBD is associated with a prominent loss of volume in the pontomesencephalic tegmentum, where cholinergic, GABAergic and glutamatergic neurons are located and implicated in the promotion of REM sleep and muscle atonia. It is additionally associated with more widespread atrophy in other subcortical and cortical regions whose loss also likely contributes to the altered regulation of sleep-wake states and motor activity underlying RBD in PD patients.
100 citations
TL;DR: REM sleep disruption and sleep fragmentation are related to higher CSF-orexin levels in patients with MCI due to AD, thus suggesting that the orexin system may be involved even in the earliest stages of AD, resulting in prolonged sleep latency, reduced sleep efficiency, and REM sleep impairment.
87 citations
TL;DR: The sleep group experienced fewer and less distressing intrusive trauma memories compared to the wake group and set the ground for early-intervention sleep studies following trauma and prevention of chronic posttrauma disorders.
Abstract: Study objectives To investigate sleep's effect in the immediate aftermath of experiencing an analog trauma in the laboratory on reducing intrusive emotional memory formation. Methods Sixty-five healthy women were exposed to an experimental laboratory trauma. They viewed a neutral and a trauma film in the laboratory and were randomly allocated to either a group that slept following film viewing or a group that remained awake. Sleep was recorded with electroencephalogram in a subgroup of participants in the sleep group. All participants recorded intrusive memories in the week following the film. Results The sleep group experienced fewer and less distressing intrusive trauma memories compared to the wake group. These effects were particularly evident toward the end of the week. Duration spent in stage N2 as opposed to light N1 sleep, a higher number of fast parietal sleep spindles and a lower rapid eye movement sleep density predicted intrusion frequency. Conclusions Our results have clinical implications and set the ground for early-intervention sleep studies following trauma and prevention of chronic posttrauma disorders.
85 citations
TL;DR: Frequency of disturbing dreams with violent and frightening content and vigorous behavioral RBD symptoms was significantly reduced, while residual nocturnal symptoms and an increase in REM-related EMG activities were observed at follow-up.
82 citations
TL;DR: In dolphins, eared seals, and manatees, unihemispheric sleep allows them to have the benefits of sleep, breathing, thermoregulation, and vigilance, but in domestic chicks, antipredation vigilance is the main function of uni Hemispheric Sleep, and it is suggested that they involve the interaction of structures of the hypothalamus, basal forebrain, and brain stem.
Abstract: Sleep is a behavior characterized by a typical body posture, both eyes’ closure, raised sensory threshold, distinctive electrographic signs, and a marked decrease of motor activity. In addition, sleep is a periodically necessary behavior and therefore, in the majority of animals, it involves the whole brain and body. However, certain marine mammals and species of birds show a different sleep behavior, in which one cerebral hemisphere sleeps while the other is awake. In dolphins, eared seals, and manatees, unihemispheric sleep allows them to have the benefits of sleep, breathing, thermoregulation, and vigilance. In birds, antipredation vigilance is the main function of unihemispheric sleep, but in domestic chicks, it is also associated with brain lateralization or dominance in the control of behavior. Compared to bihemispheric sleep, unihemispheric sleep would mean a reduction of the time spent sleeping and of the associated recovery processes. However, the behavior and health of aquatic mammals and birds does not seem at all impaired by the reduction of sleep. The neural mechanisms of unihemispheric sleep are unknown, but assuming that the neural structures involved in sleep in cetaceans, seals, and birds are similar to those of terrestrial mammals, it is suggested that they involve the interaction of structures of the hypothalamus, basal forebrain, and brain stem. The neural mechanisms promoting wakefulness dominate one side of the brain, while those promoting sleep predominates the other side. For cetaceans, unihemispheric sleep is the only way to sleep, while in seals and birds, unihemispheric sleep events are intermingled with bihemispheric and rapid eye movement sleep events. Electroencephalogram hemispheric asymmetries are also reported during bihemispheric sleep, at awakening, and at sleep onset, as well as being associated with a use-dependent process (local sleep).
78 citations
TL;DR: The results indicate that activation of MCH neurons primarily drives REM sleep and their presence may be necessary for normal expression of diurnal variation ofREM sleep and wake.
75 citations
TL;DR: A review of the current literature on autonomic impairment in common primary sleep disorders including obstructive sleep apnea, insomnia, restless legs syndrome, periodic limb movement disorder, narcolepsy, and rapid eye movement sleep behavior disorder is presented in this article.
TL;DR: Investigating waking DMN functional connectivity in patients with primary insomnia and good sleeper controls suggested that greater waking connectivity between the retrosplenial cortex/hippocampus and various nodes of the DMN was associated with lower sleep efficiency, lower amounts of rapid eye movement sleep and greater sleep-onset latency.
Abstract: © 2016 Joule Inc. or its licensors. Background: Psychological models highlight the bidirectional role of self-referential processing, introspection, worry and rumination in the development and maintenance of insomnia; however, little is known about the underlying neural substrates. Default mode network (DMN) functional connectivity has been previously linked to these cognitive processes. Methods: We used fMRI to investigate waking DMN functional connectivity in a well-characterized sample of patients with primary insomnia (PI) and good sleeper controls. Results: We included 20 patients with PI (8 men and 12 women, mean age 42.7 ± 13.4 yr) and 20 controls (8 men and 12 women, mean age 44.1 ± 10.6 yr) in our study. While no between-group differences in waking DMN connectivity were observed, exploratory analyses across all participants suggested that greater waking connectivity between the retrosplenial cortex/hippocampus and various nodes of the DMN was associated with lower sleep efficiency, lower amounts of rapid eye movement sleep and greater sleep-onset latency. Limitations: Owing to the cross-sectional nature of the study, conclusions about causality cannot be drawn. Conclusion: As sleep disturbances represent a transdiagnostic symptom that is characteristic of nearly all psychiatric disorders, our results may hold particular relevance to previous findings of increased DMN connectivity levels in patients with psychiatric disorder.
TL;DR: Findings from human sleep studies, the ethnographic record, and the ecology and evolution of mammalian sleep are integrated to better understand sleep along the human lineage and in the modern world.
Abstract: Sleep is essential to cognitive function and health in humans, yet the ultimate reasons for sleep-i.e. 'why' sleep evolved-remain mysterious. We integrate findings from human sleep studies, the ethnographic record, and the ecology and evolution of mammalian sleep to better understand sleep along the human lineage and in the modern world. Compared to other primates, sleep in great apes has undergone substantial evolutionary change, with all great apes building a sleeping platform or 'nest'. Further evolutionary change characterizes human sleep, with humans having the shortest sleep duration, yet the highest proportion of rapid eye movement sleep among primates. These changes likely reflect that our ancestors experienced fitness benefits from being active for a greater portion of the 24-h cycle than other primates, potentially related to advantages arising from learning, socializing and defending against predators and hostile conspecifics. Perspectives from evolutionary medicine have implications for understanding sleep disorders; we consider these perspectives in the context of insomnia, narcolepsy, seasonal affective disorder, circadian rhythm disorders and sleep apnea. We also identify how human sleep today differs from sleep through most of human evolution, and the implications of these changes for global health and health disparities. More generally, our review highlights the importance of phylogenetic comparisons in understanding human health, including well-known links between sleep, cognitive performance and health in humans.
TL;DR: These findings lend some physiological validity to ratings of habitual sleep quality in normal sleepers and less supportive of a physiological correlate of ratings of restoration from sleep.
Abstract: This study aimed to examine the association between polysomnographic sleep and subjective habitual sleep quality and restoration from sleep. Thirty-one normal sleepers completed the Karolinska Sleep Questionnaire and multiple home polysomnography recordings (n = 2-5). Using linear regression, sleep quality and restoration were separately analyzed as functions of standard polysomnography parameters: sleep efficiency, total sleep time, sleep latency, stage 1 and 2 sleep, slow-wave sleep, rapid eye movement sleep, wake time after sleep onset, and awakenings (n), averaged across recordings. Stage 2 and slow-wave sleep predicted worse and better sleep quality, respectively. Also, slow-wave sleep predicted less subjective restoration, although adjustment for age attenuated this relation. Our findings lend some physiological validity to ratings of habitual sleep quality in normal sleepers. Data were less supportive of a physiological correlate of ratings of restoration from sleep.
TL;DR: A pattern of electroencephalographic activation during REM sleep similar to that observed during the performance of a voluntary movement during wakefulness is reported, which may help clarify certain phenomenological aspects observed in REM sleep behavior disorder.
Abstract: When dreaming during rapid eye movement (REM) sleep, we can perform complex motor behaviors while remaining motionless. How the motor cortex behaves during this state remains unknown. Here, using intracerebral electrodes sampling the human motor cortex in pharmacoresistant epileptic patients, we report a pattern of electroencephalographic activation during REM sleep similar to that observed during the performance of a voluntary movement during wakefulness. This pattern is present during phasic REM sleep but not during tonic REM sleep, the latter resembling relaxed wakefulness. This finding may help clarify certain phenomenological aspects observed in REM sleep behavior disorder.
TL;DR: Gaps remain in knowledge of the synaptic basis by which SLD REM neurons are regulated and in turn produce REM sleep atonia, which is a critical step for treating many sleep‐related disorders including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with cataplexy.
Abstract: Rapid eye movement (REM) sleep is a recurring part of the sleep-wake cycle characterized by fast, desynchronized rhythms in the electroencephalogram (EEG), hippocampal theta activity, rapid eye movements, autonomic activation and loss of postural muscle tone (atonia). The brain circuitry governing REM sleep is located in the pontine and medullary brainstem and includes ascending and descending projections that regulate the EEG and motor components of REM sleep. The descending signal for postural muscle atonia during REM sleep is thought to originate from glutamatergic neurons of the sublaterodorsal nucleus (SLD), which in turn activate glycinergic pre-motor neurons in the spinal cord and/or ventromedial medulla to inhibit motor neurons. Despite work over the past two decades on many neurotransmitter systems that regulate the SLD, gaps remain in our knowledge of the synaptic basis by which SLD REM neurons are regulated and in turn produce REM sleep atonia. Elucidating the anatomical, cellular and synaptic basis of REM sleep atonia control is a critical step for treating many sleep-related disorders including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with cataplexy.
TL;DR: It is suggested that electroencephalographic slowing during sleep is a new promising predictive biomarker for Parkinson's disease dementia, perhaps as a marker of cholinergic denervation.
Abstract: In Parkinson's disease, electroencephalographic abnormalities during wakefulness and non-rapid eye movement sleep (spindles) were found to be predictive biomarkers of dementia. Because rapid eye movement sleep is regulated by the cholinergic system, which shows early degeneration in Parkinson's disease with cognitive impairment, anomalies during this sleep stage might mirror dementia development. In this prospective study, we examined baseline electroencephalographic absolute spectral power across three states of consciousness (non-rapid eye movement sleep, rapid eye movement sleep, and wakefulness) in 68 non-demented patients with Parkinson's disease and 44 healthy controls. All participants underwent baseline polysomnographic recordings and a comprehensive neuropsychological assessment. Power spectral analyses were performed on standard frequency bands. Dominant occipital frequency during wakefulness and ratios of slow-to-fast frequencies during rapid eye movement sleep and wakefulness were also computed. At follow-up (an average 4.5 years after baseline), 18 patients with Parkinson's disease had developed dementia and 50 patients remained dementia-free. In rapid eye movement sleep, patients with Parkinson's disease who later developed dementia showed, at baseline, higher absolute power in delta and theta bands and a higher slowing ratio, especially in temporal, parietal, and occipital regions, compared to patients who remained dementia-free and controls. In non-rapid eye movement sleep, lower baseline sigma power in parietal cortical regions also predicted development of dementia. During wakefulness, patients with Parkinson's disease who later developed dementia showed lower dominant occipital frequency as well as higher delta and slowing ratio compared to patients who remained dementia-free and controls. At baseline, higher slowing ratios in temporo-occipital regions during rapid eye movement sleep were associated with poor performance on visuospatial tests in patients with Parkinson's disease. Using receiver operating characteristic curves, we found that best predictors of dementia in Parkinson's disease were rapid eye movement sleep slowing ratios in posterior regions, wakefulness slowing ratios in temporal areas, and lower dominant occipital frequency. These results suggest that electroencephalographic slowing during sleep is a new promising predictive biomarker for Parkinson's disease dementia, perhaps as a marker of cholinergic denervation.
TL;DR: Findings have significant clinical implications for the duration of continuous positive airway pressure (CPAP) use that is needed to decrease the health risks associated with OSA.
Abstract: Purpose of reviewObstructive sleep apnea (OSA) is a highly prevalent condition that has been associated with cardiovascular morbidity and mortality, impaired glucose metabolism and daytime functional impairment. Compared with nonrapid eye movement sleep, rapid eye movement (REM) sleep is associated
TL;DR: Findings demonstrate the superiority of the REM sleep EEG in the discrimination between a-MCI and both na- MCI and control subjects.
Abstract: The basal forebrain cholinergic system, which is impaired in early Alzheimer's disease, is more crucial for the activation of rapid-eye-movement (REM) sleep electroencephalogram (EEG) than it is for wakefulness Quantitative EEG from REM sleep might thus provide an earlier and more accurate marker of the development of Alzheimer's disease in subjects with mild cognitive impairment (MCI) subjects than that from wakefulness To assess the superiority of the REM sleep EEG as a screening tool for preclinical Alzheimer's disease, 22 subjects with amnestic MCI (a-MCI; 639±77 years), 10 subjects with nonamnestic MCI (na-MCI; 641±45 years) and 32 controls (637±66 years) participated in the study Spectral analyses of the waking EEG and REM sleep EEG were performed and the [(delta+theta)/(alpha+beta)] ratio was used to assess between-group differences in EEG slowing The a-MCI subgroup showed EEG slowing in frontal lateral regions compared to both na-MCI and control groups This EEG slowing was present in wakefulness (compared to controls) but was much more prominent in REM sleep Moreover, the comparison between amnestic and nonamnestic subjects was found significant only for the REM sleep EEG There was no difference in EEG power ratio between na-MCI and controls for any of the 7 cortical regions studied These findings demonstrate the superiority of the REM sleep EEG in the discrimination between a-MCI and both na-MCI and control subjects
TL;DR: The appearance of RBD in PD may be related to regional gray matter changes in the left posterior cingulate and hippocampus but not localized to the brainstem.
TL;DR: A growing literature base has accrued on the prevalence, risk factors, and clinical impact of this condition, and a number of assessment instruments are currently available in both self-report and interview formats.
Abstract: This review summarizes the empirical and clinical literature on sleep paralysis most relevant to practitioners. During episodes of sleep paralysis, the sufferer awakens to rapid eye movement sleep-based atonia combined with conscious awareness. This is usually a frightening event often accompanied by vivid, waking dreams (ie, hallucinations). When sleep paralysis occurs independently of narcolepsy and other medical conditions, it is termed "isolated" sleep paralysis. Although the more specific diagnostic syndrome of "recurrent isolated sleep paralysis" is a recognized sleep-wake disorder, it is not widely known to nonsleep specialists. This is likely due to the unusual nature of the condition, patient reluctance to disclose episodes for fear of embarrassment, and a lack of training during medical residencies and graduate education. In fact, a growing literature base has accrued on the prevalence, risk factors, and clinical impact of this condition, and a number of assessment instruments are currently available in both self-report and interview formats. After discussing these and providing suggestions for accurate diagnosis, differential diagnosis, and patient selection, the available treatment options are discussed. These consist of both pharmacological and psychotherapeutic interventions which, although promising, require more empirical support and larger, well-controlled trials.
TL;DR: It is proposed that phasic activation associated with rapid eye movements may provide the amygdala with endogenous excitation during REM sleep, and its possible role in the bidirectional interaction between REM sleep and such sleep disorders as nightmares, anxiety and post‐traumatic sleep disorder is proposed.
Abstract: The amygdaloid complex plays a crucial role in processing emotional signals and in the formation of emotional memories. Neuroimaging studies have shown human amygdala activation during rapid eye movement sleep (REM). Stereotactically implanted electrodes for presurgical evaluation in epileptic patients provide a unique opportunity to directly record amygdala activity. The present study analysed amygdala activity associated with REM sleep eye movements on the millisecond scale. We propose that phasic activation associated with rapid eye movements may provide the amygdala with endogenous excitation during REM sleep. Standard polysomnography and stereo-electroencephalograph (SEEG) were recorded simultaneously during spontaneous sleep in the left amygdala of four patients. Time-frequency analysis and absolute power of gamma activity were obtained for 250 ms time windows preceding and following eye movement onset in REM sleep, and in spontaneous waking eye movements in the dark. Absolute power of the 44-48 Hz band increased significantly during the 250 ms time window after REM sleep rapid eye movements onset, but not during waking eye movements. Transient activation of the amygdala provides physiological support for the proposed participation of the amygdala in emotional expression, in the emotional content of dreams and for the reactivation and consolidation of emotional memories during REM sleep, as well as for next-day emotional regulation, and its possible role in the bidirectional interaction between REM sleep and such sleep disorders as nightmares, anxiety and post-traumatic sleep disorder. These results provide unique, direct evidence of increased activation of the human amygdala time-locked to REM sleep rapid eye movements.
TL;DR: HFOs near the epileptogenic zone are less suppressed during REM, and the less suppressive effect of REM may provide a specific marker of epileptogenicity in patients with drug-resistant epilepsy.
TL;DR: Melatonin is effective for treating patients with rapid eye movement sleep behavior disorder (RBD) and ramelteon may have beneficial effects on sleep disturbances, especially on RBD in patients with Parkinson's disease (PD).
Abstract: Objective Melatonin is effective for treating patients with rapid eye movement sleep behavior disorder (RBD). Ramelteon, a novel hypnotic, acts as a melatonin receptor agonist. In the current study, we investigated the effects of ramelteon on sleep disorders, including RBD, in patients with Parkinson's disease (PD). Methods We evaluated 35 patients from multiple centers with idiopathic PD accompanied by sleep disturbances (age: 69.1±11.1 years; 17 men, 18 women; PD morbidity: 6.9±5.7 years; Hoehn & Yahr stage: 2.5±0.8; levodopa dose equivalent: 561±401 mg/day). The patients received 8 mg of ramelteon before sleep once daily for 12 weeks. Motor and sleep symptoms were evaluated both before and after ramelteon administration. Results Of the 35 patients enrolled in this study, 24 (68.6%) were diagnosed with probable RBD (pRBD) using the Japanese version of the RBD screening questionnaire. Ramelteon administration reduced the severity of sleep disturbances in patients with PD. It also lowered scores on the Japanese version of the RBD questionnaire in patients with PD and pRBD. Conclusion Ramelteon may have beneficial effects on sleep disturbances, especially on RBD in patients with PD.
TL;DR: Optogenetic activation of MCH neurons increased both REM and NREM sleep at night, whereas during the day cycle, only REM sleep was increased, and Delta power, an indicator of sleep intensity, was increased.
Abstract: Neurons containing melanin-concentrating hormone (MCH) are located in the hypothalamus. In mice, optogenetic activation of the MCH neurons induces both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep at night, the normal wake-active period for nocturnal rodents [R. R. Konadhode et al. (2013) J. Neurosci., 33, 10257-10263]. Here we selectively activate these neurons in rats to test the validity of the sleep network hypothesis in another species. Channelrhodopsin-2 (ChR2) driven by the MCH promoter was selectively expressed by MCH neurons after injection of rAAV-MCHp-ChR2-EYFP into the hypothalamus of Long-Evans rats. An in vitro study confirmed that the optogenetic activation of MCH neurons faithfully triggered action potentials. In the second study, in Long-Evans rats, rAAV-MCH-ChR2, or the control vector, rAAV-MCH-EYFP, were delivered into the hypothalamus. Three weeks later, baseline sleep was recorded for 48 h without optogenetic stimulation (0 Hz). Subsequently, at the start of the lights-off cycle, the MCH neurons were stimulated at 5, 10, or 30 Hz (1 mW at tip; 1 min on - 4 min off) for 24 h. Sleep was recorded during the 24-h stimulation period. Optogenetic activation of MCH neurons increased both REM and NREM sleep at night, whereas during the day cycle, only REM sleep was increased. Delta power, an indicator of sleep intensity, was also increased. In control rats without ChR2, optogenetic stimulation did not increase sleep or delta power. These results lend further support to the view that sleep-active MCH neurons contribute to drive sleep in mammals.
TL;DR: It is vital that the normal functioning of the body in relation to sleep is well understood before proceeding on to the pathophysiology of PD correlating to its symptoms, which is the focus of this review.
Abstract: Sleep is an indispensable normal physiology of the human body fundamental for healthy functioning. It has been observed that Parkinson's disease (PD) not only exhibits motor symptoms, but also non-motor symptoms such as metabolic irregularities, altered olfaction, cardiovascular dysfunction, gastrointestinal complications and especially sleep disorders which is the focus of this review. A good understanding and knowledge of the different brain structures involved and how they function in the development of sleep disorders should be well comprehended in order to treat and alleviate these symptoms and enhance quality of life for PD patients. Therefore it is vital that the normal functioning of the body in relation to sleep is well understood before proceeding on to the pathophysiology of PD correlating to its symptoms. Suitable treatment can then be administered toward enhancing the quality of life of these patients, perhaps even discovering the cause for this disease.
TL;DR: Orexin-A is associated with increased P-Tau in normal elderly individuals and this might be a consequence of the reduction in the proportion of the deeper, more restorative slow wave sleep and rapid eye movement sleep reported with aging.
Abstract: STUDY OBJECTIVES To evaluate the role of orexin-A with respect to cerebrospinal fluid (CSF) Alzheimer disease (AD) biomarkers, and explore its relationship to cognition and sleep characteristics in a group of cognitively normal elderly individuals. METHODS Subjects were recruited from multiple community sources for National Institutes of Health supported studies on normal aging, sleep and CSF biomarkers. Sixty-three participants underwent home monitoring for sleep-disordered breathing, clinical, sleep and cognitive evaluations, as well as a lumbar puncture to obtain CSF. Individuals with medical history or with magnetic resonance imaging evidence of disorders that may affect brain structure or function were excluded. Correlation and linear regression analyses were used to assess the relationship between orexin-A and CSF AD-biomarkers controlling for potential sociodemographic and sleep confounders. RESULTS Levels of orexin-A, amyloid beta 42 (Aβ42), phosphorylated-tau (P-Tau), total-tau (T-Tau), Apolipoprotein E4 status, age, years of education, reported total sleep time, number of awakenings, apnea-hypopnea indices (AHI), excessive daytime sleepiness, and a cognitive battery were analyzed. Subjects were 69.59 ± 8.55 years of age, 57.1% were female, and 30.2% were apolipoprotein E4+. Orexin-A was positively correlated with Aβ42, P-Tau, and T-Tau. The associations between orexin-A and the AD-biomarkers were driven mainly by the relationship between orexin-A and P-Tau and were not influenced by other clinical or sleep characteristics that were available. CONCLUSIONS Orexin-A is associated with increased P-Tau in normal elderly individuals. Increases in orexin-A and P-Tau might be a consequence of the reduction in the proportion of the deeper, more restorative slow wave sleep and rapid eye movement sleep reported with aging. CLINICAL TRIAL REGISTRATION Clinicaltrials.gov registration number NCT01962779.
TL;DR: It was found that both state and trait anxiety affected non-rapid eye movement sleep parameters, predominantly associated to state anxiety while rapid eye movement parameters related to trait anxiety.
Abstract: Anxiety affects millions of people and has been shown to co-occur in combination with sleep disturbances, generating heavy medical costs and a huge socio-medico-economic burden. Sleep-studies in anxiety disorders are inconsistent and the effects of state and trait anxiety are unexplored. We selected 1083 patients from the database of a hospital sleep laboratory. The patients had polysomnography for different sleep disorders; their sleep initiation (sleep onset latency), sleep maintenance (total sleep time), non-rapid eye movement sleep-, and rapid eye movement sleep parameters; as well as their State-Trait Anxiety Inventory and Beck depression scale were measured. In order to be included in our study, individuals needed to score in the low or high range on the State and/or Trait Subscales of the State-Trait Anxiety Inventory. We found that both state and trait anxiety affected non-rapid eye movement sleep parameters. Sleep onset latency changes predominantly associated to state anxiety while rapid eye movement parameters related to trait anxiety.
TL;DR: It is suggested that the MRF is an integration center that potentially allows to fine tune waking state and locomotor signals in order to establish an efficient locomotion.
Abstract: The mesencephalic reticular formation (MRF) mainly composed by the pedunculopontine and the cuneiform nuclei is involved in the control of several fundamental brain functions such as locomotion, rapid eye movement sleep and waking state. On the one hand, the role of MRF neurons in locomotion has been investigated for decades in different animal models, including in behaving nonhuman primate (NHP) using extracellular recordings. On the other hand, MRF neurons involved in the control of waking state have been consistently shown to constitute the cholinergic component of the reticular ascending system. However, a dual control of the locomotion and waking state by the same groups of neurons in NHP has never been demonstrated in NHP. Here, using microelectrode recordings in behaving NHP, we recorded 38 neurons in the MRF that were followed during transition between wakefulness (TWS) and sleep, i.e., until the emergence of sleep episodes characterized by typical cortical slow wave activity (SWA). We found that the MRF neurons, mainly located in the pedunculopontine nucleus region, modulated their activity during TWS with a decrease in firing rate during SWA. Of interest, we could follow some MRF neurons from locomotion to SWA and found that they also modulated their firing rate during locomotion and TWS. These new findings confirm the role of MRF neurons in both functions. They suggest that the MRF is an integration center that potentially allows to fine tune waking state and locomotor signals in order to establish an efficient locomotion.
TL;DR: It is found that unilateral DBS in the GPe in rats significantly increased both non-rapid eye movement and rapid eye movement sleep compared to sham DBS stimulation, and the G Pe is potentially a better site for DBS to treat both insomnia and motor disorders caused by basal ganglia dysfunction.