Masseter EMG activity during sleep and sleep bruxism

The masseter muscle is involved in the complex and coordinated oromotor behaviors such as mastication during wakefulness. The masseter electromyographic (EMG) activity decreases but does not disappear completely during sleep: the EMG activity is generally of low level and inhomogeneous for the duration, amplitude and intervals. The decreased excitability of the masseter motoneurons can be determined by neural substrates for NREM and REM sleep. The masseter EMG activity is increased in association with the level of arousal fluctuations within either sleep state. In addition, there are some motor events such as REM twitches, swallowing and rhythmic masticatory muscle activity (RMMA), whose generation might involve the additional activation of specific neural circuits. Sleep bruxism (SB) is characterized by exaggerated occurrence of RMMA. In SB, the rhythmic activation of the masseter muscle can reflect the rhythmic motor inputs to motoneurons through, at least in part, common neural circuits for generating masticatory rhythm under the facilitatory influences of transient arousals. However, it remains elusive as to which neural circuits determine the genesis of sleep bruxism. Based on the available knowledge on the masseter EMG activity during sleep, this review presents that the variety of the masseter EMG phenotypes during sleep can result from the combinations of the quantitative, spatial and temporal neural factors eventually sending net facilitatory inputs to trigeminal motoneurons under sleep regulatory systems.     

Sleep quality in adult patients with sleep related bruxism

Sleep related bruxism (SB) is the grinding of teeth during sleep and may also be associated with various sleep disorders. However, little is known about sleep structures and disturbances of SB. This study aims to further understand sleep architectures using overnight polysomnography (PSG) in patients with SB. We analyze sleep parameters and architectures in 33 healthy subjects and 25 patients with SB. PSG and sleep questionnaires measured sleep variables including proportions of rapid eye movement (REM) sleep, non-REM sleep (N1, N2 and N3), latency to sleep onset, sleep efficiency, wake after sleep onset (WASO), apnea hypopnea index (AHI), respiratory disturbance index (RDI), and periodic limb movement index (PLMI) during sleep for both groups. Sleep efficiency and the proportion of N3 in the SB group were significantly lower than in the control group (P < 0.05). In addition latency to onset of sleep and WASO were markedly increased in the SB group (P < 0.05). AHI, RDI, and PLMI showed no differences between the groups. Epworth Sleepiness Scale was significantly higher in the SB group than in the control group (P < 0.05). In contrast to previous studies, we conclude that patients with SB are not good sleepers based on PSG study. Further studies are required to assess the relationship between sleep quality and the severity of SB.

     

Sleep apnea syndromes

Sleep apnea syndromes have been identified only relatively recently. Their most frequent form is characterized by a sleep-related upper airway obstruction resulting in apneas which may repeat themselves up to several hundred times during a night's sleep. Their mean duration is about 30 to 40 seconds, but some apneas last over one minute. Breathing resumption requires an arousal, which may be clearly identified on the EEG but usually goes unnoticed by the patient. The most immediate consequence are hypoxemia and sleep fragmentation. There may be associated arrhythmias and hemodynamic changes, especially in the pulmonary circulation. The predominant clinical signs are snoring (during the breathing resumption between the apneas) and daytime somnolence due to sleep fragmentation. In addition to the risks of work and traffic accidents, these patients run a long-term risk of cardiovascular accidents. About 20% develop pulmonary hypertension, a contributing factor to right heart failure. About 50% are hypertensive, which combined with a frequently observed polycythemia, makes them vulnerable to ischemic accidents. The treatment is based upon the use of continuous positive airway pressure (CPAP) during sleep. In case of failure, surgical alternatives may be considered.     

The effect of short-term sleep fragmentation produced by intense auditory stimuli on the arousal response to upper airway obstruction in lambs

Upper airway obstruction is recognized to cause apnoea in newborns as well as in adults. However, very little is known about factors that influence the arousal response from sleep during upper airway obstruction in newborns. Experiments were therefore done to investigate the effect of short-term sleep fragmentation on the arousal response to upper airway obstruction in six lambs aged 8 to 14 days. Each lamb was anaesthetized and instrumented for recordings of electrocorticogram, electro-oculogram, nuchal and diaphragm electromyograms and measurements of systemic arterial blood pressure and oxygen saturation (fiberoptic catheter oximeter). A tracheostomy was done and a fenestrated tracheostomy tube placed in the trachea. Experiments were not done before the third postoperative day. During a study, a 5F balloon tipped catheter was inserted into the tube so that airflow could be obstructed by inflating the balloon. Measurements were made during 30 s control periods and during experimental periods of upper airway obstruction in at least three epochs of quiet sleep and active sleep in each animal. These measurements were made following a period of uninterrupted sleep and repeated following a 36-42 h period of sleep fragmentation. Sleep fragmentation was produced by 30 s of noise separated by 2 min of quiet. Sleep fragmentation produced small but statistically significant increases in the time to arousal and decreases in the haemoglobin oxygen saturation at arousal during upper airway obstruction in quiet sleep but not active sleep. However, these changes, although consistent, were small and are of questionable biological significance. Therefore, I believe it is unlikely that short-term sleep fragmentation per se significantly impairs the arousal response to respiratory stimuli in newborns.     

Topographical EEG Mapping in a Case of Recurrent Sleep Terrors

Sleep terrors are characterized by marked CNS arousal and typically occur during stage 3-4 sleep within the first NREM cycle. Studies of the EEG during sleep terrors suggest that delta power and synchrony in the EEG may be important physiological markers of sleep terror presence and intensity. An EEG mapping study was undertaken with a single participant who experienced three sleep terror episodes in the laboratory. A one-minute section of EEG was sampled immediately prior to the onset of each of the three sleep terrors. Similar EEG sections were taken from 10 healthy sex- and age-matched controls. The sleep tenors and control (normative) data were then compared topographically with z-scores (z-mapping). The z-maps indicated that all three sleep terrors contained more total and delta power in central and frontal areas than the control EEG sections. Moreover, relative delta power in these areas for the three sleep terrors was proportional to the subjective intensity of the episode. Although this pre-arousal EEG pattern may be related to ongoing slow-wave sleep mentation that may sometimes trigger sleep terror episodes, its functional significance remains an open question. The results demonstrate the utility of EEG mapping for the quantification of brain activation during sleep terror attacks and suggest that discrete activity profiles are identifiable for different types of dreaming-related arousal.     

A Randomized Controlled Trial Comparing Neurofeedback and Cognitive-Behavioral Therapy for Insomnia Patients: Pilot Study

Insomnia is a common disease that negatively affects patients both mentally and physically. While insomnia disorder is mainly characterized by hyperarousal, a few studies that have directly intervened with cortical arousal. This study was conducted to investigate the effect of a neurofeedback protocol for reducing cortical arousal on insomnia compared to cognitive-behavioral treatment for insomnia (CBT-I). Seventeen adults with insomnia, free of other psychiatric illnesses, were randomly assigned to neurofeedback or CBT-I. All participants completed questionnaires on insomnia [Insomnia Severity Index (ISI)], sleep quality [Pittsburgh Sleep Quality Index (PSQI)], and dysfunctional cognition [Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS-16)]. The neurofeedback group showed decreases in beta waves and increases in theta and alpha waves in various areas of the electroencephalogram (EEG), indicating lowered cortical arousal. The ISI and PSQI scores were significantly decreased, and sleep efficiency and sleep satisfaction were increased compared to the pre-treatment scores in both groups. DBAS scores decreased only in the CBT-I group (NF p?=?0.173; CBT-I p?=?0.012). This study confirmed that neurofeedback training could alleviate the symptoms of insomnia by reducing cortical hyperarousal in patients, despite the limited effect in reducing cognitive dysfunction compared to CBT-I.

     

A Homeostatic Sleep-Stabilizing Pathway in Drosophila Composed of the Sex Peptide Receptor and Its Ligand,the Myoinhibitory Peptide

Sleep, a reversible quiescent state found in both invertebrate and vertebrate animals, disconnects animals from their environment and is highly regulated for coordination with wakeful activities, such as reproduction. The fruit fly, Drosophila melanogaster, has proven to be a valuable model for studying the regulation of sleep by circadian clock and homeostatic mechanisms. Here, we demonstrate that the sex peptide receptor (SPR) of Drosophila, known for its role in female reproduction, is also important in stabilizing sleep in both males and females. Mutants lacking either the SPR or its central ligand, myoinhibitory peptide (MIP), fall asleep normally, but have difficulty in maintaining a sleep-like state. Our analyses have mapped the SPR sleep function to pigment dispersing factor (pdf) neurons, an arousal center in the insect brain. MIP downregulates intracellular cAMP levels in pdf neurons through the SPR. MIP is released centrally before and during night-time sleep, when the sleep drive is elevated. Sleep deprivation during the night facilitates MIP secretion from specific brain neurons innervating pdf neurons. Moreover, flies lacking either SPR or MIP cannot recover sleep after the night-time sleep deprivation. These results delineate a central neuropeptide circuit that stabilizes the sleep state by feeding a slow-acting inhibitory input into the arousal system and plays an important role in sleep homeostasis.     

Baroreflexes of the rat. III. Open-loop gain and electroencephalographic arousal

In early studies of humans, baroreflex sensitivity was found to be higher during sleep; however, subsequent observations in several species, including humans, have been at variance with the original reports. Sleep and arousal are behavioral states, and it is difficult to accurately and repeatedly measure baroreflex sensitivity in behaving animals. However, pharmacologically immobilized (neuromuscularly blocked) rats have apparently normal sleep-wakefulness cycles, and baroreflex gain can be measured directly in this preparation. Using the delta band of the EEG (EEG(delta)) as an index of sleep and arousal and open-loop aortic depressor nerve (ADN) stimulation as a baroreflex input, we found that blood pressure (BP) level depended on arousal (r = -0.416; P < 0.0001), and BP baroreflex gain depended on BP level (r = 0.496; P < 0.0001), but that BP baroreflex gain was independent of arousal (r = 0.001; NS). Heart period (HP) was different; although HP level depended on arousal (r = 0.352; P < 0.0001), HP baroreflex gain did not depend on HP level (r = 0.029; NS), and HP baroreflex gain increased with arousal (r = 0.315; P < 0.0001). A partial-correlations analysis showed that the presence of the relationship between BP level and BP baroreflex gain probably attenuated the relationship between arousal and BP gain. The results are consistent 1) with physiological findings showing that arousal attenuates afferent transmission through the nucleus of the solitary tract and enhances sympathoinhibition at the rostral ventrolateral medulla; and 2) with observations in humans and animals showing increased cardiac baroreflex sensitivity during sleep, but little if any effect of sleep on BP baroreflex sensitivity. The findings are relevant to all methods of baroreflex gain estimation that use HP as the index of baroreflex activation.     

An Exploratory Study on the Effects of Tele-neurofeedback and Tele-biofeedback on Objective and Subjective Sleep in Patients with Primary Insomnia

Insomnia is a sleeping disorder, usually studied from a behavioural perspective, with a focus on somatic and cognitive arousal. Recent studies have suggested that an impairment of information processes due to the presence of cortical hyperarousal might interfere with normal sleep onset and/or consolidation. As such, a treatment modality focussing on CNS arousal, and thus influencing information processing, might be of interest. Seventien insomnia patients were randomly assigned to either a tele-neurofeedback (n = 9) or an electromyography tele-biofeedback (n = 8) protocol. Twelve healthy controls were used to compare baseline sleep measures. A polysomnography was performed pre and post treatment. Total Sleep Time (TST), was considered as our primary outcome variable. Sleep latency decreased pre to post treatment in both groups, but a significant improvement in TST was found only after the neurofeedback (NFB) protocol. Furthermore, sleep logs at home showed an overall improvement only in the neurofeedback group, whereas the sleep logs in the lab remained the same pre to post training. Only NFB training resulted in an increase in TST. The mixed results concerning perception of sleep might be related to methodological issues, such as the different locations of the training and sleep measurements.     

Role of Homer proteins in the maintenance of sleep-wake states

Sleep is an evolutionarily conserved process that is linked to diurnal cycles and normal daytime wakefulness. Healthy sleep and wakefulness are integral to a healthy lifestyle; this occurs when an organism is able to maintain long bouts of both sleep and wake. Homer proteins, which function as adaptors for group 1 metabotropic glutamate receptors, have been implicated in genetic studies of sleep in both Drosophila and mouse. Drosophila express a single Homer gene product that is upregulated during sleep. By contrast, vertebrates express Homer as both constitutive and immediate early gene (H1a) forms, and H1a is up-regulated during wakefulness. Genetic deletion of Homer in Drosophila results in fragmented sleep and in failure to sustain long bouts of sleep, even under increased sleep drive. However, deletion of Homer1a in mouse results in failure to sustain long bouts of wakefulness. Further evidence for the role of Homer1a in the maintenance of wake comes from the CREB alpha delta mutant mouse, which displays a reduced wake phenotype similar to the Homer1a knockout and fails to up-regulate Homer1a upon sleep loss. Homer1a is a gene whose expression is induced by CREB. Sustained behaviors of the sleep/wake cycle are created by molecular pathways that are distinct from those for arousal or short bouts, and implicate an evolutionarily-conserved role for Homer in sustaining these behaviors.     

Design and Validation of a Periodic Leg Movement Detector

Periodic Limb Movements (PLMs) are episodic, involuntary movements caused by fairly specific muscle contractions that occur during sleep and can be scored during nocturnal polysomnography (NPSG). Because leg movements (LM) may be accompanied by an arousal or sleep fragmentation, a high PLM index (i.e. average number of PLMs per hour) may have an effect on an individual’s overall health and wellbeing. This study presents the design and validation of the Stanford PLM automatic detector (S-PLMAD), a robust, automated leg movement detector to score PLM. NPSG studies from adult participants of the Wisconsin Sleep Cohort (WSC, n = 1,073, 2000–2004) and successive Stanford Sleep Cohort (SSC) patients (n = 760, 1999–2007) undergoing baseline NPSG were used in the design and validation of this study. The scoring algorithm of the S-PLMAD was initially based on the 2007 American Association of Sleep Medicine clinical scoring rules. It was first tested against other published algorithms using manually scored LM in the WSC. Rules were then modified to accommodate baseline noise and electrocardiography interference and to better exclude LM adjacent to respiratory events. The S-PLMAD incorporates adaptive noise cancelling of cardiac interference and noise-floor adjustable detection thresholds, removes LM secondary to sleep disordered breathing within 5 sec of respiratory events, and is robust to transient artifacts. Furthermore, it provides PLM indices for sleep (PLMS) and wake plus periodicity index and other metrics. To validate the final S-PLMAD, experts visually scored 78 studies in normal sleepers and patients with restless legs syndrome, sleep disordered breathing, rapid eye movement sleep behavior disorder, narcolepsy-cataplexy, insomnia, and delayed sleep phase syndrome. PLM indices were highly correlated between expert, visually scored PLMS and automatic scorings (r² = 0.94 in WSC and r² = 0.94 in SSC). In conclusion, The S-PLMAD is a robust and high throughput PLM detector that functions well in controls and sleep disorder patients.     

Respiratory instability during sleep onset.

It has been hypothesized that regulatory control in the respiratory system is state dependent. According to this view respiratory instability during sleep onset is a consequence of repeated fluctuations in arousal state. However, these speculations are based primarily on measurements during stable sleep, not during sleep onset itself. The aim of the present study was to assess changes in ventilation and gas tensions during sleep onset as a function of arousal state. Twenty-one subjects (12 males and 9 females, mean age 20 yr) were assessed over an average of 11.3 sleep onsets. The subject's state was classified as alpha, theta, body movement, or stage 2 sleep, and expiratory tidal volume, minute ventilation, respiratory rate, and end-tidal CO2 and O2 were measured by means of a face mask, valve, and pneumotachograph on a breath-by-breath basis. Respiratory instability during sleep onset was found to be a result of two factors. The first factor was a between-state effect in which transitions from alpha to theta were associated with falls, and from theta to alpha with increases, in ventilation. The magnitude of the change was a positive function of metabolic drive at the time of the state change (as indicated by alveolar PCO2 and PO2 levels). The second was a within-state effect in which ventilation fell during consecutive alpha breaths and increased during consecutive theta breaths. These changes were due to the influence of the relative hyperventilation of the alpha state and the relative hypoventilation of the theta state on metabolic drive.     

Sleep in the herring gull (Larus argentatus)

Sleep postures and eye state of free-ranging herring gulls (Larus argentatus) were studied during the breeding season. Three mutually exclusive behaviours were observed, namely sleep, rest-sleep and rest postures. Arousal thresholds, eye blink rates and eye closure time were obtained during these behaviours. Significant relationships existed between eye blinking, eye closure, and a raised threshold of arousal when birds were in the sleep and rest-sleep postures. During a natural disturbance, birds in the sleep posture remained in this posture but did not blink their eyes: this is called pseudo sleep. Male gulls also exhibited a lower threshold of arousal while in the sleep posture compared with females. We conclude that rhythmic eye blinking is a good indication of sleep in herring gulls.     

Treatment of Chronic Insomnia with Yoga: A Preliminary Study with Sleep–Wake Diaries

There is good evidence for cognitive and physiological arousal in chronic insomnia. Accordingly, clinical trial studies of insomnia treatments aimed at reducing arousal, including relaxation and meditation, have reported positive results. Yoga is a multicomponent practice that is also known to be effective in reducing arousal, although it has not been well evaluated as a treatment for insomnia. In this preliminary study, a simple daily yoga treatment was evaluated in a chronic insomnia population consisting of sleep-onset and/or sleep-maintenance insomnia and primary or secondary insomnia. Participants maintained sleep–wake diaries during a pretreatment 2-week baseline and a subsequent 8-week intervention, in which they practiced the treatment on their own following a single in-person training session with subsequent brief in-person and telephone follow-ups. Sleep efficiency (SE), total sleep time (TST), total wake time (TWT), sleep onset latency (SOL), wake time after sleep onset (WASO), number of awakenings, and sleep quality measures were derived from sleep–wake diary entries and were averaged in 2-week intervals. For 20 participants completing the protocol, statistically significant improvements were observed in SE, TST, TWT, SOL, and WASO at end-treatment as compared with pretreatment values.     

Upper airway anesthesia delays arousal from airway occlusion induced during human NREM sleep.

Six healthy subjects (5 males and 1 female, 26-40 yr old) were studied during non-rapid-eye-movement (NREM) sleep to assess the role of upper airway (UA) afferents in the arousal response to induced airway occlusion. Subjects wore an airtight face mask attached to a low-resistance one-way valve. A valve in the inspiratory circuit allowed instantaneous inspiratory airway occlusion and release; the expiratory circuit remained unoccluded at all times. Each subject was studied during two nights. On one night, occlusions were created during stable stage 2 NREM sleep before and after application of 4% lidocaine to the oral and nasal mucosa. On the other night, the protocol was duplicated with saline ("sham anesthesia") rather than lidocaine. The order of nights was randomized. Occlusions were sustained until electroencephalographic arousal. Three to 12 occlusions were performed in each subject for each of the four parts of the protocol (pre- and post-lidocaine, pre- and post-saline). The auditory threshold for arousal (1,500-Hz tone beginning at 30 dB) was also tested before and after UA lidocaine. For the group, arousal time after UA anesthesia was prolonged compared with preanesthesia arousal time (P less than 0.001); arousal time after sham anesthesia did not significantly increase from before sham anesthesia (P = 0.9). The increase in arousal time with UA anesthesia was greater than the increase with sham anesthesia (P less than 0.001). The auditory arousal threshold did not increase after UA anesthesia. Inspiratory mask pressure, arterial O2 saturation of hemoglobin, and end-tidal PCO2 during occlusions were similar before and after UA anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of repeated exposure to rapidly developing hypoxaemia on the arousal and cardiopulmonary response to rapidly developing hypoxaemia in lambs

Experiments were done on four lambs to determine if repeated exposure to rapidly developing hypoxaemia influences the cardiopulmonary and arousal response from sleep. Each lamb was anaesthetized and instrumented for sleep staging and measurements of arterial haemoglobin oxygen saturation. No sooner than three days after surgery, measurements were made in quiet sleep and active sleep during control periods when the animal was breathing 21% oxygen and during experimental periods of rapidly developing hypoxaemia when the animal was breathing 5% oxygen for approximately 100 epochs of sleep. Arousal occurred from both sleep states during rapidly developing hypoxaemia but was delayed in active sleep compared to quiet sleep. The time to arousal and the decrease in arterial haemoglobin oxygen saturation were significantly increased with repeated exposure to rapidly developing hypoxaemia during both quiet sleep and active sleep. Thus, our data provide evidence that repeated exposure to rapidly developing hypoxaemia produces an arousal response decrement in lambs. Since it is possible that alterations in the arousal response to respiratory stimuli play a role in sudden infant death, studies to investigate the mechanism of the arousal response decrement following repeated exposure to rapidly developing hypoxaemia are warranted.     

Automatic EEG arousal detection for sleep apnea syndrome

Electroencephalographic (EEG) arousals are seen in EEG recordings as an awakening response of the human brain. Sleep apnea is a serious sleep disorder. Severe sleep apnea brings about EEG arousals and sleep for patients with sleep apnea syndrome (SAS) is thus frequently interrupted. The number of respiratory-related arousals during the whole night on PSG recordings is directly related to the quality of sleep. Detecting EEG arousals in the PSG record is thus a significant task for clinical diagnosis in sleep medicine. In this paper, a method for automatic detection of EEG arousals in SAS patients was proposed. To effectively detect respiratory-related arousals, threshold values were determined according to pathological events as sleep apnea and electromyogram (EMG). If resumption of ventilation (end of the apnea interval) was detected, much lower thresholds were adopted for detecting EEG arousals, including relatively doubtful arousals. Conversely, threshold was maintained high when pathological events were undetected. The proposed method was applied to polysomnographic (PSG) records of eight patients with SAS and accuracy of EEG arousal detection was verified by comparative visual inspection. Effectiveness of the proposed method in clinical diagnosis was also investigated.     

Relationship with excessive daytime sleepiness and serum substance P levels in OSAS patients and the effect of PAP treatment

Sleep and Biological Rhythms - Obstructive sleep apnea syndrome (OSAS) is a commonly seen disorder characterized by repeated episodes of upper airway obstruction during sleep leading to...     

Experienced Mindfulness Meditators Exhibit Higher Parietal-Occipital EEG Gamma Activity during NREM Sleep

Over the past several years meditation practice has gained increasing attention as a non-pharmacological intervention to provide health related benefits, from promoting general wellness to alleviating the symptoms of a variety of medical conditions. However, the effects of meditation training on brain activity still need to be fully characterized. Sleep provides a unique approach to explore the meditation-related plastic changes in brain function. In this study we performed sleep high-density electroencephalographic (hdEEG) recordings in long-term meditators (LTM) of Buddhist meditation practices (approximately 8700 mean hours of life practice) and meditation naive individuals. We found that LTM had increased parietal-occipital EEG gamma power during NREM sleep. This increase was specific for the gamma range (25–40 Hz), was not related to the level of spontaneous arousal during NREM and was positively correlated with the length of lifetime daily meditation practice. Altogether, these findings indicate that meditation practice produces measurable changes in spontaneous brain activity, and suggest that EEG gamma activity during sleep represents a sensitive measure of the long-lasting, plastic effects of meditative training on brain function.     

Arousal responses to airway occlusion in sleeping dogs: comparison of nasal and tracheal occlusions

Previous studies have shown that the arousal threshold to hypoxia, hypercapnia, and tracheal occlusions is greatly depressed in rapid-eye-movement (REM) sleep compared with slow-wave sleep (SWS). The aim of this study was to compare the arousal thresholds in SWS and REM sleep in response to an upper airway pressure stimulus. We compared the waking responses to tracheal (T) vs. nasal (N) occlusion in four unanesthetized, naturally sleeping dogs. The dogs either breathed through a tracheal fistula or through the snout using a fiberglass mask. A total of 295 T and 160 N occlusion tests were performed in SWS and REM sleep. The mean time to arousal during N and T tests was variable in the same dog and among the dogs. The mean time to arousal in SWS-tracheal occlusion was longer than that in N tests in only two of the four dogs. The total number of tests inducing arousal within the first 15 s of SWS-nasal occlusion tests was significantly more than that of T tests (N: 47%; T: 27%). There was a marked depression of arousal within the initial 15 s of REM sleep in T tests compared with N tests (N: 21%; T: 0%). The frequency of early arousals in REM tests was less than that of SWS for both N and T tests. The early arousal in N occlusion is in sharp contrast to the well-described depressed arousal responses to hypoxia, hypercapnia, and asphyxia. This pattern of arousal suggests that the upper airway mechanoreceptors may play an important role in the induction of an early arousal from nasal occlusion.