Characteristics Of Sleep Architecture Research Articles

Sleep architecture as a candidate for phenotyping sleep bruxism: A narrative physiological review.

Sleep bruxism (SB), an oral behaviour in otherwise healthy individuals, is characterised by frequent rhythmic masticatory muscle activity (RMMA) during sleep. RMMA/SB episodes occur over various sleep stages (N1-N3 and rapid eye movement (REM)), sleep cycles (non-REM to REM), and frequently with microarousals. It currently remains unclear whether these characteristics of sleep architecture are phenotype candidates for the genesis of RMMA/SB. This narrative review investigated the relationship between sleep architecture and the occurrence of RMMA as a SB phenotype candidate. PubMed research was performed using keywords related to RMMA/SB and sleep architecture. In non-SB and SB healthy individuals, RMMA episodes were most frequent in the light non-REM sleep stages N1 and N2, particularly during the ascending phase of sleep cycles. The onset of RMMA/SB episodes in healthy individuals was preceded by a physiological arousal sequence of autonomic cardiovascular to cortical activation. It was not possible to extract a consistent sleep architecture pattern in the presence of sleep comorbidities. The lack of standardisation and variability between subject complexified the search for specific sleep architecture phenotype(s). In otherwise healthy individuals, the genesis of RMMA/SB episodes is largely affected by oscillations in the sleep stage and cycle as well as the occurrence of microarousal. Furthermore, a specific sleep architecture pattern cannot be confirmed in the presence of sleep comorbidity. Further studies are needed to delineate sleep architecture phenotype candidate(s) that contribute to the more accurate diagnosis of SB and treatment approaches using standardised and innovative methodologies.

Sleep architecture of short sleep time in patients with obstructive sleep apnea: a retrospective single-facility study.

Sleep architecture consists of rapid eye movement (REM) sleep and non-REM sleep time. Non-REM sleep time is further classified into three stages by depth (stage N1-N3). Some studies have reported that short sleep time predicts all-cause mortality. Short sleep time can have characteristics of sleep architecture which contribute to poor prognosis. Obstructive sleep apnea (OSA) is a disease which causes cessation or decline of ventilation during sleep due to upper airway stenosis and affects sleep architecture. Few studies have reported on the sleep architecture of short sleep time in patients withOSA. Therefore, we aimed to observe this phenomenon. From May 2008 to September 2021, patients diagnosed with OSA at our facility were assessed for clinical history and underwentfull-night polysomnography (PSG). These patients were classified into two groups: total sleep time (TST) recorded on PSG consisting of a short TST (< 7h) group and a not short TST (≥ 7h) group. Of 266 patients with OSA, compared to the not short TST group (n = 131), the short TST group(n = 135) had a lower REM sleep time (%) and a higher stage N1 sleep time (%). There was a significant difference in age betweenthe two groups, so sub-analyses classified thepatients by age: non-elderly patients (< 65years) and elderly patients (≥ 65years) to adjust for age. Both sub-analyses showed similar results to the analysis for the combined ages regarding sleep architecture. Patients with OSA who hadshort sleep time had disordered sleep architecture with a lower REM sleep time (%) and more stage N1 sleep time.

Diurnal Emotional States Impact the Sleep Course.

BackgroundDiurnal emotional experiences seem to affect several characteristics of sleep architecture. However, this influence remains unclear, especially for positive emotions. In addition, electrodermal activity (EDA), a sympathetic robust indicator of emotional arousal, differs depending on the sleep stage. The present research has a double aim: to identify the specific effects of pre-sleep emotional states on the architecture of the subsequent sleep period; to relate such states to the sympathetic activation during the same sleep period.MethodsTwelve healthy volunteers (20.1 ± 1.0 yo.) participated in the experiment and each one slept 9 nights at the laboratory, divided into 3 sessions, one per week. Each session was organized over three nights. A reference night, allowing baseline pre-sleep and sleep recordings, preceded an experimental night before which participants watched a negative, neutral, or positive movie. The third and last night was devoted to analyzing the potential recovery or persistence of emotional effects induced before the experimental night. Standard polysomnography and EDA were recorded during all the nights.ResultsFirstly, we found that experimental pre-sleep emotional induction increased the Rapid Eye Movement (REM) sleep rate following both negative and positive movies. While this increase was spread over the whole night for positive induction, it was limited to the second half of the sleep period for negative induction. Secondly, the valence of the pre-sleep movie also impacted the sympathetic activation during Non-REM stage 3 sleep, which increased after negative induction and decreased after positive induction.ConclusionPre-sleep controlled emotional states impacted the subsequent REM sleep rate and modulated the sympathetic activity during the sleep period. The outcomes of this study offer interesting perspectives related to the effect of diurnal emotional influences on sleep regulation and open new avenues for potential practices designed to alleviate sleep disturbances.

Sleep Quality, Short-Term and Long-Term CPAP Adherence

Adherence to CPAP therapy is low in patients with obstructive sleep apnea/hypopnea syndrome (OSAHS). The purpose of the present study was to evaluate the utility of measures of sleep architecture and sleep continuity on the CPAP titration study as predictors of both short- and long-term CPAP adherence. 93 patients with OSAHS (RDI 42.8 ± 34.3/h) underwent in-laboratory diagnostic polysomnography, CPAP titration, and follow-up polysomnography (NPSG) on CPAP. Adherence to CPAP was objectively monitored. Short-term (ST) CPAP adherence was averaged over 14 days immediately following the titration study. Long-term (LT) CPAP adherence was obtained in 56/93 patients after approximately 2 months of CPAP use. Patients were grouped into CPAP adherence groups for ST (< 2 h, 2-4 h, and > 4 h) and LT adherence (< 4 h, > 4 h). Sleep architecture, sleep disordered breathing (SDB) indices, and daytime outcome variables from the diagnostic and titration NPSGs were compared between CPAP adherence groups. There was a significant relationship between ST and LT CPAP adherence (r = 0.81, p < 0.001). Neither ST nor LT adherence were related to demographic variables, baseline severity of untreated SDB, sleep architecture, or measures of daytime impairment. Good CPAP adherence groups had significantly lower %N2 and greater %REM on the titration NPSG. A model combining change in sleep efficiency and change in sleep continuity between the diagnostic and titration NPSGs predicted 17% of the variance in LT adherence (p = 0.006). These findings demonstrate that characteristics of sleep architecture, even on the titration NPSG, may predict some of the variance in CPAP adherence. Better sleep quality on the titration night was related to better CPAP adherence, suggesting that interventions to improve sleep on/prior to the CPAP titration study might be used as a therapeutic intervention to improve CPAP adherence.

Schizophrenia as a possible dysfunction of the suprachiasmatic nucleus

Psychosis and dreaming have many similarities, including delusions, hallucinations, bizarre thinking and perceptual distortions. This clinical observation has lead us to hypothesize that the suprachiasmatic nucleus (SCN), a hypothalamic center regulating sleep and wakefulness, is involved in the pathogenesis of schizophrenia. Schizophrenic patients have certain sleep architecture characteristics, and distinctive biological markers suggesting abnormity of the SCN, including irregular pattern of melatonin secretion, abnormal actigraphyic studies, D1-dopamine receptors involvement in the process of entraining the SCN and vulnerability to psychotic exacerbation due to jet lag. In addition, SCN lesions in rodents are associated with pathologic day-time sleep pattern, very similar to the sleeping pattern in patients with schizophrenia. We introduce the concept of REM sleep abnormity as a possible etiological factor in development of psychosis. We hypothesize that the proposed dysfunction of the SCN may contribute to schizophrenia through several different, not necessarily mutually exclusive, mechanisms, including "REM sleep (dream) rebound" phenomenon, damaged neuronal pathways connecting SCN to the brain regions affected by schizophrenia, and the SCN dysfunction induced dysregulation of gene expression in different parts of the body, including the brain. Moreover, the influenza virus, which has been implicated in the etiology of schizophrenia, is capable of resetting the SCN, the ultimate processor of light signals, suggesting the explanation for chronological variability of incidence of schizophrenia. Future investigation of the proposed mechanisms will provide the ultimate test of our hypothesis that lesions of the suprachiasmatic nucleus play an important role in the etiology of schizophrenia.

Plasma visfatin levels in severe obstructive sleep apnea—hypopnea syndrome

Obstructive sleep apnea syndrome (OSAS) is associated with obesity and insulin resistance. Visfatin is an insulin-mimicking adipokine, which is considered a link between obesity and insulin resistance. Aim of this study was to evaluate levels of plasma visfatin in patients with severe OSAS and examine their potential correlation with sleep characteristics and several biochemical parameters. Nondiabetic patients with severe OSAS (Apnea Hypopnea Index > 30/h, n = 32) and healthy controls (Apnea Hypopnea Index < 5/h, n = 12), examined with polysomnography, underwent a biochemical analysis to estimate fasting levels of visfatin, glucose, insulin, C-peptide, and lipid profile. The two groups were matched for age and body mass index (BMI). OSAS patients had significantly higher fasting insulin levels (p = 0.045), but no difference was shown in visfatin between patients and controls (p = 0.585). In OSAS patients, visfatin levels correlated positively with sleep latency (r = 0.539, p = 0.01) and triglyceride levels (r = 0.584, p = 0.036) and negatively with total sleep time, percentage of stage 2 and REM sleep, and LDL-cholesterol levels (r = -0.659 and p = 0.001; r = -0.496 and p = 0.019; r = -0.577 and p = 0.005; r = -0.804 and p = 0.003, respectively). No association was found, however, between visfatin levels and HOMA index or indices of nocturnal hypoxia. In patients with severe OSAS, visfatin levels are associated with characteristics of sleep architecture. However, there is no correlation between visfatin and insulin resistance or nocturnal hypoxia.

The Feasibility of Adding Fetal Heart Rate to the Nocturnal Polysomnogram

To demonstrate that fetal heart rate measured by ultrasound can be successfully captured and monitored throughout the nocturnal polysomnogram. Fetal heart rate by ultrasound using an abdominal belt (Hewlett Packard Fetal Monitor 8040A) was measured during 1 overnight polysomnogram in volunteers in late pregnancy and added to a digitized polysomnography system (Alice 4, Respironics). In 6 women with a single fetus in their third trimester, the fetal heart rate monitor band only infrequently needed to be readjusted. Fetal kicks and movements resulted in signal loss, usually with subsequent recapture without having to awaken the mother. Fetal heart rate, 1 of the classic signals of fetal distress, can be added to the nocturnal polysomnogram with minimal disruption of maternal sleep and with signal capture throughout the night.

Sleep characteristics of persons with chronic fatigue syndrome and non-fatigued controls: results from a population-based study

BackgroundThe etiology and pathophysiology of chronic fatigue syndrome (CFS) remain inchoate. Attempts to elucidate the pathophysiology must consider sleep physiology, as unrefreshing sleep is the most commonly reported of the 8 case-defining symptoms of CFS. Although published studies have consistently reported inefficient sleep and documented a variable occurrence of previously undiagnosed primary sleep disorders, they have not identified characteristic disturbances in sleep architecture or a distinctive pattern of polysomnographic abnormalities associated with CFS.MethodsThis study recruited CFS cases and non-fatigued controls from a population based study of CFS in Wichita, Kansas. Participants spent two nights in the research unit of a local hospital and underwent overnight polysomnographic and daytime multiple sleep latency testing in order to characterize sleep architecture.ResultsApproximately 18% of persons with CFS and 7% of asymptomatic controls were diagnosed with severe primary sleep disorders and were excluded from further analysis. These rates were not significantly different. Persons with CFS had a significantly higher mean frequency of obstructive apnea per hour (p = .003); however, the difference was not clinically meaningful. Other characteristics of sleep architecture did not differ between persons with CFS and controls.ConclusionAlthough disordered breathing during sleep may be associated with CFS, this study generally did not provide evidence that altered sleep architecture is a critical factor in CFS. Future studies should further scrutinize the relationship between subjective sleep quality relative to objective polysomnographic measures.

Sleep Characteristics Following Adenotonsillectomy in Children With Obstructive Sleep Apnea Syndrome

To compare the effect of adenotonsillectomy on rapid eye movement (REM)- and non-REM-related respiratory and sleep architecture characteristics in children with obstructive sleep apnea syndrome (OSAS). This prospective study evaluated 36 children (median age, 6.9 years; range, 1.8 to 12.6 years) with OSAS using polysomnography before and a few months after adenotonsillectomy. Primary outcomes included the number of obstructive apnea and hypopnea and arousals per hour of sleep. At 4.6 months (range, 1 to 16 months) after adenotonsillectomy, there was a significant improvement of all respiratory parameters. The median respiratory disturbance index (RDI) decreased from 4.1/h (range, 0 to 85/h) to 0.9/h (range, 0 to 13/h) after adenotonsillectomy (p < 0.0001). The median non-REM RDI decreased from 3.0/h (range, 0 to 89/h) to 0.4/h (range, 0 to 13/h) [p < 0.001] as compared with REM RDI, which decreased from 7.8/h (range, 0 to 69/h) to 2.3/h (range, 0 to 54/h) after adenotonsillectomy (p < 0.01). Median arousal index decreased following adenotonsillectomy from 17.5/h (range, 7 to 57/h) to 14.0/h (range, 6 to 47/h) [p < 0.03]. Adenotonsillectomy resulted in a greater improvement in non-REM RDI as compared with REM-RDI, and a decrease in the number of arousals.