Daily experiences affect the timing rather than the structure of sleep

Effects of aging on sleep structure throughout adulthood: a population-based study

We want to evaluate the effect of sertraline on polysomnogram (PSG) and clinical variables in depression. An 8-week and open-label trial (n = 31) was applied. The primary outcome was mean baseline-to-visit changes in PSG variables. The secondary outcomes were clinical improvement, side-effects, and the subjective sleepiness. Rapid eye movement (REM) latency was prolonged significantly over the course of the study. The arousal index reached the highest level on the 1st day (13.8 _ 7.2). From the 14th day onward, the sleep latency (SL) and wake after sleep onset (WASO) decreased significantly. The percentage of stage 3 sleep increased in this trial. The Hamilton Rating Scale for Depression (HRSD) and Clinical Global Impression (CGI) scores on the 14th, 28th, and 56th days were significantly lower than baseline. Furthermore, a significant correlation was shown between the decreasing score rate of HRSD on the 56th day and the decreasing score rate of REM latency on the 1st day (r = -0.733, P = 0.003). The effectiveness of sertraline positively correlated with the reduction of REM latency. The final clinical improvement could be predicted by the extent of the prolongation of REM latency on the first night.

Objective To investigate the sleep structure of children with attention deficit hyperactivity disorder(ADHD) and the differences among subtypes of ADHD. Methods Ninety children with ADHD were diagnosed in Department of Neurology, the Children's Hospital Affiliated to Capital Institute of Pediatrics between June 2012 and June 2013, including 75 boys and 15 girls, 6-14 years old[(9.5±2.4) years old], and among them there were 55 cases of ADHD-combined type, 25 cases of ADHD-inattentive type, and 10 cases of ADHD-hyperactive impulsive type.Thirty healthy children whose age and sex matched with ADHD group, came from Beijing and the surrounding area, were selected as the healthy control group, including 23 boys and 7 girls, 6-14 years old [(9.2 ± 2.9) years old]. Two groups underwent full overnight sleep assessment. Results The latency of rapid eye movement(REM) in children with ADHD was (146.58±47.28) minutes, and the sleep latency was 19.00 minutes[(8.25-37.50)minutes]; while the latency of REM in healthy control group was(87.55±13.59) minutes, and the sleep latency was 9.00 minutes[(3.50-13.63)minutes]. Compared with healthy control group, children with ADHD demonstrated the increased latency REM and sleep latency, and decreased sleep efficiency, the increasing times of awakening and total duration, and these differences were all statistically significant(all P<0.05). The percentage of non-rapid eye movement(NREM) phase Ⅱ in ADHD hybrid was lower than the ADHD attention-deficit(t=2.012, P<0.05). Sleep latency in ADHD attention-deficit was longer than the ADHD hybrid(t=2.964, P<0.05). No statistical differences were found among the various types in other indicators.The prevalence of periodic limb movements in sleep(PLMS) was 27.78%(25/90 cases) in ADHD group and the prevalence of PLMS was 3.30% (1/30 cases) in the healthy control group.The diffe-rences in prevalence between 2 groups were statistically significant(χ2=8.053, P<0.05). Conclusions Children with ADHD significantly display more problems with sleep.Sleep latency and NREMⅡ are different between ADHD attention-deficit and ADHD hybrid. Key words: Attention deficit hyperactivity disorder; Sleep structure; Child

The effect of a small amount of alcohol on the sleep structure in relation to alcohol sensitivity was examined using polysomnography (PSG). Alcohol sensitivity was evaluated using alcohol patch test for all subjects. PSGs were performed on three nights after one night for acclimation, and subjects consumed no alcohol, 0.28 or 0.69 g ethanol/kg body weight, respectively, before going to bed. The percentages of sleep time in each sleep stage of 1, 2, 3+4 and rapid eye movement (REM), REM latency, and REM cycle were calculated. Thirteen healthy female students (age 21.1 +/- 0.7 years) were enrolled in this study. In all subjects, there were no significant differences in any of the sleep parameters between baseline night and alcohol nights. Six of the 13 subjects were sensitive to alcohol, in whom %stage REM was significantly decreased by alcohol consumption (baseline night: 18.3 +/- 6.2%, alcohol night I: 9.8 +/- 5.1% and alcohol night II: 11.0 +/- 2.8%), and the REM latency was significantly prolonged. The standard deviation of REM cycle was significantly greater on alcohol nights I and II than baseline night. There were no significant differences in other sleep parameters. In the other seven subjects who were insensitive to alcohol, none of the sleep parameters were significantly affected by alcohol consumption. REM sleep was adversely affected by a small amount of alcohol in alcohol-sensitive healthy young women. Alcohol sensitivity might play some important role in impaired REM sleep by an ingestion of a small amount of alcohol.

IntroductionThe onset of puberty is associated with a shift in the circadian timing of sleep, leading to delayed sleep initiation [i.e., later sleep onset time (SOT)] due to later bedtimes and/or longer sleep onset latency (SOL). Several genome-wide association studies (GWAS) have identified genes that may be involved in the etiology of sleep phenotypes. However, circadian rhythms are also epigenetically regulated; therefore, epigenetic biomarkers may provide insight into the physiology of the pubertal sleep onset shift and the pathophysiology of prolonged or delayed sleep initiation.ResultsThe gene-wide analysis indicated differential methylation within or around 1818 unique genes across the sleep initiation measurements using self-report, actigraphy (ACT), and polysomnography (PSG), while GWAS-informed analysis yielded 67 genes. Gene hits were identified for bedtime (PSG), SOL (subjective, ACT and PSG) and SOT (subjective and PSG). DNA methylation within 12 genes was associated with both subjective and PSG-measured SOL, 31 with both ACT- and PSG-measured SOL, 19 with both subjective and ACT-measured SOL, and one gene (SMG1P2) had methylation sites associated with subjective, ACT- and PSG-measured SOL.ConclusionsObjective and subjective sleep initiation in adolescents is associated with altered DNA methylation in genes previously identified in adult GWAS of sleep and circadian phenotypes. Additionally, our data provide evidence for a potential epigenetic link between habitual (subjective and ACT) SOL and in-lab SOT and DNA methylation in and around genes involved in circadian regulation (i.e., RASD1, RAI1), cardiometabolic disorders (i.e., FADS1, WNK1, SLC5A6), and neuropsychiatric disorders (i.e., PRR7, SDK1, FAM172A). If validated, these sites may provide valuable targets for early detection and prevention of disorders involving prolonged or delayed SOT, such as insomnia, delayed sleep phase, and their comorbidity.

Mid-morning Tryptophan Depletion Delays REM Sleep Onset in Healthy Subjects

Several previous studies have observed short rapid eye movement (REM) latencies in schizophrenic patients without major affective disorder. This study was designed to meet several of the criticisms of those previous studies. Using Research Diagnostic Criteria, we compared the sleep patterns of schizophrenic patients with those of normal controls and patients with major depressive disorder and schizoaffective disorder. All patients were medication free, and REM latency was explicitly defined using both strict and lenient criteria. Chronically ill paranoid or undifferentiated schizophrenics could not be distinguished from patients with major depressive disorder or schizoaffective disorder using any definition of REM latency. These results were not due to longer REM latency in the particular sample of patients with major depressive disorder. They had abnormally low REM latencies; however, the schizophrenic patients showed similar decrements. These data cast serious doubt on the specificity of short REM latency as a biological marker for major depressive disorder.

Objective To explore the rapid eye movement (REM) sleep characteristics of different episode types of depression and post-stroke depression (PSD) patients and provide support for clinical diagnosis, treatment and prognosis. Methods Patients with single-episode depression (group A, n=22), patients with recurrent depression (≥2 episodes, group B, n=26) and patients with PSD (group C, n=19) were included from Henan Provincial Mental Hospital. 20 healthy volunteers were assigned to control group.Participants in the 4 groups were performed polysomnographic recordings (PSG) from 9 PM to 6 AM before treatment.The 3 patients groups were performed the second PSG recordings and HAMD score at the end of 6 week SSRIs treatment. The REM indexes of 4 groups were compared and analyzed. Results First PSG detection showed that REM sleep latencies (RL) were shorter in group A and B (A: (65.57±18.29) min, B: (66.32±15.46) min) than that in group C ( (79.17±20.18) min ) and control group( (87.24±16.55) min); REM activity (RA) (A: (99.82±25.71) u, B: (104.70±28.23) u)and REM density (RD) (A: (81.06±19.35)%, B: (86.61±23.83)%) were increased more significantly in group A and B than those in control group ((79.61±18.40) u; (68.11±17.54)%); REM sleep time (RT) were decreased more significantly in group C ((51.66±22.26) min) than that in group A((71.43±20.70) min), group B((74.81±17.52) min) and control group ((70.46±16.35) min)(P 0.05). There was no significant difference in the indexes of REM in group C; RT was prolonged ((51.66±22.26) min vs(68.37±20.16) min)in group C, the difference was statistically significant (P<0.05). Conclusion Most of depression patients with different episode types have REM disinhibition phenomenon. RD increase may be REM characteristic type of depression patient. Sleep disorders of PSD patients are mainly poor sleep process and sleep continuity and have no characteristics of REM sleep disorder of depression ones. Key words: Depression; Post-stroke depression; Sleep disorders; Rapid eye movement sleep; Polysomnogram

Night-to-night variability in sleep in cystic fibrosis

The purpose of this study was to describe objective sleep-wake characteristics and glycemia over 7-14 days in young adults with type 1 diabetes. In addition, person-level associations among objective sleep-wake characteristics (total sleep time, sleep variability, and sleep fragmentation index), daytime sleepiness, and glycemia (glycemic control and glucose variability) were examined. In this cross-sectional study, objective sleep-wake characteristics were measured via actigraphy and glucose variability via continuous glucose monitoring over 6-14 days. At baseline, participants completed the Psychomotor Vigilance Test, the Trail Making Test, and questionnaires on daytime sleepiness, sleep quality, and sleep disturbance including sleep diaries. Forty-six participants (mean age, 22.3 ± 3.2 years) wore a wrist actigraph and underwent continuous glucose monitoring concurrently for 6-14 days. Greater sleep variability was directly associated with greater glucose variability (mean of daily differences; r = .33, P = .036). Higher daytime sleepiness was directly associated with greater glucose variability (mean of daily differences; r = .50, P = .001). The association between sleep variability and glucose variability (mean of daily differences) was no longer significant when accounting for daytime sleepiness and controlling for type 1 diabetes duration (P > .05). A higher sleep fragmentation index was associated with greater glucose variability (B = 1.27, P = .010, pr2 = 0.40) after controlling for type 1 diabetes duration and accounting for higher daytime sleepiness. Sleep-wake variability, sleep fragmentation, daytime sleepiness, and the associations with glycemia are new dimensions to consider in young adults with type 1 diabetes. Sleep habits in this population may explain higher glucose variability, and optimizing sleep may improve overall diabetes management. Griggs S, Hickman RL Jr, Strohl KP, Redeker NS, Crawford SL, Grey M. Sleep-wake characteristics, daytime sleepiness, and glycemia in young adults with type 1 diabetes. J Clin Sleep Med. 2021;17(9):1865-1874.

Repeated exposure to an anxiogenic stressor (AS) is a known environmental factor for the development of depression, yet the progression of sleep-wake (S-W) changes associated with the onset of AS-induced depression (ASID) is not completely understood. Thus, the aim of this study was to identify these progressive S-W changes by developing ASID in rats, via repeated exposure to an AS, and compare this ASID-associated sleep phenotype with the sleep phenotype of human depression. To achieve this aim, rats were first recorded for a 6 h period of baseline S-W activity without AS. Then, rats were subjected to 5 days of AS [Day 1: inescapable foot-shock; 5 trials of 3 s foot-shocks (1.0 mA) at 3 min intervals; Days 3–5: 15 trials of 5 s foot-shocks at 45 s intervals]. S-W activity was recorded for 6 h immediately after each AS treatment session. Two days later rats were again recorded for 6 h of S-W activity, but with no exposure to the AS (NASD). Compared to the baseline day: Day 1 of AS (ASD-1) increased wakefulness, slow-wave sleep (SWS) latency, and rapid-eye movement (REM) sleep latency, but decreased the total amount of REM sleep; ASD-2 animals remained awake throughout the 6 h S-W recording period; ASD-3, ASD-4, and ASD-5 (ASDs-3–5) decreased wakefulness, SWS latency, and REM sleep latency, but increased the total amount of REM sleep. Interestingly, these results reveal that initial exposure to the AS versus later, repeated exposure to the AS produced opposing S-W changes. On NASD, animals exhibited baseline-like S-W activity, except slightly less REM sleep. These results suggest that repeated AS produces a sleep phenotype that resembles the sleep phenotype of depression in humans, but consistent re-exposure to the AS is required. These results are promising because the methodological simplicity and reversibility of the ASID-associated S-W phenotype could be more advantageous than other animal models for studying the pathophysiological mechanisms that underlie the expression of ASID.

To continuously and dynamically monitor the sleep status of patients in the acute phase of cerebral infarction, and to investigate the characteristics of acute cerebral infarction(ACI)associated with sleep-disordered breathing (SDB), variations in sleep structure, and changes in sleep circadian rhythms. Patients with ACI within 48h of onset who were admitted to the Department of Neurology at Kailuan General Hospital from November 2020 to December 2022 were selected. Detailed baseline information such as age, gender, smoking history, drinking history, were recorded for the selected participants. From the beginning of their hospitalization, the selected participants were monitored for their sleep status continuously for 5 days using the Intelligent Mattress-based Sleep Monitoring Platform System(IMSMPS). Based on the heart rate data obtained from the monitoring, the interdaily stability (IS) and intradaily variability (IV) of the sleep circadian rhythm were calculated. 1,367 patients with ACI were selected. Monitoring results over 5 days indicated 147 cases (10.75%) without SDB, and 1,220 cases (89.25%) with SDB. Among the group with SDB, there were 248 cases (18.14%) with continuous mild SDB, 395 cases (28.90%) with moderate SDB, 295 cases (21.58%) with severe SDB, and 282 cases (20.63%) that fluctuated between different severity levels. Within this fluctuating group, 152 cases (53.90%) fluctuated between two severity levels, 120 cases (42.55%) between three levels, and 10 cases (3.55%) among all four levels. There were statistically significant differences (P < 0.05) in the sleep latency, sleep efficiency, non-rapid eye movement stages 1-2, rapid eye movement, proportion of non-rapid eye movement, proportion of rapid eye movement, wake after sleep onset, time out of bed, number of awakenings, respiratory variability index, and heart rate variability index among patients with ACI monitored from day 1 to 5. However, other monitored sleep structure parameters did not show statistically significant differences (P > 0.05). The coefficient of variation for all sleep monitoring parameters ranged between 14.54 and 36.57%. The IV in the SDB group was higher than in the group without SDB (P < 0.05), and the IS was lower than in the group without SDB (P < 0.05). Patients in the acute phase of cerebral infarction have a high probability of accompanying SDB. The sleep structure of these patients shows significant variability based on the onset time of the stroke, and some patients experience fluctuations among different severity levels of SDB. ACI accompanied by SDB can further reduce the IS of a patient's sleep circadian rhythm and increase its IV.

Sleep quality in patients studied with laboratory-based polysomnography may differ from sleep quality in patients studied at home but remains clinically relevant and important to describe. We assessed objective sleep quality and explored factors associated with poor sleep in patients undergoing laboratory-based polysomnography. We reviewed diagnostic polysomnography studies from a 10-year period at a single sleep center. Total sleep time (TST) and sleep efficiency (SE) were assessed as markers of sleep quality. Poor sleep was defined as TST ≤ 4 hours or SE ≤ 50%. Multivariable analysis was performed to determine associations between objective sleep quality as an outcome and multiple candidate predictors including age, sex, race, body mass index, comorbidities, severity of obstructive sleep apnea, and central nervous system medications. Among 4957 patients (age 53 ± 15 years), average TST and median SE were 5.8 hours and 79%, respectively. There were 556 (11%) and 406 (8%) patients who had poor sleep based on TST and SE, respectively. In multivariable analysis, those who were older (per 10 years: 1.48 [1.34, 1.63]), male (1.38 [1.14,1.68]), and had severe obstructive sleep apnea (1.76 [1.28, 2.43]) were more likely to have short sleep. Antidepressant use was associated with lower odds of short sleep (0.77 [0.59,1.00]). Older age (per 10 years: 1.48 [1.34, 1.62]), male sex (1.34 [1.07,1.68]), and severe obstructive sleep apnea (2.16 [1.47, 3.21]) were associated with higher odds of poor SE. We describe TST and SE from a single sleep center cohort. Multiple demographic characteristics were associated with poor objective sleep in patients during laboratory-based polysomnography. Harrison EI, Roth RH, Lobo JM, et al. Sleep time and efficiency in patients undergoing laboratory-based polysomnography. J Clin Sleep Med. 2021;17(8):1591-1598.

Objective To quantitatively research the chin electromyography (EMG) increasing level of narcolepsy in rapid eye movement(REM) period, and analyze its association with clinical features and rapid eye movement sleep without atonia (RSWA). Methods Sixty-six patients with narcolepsy underwent video-polysomnography (video-PSG) and multiple sleep latency test (MSLT), and were grouped by quantitative research of the chin EMG levels during overnight REM (patients with elevated level belongs to RSWA group(n=31)). The data from general clinical data, video-PSG and MSLT and neuro-psychological assessment (Epworth Sleepiness Scale (ESS) and Montreal Cognitive Assessment) were analyzed statistically. Results Compared with narcolepsy without RSWA group (n=35), narcolepsy with RSWA group showed higher ESS score (17.9±4.1 vs 15.4±4.9, t=2.236, P=0.029), longer average time (min) per drowsiness (38.3±28.4 vs 19.2±11.2, t=2.931, P=0.030), higher incidence of cataplexy (58.1%(18/31) vs 28.6%(10/35); χ2=6.281, P=0.012). In the polysomnography parameters, narcolepsy with RSWA group had shorter sleep latency (2.00(0.50, 3.50) min vs 3.00(1.75, 9.50) min; Z=3.007, P=0.003), higher total arousal index (31.4±14.4 vs 22.9±13.1; t=2.368, P=0.021), and micro arousal index ((13.0±7.19)/h vs (9.2±6.5)/h; t=2.080, P=0.042) and spontaneous arousal index((11.9±7.1)/h vs(8.1±5.4)/h; t=2.500, P=0.015). There was no significant difference in sleep structure between the narcolepsy with RSWA group and narcolepsy without RSWA group. In MSLT parameters, shorter average REM sleep latency (min) appeared in narcolepsy with RSWA group(3.5±1.7 vs 5.3±4.5, t=-2.190, P=0.027). Logistic regression analysis showed that the phase of the chin EMG (OR=1.103, 95% CI 1.008-1.207, P=0.033) and tension chin EMG (OR=1.339, 95% CI 1.111-1.615, P=0.002)were significantly associated with cataplexy. Conclusions Narcolepsy with RSWA group showed sleep fragmentation, severer daytime sleepiness, and higher risk of cataplexy. Therefore, narcolepsy patients with high chin EMG had a higher prevalence of cataplexy. Key words: Narcolepsy; Electrophysiology; Polysomnography; Rapid eye movement sleep without atonia

Short sleep appears to elevate obesity risk in youth; however, sleep is a multidimensional construct, and few studies have investigated parameters beyond duration. The objective of this study was to investigate if sleep onset time, duration, latency and night waking frequency are independently associated with adiposity and weight status in UK adolescents. This was a cross-sectional observational study of 10,619, 13-15years olds. Adjusted linear and logistic regressions were used to investigate associations of self-reported sleep characteristics with adiposity markers (body mass index z-score and percent body fat) and weight status. Compared with a sleep onset before 10pm, later sleep timing was associated with higher adiposity and higher likelihood of overweight and obesity in boys (after midnight, odds ratio [95% confidence interval]: 1.76 [1.19-2.60]) and girls (between 11pm and 11:59pm: 1.36 [1.17-1.65]). Sleeping ≤ 8hr, compared with > 9-10hr, was associated with higher odds of overweight and obesity in both sexes (boys: 1.80 [1.38-2.35]; girls: 1.38 [1.06-1.79]), and so too was sleeping > 10hr in girls (1.31 [1.06-1.62]), indicating evidence for a U-shaped association. Also in girls, compared to a sleep latency of 16-30 min, sleep latencies ≥ 46min were associated with higher adiposity (46-60min, beta coefficient [95% confidence interval], percent body fat: 1.47 [0.57-2.36]) and higher likelihood of overweight and obesity (46-60min: 1.39 [1.05-1.83]), and often as opposed to never waking in the night was associated with higher adiposity (body mass index z-score: 0.24 [0.08-0.41]; percent body fat: 1.44 [0.44-2.44]). Sleep duration and timing in both sexes, and sleep quality in girls, appear to be independently associated with adiposity and weight status in adolescence, and may be important targets for obesity prevention.