Sleep最新文献

Study objectives: The tendency to procrastinate bedtime is associated with poorer sleep and wellbeing. However, day-specific effects of bedtime procrastination are rarely studied and may differ by whether an individual has school/work the next day versus the flexibility to wake up later. We tested the hypothesis that going to bed later than intended would be associated with shorter sleep and worse next-day mood on school nights, but not non-school nights, in residential college students.

Methods: Actigraphy-estimated sleep timing and duration were measured for 2 weeks in 104 university students. Daily diaries recorded instances of going to bed later than intended, morning mood, and daytime sleepiness. Mixed effects models tested associations of delaying bedtime with same-night sleep duration and next-day mood and sleepiness, adjusting for demographics, chronotype, and school start time.

Results: Students went to bed later than intended on 54% of all nights. Individuals who delayed their bedtime more frequently had poorer self-rated sleep, higher pre-sleep arousal, and higher depression scores. Going to bed later than intended was associated with shorter sleep by 0.91 h on school nights and 0.86 h on non-school nights because there was no compensatory delay in wake-up time. Next-morning mood and daytime sleepiness were worse compared with nights with no bedtime delay.

Conclusions: Residential college students who went to bed later than intended showed deficits in sleep duration and wellbeing irrespective of whether they needed to wake up for classes. Interventions to prevent bedtime procrastination may help students to achieve better sleep and mental health.

Alterations in sleep-wake patterns are well-recognized features of overt alpha-synucleinopathies. However, their presence in prodromal stages, characterised by isolated REM sleep behavior disorder (iRBD), remains controversial, and their association with clinical symptoms and imaging risk factors has been underexplored. In this study, we used seven-day ambulatory circadian monitoring to characterize circadian and sleep-wake disturbances in a well-characterised sample of forty-two patients with video-polysomnography-confirmed iRBD and twenty-three healthy controls (HC). We investigated the associations between circadian disturbances and non-motor clinical symptoms, assessed in a comprehensive neuropsychological protocol, alongside imaging proxies of glymphatic system functioning, namely the Diffusion Tensor Imaging Along the Perivascular Spaces (DTI-ALPS) index, and volume of perivascular spaces and choroid plexuses. Moreover, we assessed the associations between circadian alterations and striatal dopaminergic uptake in the most affected putamen, a well-established risk factor for conversion to alpha-synucleinopathies, as assessed with presynaptic dopaminergic imaging. Patients with iRBD exhibited reduced diurnal physical activity, along with reduced amplitude and increased fragmentation of the sleep probability and motor activity rhythms. Circadian alterations correlated with greater neuropsychiatric symptoms and reduced psychomotor and mental speed. Patients with iRBD exhibited a decreased DTI-ALPS and larger volume of perivascular spaces, but only the former was associated with sleep impairment. Decreased putaminal dopaminergic uptake was associated with rest-activity rhythm fragmentation. These results show that circadian alterations are observed in early stages of neurodegeneration and are associated with clinical and imaging risk markers of conversion to alpha-synucleinopathies, posing them as possible targets for intervention in prodromal disease stages.

Study objectives: This study examined whether basal electromyographic (EMG) amplitude during sleep is altered in patients with isolated REM sleep behavior disorder (iRBD) and its relationship to disease progression, as well as changes across the sleep cycle.

Methods: Baseline polysomnograms collected from 95 iRBD patients (15 converters, 80 non-converters) and matched 24 controls were analyzed. EMG amplitude was calculated from submentalis recordings across all sleep stages using 3-second mini-epochs, with REM sleep further classified as REM sleep without atonia (RWA) and non-RWA (RA) according to the presence of "any" RWA events. Kaplan-Meier analysis assessed phenoconversion risk, and EMG amplitude was compared between early and late sleep cycles within each group.

Results: Group comparisons with post-hoc adjustment showed that EMG amplitude in RA and RWA was higher in non-converters than controls (adj-p<.001), while converters showed further increases of EMG amplitude in N2 and N3 (adj-p<.045). RA amplitude was higher in converters than non-converters (adj-p=.02). Increased EMG amplitude in N2, N3, and RA was associated with higher phenoconversion risk (p<.05). EMG amplitude remained stable between early and late cycles during RA in both iRBD and controls. In contrast, iRBD patients showed a significant decrease in EMG amplitude during late cycles in N2 (p<.009).

Conclusions: Elevated basal EMG amplitude during both REM and NREM sleep in iRBD patients shows potential as a prognostic marker, indicating muscle tone dysregulation beyond REM atonia loss and underscoring the need to consider broader sleep stages in iRBD evaluation.

Rapid eye movement (REM) sleep is believed to reduce physiological reactivity to emotional experiences. While REM sleep fragmentation has been associated with maladaptive emotional processing in clinical and animal models, its causal role has not been experimentally isolated in healthy humans. In this study, we tested whether selectively fragmenting REM sleep impairs overnight psychophysiological habituation in healthy individuals, aiming to identify the cortical dynamics involved. Seventeen participants (mean age±SD, 23.18±3.94, 14 females) completed two counterbalanced conditions (Fragmentation and Control) each encompassing a baseline assessment of emotional memory/reactivity, a nocturnal polysomnography with or without wrist-applied vibrotactile stimulation during REM sleep, a post-sleep emotional memory/reactivity reassessment, and a 48-hour follow-up evaluation. Emotional memory was evaluated using an old/new paradigm, while emotional reactivity was assessed through self-report and physiological measures (electrodermal activity and heart rate deceleration-HRD). The stimulation procedure elicited cortical arousal during REM sleep, increasing REM sleep fragmentation without altering total sleep time, sleep efficiency, and wake after sleep onset. Stimulations reliably induced a distinct cortical arousal signature, characterised by increased higher EEG frequencies (alpha, sigma, beta, gamma). REM sleep fragmentation compromised HRD habituation to emotional stimuli at both post-sleep assessments without impacting electrodermal response, self-report evaluation, and recognition memory. Crucially, the degree of impaired cardiac habituation at both timepoints was strongly predicted by the magnitude of stimulation-induced alpha power over parieto-occipital regions. These findings indicated the importance of unperturbed REM sleep continuity for proper psychophysiological habituation to emotional events, suggesting alpha intrusions as a potential cortical correlate of impaired habituation.

Twitches are discrete movements that characterize REM sleep. However, recent work showed that twitches also occur during NREM sleep in human infants beginning around 3 months of age, a time when sleep spindles and the cortical delta rhythm are also emerging. Further, NREM twitches are coupled with sleep spindles, suggesting a unique contribution to sensorimotor development. Given that NREM sleep is composed of distinct substages, we investigated whether twitching and twitch-spindle coupling are differentially expressed during N2 and N3 sleep. In 6-month-old human infants (n=21; 7 females), we recorded EEG, respiration, and video during daytime sleep. We found high-intensity twitching during N2 and REM but not N3 sleep. In contrast, sleep spindles exhibited similar temporal characteristics during N2 and N3. Also, despite differences in the intensity of twitching during N2 and N3, significant twitch-spindle coupling occurred in both stages. Finally, the rate of twitching was inversely related to delta power across NREM periods. These findings suggest that although twitching occurs during REM, N2, and N3 sleep at this age, its expression is compatible with some sleep components (e.g., rapid eye movements, sleep spindles) but not others (e.g., cortical delta), highlighting the continuing need to better understand the dynamic organization of sleep and its individual components in early development.

Study objectives: Alcohol-induced memory loss (also known as "blackout") is prevalent and confers risk for other adverse drinking outcomes. Sleep health is implicated in memory and cognitive functioning broadly, but proximal impacts of sleep on next-day memory loss are understudied. We hypothesized that worse sleep health the night before drinking (fewer hours, misaligned timing, worse sleep quality, greater sleepiness) would (a) increase the odds of next-day memory loss and (b) moderate day-level associations between estimated blood alcohol concentration (eBAC) and blackouts, such that lower eBACs would be required to experience memory loss following nights of worse sleep.

Methods: Heavy-drinking young adults (N=203, 57% female) in the United States completed baseline self-report measures, followed by 28 days of ecological momentary assessments.

Results: Memory loss was reported on 15.4% (n=366) of drinking days (n=2380). Multilevel models, controlling for eBAC, indicated that fewer hours of sleep [OR=0.84 (95% CI: 0.76, 0.92), p<.001], more deviation than usual from midsleep timing [OR=1.43 (1.25, 1.65), p<.001], and worse sleep quality [OR=0.72 (0.60, 0.85), p<.001] on the night before drinking significantly increased the odds of next-day memory loss. Sleepiness at the start of drinking events was unrelated to memory loss [OR=0.91 (0.81, 1.03), p=.13]. Sleep parameters did not significantly moderate associations between eBAC and memory loss (p≥.08).

Conclusions: Prior-night sleep health increases risk for alcohol-induced memory loss. These behavioral data extend experimental findings to young adults' real-time drinking outcomes. We encourage prevention and intervention efforts highlighting poor sleep as a potential contributor to alcohol-induced memory impairment.