Local slow wave activity in regular sleep reveals individual risk preferences

In many everyday life situations, we have to make decisions under varying degrees of risk. Even though previous research has shown that the manipulation of sleep affects risky decision-making, it yet remains to be understood how regular, healthy sleep relates to risk preferences. Therefore, we investigated the relationship between individual, temporally stable neural sleep characteristics and individual differences in risk preferences in healthy adults. Sleep data were collected using a portable high-density EEG system at participants’ home. Results revealed a significant negative correlation between local sleep depth, as reflected in slow-wave activity (SWA) in a cluster of 5 electrodes located over the right prefrontal cortex and risk-taking behavior. This finding remained significant when controlling for total sleep time. Moreover, the association between SWA over the right prefrontal cortex and risk preferences was very similar in all sleep cycles. Our findings suggest that sleep depth in the right prefrontal cortex, an area involved in self-regulation, might serve as a dispositional indicator of lower self-regulatory abilities, which is expressed in greater risk-taking behavior

Local slow-wave activity over the right prefrontal cortex reveals individual risk preferences.

In everyday life, we have to make decisions under varying degrees of risk. Even though previous research has shown that the manipulation of sleep affects risky decision-making, it remains unknown whether individual, temporally stable neural sleep characteristics relate to individual differences in risk preferences. Here, we collected sleep data under normal conditions in fifty-four healthy adults using a portable high-density EEG at participants' home. Whole-brain corrected for multiple testing, we found that lower slow-wave activity (SWA, an indicator of sleep depth) in a cluster of electrodes over the right prefrontal cortex is associated with higher individual risk propensity. Importantly, the association between local sleep depth and risk preferences remained significant when controlling for total sleep time and for time spent in deep sleep, i.e., sleep stages N2 and N3. Moreover, the association between risk preferences and SWA over the right prefrontal cortex was very similar in all sleep cycles. Because the right prefrontal cortex plays a central role in cognitive control functions, we speculate that local sleep depth in this area, as reflected by SWA, might serve as a dispositional indicator of self-regulatory ability, which in turn reflects risk preferences

Reduced Regional NREM Sleep Slow-Wave Activity Is Associated With Cognitive Impairment in Parkinson Disease

Growing evidence implicates a distinct role of disturbed slow-wave sleep in neurodegenerative diseases. Reduced non-rapid eye movement (NREM) sleep slow-wave activity (SWA), a marker of slow-wave sleep intensity, has been linked with age-related cognitive impairment and Alzheimer disease pathology. However, it remains debated if SWA is associated with cognition in Parkinson disease (PD). Here, we investigated the relationship of regional SWA with cognitive performance in PD. In the present study, 140 non-demented PD patients underwent polysomnography and were administered the Montréal Cognitive Assessment (MoCA) to screen for cognitive impairment. We performed spectral analysis of frontal, central, and occipital sleep electroencephalography (EEG) derivations to measure SWA, and spectral power in other frequency bands, which we compared to cognition using linear mixed models. We found that worse MoCA performance was associated with reduced 1–4 Hz SWA in a region-dependent manner (F2, 687 =11.67, p < 0.001). This effect was driven by reduced regional SWA in the lower delta frequencies, with a strong association of worse MoCA performance with reduced 1–2 Hz SWA (F2, 687 =18.0, p < 0.001). The association of MoCA with 1–2 Hz SWA (and 1–4 Hz SWA) followed an antero-posterior gradient, with strongest, weaker, and absent associations over frontal (rho = 0.33, p < 0.001), central (rho = 0.28, p < 0.001), and occipital derivations, respectively. Our study shows that cognitive impairment in PD is associated with reduced NREM sleep SWA, predominantly in lower delta frequencies (1–2 Hz) and over frontal regions. This finding suggests a potential role of reduced frontal slow-wave sleep intensity in cognitive impairment in PD

Benchmarking Real-Time Algorithms for In-Phase Auditory Stimulation of Low Amplitude Slow Waves With Wearable EEG Devices During Sleep

OBJECTIVE: In-phase stimulation of EEG slow waves (SW) during deep sleep has shown to improve cognitive function. SW enhancement is particularly desirable in subjects with low-amplitude SW such as older adults or patients suffering from neurodegeneration. However, existing algorithms to estimate the up-phase of EEG suffer from a poor phase accuracy at low amplitudes and when SW frequencies are not constant. METHODS: We introduce two novel algorithms for real-time EEG phase estimation on autonomous wearable devices, a phase-locked loop (PLL) and, for the first time, a phase vocoder (PV). We compared these phase tracking algorithms with a simple amplitude threshold approach. The optimized algorithms were benchmarked for phase accuracy, the capacity to estimate phase at SW amplitudes between 20 and 60 μV, and SW frequencies above 1 Hz on 324 home-based recordings from healthy older adults and Parkinson disease (PD) patients. Furthermore, the algorithms were implemented on a wearable device and the computational efficiency and the performance was evaluated in simulation and with a PD patient. RESULTS: All three algorithms delivered more than 70% of the stimulation triggers during the SW up-phase. The PV showed the highest capacity on targeting low-amplitude SW and SW with frequencies above 1 Hz. The hardware testing revealed that both PV and PLL have marginal impact on microcontroller load, while the efficiency of the PV was 4% lower. Active stimulation did not influence the phase tracking. CONCLUSION: This work demonstrated that phase-accurate auditory stimulation can also be delivered during fully remote sleep interventions in populations with low-amplitude SW

Increased sleep need and daytime sleepiness 6 months after traumatic brain injury: a prospective controlled clinical trial

In a controlled, prospective, electrophysiological study, Imbach et al. demonstrate increased sleep need and excessive daytime sleepiness 6 months after traumatic brain injury. Sleep is more consolidated after brain trauma, and an increase in sleep need is associated with intracranial haemorrhage. Trauma patients underestimate their increased sleep need and sleepines

Human prosocial preferences are related to slow-wave activity in sleep

Prosocial behavior is crucial for the smooth functioning of society. Yet, individuals differ vastly in the propensity to behave prosocially. Here we try to explain these individual differences under normal sleep conditions without any experimental modulation of sleep. Using a portable high-density EEG we measured sleep data in 54 healthy adults (28 females) during a normal night's sleep at participants’ homes. To capture prosocial preferences, participants played an incentivised public goods game in which they faced real monetary consequences. Whole-brain analyses showed that higher relative slow-wave activity (SWA, an indicator of sleep depth) in a cluster of electrodes over the right temporo-parietal junction (TPJ) was associated with increased prosocial preferences. Source localization and CSD analyses further support these findings. Recent sleep deprivation studies imply that sleeping enough makes us more prosocial; the present findings suggest that it is not only sleep duration, but particularly sufficient sleep depth in the TPJ that is positively related to prosociality. Because the TPJ plays a central role in social cognitive functions, we speculate that sleep depth in the TPJ, as reflected by relative SWA, might serve as a dispositional indicator of social cognition ability, which is reflected in prosocial preferences. These findings contribute to the emerging framework explaining the link between sleep and prosocial behavior by shedding light on the underlying mechanisms. Significance Statement Sleep deprivation reportedly hampers prosocial behavior. Yet, sleep loss is not a regular occurrence. We studied participants without experimentally manipulating their sleep and conducted polysomnography along with a prosocial economic task. We found that higher relative slow-wave activity (an indicator of sleep depth) in the right TPJ – a brain region involved in social cognition – is associated with increased prosociality. This demonstrates a novel link between deep sleep neural markers and prosocial preferences. Furthermore, our study provides evidence about a possible neural mechanism that underlies the behavioral findings of previous studies on sleep deprivation and prosocial behavior. Our findings highlight the significance of sleep quality in shaping prosociality and the potential benefits of interventions targeting sleep quality to promote social capital

Human prosocial preferences are related to slow-wave activity in sleep.

Prosocial behavior is crucial for the smooth functioning of society. Yet, individuals differ vastly in the propensity to behave prosocially. Here we try to explain these individual differences under normal sleep conditions without any experimental modulation of sleep. Using a portable high-density EEG we measured sleep data in 54 healthy adults (28 females) during a normal night's sleep at participants' homes. To capture prosocial preferences, participants played an incentivised public goods game in which they faced real monetary consequences. Whole-brain analyses showed that higher relative slow-wave activity (SWA, an indicator of sleep depth) in a cluster of electrodes over the right temporo-parietal junction (TPJ) was associated with increased prosocial preferences. Source localization and CSD analyses further support these findings. Recent sleep deprivation studies imply that sleeping enough makes us more prosocial; the present findings suggest that it is not only sleep duration, but particularly sufficient sleep depth in the TPJ that is positively related to prosociality. Because the TPJ plays a central role in social cognitive functions, we speculate that sleep depth in the TPJ, as reflected by relative SWA, might serve as a dispositional indicator of social cognition ability, which is reflected in prosocial preferences. These findings contribute to the emerging framework explaining the link between sleep and prosocial behavior by shedding light on the underlying mechanisms.Significance Statement Sleep deprivation reportedly hampers prosocial behavior. Yet, sleep loss is not a regular occurrence. We studied participants without experimentally manipulating their sleep and conducted polysomnography along with a prosocial economic task. We found that higher relative slow-wave activity (an indicator of sleep depth) in the right TPJ - a brain region involved in social cognition - is associated with increased prosociality. This demonstrates a novel link between deep sleep neural markers and prosocial preferences. Furthermore, our study provides evidence about a possible neural mechanism that underlies the behavioral findings of previous studies on sleep deprivation and prosocial behavior. Our findings highlight the significance of sleep quality in shaping prosociality and the potential benefits of interventions targeting sleep quality to promote social capital

Exploring the impact of experimental sleep restriction and sleep deprivation on subjectively perceived sleep parameters

We aimed to investigate the effect of increased sleep pressure and shortened sleep duration on subjective sleep perception in relation to electroencephalographic sleep measures. We analyzed the data from a study in which 14 healthy male volunteers had completed a baseline assessment with 8 hr time in bed, a sleep deprivation (40 hr of wakefulness) and a sleep restriction protocol with 5 hr time in bed during 7 nights. In this work, we assessed perception index, derived through dividing the subjectively perceived total sleep time, wake after sleep onset and sleep latency duration by the objectively measured one at each condition. We found that total sleep time was subjectively underestimated at baseline and shifted towards overestimation during sleep restriction and after deprivation. This change in accuracy of subjective estimates was not associated with any changes in sleep architecture or sleep depth. Wake after sleep onset was significantly underestimated only during sleep restriction. Sleep latency was always overestimated subjectively without any significant change in this misperception across conditions. When comparing accuracy of subjective and actimetry estimates, subjective estimates regarding total sleep time and wake after sleep onset deviated less from electroencephalography derived measures during sleep restriction and after deprivation. We conclude that self-assessments and actimetry data of patients with chronic sleep restriction should be interpreted cautiously. The subjectively decreased perception of wake after sleep onset could lead to overestimated sleep efficiency in such individuals, whereas the underestimation of sleep time and overestimation of wake after sleep onset by actimetry could lead to further underestimated sleep duration