Duration of N1 sleep is a factor for excessive daytime sleepiness in epilepsy patients with interictal epileptiform discharges: A polysomnographic study.

Purpose: This study aimed to identify the occurrence of excessive daytime sleepiness (EDS) in epilepsy patients with interictal epileptiform discharges and to explore the impact of interictal sleep architecture and sleep-related events on EDS. Methods: This study included 101 epilepsy patients with interictal epileptiform discharges (IED) and 100 control patients who underwent simultaneous polysomnography and video ambulatory electroencephalography for >7 h throughout a single night. Multiple sleep latency tests were used to assess EDS. Comorbid EDS was present in 25 and 11 patients in the IED epilepsy and control groups, respectively. In addition, univariate and multivariate logistic regression analyses were performed to explore the factors influencing EDS. Results: The epilepsy group had a higher prevalence of comorbid EDS and shorter R sleep duration. Univariate logistic regression analysis indicated that an increased risk of EDS may be associated with prolonged N1 sleep duration, higher arousal index, lower mean saturation (mSaO2), higher oxygen desaturation index (ODI), and duration of wake after sleep onset (WASO). Multivariate logistic regression analysis revealed that N1 sleep duration was significantly correlated with EDS. Conclusion: In epilepsy patients with IED, the arousal index, mSaO2, ODI, and duration of WASO were weakly correlated with EDS, and the duration of N1 sleep demonstrated a significant positive correlation with EDS, which requires further research.

Embracing sleep-onset complexity.

Sleep is crucial for many vital functions and has been extensively studied. By contrast, the sleep-onset period (SOP), often portrayed as a mere prelude to sleep, has been largely overlooked and remains poorly characterized. Recent findings, however, have reignited interest in this transitional period and have shed light on its neural mechanisms, cognitive dynamics, and clinical implications. This review synthesizes the existing knowledge about the SOP in humans. We first examine the current definition of the SOP and its limits, and consider the dynamic and complex electrophysiological changes that accompany the descent to sleep. We then describe the interplay between internal and external processing during the wake-to-sleep transition. Finally, we discuss the putative cognitive benefits of the SOP and identify novel directions to better diagnose sleep-onset disorders.

A two-branch trade-off neural network for balanced scoring sleep stages on multiple cohorts.

Introduction: Automatic sleep staging is a classification process with severe class imbalance and suffers from instability of scoring stage N1. Decreased accuracy in classifying stage N1 significantly impacts the staging of individuals with sleep disorders. We aim to achieve automatic sleep staging with expert-level performance in both N1 stage and overall scoring. Methods: A neural network model combines an attention-based convolutional neural network and a classifier with two branches is developed. A transitive training strategy is employed to balance universal feature learning and contextual referencing. Parameter optimization and benchmark comparisons are conducted using a large-scale dataset, followed by evaluation on seven datasets in five cohorts. Results: The proposed model achieves an accuracy of 88.16%, Cohen's kappa of 0.836, and MF1 score of 0.818 on the SHHS1 test set, also with comparable performance to human scorers in scoring stage N1. Incorporating multiple cohort data improves its performance. Notably, the model maintains high performance when applied to unseen datasets and patients with neurological or psychiatric disorders. Discussion: The proposed algorithm demonstrates strong performance and generalizablility, and its direct transferability is noteworthy among similar studies on automated sleep staging. It is publicly available, which is conducive to expanding access to sleep-related analysis, especially those associated with neurological or psychiatric disorders.

Memory loss at sleep onset.

Every night, we pass through a transitory zone at the borderland between wakefulness and sleep, named the first stage of nonrapid eye movement sleep (N1). N1 sleep is associated with increased hippocampal activity and dream-like experiences that incorporate recent wake materials, suggesting that it may be associated with memory processing. Here, we investigated the specific contribution of N1 sleep in the processing of memory traces. Participants were asked to learn the precise locations of 48 objects on a grid and were then tested on their memory for these items before and after a 30-min rest during which participants either stayed fully awake or transitioned toward N1 or deeper (N2) sleep. We showed that memory recall was lower (10% forgetting) after a resting period, including only N1 sleep compared to N2 sleep. Furthermore, the ratio of alpha/theta power (an electroencephalography marker of the transition toward sleep) correlated negatively with the forgetting rate when taking into account all sleepers (N1 and N2 groups combined), suggesting a physiological index for memory loss that transcends sleep stages. Our findings suggest that interrupting sleep onset at N1 may alter sleep-dependent memory consolidation and promote forgetting.

Predicting the loss of responsiveness when falling asleep in humans.

Falling asleep is a dynamical process that is poorly defined. The period preceding sleep, characterized by the progressive alteration of behavioral responses to the environment, which may last several minutes, has no electrophysiological definition, and is embedded in the first stage of sleep (N1). We aimed at better characterizing this drowsiness period looking for neurophysiological predictors of responsiveness using electro and magneto-encephalography. Healthy participants were recorded when falling asleep, while they were presented with continuous auditory stimulations and asked to respond to deviant sounds. We analysed brain responses to sounds and markers of ongoing activity, such as information and connectivity measures, in relation to rapid fluctuations of brain rhythms observed at sleep onset and participants' capabilities to respond. Results reveal a drowsiness period distinct from wakefulness and sleep, from alpha rhythms to the first sleep spindles, characterized by diverse and transient brain states that come on and off at the scale of a few seconds and closely reflects, mainly through neural processes in alpha and theta bands, decreasing probabilities to be responsive to external stimuli. Results also show that the global P300 was only present in responsive trials, regardless of vigilance states. A better consideration of the drowsiness period through a formalized classification and its specific brain markers such as described here should lead to significant advances in vigilance assessment in the future, in medicine and ecological environments.