Influencing dreams through sensory stimulation: A systematic review.

Sleep is typically considered a state of disconnection from the environment, yet instances of external sensory stimuli influencing dreams have been reported for centuries. Explaining this phenomenon could provide valuable insight into dreams' generative and functional mechanisms, the factors that promote sleep continuity, and the processes that underlie conscious awareness. Moreover, harnessing sensory stimuli for dream engineering could benefit individuals suffering from dream-related alterations. This PRISMA-compliant systematic review assessed the current evidence concerning the influence of sensory stimulation on sleep mentation. We included 51 publications, of which 21 focused on auditory stimulation, ten on somatosensory stimulation, eight on olfactory stimulation, four on visual stimulation, two on vestibular stimulation, and one on multimodal stimulation. Furthermore, nine references explored conditioned associative stimulation: six focused on targeted memory reactivation protocols and three on targeted lucid reactivation protocols. The reported frequency of stimulus-dependent dream changes across studies ranged from 0 to ∼80%, likely reflecting a considerable heterogeneity of definitions and methodological approaches. Our findings highlight a lack of comprehensive understanding of the mechanisms, functions, and neurophysiological correlates of stimulus-dependent dream changes. We suggest that a paradigm shift is required for meaningful progress in this field.

Maturation-dependent changes in cortical and thalamic activity during sleep slow waves: Insights from a combined EEG-fMRI study.

INTRODUCTION: Studies using scalp EEG have shown that slow waves (0.5-4 Hz), the most prominent hallmark of NREM sleep, undergo relevant changes from childhood to adulthood, mirroring brain structural modifications and the acquisition of cognitive skills. Here we used simultaneous EEG-fMRI to investigate the cortical and subcortical correlates of slow waves in school-age children and determine their relative developmental changes. METHODS: We analyzed data from 14 school-age children with self-limited focal epilepsy of childhood who fell asleep during EEG-fMRI recordings. Brain regions associated with slow-wave occurrence were identified using a voxel-wise regression that also modelled interictal epileptic discharges and sleep spindles. At the group level, a mixed-effects linear model was used. The results were qualitatively compared with those obtained from 2 adolescents with epilepsy and 17 healthy adults. RESULTS: Slow waves were associated with hemodynamic-signal decreases in bilateral somatomotor areas. Such changes extended more posteriorly relative to those in adults. Moreover, the involvement of areas belonging to the default mode network changes as a function of age. No significant hemodynamic responses were observed in subcortical structures. However, we identified a significant correlation between age and thalamic hemodynamic changes. CONCLUSIONS: Present findings indicate that the somatomotor cortex may have a key role in slow-wave expression throughout the lifespan. At the same time, they are consistent with a posterior-to-anterior shift in slow-wave distribution mirroring brain maturational changes. Finally, our results suggest that slow-wave changes may not reflect only neocortical modifications but also the maturation of subcortical structures, including the thalamus.

Pulse Wave Amplitude Drops Index: A Biomarker of Cardiovascular Risk in Obstructive Sleep Apnea.

Rationale: It is currently unclear which patients with obstructive sleep apnea (OSA) are at increased cardiovascular risk. Objective: To investigate the value of pulse wave amplitude drops (PWADs), reflecting sympathetic activations and vasoreactivity, as a biomarker of cardiovascular risk in OSA. Methods: PWADs were derived from pulse oximetry-based photoplethysmography signals in three prospective cohorts: HypnoLaus (N = 1,941), the Pays-de-la-Loire Sleep Cohort (PLSC; N = 6,367), and "Impact of Sleep Apnea syndrome in the evolution of Acute Coronary syndrome. Effect of intervention with CPAP" (ISAACC) (N = 692). The PWAD index was the number of PWADs (>30%) per hour during sleep. All participants were divided into subgroups according to the presence or absence of OSA (defined as ⩾15 or more events per hour or <15/h, respectively, on the apnea-hypopnea index) and the median PWAD index. Primary outcome was the incidence of composite cardiovascular events. Measurements and Main Results: Using Cox models adjusted for cardiovascular risk factors (hazard ratio; HR [95% confidence interval]), patients with a low PWAD index and OSA had a higher incidence of cardiovascular events compared with the high-PWAD and OSA group and those without OSA in the HypnoLaus cohort (HR, 2.16 [1.07-4.34], P = 0.031; and 2.35 [1.12-4.93], P = 0.024) and in the PLSC (1.36 [1.13-1.63], P = 0.001; and 1.44 [1.06-1.94], P = 0.019), respectively. In the ISAACC cohort, the low-PWAD and OSA untreated group had a higher cardiovascular event recurrence rate than that of the no-OSA group (2.03 [1.08-3.81], P = 0.028). In the PLSC and HypnoLaus cohorts, every increase of 10 events per hour in the continuous PWAD index was negatively associated with incident cardiovascular events exclusively in patients with OSA (HR, 0.85 [0.73-0.99], P = 0.031; and HR, 0.91 [0.86-0.96], P < 0.001, respectively). This association was not significant in the no-OSA group and the ISAACC cohort. Conclusions: In patients with OSA, a low PWAD index reflecting poor autonomic and vascular reactivity was independently associated with a higher cardiovascular risk.

Origin, synchronization, and propagation of sleep slow waves in children.

STUDY OBJECTIVES: Sleep slow wave activity, as measured using EEG delta power (<4 Hz), undergoes significant changes throughout development, mirroring changes in brain function and anatomy. Yet, age-dependent variations in the characteristics of individual slow waves have not been thoroughly investigated. Here we aimed at characterizing individual slow wave properties such as origin, synchronization, and cortical propagation at the transition between childhood and adulthood. METHODS: We analyzed overnight high-density (256 electrodes) EEG recordings of healthy typically developing children (N = 21, 10.3 ± 1.5 years old) and young healthy adults (N = 18, 31.1 ± 4.4 years old). All recordings were preprocessed to reduce artifacts, and NREM slow waves were detected and characterized using validated algorithms. The threshold for statistical significance was set at p = 0.05. RESULTS: The slow waves of children were larger and steeper, but less widespread than those of adults. Moreover, they tended to mainly originate from and spread over more posterior brain areas. Relative to those of adults, the slow waves of children also displayed a tendency to more strongly involve and originate from the right than the left hemisphere. The separate analysis of slow waves characterized by high and low synchronization efficiency showed that these waves undergo partially distinct maturation patterns, consistent with their possible dependence on different generation and synchronization mechanisms. CONCLUSIONS: Changes in slow wave origin, synchronization, and propagation at the transition between childhood and adulthood are consistent with known modifications in cortico-cortical and subcortico-cortical brain connectivity. In this light, changes in slow-wave properties may provide a valuable yardstick to assess, track, and interpret physiological and pathological development.

Crossmodal plasticity following short-term monocular deprivation.

A brief period of monocular deprivation (MD) induces short-term plasticity of the adult visual system. Whether MD elicits neural changes beyond visual processing is yet unclear. Here, we assessed the specific impact of MD on neural correlates of multisensory processes. Neural oscillations associated with visual and audio-visual processing were measured for both the deprived and the non-deprived eye. Results revealed that MD changed neural activities associated with visual and multisensory processes in an eye-specific manner. Selectively for the deprived eye, alpha synchronization was reduced within the first 150 ms of visual processing. Conversely, gamma activity was enhanced in response to audio-visual events only for the non-deprived eye within 100-300 ms after stimulus onset. The analysis of gamma responses to unisensory auditory events revealed that MD elicited a crossmodal upweight for the non-deprived eye. Distributed source modeling suggested that the right parietal cortex played a major role in neural effects induced by MD. Finally, visual and audio-visual processing alterations emerged for the induced component of the neural oscillations, indicating a prominent role of feedback connectivity. Results reveal the causal impact of MD on both unisensory (visual and auditory) and multisensory (audio-visual) processes and, their frequency-specific profiles. These findings support a model in which MD increases excitability to visual events for the deprived eye and audio-visual and auditory input for the non-deprived eye.

Memory reactivations during sleep: a neural basis of dream experiences?

Newly encoded memory traces are spontaneously reactivated during sleep. Since their discovery in the 1990s, these memory reactivations have been discussed as a potential neural basis for dream experiences. New results from animal and human research, as well as from the rapidly growing field of sleep and dream engineering, provide essential insights into this question, and reveal both strong parallels and disparities between the two phenomena. We suggest that, although memory reactivations may contribute to subjective experiences across different states of consciousness, they are not likely to be the primary neural basis of dreaming. We identify important limitations in current research paradigms and suggest novel strategies to address this question empirically.

EEG cortical activity and connectivity correlates of early sympathetic response during cold pressor test.

Previous studies have identified several brain regions involved in the sympathetic response and its integration with pain, cognition, emotions and memory processes. However, little is known about how such regions dynamically interact during a sympathetic activation task. In this study, we analyzed EEG activity and effective connectivity during a cold pressor test (CPT). A source localization analysis identified a network of common active sources including the right precuneus (r-PCu), right and left precentral gyri (r-PCG, l-PCG), left premotor cortex (l-PMC) and left anterior cingulate cortex (l-ACC). We comprehensively analyzed the network dynamics by estimating power variation and causal interactions among the network regions through the direct directed transfer function (dDTF). A connectivity pattern dominated by interactions in [Formula: see text] (8-12) Hz band was observed in the resting state, with r-PCu acting as the main hub of information flow. After the CPT onset, we observed an abrupt suppression of such [Formula: see text]-band interactions, followed by a partial recovery towards the end of the task. On the other hand, an increase of [Formula: see text]-band (1-4) Hz interactions characterized the first part of CPT task. These results provide novel information on the brain dynamics induced by sympathetic stimuli. Our findings suggest that the observed suppression of [Formula: see text] and rise of [Formula: see text] dynamical interactions could reflect non-pain-specific arousal and attention-related response linked to stimulus' salience.

Sleep Power Topography in Children with Attention Deficit Hyperactivity Disorder (ADHD).

OBJECTIVE: Recent years saw an increasing interest towards sleep microstructure abnormalities in attention-deficit/hyperactivity disorder (ADHD). However, the existing literature on sleep electroencephalographic (EEG) power in ADHD is still controversial, often based on single electrode recordings, and mainly focused on slow wave activity (SWA) during NREM sleep. This study aimed to systematically investigate sleep power topography in all traditional frequency bands, in all sleep stages and across sleep cycles using high-density EEG (HD-EEG). METHOD: Thirty drug-naïve children with ADHD (10.5 ± 2.1 years, 21 male) and 23 typically developing (TD) control participants (mean age: 10.2 ± 1.6 years, 13 male) were included in the current analysis. Signal power topography was computed in classical frequency bands during sleep, contrasted between groups and sleep cycles, and correlated with measures of ADHD severity, cognitive functioning and estimated total sleep time. RESULTS: Compared to TD subjects, patients with ADHD consistently displayed a widespread increase in low-frequency activity (between 3 and 10 Hz) during NREM sleep, but not during REM sleep and wake before sleep onset. Such a difference involved a wide centro-posterior cluster of channels in the upper SWA range, in Theta, and low-Alpha. Between-group difference was maximal in sleep stage N3 in the first sleep cycle, and positively correlated with average total sleep time. CONCLUSIONS: These results support the concept that children with ADHD, compared to TD peers, have a higher sleep pressure and altered sleep homeostasis, which possibly interfere with (and delay) cortical maturation.

Local sleep: A new concept in brain plasticity.

Traditionally, sleep and wakefulness have been considered as two global, mutually exclusive states. However, this view has been challenged by the discovery that sleep and wakefulness are actually locally regulated and that islands of these two states may often coexist in the same individual. Importantly, such a local regulation seems to be the key for many essential functions of sleep, including the maintenance of cognitive efficiency and the consolidation of new skills and memories. Indeed, local changes in sleep-related oscillations occur in brain areas that are used and involved in learning during wakefulness. In turn, these changes directly modulate experience-dependent brain adaptations and the consolidation of newly acquired memories. In line with these observations, alterations in the regional balance between wake- and sleep-like activity have been shown to accompany many pathologic conditions, including psychiatric and neurologic disorders. In the last decade, experimental research has started to shed light on the mechanisms involved in the local regulation of sleep and wakefulness. The results of this research have opened new avenues of investigation regarding the function of sleep and have revealed novel potential targets for the treatment of several pathologic conditions.

Emotion Regulation Failures Are Preceded by Local Increases in Sleep-like Activity.

Emotion self-regulation relies both on cognitive and behavioral strategies implemented to modulate the subjective experience and/or the behavioral expression of a given emotion. Although it is known that a network encompassing fronto-cingulate and parietal brain areas is engaged during successful emotion regulation, the functional mechanisms underlying failures in emotion suppression (ES) are still unclear. In order to investigate this issue, we analyzed video and high-density EEG recordings of 20 healthy adult participants during an ES and a free expression task performed on two consecutive days. Changes in facial expression during ES, but not free expression, were preceded by local increases in sleep-like activity (1-4 Hz) in brain areas responsible for emotional suppression, including bilateral anterior insula and anterior cingulate cortex, and in right middle/inferior frontal gyrus (p < .05, corrected). Moreover, shorter sleep duration the night before the ES experiment correlated with the number of behavioral errors (p = .03) and tended to be associated with higher frontal sleep-like activity during ES failures (p = .09). These results indicate that local sleep-like activity may represent the cause of ES failures in humans and may offer a functional explanation for previous observations linking lack of sleep, changes in frontal activity, and emotional dysregulation.

The Language of Dreams: Application of Linguistics-Based Approaches for the Automated Analysis of Dream Experiences.

The study of dreams represents a crucial intersection between philosophical, psychological, neuroscientific, and clinical interests. Importantly, one of the main sources of insight into dreaming activity are the (oral or written) reports provided by dreamers upon awakening from their sleep. Classically, two main types of information are commonly extracted from dream reports: structural and semantic, content-related information. Extracted structural information is typically limited to the simple count of words or sentences in a report. Instead, content analysis usually relies on quantitative scores assigned by two or more (blind) human operators through the use of predefined coding systems. Within this review, we will show that methods borrowed from the field of linguistic analysis, such as graph analysis, dictionary-based content analysis, and distributional semantics approaches, could be used to complement and, in many cases, replace classical measures and scales for the quantitative structural and semantic assessment of dream reports. Importantly, these methods allow the direct (operator-independent) extraction of quantitative information from language data, hence enabling a fully objective and reproducible analysis of conscious experiences occurring during human sleep. Most importantly, these approaches can be partially or fully automatized and may thus be easily applied to the analysis of large datasets.

Role of corpus callosum in sleep spindle synchronization and coupling with slow waves.

Sleep spindles of non-REM sleep are transient, waxing-and-waning 10-16 Hz EEG oscillations, whose cortical synchronization depends on the engagement of thalamo-cortical loops. However, previous studies in animal models lacking the corpus callosum due to agenesis or total callosotomy and in humans with agenesis of the corpus callosum suggested that cortico-cortical connections may also have a relevant role in cortical (inter-hemispheric) spindle synchronization. Yet, most of these works did not provide direct quantitative analyses to support their observations. By studying a rare sample of callosotomized, split-brain patients, we recently demonstrated that the total resection of the corpus callosum is associated with a significant reduction in the inter-hemispheric propagation of non-REM slow waves. Interestingly, sleep spindles are often temporally and spatially grouped around slow waves (0.5-4 Hz), and this coordination is thought to have an important role in sleep-dependent learning and memory consolidation. Given these premises, here we set out to investigate whether total callosotomy may affect the generation and spreading of sleep spindles, as well as their coupling with sleep slow waves. To this aim, we analysed overnight high-density EEG recordings (256 electrodes) collected in five patients who underwent total callosotomy due to drug-resistant epilepsy (age 40-53, two females), three non-callosotomized neurological patients (age 44-66, two females), and in a sample of 24 healthy adult control subjects (age 20-47, 13 females). Individual sleep spindles were automatically detected using a validated algorithm and their properties and topographic distributions were computed. All analyses were performed with and without a regression-based adjustment accounting for inter-subject age differences. The comparison between callosotomized patients and healthy subjects did not reveal systematic variations in spindle density, amplitude or frequency. However, callosotomized patients were characterized by a reduced spindle duration, which could represent the result of a faster desynchronization of spindle activity across cortical areas of the two hemispheres. In contrast with our previous findings regarding sleep slow waves, we failed to detect in callosotomized patients any clear, systematic change in the inter-hemispheric synchronization of sleep spindles. In line with this, callosotomized patients were characterized by a reduced extension of the spatial association between temporally coupled spindles and slow waves. Our findings are consistent with a dependence of spindles on thalamo-cortical rather than cortico-cortical connections in humans, but also revealed that, despite their temporal association, slow waves and spindles are independently regulated in terms of topographic expression.

Cortical and subcortical hemodynamic changes during sleep slow waves in human light sleep.

EEG slow waves, the hallmarks of NREM sleep are thought to be crucial for the regulation of several important processes, including learning, sensory disconnection and the removal of brain metabolic wastes. Animal research indicates that slow waves may involve complex interactions within and between cortical and subcortical structures. Conventional EEG in humans, however, has a low spatial resolution and is unable to accurately describe changes in the activity of subcortical and deep cortical structures. To overcome these limitations, here we took advantage of simultaneous EEG-fMRI recordings to map cortical and subcortical hemodynamic (BOLD) fluctuations time-locked to slow waves of light sleep. Recordings were performed in twenty healthy adults during an afternoon nap. Slow waves were associated with BOLD-signal increases in the posterior brainstem and in portions of thalamus and cerebellum characterized by preferential functional connectivity with limbic and somatomotor areas, respectively. At the cortical level, significant BOLD-signal decreases were instead found in several areas, including insula and somatomotor cortex. Specifically, a slow signal increase preceded slow-wave onset and was followed by a delayed, stronger signal decrease. Similar hemodynamic changes were found to occur at different delays across most cortical brain areas, mirroring the propagation of electrophysiological slow waves, from centro-frontal to inferior temporo-occipital cortices. Finally, we found that the amplitude of electrophysiological slow waves was positively related to the magnitude and inversely related to the delay of cortical and subcortical BOLD-signal changes. These regional patterns of brain activity are consistent with theoretical accounts of the functions of sleep slow waves.

Cross-participant prediction of vigilance stages through the combined use of wPLI and wSMI EEG functional connectivity metrics.

Functional connectivity (FC) metrics describe brain inter-regional interactions and may complement information provided by common power-based analyses. Here, we investigated whether the FC-metrics weighted Phase Lag Index (wPLI) and weighted Symbolic Mutual Information (wSMI) may unveil functional differences across four stages of vigilance-wakefulness (W), NREM-N2, NREM-N3, and REM sleep-with respect to each other and to power-based features. Moreover, we explored their possible contribution in identifying differences between stages characterized by distinct levels of consciousness (REM+W vs. N2+N3) or sensory disconnection (REM vs. W). Overnight sleep and resting-state wakefulness recordings from 24 healthy participants (27 ± 6 years, 13F) were analyzed to extract power and FC-based features in six classical frequency bands. Cross-validated linear discriminant analyses (LDA) were applied to investigate the ability of extracted features to discriminate (1) the four vigilance stages, (2) W+REM vs. N2+N3, and (3) W vs. REM. For the four-way vigilance stages classification, combining features based on power and both connectivity metrics significantly increased accuracy relative to considering only power, wPLI, or wSMI features. Delta-power and connectivity (0.5-4 Hz) represented the most relevant features for all the tested classifications, in line with a possible involvement of slow waves in consciousness and sensory disconnection. Sigma-FC, but not sigma-power (12-16 Hz), was found to strongly contribute to the differentiation between states characterized by higher (W+REM) and lower (N2+N3) probabilities of conscious experiences. Finally, alpha-FC resulted as the most relevant FC-feature for distinguishing among wakefulness and REM sleep and may thus reflect the level of disconnection from the external environment.

Risk factors of excessive daytime sleepiness in a prospective population-based cohort.

Although excessive daytime sleepiness is commonly evaluated in clinical and research settings using the Epworth Sleepiness Scale, few studies have assessed the factors associated with its incidence in the general population. We prospectively investigated the predictors of incident and persistent excessive daytime sleepiness in 2,751 subjects (46.1% men, mean age 56.0 ± 9.8 years) from the CoLaus-PsyCoLaus population-based cohort (Lausanne, Switzerland) over 5 years. Participants completed the Epworth Sleepiness Scale and the Pittsburgh Sleep Quality Index, and underwent a full clinical evaluation at baseline and 5 years afterwards. Ambulatory polysomnography was performed at baseline in a sub-sample of 1,404 subjects. Among the 2,438 subjects without excessive daytime sleepiness (Epworth Sleepiness Scale ≤ 10) at baseline, the 5-year incidence of excessive daytime sleepiness was 5.1% (n = 124). Multivariate logistic regression revealed that male sex, depressive symptoms, reported poor sleep quality and moderate to severe obstructive sleep apnea were independent predictors of incident excessive daytime sleepiness, while older age, moderate coffee consumption, periodic leg movement during sleep and hypertension were independent protective factors. Stratified analysis according to sex and age showed some distinctive associations. Among the 313 patients with excessive daytime sleepiness at baseline, 137 (43.8%) had persistent excessive daytime sleepiness 5 years later. Our findings provide new insights into the predictors of incident excessive daytime sleepiness, but interventional studies are needed to understand the impact of treating these risk factors on the incidence of excessive daytime sleepiness.

Integrity of Corpus Callosum Is Essential for theCross-Hemispheric Propagation of Sleep Slow Waves:A High-Density EEG Study in Split-Brain Patients.

The slow waves of non-rapid eye movement (NREM) sleep reflect experience-dependent plasticity and play a direct role in the restorative functions of sleep. Importantly, slow waves behave as traveling waves, and their propagation is assumed to occur through cortico-cortical white matter connections. In this light, the corpus callosum (CC) may represent the main responsible for cross-hemispheric slow-wave propagation. To verify this hypothesis, we performed overnight high-density (hd)-EEG recordings in five patients who underwent total callosotomy due to drug-resistant epilepsy (CPs; two females), in three noncallosotomized neurologic patients (NPs; two females), and in a sample of 24 healthy adult subjects (HSs; 13 females). In all CPs slow waves displayed a significantly reduced probability of cross-hemispheric propagation and a stronger inter-hemispheric asymmetry. In both CPs and HSs, the incidence of large slow waves within individual NREM epochs tended to differ across hemispheres, with a relative overall predominance of the right over the left hemisphere. The absolute magnitude of this asymmetry was greater in CPs relative to HSs. However, the CC resection had no significant effects on the distribution of slow-wave origin probability across hemispheres. The present results indicate that CC integrity is essential for the cross-hemispheric traveling of slow waves in human sleep, which is in line with the assumption of a direct relationship between white matter integrity and slow-wave propagation. Our findings also revealed a residual cross-hemispheric slow-wave propagation that may rely on alternative pathways, including cortico-subcortico-cortical loops. Finally, these data indicate that the lack of the CC does not lead to differences in slow-wave generation across brain hemispheres.SIGNIFICANCE STATEMENT The slow waves of NREM sleep behave as traveling waves, and their propagation has been suggested to reflect the integrity of white matter cortico-cortical connections. To directly assess this hypothesis, here we investigated the role of the corpus callosum in the cortical spreading of NREM slow waves through the study of a rare population of totally callosotomized patients. Our results demonstrate a causal role of the corpus callosum in the cross-hemispheric traveling of sleep slow waves. Additionally, we found that callosotomy does not affect the relative tendency of each hemisphere at generating slow waves. Incidentally, we also found that slow waves tend to originate more often in the right than in the left hemisphere in both callosotomized and healthy adult individuals.

Electroencephalographic changes associated with subjective under- and overestimation of sleep duration.

Feeling awake although sleep recordings indicate clear-cut sleep sometimes occurs in good sleepers and to an extreme degree in patients with so-called paradoxical insomnia. It is unknown what underlies sleep misperception, as standard polysomnographic (PSG) parameters are often normal in these cases. Here we asked whether regional changes in brain activity could account for the mismatch between objective and subjective total sleep times (TST). To set cutoffs and define the norm, we first evaluated sleep perception in a population-based sample, consisting of 2,092 individuals who underwent a full PSG at home and estimated TST the next day. We then compared participants with a low mismatch (normoestimators, n = 1,147, ±0.5 SD of mean) with those who severely underestimated (n = 52, <2.5th percentile) or overestimated TST (n = 53, >97.5th percentile). Compared with normoestimators, underestimators displayed higher electroencephalographic (EEG) activation (beta/delta power ratio) in both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep, while overestimators showed lower EEG activation (significant in REM sleep). To spatially map these changes, we performed a second experiment, in which 24 healthy subjects and 10 insomnia patients underwent high-density sleep EEG recordings. Similarly to underestimators, patients displayed increased EEG activation during NREM sleep, which we localized to central-posterior brain areas. Our results indicate that a relative shift from low- to high-frequency spectral power in central-posterior brain regions, not readily apparent in conventional PSG parameters, is associated with underestimation of sleep duration. This challenges the concept of sleep misperception, and suggests that instead of misperceiving sleep, insomnia patients may correctly perceive subtle shifts toward wake-like brain activity.