Distinguishing epileptic seizures from parasomnias is challenging due to overlapping motor features. This study evaluated a SlowFast deep learning model using video recordings of 167 individuals to classify Sleep-Related Hypermotor Epilepsy, Disorders of Arousal, and REM Sleep Behavior Disorder. The model achieved a mean accuracy of 83.3% across three data splits. This work represents an initial step toward developing automated tools to support clinicians in assessing sleep-related motor events.
Parkinson's disease (PD) can progress to an advanced stage characterized by motor fluctuations and or levodopa-induced dyskinesia (LID). Although both motor fluctuations and LID reflect altered dopaminergic reactivity, LID has been specifically linked to disrupted synaptic plasticity. Slow wave sleep (N3) reflects homeostatic processes and may offer neurophysiological markers related to the motor phenotype in PD. This study tested whether overnight dynamics of N3 slow-wave activity (SWA) and cortical complexity, i.e., sample entropy (SampEn) differ between PD patients with and without dyskinesia, and whether these dynamics relate to dyskinesia severity. Polysomnography (PSG) was analyzed in seven healthy volunteers and two PD cohorts: non-dyskinetic (PDdys-, n = 8), and dyskinetic (PDdys+, n = 10). NREM sleep was divided into 10 segments; SWA and SampEn were mapped across the scalp and summarized in Early/Late N3 windows. Within-group Late-Early changes were assessed using paired permutation tests with TFCE correction. Late-Early changes were then compared between groups, and associations with the functional impact of dyskinesia (MDS-UPDRS-Part IV- item4.2) were examined in PDdys+. In CTL, SWA decreased and SampEn increased overnight (pTFCE < 0.001). PDdys- showed a similar but more restricted pattern, whereas PDdys+ showed no significant Late-Early change in either metric. In PDdys+, Late-Early SampEn change was inversely related to dyskinesia severity (r = -0.75, pHolm = 0.068) and remained strong after adjustment for SWA (r = -0.90, pHolm = 0.018). These findings suggest that entropy-based measures capture dyskinesia-related alterations in nocturnal dynamics beyond SWA, providing a quantitative link between sleep neurophysiology and daytime motor complications in PD.
PURPOSE:Positional obstructive sleep apnea (POSA) is the most common phenotype of obstructive sleep apnea, yet patient selection for positional therapy (PT) remains suboptimal. With this analysis we aimed to clarify how many patients with POSA may not require PT because they do not habitually sleep supine at home, and how many fail vibrotactile PT despite appropriate indication. METHODS:We conducted a retrospective observational study of consecutive adults with POSA evaluated at a tertiary sleep center between 2021 and 2024. All patients underwent a home-based trial with a neck-based vibrotactile positional therapy device (Night Shift™), consisting of monitoring mode followed by therapy mode. Outcomes included the proportion of non-supine sleepers at home, failure rate of vibrotactile PT, device compliance and differences in supine sleep time between diagnostic testing and home monitoring. RESULTS:Of 92 screened patients, 74 met inclusion criteria (mean age 60.3 ± 13.2 years; mean AHI 22.9 ± 13.3 events/h). Fifteen percent (11/74) did not habitually sleep supine at home, indicating no clinical need for PT, and an additional 14.8% (11/74) failed vibrotactile PT. Overall, 30% of patients were either unlikely to benefit from PT or failed therapy. Non-response was frequently associated with psychotropic or sedative medication use and neurological or sleep-related comorbidities. CONCLUSION:A substantial proportion of patients diagnosed with POSA either do not require or fail vibrotactile treatment in real-world conditions. Incorporating a brief home monitoring and therapy trial into routine clinical practice may optimize patient selection, reduce unnecessary costs, and improve personalized management of POSA.
Disorders of arousal (DOA), including sleepwalking, sleep terrors, and confusional arousals, are characterized by complex behaviors emerging from non-rapid eye movement (NREM) sleep. Although these conditions are defined by abnormal arousal, their neurobiological basis remains poorly understood, and the contribution of neuromodulatory systems, particularly the locus coeruleus-noradrenaline (LC-NA) system, has received limited attention. Here, we present a hypothesis-driven conceptual framework integrating existing evidence from neurophysiology, neuroimaging, autonomic regulation, and genetics. The LC-NA is organized into partially segregated modules projecting to distinct cortical and subcortical targets with different kinetics. We propose that under conditions such as sleep deprivation or stress, these modules become asynchronously engaged due to use-dependent fatigue. Motor- and limbic-projecting ensembles reactivate more readily, while prefrontal-projecting neurons remain functionally disengaged. This imbalance produces asynchronous cortical arousal, allowing complex motor and emotional behaviors to occur without full cognitive integration. This framework generates testable predictions and conceptualizes DOA as manifestations of arousal instability during NREM sleep, driven by intrinsic modular LC dynamics that modulate transitions between sleep and wakefulness. More broadly, it provides insight into how disrupted neuromodulatory coordination affects the integration of conscious states.
Abstract Slow-wave activity during sleep facilitates synaptic downscaling, while theta activity during wakefulness reflects synaptic upscaling, and both processes may be altered in levodopa-induced dyskinesia (LID) in Parkinson’s disease (PD). We compared actigraphy and high-density EEG in 12 healthy volunteers and three PD cohorts: early stage (EPD, n = 12), advanced non-dyskinetic (ADV, n = 13), and advanced dyskinetic (DYS, n = 11). Participants completed one week of actigraphy monitoring, followed by two resting-state EEG recordings conducted separately in the morning and evening. Wake-theta activity was analyzed using both linear and linear mixed-effects models, adjusted for age/sex, plus cluster-based non-parametric statistics, then related to clinical variables, and actigraphy-derived sleep metrics via partial correlations. Dyskinetic patients showed marked sleep disruption, elevated morning theta compared with controls (p = 0.006, d = 1.54) and EPD (p = 0.03, d = 0.85), along with a significantly reduced diurnal theta build-up compared with controls (p = 0.009, d = 1.57). EPD and ADV groups showed preserved diurnal increases. In dyskinetic patients, a higher levodopa equivalent daily dose (LEDD) was correlated with higher morning theta (ρ = 0.70, p = 0.023, pFDR=0.046) and smaller diurnal theta increases (ρ = −0.77, p = 0.009, pFDR=0.046). Relationships between theta and actigraphy-derived sleep metrics were weaker and inconsistent across groups. These findings suggest a dyskinesia-specific profile of impaired wake-related theta homeostasis, motivating longitudinal studies combining polysomnography and waking EEG.
BACKGROUND:The cyclic alternating pattern (CAP) is a key marker of NREM sleep microstructure, reflecting the balance between sleep-protective (A1) and arousal-promoting (A2/A3) processes. However, normative spectral and topographic data for CAP subtypes during development are limited, and high-density EEG (HD-EEG) mapping in children is lacking. This study aimed to characterize the scalp topography and spectral properties of CAP A subtypes in typically developing children and to assess their overnight dynamics. METHODS:Nineteen typically developing children (mean age 10.2 years, range 8-13.7; 10 females) underwent overnight video-polysomnography with 256-channel HD-EEG. Power spectral density was estimated using Welch's method for CAP A1 (0.5-2.5 Hz), A2-low (0.5-2.5 Hz), A2-high (11-14 Hz), and A3 (11-14 Hz). Topographic distributions were computed across the night and compared between early and late NREM sleep using linear mixed-effects models with permutation-based TFCE correction. RESULTS:A1 and A2-low activity showed maximal power over fronto-central and centro-parietal midline regions and was significantly higher during early compared to late night. In contrast, A2-high and A3 activity displayed a predominantly frontal distribution and increased during the late night. High-frequency components of A2 and A3 peaked within the 11-14 Hz range, differing from the alpha-band activity typically reported in adults. CONCLUSIONS:This exploratory study characterises the scalp topography and spectral properties of CAP A subtypes in typically developing children using HD-EEG. Slow-frequency CAP activity declined across the night, consistent with homeostatic processes, whereas faster components showed a frontal predominance and a late-night increase. These findings highlight developmental differences in CAP organization and provide preliminary reference data for paediatric sleep research, which require confirmation in larger, multicentre cohorts.
Disorders of arousal (DOA) are parasomnias occurring during Non-REM Sleep (NREM), stemming from incomplete arousal from slow wave sleep and resulting in diverse, complex emotional and motor behaviours. Growing evidence suggests that distinct psychopathological traits play a role in the multifaceted genesis of these occurrences. This multicentre study aims to characterize the personality profiles of adults with and without DOA using the Temperament and Character Inventory-Revised. We included 39 patients diagnosed with DOA (mean age = 30.9 ± 10.2 years, 22 females) and 40 healthy control subjects matched for age and gender (mean age of 32.4 ± 11.6 years, 21 females). Participants completed the Paris Arousal Disorder Severity Scale, the Epworth Sleepiness Scale, the Sleep Condition Indicator, and the Temperament and Character Inventory-Revised. Higher levels of Harm Avoidance, Reward Dependence, and Persistence were predictive of the occurrence of DOA, as were elevated Anticipatory Worry and Attachment, and low Self-directedness. These findings support the hypothesis that certain psychobiological personality traits may be associated with the occurrence of DOA. To deepen our understanding, prospective studies are essential, aiming to delve into the causal relationship between the psychopathological profile and the clinical manifestation of DOA and assess the impact of targeted psychological interventions on DOA symptomatology.
STUDY OBJECTIVES:To characterize source-level cortical oscillatory dynamics before and during disorders of arousal (DoA) compared with physiological motor arousals in children and adults. MATERIALS AND METHODS:Nineteen children (10.9 ± 3.0 years) and 22 adults (30.3 ± 5.2 years) with DoA underwent 256-channel high-density EEG with video-polysomnography. Source-space spectral analysis in delta (0.5-4 Hz) and beta (18-30 Hz) bands was computed during stable slow-wave-sleep (-3 to -2 minutes before movement onset) and from -5 seconds to +15 seconds around movement onset for 84 DoA episodes and 146 physiological motor arousals. Linear mixed-effects models with permutation-based cluster correction were applied. RESULTS:Four reproducible cortical hallmarks emerged across age groups: (1) a widespread pre-onset increase in beta and delta relative to slow-wave-sleep; (2) sustained frontal delta enhancement over anterior cingulate, dorsomedial and ventromedial prefrontal, frontopolar, and orbitofrontal cortices; (3) concurrent centro-parietal delta suppression spanning posterior cingulate, precuneus, superior parietal, sensorimotor, and supplementary motor regions; and (4) persistent bilateral beta enhancement. Compared with physiological arousals, DoA arose from a "sleepier" background (higher delta, lower beta) and displayed greater beta coexisting with frontal delta persistence. Children showed broader pre-onset delta effects and more diffuse post-onset persistence, whereas adults exhibited a more anteriorly confined pattern. CONCLUSION:DoA display a reproducible, age-invariant cortical signature, consistent with a spatially organized failure of arousal integration: posterior sensorimotor and awareness circuits partially reactivate, while anterior executive and emotion-regulatory regions remain sleep-like. These spatiotemporal fingerprints position hd-EEG source analysis as a translational tool for mechanistically informed diagnostic and therapeutic development.
Insufficient sleep syndrome (ISS) and narcolepsy type 1 (NT1) both feature excessive daytime sleepiness (EDS), yet they differ in etiology and nighttime sleep architecture. We compared clinical characteristics, video-polysomnography (v-PSG), Multiple Sleep Latency Test (MSLT), and actigraphy in ISS and NT1, to better define ISS and differentiate the two disorders. We retrospectively screened patients from a Sleep Medicine Unit who had a confirmed diagnosis of ISS (n = 23) or NT1 (n = 9) and underwent v-PSG, MSLT, and actigraphy. All patients were drug-free, and those with comorbid sleep disorders were excluded. Clinical data were collected through structured interviews, sleep diaries, and standardized questionnaires. Subjective EDS, reported by both ISS and NT1 groups, was similar in severity. MSLT showed that nearly one-third of ISS patients exhibited sleep-onset REM periods (SOREMPs), highlighting the risk of overlap with NT1. In v-PSG, ISS was characterized by high sleep efficiency and a low arousal index; no major differences in sleep parameters emerged between ISS and NT1. Actigraphy provided relevant data: ISS displayed weekday sleep restriction with weekend compensation, whereas NT1 showed fragmented but prolonged nighttime sleep and more frequent daytime naps. Overall, the variability in sleep patterns (time in bed and total sleep time) was more pronounced in ISS on weekends, whereas NT1's hallmark was nighttime fragmentation. While ISS and NT1 overlap in EDS, they differ in the organization of sleep-wake rhythms. Actigraphy, highlighting weekday-weekend changes in ISS and fragmented nighttime sleep in NT1, may be pivotal for differential diagnosis.
Although not included in current diagnostic criteria, sleep disturbances are common in patients with schizophrenia (SCZ) and significantly impact their cognitive function and clinical outcomes. Among sleep disturbances, abnormalities in sleep spindles—non-rapid eye movement thalamocortical oscillations essential for sleep stability and memory consolidation—have emerged as potential neurophysiological biomarkers of SCZ.Sleep spindle deficits, particularly reduced density and duration, are consistently observed across illness stages and correlate with cognitive impairments, including working memory and attentional deficits, in individuals with SCZ. Spindle abnormalities reflect disruptions in thalamocortical connectivity, especially within the thalamic reticular nucleus, and are linked to dysfunction in GABAergic (gamma-aminobutyric acidergic) and glutamatergic signaling. Genetic studies further indicate that sleep spindle characteristics are associated with SCZ risk variants, reinforcing their putative role as heritable biomarkers of the disorder.Despite strong evidence supporting the role of spindle deficits in the development and manifestation of SCZ, methodological inconsistencies and a lack of standardized assessment protocols limit their clinical application. In this review, we summarize the neurophysiological basis of spindle deficits in SCZ, discuss their cognitive and clinical implications, highlight the need for standardized spindle measurements, and evaluate emerging therapeutic strategies, including pharmacological modulation, transcranial stimulation, and closed-loop auditory stimulation. Although preliminary, the reviewed evidence suggests that future spindle-informed research could enhance diagnostic precision and potentially lead to the discovery of novel therapeutic strategies for SCZ.
Disorders of arousal (DoA), a group of Non-Rapid Eye Movement parasomnias—including sleepwalking, night terrors, and confusional arousals—arise from incomplete awakenings during slow-wave sleep, yet their neural signatures remain poorly defined. Using high-density EEG and source-space spectral analysis in both children and adults, we mapped cortical dynamics in the seconds before and after DoA onset and compared them to physiological motor arousals. Across ages, DoA episodes emerged from a globally less activated cortical state, with pre-onset surges in delta and beta power peaking in premotor, orbitofrontal, and anterior cingulate cortices. After onset, episodes showed widespread beta enhancement and focal delta suppression in sensorimotor and parietal associative regions relative to stable slow-wave sleep, alongside sustained frontal delta and beta activity compared with physiological motor arousals. These age-invariant spatial patterns identify a stable neurophysiological signature of DoA, supporting the concept of local sleep–wake dissociation. Our findings provide a framework for mechanistic models and potential biomarkers to modulate, predict, and differentiate DoA from other nocturnal events. ### Competing Interest Statement The authors have declared no competing interest. EOC Young Researchers Grant 2023
BACKGROUND:While changes in sleep architecture during depression and mania are well-established, the extent to which they persist during euthymia in Bipolar Disorders (BD) remains unclear. Here we investigate pre-sleep cortical arousal and its correlation with sleep architecture and subjective sleep quality in BD patients. METHODS:Subjective sleep measures and whole-night, high-density sleep electroencephalography (EEG) recordings were obtained from 16 euthymic BD patients and 16 age and sex-matched healthy control subjects. Sleep architecture was determined according to standard guidelines and power analysis was computed to compare mean group 0.5-80 Hz frequency bands in the EEG signal preceding sleep onset. RESULTS:Despite the absence of disturbances in subjective sleep, euthymic BD patients exhibited heightened sleep onset latency (52,91 ± 60,3 vs 21,76 ± 29,71, p = 0,018), REM density (2,65 ± 1,47 vs 1,52 ± 1,17, p = 0,022), and poorer sleep efficiency (0,64 ± 0,15 vs 0,74 ± 0,21, p = 0,032) compared to healthy controls. Total sleep time and durations of sleep substages did not differ between the groups. Additionally, our findings revealed increased pre-sleep gamma power in left frontotemporal areas among BD patients (p = 0.005), which exhibited an inverse relationship with sleep efficiency that approached significance (r = -0.497, p = 0.050). CONCLUSION:Our findings suggest an alteration in sleep onset, efficiency, and REM density in euthymic BD patients, in the context of a preserved sleep duration. Some of these changes may be associated with a neural signature of cortical arousal that influences sleep quality.
This systematic review analyzed 37 studies on sleep-disordered breathing during pregnancy, involving over 7000 women, predominantly pregnant, with a subgroup of non-pregnant controls. Most studies were conducted in the United States, using in-laboratory polysomnography and focusing on the third trimester. The meta-analysis estimated a prevalence of nearly 20 %, although results showed considerable heterogeneity, reflecting variations in study methodologies, diagnostic criteria, and sample characteristics.Sleep-disordered breathing was generally mild, with body mass index identified as the main risk factor, while age did not appear to significantly influence prevalence. Monitoring body mass index throughout pregnancy and screening for sleep-disordered breathing in women with gestational diabetes or hypertensive disorders is crucial, as these conditions are associated with higher prevalence.Findings highlight the need for future studies to adhere to standardized guidelines, use objective diagnostic tools, and include larger, well-characterized samples of normal pregnancies. Comparative studies with matched non-pregnant controls by body mass index and age, longitudinal cohort designs, and interventional trials using continuous positive airway pressure for moderate-to-severe obstructive sleep apnea are essential to enhance understanding and improve maternal-fetal outcomes.
BACKGROUND:Insufficient sleep syndrome (ISS) represents an emerging health concern but remains poorly defined as a diagnostic entity, though included in the international classification of sleep disorders. In the present study, we aimed to clarify the longitudinal course of ISS and to identify prognostic factors by comparing remitting and non-remitting patients. METHODS:A chart-review was realized, retrieving fifty-five patients with ISS (aged 39.8 ± 16.6 years, with 44.6 % of women) who underwent a comprehensive clinical evaluation at baseline and during a follow-up visit after 3-6 months. This evaluation included sleep symptoms, sleep logs, medications, and comorbidities. Additionally, actigraphy, video-polysomnography, and a multiple sleep latency test were conducted at baseline, and at the same moment standard psychoeducation on sleep was provided. RESULTS:During the follow-up visit, 69 % of patients still met the criteria for a clinical diagnosis of ISS, experiencing symptoms such as daytime sleepiness, disrupted nighttime sleep, unrefreshing sleep, and sleep attacks. Comparing sleep patterns of remitters and non-remitters based on sleep diaries, we observed that remission is associated with not only an increase in total sleep time but also a more regular sleep schedule. This regularity includes a reduction in napping and a lesser difference in sleep timings between weekdays and weekends. However, comparing baseline clinical and instrumental data between remitters and non-remitters revealed no significant differences, hindering the use of these features as prognostic factors. CONCLUSIONS:Given the low remission rate with standard treatment (i.e. psychoeducation on sleep), we propose the following: (1) Criterion E (extension of total sleep time results in resolution of the symptoms of sleepiness) should be considered as a therapeutic advice, and supportive rather than necessary for the diagnosis; (2) specific cognitive-behavioral therapy protocols targeting the cognitive factors underlying sleep-depriving behaviors are required, as single routine behavioral interventions are insufficient.
BACKGROUND:Increasing attention to the early stages of psychosis and the identification of symptomatic prodromal states have led to the development of a growing number of screening tools. The 16-item version of the Prodromal Questionnaire (PQ-16) is a worldwide used self-administered tool for this purpose. However, to date, fundamental psychometric properties of PQ-16 were not thoroughly investigated. This study aimed to examine the structural validity, measurement invariance, reliability and other psychometrical properties of the Italian version of the PQ-16 (iPQ-16) in help-seeking individuals and in the general population. METHODS:The iPQ-16 was administered to 449 young outpatients attending six community mental health services and to 318 control participants enrolled in educational environment. Confirmatory factor analyses (CFAs), measurement invariance (MI) between the help-seeking group and the general population sample, convergent validity, test-retest reliability, internal consistency, and prevalence analyses were performed. Lastly, the validity of the adopted PQ-16 cut-offs through Receiver Operating Characteristic (ROC) curves plotted against CAARMS diagnoses was also tested. RESULTS:CFAs confirmed the single-factor structure for the iPQ-16 and scalar MI was reached. The iPQ-16 showed high internal consistency, test-retest reliability, convergent validity, and acceptable diagnostic accuracy. ROC analysis suggested a score of ≥4 as best cut-off. CONCLUSIONS:The iPQ-16 represents a valid and reliable questionnaire for the assessment of high mental risk in both Italian outpatients and general student population. It has good psychometric properties and is easy to implement as UHR screening for clinical as well as research purposes.
This review critically analyzes the forensic application of the Parasomnia Defense in homicidal incidents, drawing from medical literature on disorders of arousal (DOA) and rapid-eye-movement sleep behavior disorder (RBD). A systematic search of PubMed, Scopus, Embase, and Cochrane databases was conducted until October 16, 2022. We screened English-language articles in peer-reviewed journals discussing murders committed during sleep with a Parasomnia Defense. We followed PRISMA guidelines, extracting event details, diagnosis methods, factors influencing the acts, perpetrator behavior, timing, motives, concealment, mental experiences, victim demographics, and court verdicts. Three sleep experts evaluated each case. We selected ten homicides, four attempted homicides, and one homicide/attempted homicide that met inclusion/exclusion criteria. Most cases were suspected DOA as unanimously confirmed by experts. RBD cases were absent. Among aggressors, a minority reported dream-like experiences. Victims were primarily female family members killed in or near the bed by hands and/or with sharp objects. Objective sleep data and important crime scene details were often missing. Verdicts were ununiform. Homicides during DOA episodes, though rare, are documented, validating the Parasomnia Defense's use in forensics. RBD-related fatal aggression seems very uncommon. However, cases often lack diagnostic clarity. We propose updated guidelines to enhance future reporting and understanding of such incidents.
Schizophrenia is thought to reflect aberrant connectivity within cortico-cortical and reentrant thalamo-cortical loops, which physiologically integrate and coordinate the function of multiple cortical and subcortical structures. Despite extensive research, reliable biomarkers of such "dys-connectivity" remain to be identified at the onset of psychosis, and before exposure to antipsychotic drugs. Because slow waves travel across the brain during sleep, they represent an ideal paradigm to study pathological conditions affecting brain connectivity. Here, we provide proof–of–concept evidence for a novel approach to investigate slow wave traveling properties in First-Episode Psychosis (FEP) with high-density electroencephalography (EEG). Whole–night sleep recordings of 5 drug-naïve FEP and 5 age- and gender-matched healthy control subjects were obtained with a 256-channel EEG system. One patient was re-recorded after 6 months and 3 years of continuous clozapine treatment. Slow wave detection and traveling properties were obtained with an open-source toolbox. Slow wave density and slow wave traveled distance (measured as the line of longest displacement) were significantly lower in patients (p < 0.05). In the patient who was tested longitudinally during effective clozapine treatment, slow wave density normalized, while traveling distance only partially recovered. These preliminary findings suggest that slow wave traveling could be employed in larger samples to detect cortical "dys-connectivity" at psychosis onset.