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Eveningness preference is associated with measures of poor wellbeing. However, recent research has found that Morning Affect (sleep inertia) and Distinctness (amplitude of diurnal variations in functioning) may be more strongly related to wellbeing indices. The current study investigated associations between Eveningness, Morning Affect, Distinctness, academic achievement, and student wellbeing (assessed with the College Student Subjective Wellbeing Questionnaire). Data was obtained from an online survey of 232 Chinese university students aged 19–27 (mean = 20.65; SD = 1.365); additional measures included conscientiousness, mind wandering, sleep quality, life satisfaction, substance use, and use of electronic devices at night. Morning Affect (MA) was positively correlated with academic achievement, Academic Satisfaction and Academic Efficacy; Eveningness was positively correlated with School Connectedness and School Gratitude; Distinctness was negatively correlated with Academic Efficacy. The negative correlation between Eveningness and academic achievement was mediated by lower MA. The negative correlation between Eveningness and MA was mediated by more use of electronic devices at night, and also the negative correlation between use of electronic devices at night and MA was mediated by Eveningness. These results suggest potentially important relationships between use of electronic devices at night, circadian functioning, student wellbeing, and academic achievement. [ABSTRACT FROM AUTHOR]

The diagnosis of Parkinson's disease (PD) is mainly based on the assessment of motor symptoms, although the influence of non-motor symptoms sometimes may be more significant on the patient's disability than the cardinal clinical signs of the disease. The predominant subtype of postural instability and gait disturbance is known to be associated with more severe non-motor symptoms of Parkinson's disease. Yet, the association between motor subtypes and specific mood symptoms remains understudied. The study aimed to analyze an association between sleep and chronotype signs, motor subtypes, with the severity of depressive symptoms in PD patients. We have included 64 patients in the clinical study. The studied population was divided into the following groups: PIGD group – patients with PD and dominance of postural instability and gait disorders; non-PIGD group – patients with PD and dominance of tremor or intermediate motor subtype. We used the Unified Parkinson's Disease Rating Scale, Beck Depression Inventory, Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, and Munich Chronotype Questionnaire. Patients with the PIGD subtype have higher levels of depressive symptoms and excessive daytime sleepiness, poorer sleep quality, later sleep onset and mid-sleep, longer sleep latency, and sleep inertia. PIGD motor subtype (p < 0.001), poor sleep quality (p < 0.001), mid-sleep (p = 0.016), and sleep latency (p = 0.025) had a significant impact on the level of depression in univariate regression analysis. Still, only mid-sleep (p = 0.019) and poor sleep quality (p = 0.003) increased the probability of higher severity of depression in the multivariate model. Poor sleep quality and later mid-sleep may be predictors of more severe depressive symptoms in PD. • Patients with Parkinson's disease and PIGD subtype experience higher depressive symptoms. • Poor sleep quality and later mid-sleep are predictors of more severe depressive symptoms in PD patients. • PIGD patients report worse sleep quality, greater daytime sleepiness, and longer sleep latency compared to non-PIGD. • Study emphasizes the importance of assessing sleep and motor subtype to manage depression in PD patients effectively. [ABSTRACT FROM AUTHOR]

To evaluate factors associated with feeling supported in adjusting to life when diagnosed with narcolepsy or idiopathic hypersomnia. An online survey was disseminated by nonprofit organization Project Sleep via email and social networks. Intended recipients were adults (≥18 years old) diagnosed with narcolepsy or idiopathic hypersomnia. Multivariable regression was used to assess predictors of feeling supported in adjusting to life with these conditions. The survey was completed by 1308 individuals (narcolepsy type 1, 48.4 %; narcolepsy type 2, 28.7 %; idiopathic hypersomnia, 22.9 %). Overall, 68.7 % of respondents were ≤40 years of age; 87.7 % were female; and 88.8 % were White. Respondents lived in 38 different countries (65.5 % in the United States). At time of diagnosis, most (91.1 %) did not know anyone with the same diagnosis. At time of the survey, 486 respondents (37.2 %) still did not know anyone with their diagnosis. Only 32.3 % of respondents felt supported in adjusting to life with narcolepsy or idiopathic hypersomnia. Knowing someone with the same diagnosis at the time of the survey was a significant predictor of perceived support. Younger age (18–30 years) and being married were also associated with greater perceived support, whereas a diagnosis of narcolepsy type 2 or idiopathic hypersomnia (versus narcolepsy type 1) and living outside the US were associated with less perceived support. People with narcolepsy or idiopathic hypersomnia often do not know others living with the same condition, even though this is associated with feeling supported. Clinicians should assess for social support and assist with resource identification. [Display omitted] • Narcolepsy and idiopathic hypersomnia have detrimental effects on quality of life. • Knowing other people with the same diagnosis is an important source of support. • Nonprofit advocacy organizations and online sources help patients form connections. • Clinicians should ask patients whether they know someone with the same condition. • Clinicians can facilitate support by connecting patients with available resources. [ABSTRACT FROM AUTHOR]

Summary Seasonality of excessive daytime sleepiness has been proposed, yet no research has specifically investigated its impact on daytime sleepiness and cataplexy in central disorders of hypersomnolence. This study examined seasonal variations in daytime sleepiness and cataplexy in narcolepsy type 1, narcolepsy type 2 and idiopathic hypersomnia. Patients included in the study were on stable pharmacological treatment, and participated in sleep medicine interviews to assess diurnal sleepiness and daytime napping and completed the Epworth Sleepiness Scale to assess excessive daytime sleepiness (Epworth Sleepiness Scale ≥ 10). Patients with narcolepsy type 1 also maintained a cataplexy diary. Evaluations were conducted in autumn, winter, spring and summer. The study included 29 patients with narcolepsy type 1, 16 patients with narcolepsy type 2 and 10 patients with idiopathic hypersomnia. Patients with narcolepsy type 1 and narcolepsy type 2 showed higher Epworth Sleepiness Scale scores in summer compared with other seasons, while patients with idiopathic hypersomnia showed no changes in excessive daytime sleepiness across the four seasons. Epworth Sleepiness Scale scores were higher in idiopathic hypersomnia patients compared to narcolepsy type 1 and narcolepsy type 2 patients in spring, autumn, and winter; conversely, in summer there were no differences in Epworth Sleepiness Scale scores among the three groups. No significant differences in Epworth Sleepiness Scale scores were noted between patients with narcolepsy type 1 and narcolepsy type 2 throughout the year. Furthermore, no seasonal effect on cataplexy frequency was found in patients with narcolepsy type 1. This study demonstrates that seasonality may influence daytime sleepiness in patients with narcolepsy type 1 and narcolepsy type 2 but not in patients with idiopathic hypersomnia, while cataplexy symptoms remain unaffected by seasonal changes. The underlying mechanisms linking excessive daytime sleepiness to seasonality have yet to be explored, though social factors and vacation time may contribute to increased excessive daytime sleepiness in narcolepsy. [ABSTRACT FROM AUTHOR]

Summary There is a growing consensus regarding the significant individual differences in responses to sleep inertia. However, little is known about the longitudinal trajectories of sleep inertia. Therefore, we aimed to investigate the incidence rates of sleep inertia, longitudinal trajectories, influencing factors and outcomes among intern nurses with shift work. A total of 1079 intern nurses with shift work completed online surveys at 2 weeks (T1) and 16 weeks (T2) after their clinical internship, respectively. The demographics and willingness to continue working as nurses, circadian type, sleep problems and emotional problems were measured. Hierarchical logistic regressions were used to examine predictors for the distinct longitudinal trajectory of sleep inertia, and binary logistic regressions were used to examine the predictive effects of trajectory memberships of sleep inertia on mental health problems (daytime sleepiness, anxiety, depression) at follow‐up. Overall, the incidence rates of severe sleep inertia increased significantly from 20.4% at T1 to 25.3% at T2 among intern nurses with shift work. All participants were classified into four trajectory memberships. Multiple factors were significant predictors of distinct trajectories of sleep inertia. Additionally, individuals with deteriorated and persistent‐high sleep inertia were more likely to develop mental health problems at the subsequent point. Sleep inertia is prevalent among intern nurses with shift work, and its distinct change patterns were associated with multiple risk factors and various adverse outcomes. Therefore, these factors should be considered when designing individualized and appropriate interventions for sleep inertia among medical staff. [ABSTRACT FROM AUTHOR]

Hypersomnolence, a broad presentation encompassing excessive daytime sleepiness, hypersomnia and sleep inertia, affects around 25 % of patients with a major depressive disorder. Yet, hypersomnolence is often overlook in clinical settings – which can prevent remission of the mood disorder in addition to significantly interfering with quality of life. Clinical guidelines are lacking to support clinicians in the diagnosis and treatment of hypersomnolence in depression. Pharmacological treatment with selective serotonin reuptake inhibitors is insufficient and noradrenaline and dopamine reuptake inhibitors or similar molecules are generally indicated. Low-sodium oxybate was recently approved for Idiopathic Hypersomnia, but studies are needed to assess its efficacy in patients with comorbid depression. In parallel, cognitive behavioral therapy for hypersomnia is being developed as adjunct non-pharmacological treatment. Light therapy might also be beneficial in these populations. This narrative review aims at proposing a diagnostic approach reconciliating psychiatry and sleep medicine nosologies, as well as offering a multimodal treatment algorithm for hypersomnolence in depression. • Up to 25 % of patients with depression experience hypersomnolence. • Psychiatry and sleep medicine definitions of hypersomnolence need alignment. • Limited access to diagnostic tools in psychiatry affects hypersomnolence diagnosis. • Differentiating clinophilia from hypersomnolence is critical in research and practice. • Chronotherapies and neuromodulation show potential for treating hypersomnolence in depression. [ABSTRACT FROM AUTHOR]

Summary: The differential diagnosis of narcolepsy type 1, a rare, chronic, central disorder of hypersomnolence, is challenging due to overlapping symptoms with other hypersomnolence disorders. While recent years have seen significant growth in our understanding of nocturnal polysomnography narcolepsy type 1 features, there remains a need for improving methods to differentiate narcolepsy type 1 nighttime sleep features from those of individuals without narcolepsy type 1. We aimed to develop a machine learning framework for identifying sleep features to discriminate narcolepsy type 1 from clinical controls, narcolepsy type 2 and idiopathic hypersomnia. The population included polysomnography data from 350 drug‐free individuals (114 narcolepsy type 1, 90 narcolepsy type 2, 105 idiopathic hypersomnia, and 41 clinical controls) collected at the National Reference Centers for Narcolepsy in Montpelier, France. Several sets of nocturnal sleep features were explored, as well as the value of time‐resolving sleep architecture by analysing sleep per quarter‐night. Several patterns of nighttime sleep evolution emerged that differed between narcolepsy type 1, clinical controls, narcolepsy type 2 and idiopathic hypersomnia, with increased nighttime instability observed in patients with narcolepsy type 1. Using machine learning models, we identified rapid eye movement sleep onset as the best single polysomnography feature to distinguish narcolepsy type 1 from controls, narcolepsy type 2 and idiopathic hypersomnia. By combining multiple feature sets capturing different aspects of sleep across quarter‐night periods, we were able to further improve between‐group discrimination and could identify the most discriminative sleep features. Our results highlight salient polysomnography features and the relevance of assessing their time‐dependent changes during sleep that could aid diagnosis and measure the impact of novel therapeutics in future clinical trials. [ABSTRACT FROM AUTHOR]

Background/Objectives: The aim of this study is to shed light on activity-based prospective memory upon the awakening and its association with motor sleep inertia in different phenotypes of insomnia disorder. Methods: To this end, 67 patients with insomnia and 51 healthy controls took part in the study. After enrollment, previously proposed actigraphic quantitative criteria were adopted, and the following phenotypes of insomnia disorder were observed in the patient sample: sleep onset (n = 12), maintenance (n = 19), mixed (n = 17), and negative misperception (n = 19). Each participant had used the Micro Motionlogger Watch (Ambulatory Monitoring, Inc., Ardsley, NY, USA) actigraph for one week. Actigraphic recording allowed for a description of both the activity-based prospective memory performance upon the awakening—by computing the time interval between sleep end and the time participants actually remembered to push the event-marker button of the actigraph—and the motor sleep inertia, i.e., the mean motor activity, minute-by-minute, in the first 60 min after sleep end in the morning. Results: Compared to healthy controls, a longer time interval was observed between sleep end and activity-based prospective memory performance in patients with mixed and maintenance insomnia. Moreover, a significant association was highlighted between motor sleep inertia and the activity-based prospective memory performance: higher levels of motor activity in those who remembered to perform the memory task early after sleep end, that spread over a longer time interval in maintenance and mixed insomnia. Conclusions: Overall, the present results seem to highlight a more marked cognitive inertia in patients with mixed and maintenance insomnia as well as a significant association between motor and cognitive inertia that spreads over a different time interval according to the phenotype of insomnia. [ABSTRACT FROM AUTHOR]

Summary Differential diagnosis of narcolepsy type 2 and idiopathic hypersomnia relies on the frequency of sleep‐onset rapid eye movement periods observed on the Multiple Sleep Latency Test. This study investigated whether variations in sleep schedules, particularly delayed sleep–wake patterns, contribute to the diagnostic distinction between narcolepsy type 2 and idiopathic hypersomnia. The study included 871 patients aged 18–39 years (316 with narcolepsy type 2, 555 with idiopathic hypersomnia). These patients were diagnosed based on MSLT results following polysomnography from November 2013 to November 2017. Patients' sleep habits, including bedtime and wake‐up times on weekdays and weekends during the 2 weeks preceding the polysomnography/Multiple Sleep Latency Test, were assessed using self‐reported sleep logs. A multivariate logistic regression analysis was conducted to identify factors associated with narcolepsy type 2 diagnosis. The analysis revealed that being male (p < 0.001), younger age (p < 0.001), shorter weekday sleep duration (p < 0.05), and a delayed weekday sleep midpoint time (p < 0.01) were significantly associated with a diagnosis of narcolepsy type 2. The study suggests that the conventionally fixed schedule of polysomnography and Multiple Sleep Latency Test administration may have contributed to the increased occurrence of sleep‐onset rapid eye movement periods particularly in individuals with a delayed sleep–wake schedule. [ABSTRACT FROM AUTHOR]

Background and Objective: Although there are several treatments for narcolepsy type 2 and idiopathic hypersomnia, studies that assess amphetamines, symptoms beyond sleepiness, and comparative effectiveness are needed. We performed a randomized, fully blinded, noninferiority trial of modafinil versus amphetamine–dextroamphetamine in these disorders. Methods: Forty-four adults were randomized to modafinil or amphetamine–dextroamphetamine, individually titrated to a maximum of modafinil 200 mg twice daily or amphetamine–dextroamphetamine 20 mg twice daily, for 12 weeks. Primary outcome was change in Epworth from baseline to week 12, with a noninferiority threshold of 2 points. Secondary outcomes were (1) patient global impression of change measures of disease severity, sleepiness, sleep inertia, and cognition; (2) change from baseline in Hypersomnia Severity Index; and (3) change from baseline in Sleep Inertia Questionnaire. Adverse events were compared between groups. Results: Epworth improved 5.0 [± standard deviation (SD) 2.7] points with modafinil and 4.4 (± SD 4.7) with amphetamine–dextroamphetamine; noninferiority of amphetamine–dextroamphetamine was not demonstrated (P = 0.11). Noninferiority of amphetamine-dextroamphetamine was demonstrated for change scores of severity, sleepiness, sleep inertia, Hypersomnia Severity Index, and Sleep Inertia Questionnaire. Dropouts due to adverse events were 31.8% for modafinil (including two severe events) and 9.1% for amphetamine–dextroamphetamine, P = 0.13. Anxiety was more common with modafinil and appetite suppression with amphetamine-dextroamphetamine. Conclusion: Noninferiority of amphetamine–dextroamphetamine to modafinil was not demonstrated for the primary outcome. However, amphetamine–dextroamphetamine was noninferior on multiple secondary measures of disease severity and symptomatology. These data may inform shared decision-making regarding treatment for idiopathic hypersomnia and narcolepsy type 2. Registration: Clinicaltrials.gov Registration (NCT03772314) 12/10/18.. [ABSTRACT FROM AUTHOR]

Abstract Background Sleep disorders are a common health problem that can be classified into many types that are distinguished by their history and characteristics. In this case report, we discuss a case of a patient suffering from recurrent unusual prolonged sleep attacks lasting up to 9 days that responded excellently to levetiracetam. Case presentation An 18-year-old Syrian male patient presented to the neurology department complaining of recurrent prolonged sleep episodes lasting for 9 days. Although Kleine–Levin syndrome was suspected, the history and investigations ruled it out. The patient was then treated with levetiracetam as a trial, and the response was excellent. Conclusion This case is a rare and unusual sleep disorder that does not match any of the known sleep disorders. What makes the case unique is the unexpected response to levetiracetam.

Summary Central disorders of hypersomnolence (CDH) are chronic diseases that significantly impact the lives of affected individuals. We aimed to explore the perspectives of individuals with narcolepsy type 1 (NT1), narcolepsy type 2 (NT2), and idiopathic hypersomnia (IH), and the challenges they encounter in their daily lives and within the healthcare systems in the Nordics. Interviews with patients (N = 41) and healthcare professionals (n = 14) and a patient survey (n = 70) were conducted in 2022 in Denmark, Sweden, Finland, and Norway to develop a patient journey map that visualises the patient with CDH journey and provides insights into the difficulties faced by these individuals. The patient journey mapping approach was chosen to focus on the processes and experiences of patients, highlighting the challenges they confront. Our findings revealed that the process of receiving a CDH diagnosis, as well as subsequent misdiagnoses and treatment, can be protracted and burdensome. CDH diagnoses remain poorly understood by neurologists, general practitioners, and the public, resulting in adverse consequences, with patients reporting a mean (standard deviation [SD]) time from symptom onset to diagnosis of 8.4 (5.11) years and a mean (SD) of 5.5 (4.17) productive hours lost/day. The available non‐pharmaceutical support for patients with CDH, encompassing medical, psychological, educational, and professional assistance, was insufficient. The generalisability of the findings to one specific diagnosis is limited due to the collective analysis of the CDH. These findings are invaluable for identifying disruptions in the patient with CDH journeys and for designing improved pathways for those with NT1, NT2, and IH in the future. [ABSTRACT FROM AUTHOR]

Summary: We aim to identify genetic markers associated with idiopathic hypersomnia, a disabling orphan central nervous system disorder of hypersomnolence that is still poorly understood. In our study, DNA was extracted from 79 unrelated patients diagnosed with idiopathic hypersomnia with long sleep time at the National Reference Center for Narcolepsy‐France according to very stringent diagnostic criteria. Whole exome sequencing on the first 30 patients with idiopathic hypersomnia (25 females and 5 males) allowed the single nucleotide variants to be compared with a control population of 574 healthy subjects from the French Exome project database. We focused on the identification of genetic variants among 182 genes related to the regulation of sleep and circadian rhythm. Candidate variants obtained by exome sequencing analysis were then validated in a second sample of 49 patients with idiopathic hypersomnia (37 females and 12 males). Our study characterised seven variants from six genes significantly associated with idiopathic hypersomnia compared with controls. A targeted sequencing analysis of these seven variants on 49 other patients with idiopathic hypersomnia confirmed the relative over‐representation of the A➔C variant of rs2859390, located in a potential splicing‐site of PER3 gene. Our findings support a genetic predisposition and identify pathways involved in the pathogeny of idiopathic hypersomnia. A variant of the PER3 gene may predispose to idiopathic hypersomnia with long sleep time. [ABSTRACT FROM AUTHOR]

Optimal measurement tools for problematic sleep inertia, common in some central disorders of hypersomnolence (CDH), have not yet been determined. We evaluated the performance of the Sleep Inertia Questionnaire (SIQ) in CDH, and how well it distinguished hypersomnolent groups from controls, and IH (idiopathic hypersomnia) from narcolepsy type 1 (NT1). This prospective, bi-centric study included 63 control, 84 IH, 16 NT1, 18 narcolepsy type 2 (NT2), and 88 subjective excessive daytime sleepiness (sEDS) participants, using ICSD-3 criteria. 126 (47.2 %) participants were on any medication at the time of SIQ completion. We assessed construct validity of SIQ scores, and sleep inertia duration (SID), and compared them across diagnoses, controlling for age and center. We derived cutpoints to distinguish hypersomnolent patients from controls and IH from NT1. Sensitivity analyses for depression, chronotype, and medication were performed. The SIQ sum and composite score were significantly lower in controls than in other groups (p < 0.0001), demonstrating outstanding ability to distinguish patients from controls (AUCs 0.92), without differences among hypersomnolent groups. SID (AUC 0.76) was significantly shorter in controls than in all hypersomnolent groups except NT1, and was shorter in NT1 than in IH or sEDS. Optimal SIQ sum cutpoint was 42 (J = 0.71) for patients versus controls. Optimal SID cutpoint in distinguishing IH from NT1 was 25 min (J = 0.39). The SIQ has excellent ability to distinguish hypersomnolent patients from healthy controls, after controlling for depression, eveningness, and medication. SID is best at distinguishing IH from NT1. • Sleep inertia can be disabling in some central disorders of hypersomnolence. • Optimal tools to measure sleep inertia severity have not yet been determined. • The Sleep Inertia Questionnaire (SIQ) distinguishes sleepy patients from controls. • Optimal SIQ sum cutpoint to distinguish patients from controls was 42 (J = 0.71). • Sleep inertia duration distinguishes Idiopathic Hypersomnia from Narcolepsy Type 1. [ABSTRACT FROM AUTHOR]

Abstract Background Although central disorders of hypersomnolence (CDH) and attention‐deficit/hyperactivity disorder (ADHD) are frequently comorbid, they often remain underdiagnosed, leading to insufficient treatment and sociopsychological outcomes. Case Presentation Here, we present a case of a male in his late 20s with ADHD and autism spectrum disorder who exhibited symptoms suggestive of idiopathic hypersomnia (IH), a subtype of CDH. The patient experienced difficulty waking up and dropped out of university. Additionally, although methylphenidate extended‐release was prescribed, he often forgot to take his medication, resulting in difficulty waking up until late afternoon. No symptoms related to rapid eye movements sleep were observed. Considering the possibility of concurrent hypersomnia with neurodevelopmental disorders, we conducted 24‐h polysomnography (PSG). The results demonstrated total sleep time of 774.5 min (≥660 min). Together with other criteria, we diagnosed him as having IH. Following discharge and discussion with the patient, we provided sleep hygiene education for him, and he resumed day care attendance to establish a social routine. Conclusion In cases where hypersomnia may co‐occur with neurodevelopmental disorders, active utilization of 24‐h PSG enables detailed evaluation of sleep–wake patterns and behaviors, facilitating effective guidance on sleep hygiene and promoting improvements in social rhythms and sociability.

Summary Hypersomnia spectrum disorders are underdiagnosed and poorly treated due to their heterogeneity and absence of biomarkers. The electroretinography has been proposed as a proxy of central dysfunction and has proved to be valuable to differentiate certain psychiatric disorders. Hypersomnolence is a shared core feature in central hypersomnia and psychiatric disorders. We therefore aimed to identify biomarkers by studying the electroretinography profile in patients with narcolepsy type 1, idiopathic hypersomnia and in controls. Cone, rod and retinal ganglion cells electrical activity were recorded with flash‐electroretinography in non‐dilated eye of 31 patients with idiopathic hypersomnia (women 84%, 26.6 ± 5.9 years), 19 patients with narcolepsy type 1 (women 63%, 36.6 ± 12.7 years) and 43 controls (women 58%, 30.6 ± 9.3 years). Reduced cone a‐wave amplitude (p = 0.039) and prolonged cone (p = 0.022) and rod b‐wave (p = 0.009) latencies were observed in patients with narcolepsy type 1 as compared with controls, while prolonged photopic negative response‐wave latency (retinal ganglion cells activity) was observed in patients with idiopathic hypersomnia as compared with controls (p = 0.033). The rod and cone b‐wave latency clearly distinguished narcolepsy type 1 from idiopathic hypersomnia and controls (area under the curve > 0.70), and the photopic negative response‐wave latency distinguished idiopathic hypersomnia and narcolepsy type 1 from controls with an area under the curve > 0.68. This first original study shows electroretinography anomalies observed in patients with hypersomnia. Narcolepsy type 1 is associated with impaired cone and rod responses, whereas idiopathic hypersomnia is associated with impaired retinal ganglion cells response, suggesting different phototransduction alterations in both hypersomnias. Although these results need to be confirmed with a larger sample size, the electroretinography may be a promising tool for clinicians to differentiate hypersomnia subtypes. [ABSTRACT FROM AUTHOR]

Idiopathic hypersomnia typically is a chronic and potentially debilitating neurologic sleep disorder, and is characterized by excessive daytime sleepiness. In addition to excessive daytime sleepiness, idiopathic hypersomnia symptoms can include severe sleep inertia; long, unrefreshing naps; long sleep time; and cognitive dysfunction. Patients with idiopathic hypersomnia may experience a significant impact on their quality of life, work or school performance, earnings, employment, and overall health. Given the complex range of symptoms associated with idiopathic hypersomnia and the array of treatments available, there is a need to provide guidance on the treatment of idiopathic hypersomnia and the clinically relevant recommendations that enhance effective disease management. Identifying appropriate treatment options for idiopathic hypersomnia requires timely and accurate diagnosis, consideration of individual patient factors, and frequent reassessment of symptom severity. In 2021, low-sodium oxybate was the first treatment to receive approval by the US Food and Drug Administration for the treatment of idiopathic hypersomnia in adults. However, many off-label treatments continue to be used. Adjunct nonpharmacologic therapies, including good sleep hygiene, patient education and counseling, and use of support groups, should be recognized and recommended when appropriate. This narrative review describes optimal treatment strategies that take into account patient-specific factors, as well as the unique characteristics of each medication and the evolution of a patient's response to treatment. Perspectives on appropriate symptom measurement and management, and potential future therapies, are also offered. [Display omitted] • Treatment options and strategies considering patient-specific factors are reviewed. • Low-sodium oxybate is the only FDA-approved medication for idiopathic hypersomnia. • Clinical experience in and perspectives on proper symptom management are discussed. • Interactions between medications used to treat idiopathic hypersomnia are summarized. [ABSTRACT FROM AUTHOR]

Summary Patients with idiopathic hypersomnia frequently report having unrefreshing naps. However, whether they have abnormal sleep architecture during naps that may explain their unrefreshing aspect is unknown. We compared sleep architecture during short daytime naps in patients with idiopathic hypersomnia reporting unrefreshing and refreshing naps. One‐hundred and thirty‐four patients tested with one‐night polysomnography, followed by an adapted version of the Multiple Sleep Latency Test with four naps, were included. They were asked about the refreshing aspect of their habitual naps during a clinical interview. They were classified as having objective (Multiple Sleep Latency Test ≤ 8 min) or subjective idiopathic hypersomnia (Multiple Sleep Latency Test > 8 min), and as presenting refreshing or unrefreshing naps. We tested Group differences (refreshing versus unrefreshing naps) on nap sleep architecture in the whole sample and for subjective and objective idiopathic hypersomnia subgroups separately using ANCOVAs. No Group effects were observed in the Multiple Sleep Latency Test architecture in the whole sample and in objective and subjective idiopathic hypersomnia subgroups. This study provides preliminary evidence that reporting unrefreshing naps is not associated with clinically significant findings in Multiple Sleep Latency Test sleep architecture in patients with idiopathic hypersomnia. Given that naps taken by patients with idiopathic hypersomnia are typically long, future studies should investigate longer daytime sleep episodes. [ABSTRACT FROM AUTHOR]

Introduction: Low-sodium oxybate (LXB) is approved for treatment of narcolepsy in patients aged 7 years and older and treatment of idiopathic hypersomnia in adults. LXB contains the same active moiety with 92% less sodium than sodium oxybate (SXB). As the indication for oxybate treatment in patients with idiopathic hypersomnia is new and allows for individualized dosing optimization, guidance for beginning LXB treatment is needed. In particular, clinicians may benefit from guidance regarding treatment initiation, dosing/regimen options, potential challenges, and treatment expectations. Additionally, pharmacokinetic profiles differ slightly between both treatments, and further guidance on transitioning from SXB to LXB in patients with narcolepsy may aid clinicians. Methods: An expert panel of five sleep specialists was convened to obtain consensus on recommendations for these topics using a modified Delphi process. Results: Across two virtual meetings, the panel agreed on 31 recommendations with a high degree of consensus that fell into four overarching topics: (1) introducing LXB to patients; (2) initiating LXB for adult narcolepsy and idiopathic hypersomnia; (3) addressing challenges in using LXB; and (4) transitioning from SXB to LXB. The panel recommended that clinicians provide a clear overview of how LXB works for treating symptoms in narcolepsy or idiopathic hypersomnia, as appropriate for their patients, explain safety aspects, and set expectations prior to initiating LXB treatment. Strategies for initial dosing and regimen are provided. Strategies for adjusting the dose, regimen, timing, and consideration of individual factors were developed for specific instances in which patients may have trouble staying asleep or waking up, as well as guidance for addressing potential adverse events, such as nausea, dizziness, anxiety, and depression. Discussion points based on existing literature and clinical experience were included as relevant for each statement. Conclusion: Clinicians may use this resource to guide LXB dosing optimization with patients. [ABSTRACT FROM AUTHOR]

Summary: Excessive daytime sleepiness is the core symptom of central disorders of hypersomnolence (CDH) and can directly impair driving performance. Sleepiness is reflected in relative alterations in distal and proximal skin temperature. Therefore, we examined the predictive value of skin temperature on driving performance. Distal and proximal skin temperature and their gradient (DPG) were continuously measured in 44 participants with narcolepsy type 1, narcolepsy type 2 or idiopathic hypersomnia during a standardised 1‐h driving test. Driving performance was defined as the standard deviation of lateral position (SDLP) per 5 km segment (equivalent to 3 min of driving). Distal and proximal skin temperature and DPG measurements were averaged over each segment and changes over segments were calculated. Mixed‐effect model analyses showed a strong, quadratic association between proximal skin temperature and SDLP (p < 0.001) and a linear association between DPG and SDLP (p < 0.021). Proximal skin temperature changes over 3 to 15 min were predictive for SDLP. Moreover, SDLP increased over time (0.34 cm/segment, p < 0.001) and was higher in men than in women (3.50 cm, p = 0.012). We conclude that proximal skin temperature is a promising predictor for real‐time assessment of driving performance in people with CDH. [ABSTRACT FROM AUTHOR]

It is hypothesized that narcolepsy type 1 (NT1) develops in genetically susceptible people who encounter environmental triggers leading to immune-mediated hypocretin-1 deficiency. The pathophysiologies of narcolepsy type 2 (NT2) and idiopathic hypersomnia (IH) remain unknown. The main aim of this study was to collect all reported immunological events before onset of a central disorder of hypersomnolence. Medical records of 290 people with NT1, and 115 with NT2 or IH were retrospectively reviewed to extract infection and influenza vaccination history. Prevalence, distribution of immunological events, and time until hypersomnolence onset were compared between NT1 and the combined group of NT2 and IH. Immunological events were frequently reported before hypersomnolence disorder onset across groups. Flu and H1N1 influenza vaccination were more common in NT1, and Epstein–Barr virus and other respiratory and non-respiratory infections in NT2 and IH. Distributions of events were comparable between NT2 and IH. Rapid symptom onset within one month of infection was frequent across groups, especially after flu infection in NT1. Hypersomnolence disorder progression after an immunological event was reported in ten individuals. Our findings suggest a variety of immunological triggers potentially related to NT1, including H1N1 influenza infection or vaccination, infection with other flu types, and other respiratory and non-respiratory infections. Frequent reports of immunological events (other than those reported in NT1) immediately prior to the development of NT2 and IH support the specificity of triggers for NT1, and open important new research avenues into possible underlying immunological mechanisms in NT2 and IH. • We studied possible immunological triggers for central disorders of hypersomnolence. • Flu and H1N1 influenza vaccination were more common before narcolepsy type 1 onset. • Non-flu infections were common before narcolepsy type 2/idiopathic hypersomnia onset. • Rapid hypersomnolence onset within one month was frequent across groups. [ABSTRACT FROM AUTHOR]

Summary: Little attention has been paid to the long‐term development of idiopathic hypersomnia symptoms and idiopathic hypersomnia comorbidities. The aim of this study was to describe the general health of patients with idiopathic hypersomnia years after the initial diagnosis, focusing on current subjective hypersomnolence and the presence of its other possible causes. Adult patients diagnosed with idiopathic hypersomnia ≥ 3 years ago at sleep centres in Prague and Kosice were invited to participate in this study. A total of 60 patients were examined (age 47.3 ± SD = 13.2 years, 66.7% women). In all participants, their hypersomnolence could not be explained by any other cause but idiopathic hypersomnia at the time of diagnosis. The mean duration of follow‐up was 9.8 + 8.0 years. Fifty patients (83%) reported persisting hypersomnolence, but only 33 (55%) had no other disease that could also explain the patient's excessive daytime sleepiness and/or prolonged sleep. In two patients (3%), the diagnosis in the meantime had changed to narcolepsy type 2, and 15 patients (25%) had developed a disease or diseases potentially causing hypersomnolence since the initial diagnosis. Complete hypersomnolence resolution without stimulant treatment lasting longer than 6 months was reported by 10 patients (17%). To conclude, in a longer interval from the diagnosis of idiopathic hypersomnia, hypersomnolence may disappear or may theoretically be explained by another newly developed disease, or the diagnosis may be changed to narcolepsy type 2. Thus, after 9.8 years, only 55% of the examined patients with idiopathic hypersomnia had a typical clinical picture of idiopathic hypersomnia without doubts about the cause of the current hypersomnolence. [ABSTRACT FROM AUTHOR]

Introduction: Fatigue is the most commonly reported post-COVID symptom. A minority of patients also report excessive daytime sleepiness, which could be a target for treatment. Methods: Among 530 patients with a post-COVID condition, those with excessive daytime sleepiness were systematically assessed for objective central hypersomnia, with exclusion of all cases not clearly attributable to SARS-CoV-2 infection. Results: Four cases of post-COVID central hypersomnia were identified, three fulfilling the criteria of the 3rd International Classification of Sleep Disorders for idiopathic hypersomnia, and one for type II narcolepsy. We report here their clinical history, sleep examination data and treatment, with a favorable response to methylphenidate in three cases and spontaneous resolution in one case. Conclusion: We highlight the importance of identifying cases of post-COVID central hypersomnia, as it may be a treatable trait of a post-COVID condition. [ABSTRACT FROM AUTHOR]