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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]

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]

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]

Abstract 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.

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]

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]

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]

In recent years, there has been an increased interest in elucidating the influence of the gut microbiota on sleep physiology. The gut microbiota affects the central nervous system by modulating neuronal pathways through the neuroendocrine and immune system, the hypothalamus-pituitary-adrenal axis, and various metabolic pathways. The gut microbiota can also influence circadian rhythms. In this study, we observed the gut microbiota composition of patients suffering from narcolepsy type 1, narcolepsy type 2, and idiopathic hypersomnia. We did not observe any changes in the alpha diversity of the gut microbiota among patient groups and healthy controls. We observed changes in beta diversity in accordance with Jaccard dissimilarities between the control group and groups of patients suffering from narcolepsy type 1 and idiopathic hypersomnia. Our results indicate that both these patient groups differ from controls relative to the presence of rare bacterial taxa. However, after adjustment for various confounding factors such as BMI, age, and gender, there were no statistical differences among the groups. This indicates that the divergence in beta diversity in the narcolepsy type 1 and idiopathic hypersomnia groups did not arise due to sleep disturbances. This study implies that using metabolomics and proteomics approaches to study the role of microbiota in sleep disorders might prove beneficial. • The gut microbiota of patients with central hypersomnia varies from controls due to BMI, age, gender, and diet differences. • Our study supports the hypothesis that narcolepsy type 2 and idiopathic hypersomnia could form one diagnostic unit. • We did not find any significant effect of the sleep predictors on the gut microbiota. [ABSTRACT FROM AUTHOR]

Abstract Introduction Patients with either Idiopathic Hypersomnia or Narcolepsy demonstrate excessive daytime somnolence (EDS) with resultant inattention mimicking Attention Deficit Hyperactivity Disorder (ADHD). Patients with ADHD also often express sleep problems including EDS. Thus, patients with ADHD and patients with idiopathic hypersomnia or narcolepsy may share inattention and daytime drowsiness as common features. However, it is not known whether EDS patients with idiopathic hypersomnia or narcolepsy also have increased movement (hyperactivity) like ADHD patients, the determination of which is the purpose of this study. Methods We studied 12 patients (7 Narcolepsy type 2 and 5 Idiopathic Hypersomnia) with EDS as shown by Multiple Sleep Latency Test which served as the gold standard for entry into the study. Twelve subjects without symptoms of EDS served as the control group. None of the participants had a previous history of ADHD. Each participant underwent a one-hour session laying at 45 degrees with surveys about the need to move and actigraphy as an objective measure of movement. Results Sleep-disordered patients with EDS reported more symptoms of inattention and hyperactivity on the ADHD Self-Report Scale. At each of the time points patients with EDS had a clear trend to express the need to move more than controls on the Suggested Immobilization Test (SIT). For the total 60 min, a large effect size for the need to move during the SIT test was found between patients and controls (Cohen’s d = 0.61, p = 0.01). Patients with EDS did not express a need to move more to combat drowsiness than controls, nor did actigraphy show any difference in objective movement between patients and controls during the SIT. Conclusion Patients with EDS express inattention and a need to move more than controls. However, hyperactivity was not verified by objective measurement, nor did the EDS patients express a need to move to combat drowsiness more than controls. Thus, a hypothesis to be further tested, is whether narcolepsy and idiopathic hypersomnia may be more a model of the inattentive form of ADHD rather than the combined or inattentive/hyperactive form of ADHD. Further studies are needed to explore the relationship between EDS and hyperactivity.

IntroductionFatigue is the most commonly reported post-COVID symptom. A minority of patients also report excessive daytime sleepiness, which could be a target for treatment.MethodsAmong 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.ResultsFour 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.ConclusionWe highlight the importance of identifying cases of post-COVID central hypersomnia, as it may be a treatable trait of a post-COVID condition.

BackgroundHypersomnia poses major challenges to treatment providers given the limitations of available treatment options. In this context, the application of non-invasive brain stimulation techniques such as transcranial electrical stimulation (tES) may open up new avenues to effective treatment. Preliminary evidence suggests both acute and longer-lasting positive effects of transcranial direct current stimulation (tDCS) on vigilance and sleepiness in hypersomniac patients. Based on these findings, the present study sought to investigate short-term effects of single sessions of tDCS and transcranial random noise stimulation (tRNS) on sleepiness in persons suffering from hypersomnia.MethodsA sample of 29 patients suffering from narcolepsy or idiopathic hypersomnia (IH) was recruited from the Regensburg Sleep Disorder Center and underwent single sessions of tES (anodal tDCS, tRNS, sham) over the left and right dorsolateral prefrontal cortex on three consecutive days in a double-blind, sham-controlled, pseudorandomized crossover trial. The primary study endpoint was the mean reaction time measured by the Psychomotor Vigilance Task (PVT) before and directly after the daily tES sessions. Secondary endpoints were additional PVT outcome metrics as well as subjective outcome parameters (e.g., Karolinska Sleepiness Scale; KSS).ResultsThere were no significant treatment effects neither on objective (i.e., PVT) nor on subjective indicators of sleepiness.ConclusionWe could not demonstrate any clinically relevant effects of single sessions of tDCS or tRNS on objective or subjective measures of sleepiness in patients with hypersomnia. However, we cannot exclude that repeated sessions of tES may affect vigilance or sleepiness in hypersomniac patients.

Background: Hypersomnias of central origin (HOCO) are diverse in origin and symptomatology and remain poorly described in an Australian population. We hypothesised that the rate of human leukocyte antigen (HLA) DQB1*0602 positivity in the Australian cohort would be comparable to international registries. Aims: The current study aims to evaluate epidemiological and clinical characteristics of Australian patients with HOCO, including prevalence of HLA DQB1*0602 positivity, the most specific HLA marker associated with narcolepsy. Methods: This is a retrospective study. Patients ≥ 16 years of age presenting with symptoms of hypersomnolence who attended one of two Australian sleep centres (New South Wales and Queensland) in the preceding 24 months and had undergone both HLA serology and multiple sleep latency tests (MSLTs) were included. Main outcome measures included demographics, HLA DQB1*0602 positivity, MSLT, and clinical parameters (presence of auxiliary narcolepsy symptoms, laboratory tests, relevant prescribed medications). Results: Eighty‐eight patients were included. HLA DQB1*0602 positivity was highest in those with type 1 narcolepsy (NT1) (95.7%) and lowest in those without a classifiable disorder (9.1%). Mean sleep latency was lowest and number of sleep‐onset rapid eye movement periods (SOREMPs) highest in the NT1 group. Comorbid disorders, particularly depression and overweight/obesity, were prevalent in all cohorts. Across all diagnostic groups, dexamphetamine was the most commonly prescribed agent for excessive daytime sleepiness. Conclusions: Patients with HOCO assessed in two specialised Australian clinics demonstrate comparable clinical characteristics to other published cohorts internationally; however, available pharmacological agents in Australia do not reflect international standards of care. [ABSTRACT FROM AUTHOR]

Summary: Idiopathic hypersomnia is poorly diagnosed in the absence of biomarkers to distinguish it from other central hypersomnia subtypes. Given that light plays a main role in the regulation of sleep and wake, we explored the retinal melanopsin‐based pupil response in patients with idiopathic hypersomnia and narcolepsy type 1, and healthy subjects. Twenty‐seven patients with narcolepsy type 1 (women 59%, 36 ± 11.5 years old), 36 patients with idiopathic hypersomnia (women 83%, 27.2 ± 7.2 years old) with long total sleep time (> 11/24 hr), and 43 controls (women 58%, 30.6 ± 9.3 years old) were included in this study. All underwent a pupillometry protocol to assess pupil diameter, and the relative post‐illumination pupil response to assess melanopsin‐driven pupil responses in the light non‐visual input pathway. Differences between groups were assessed using logistic regressions adjusted on age and sex. We found that patients with narcolepsy type 1 had a smaller baseline pupil diameter as compared with idiopathic hypersomnia and controls (p < 0.05). In addition, both narcolepsy type 1 and idiopathic hypersomnia groups had a smaller relative post‐illumination pupil response (respectively, 31.6 ± 13.9% and 33.2 ± 9.9%) as compared with controls (38.7 ± 9.7%), suggesting a reduced melanopsin‐mediated pupil response in both types of central hypersomnia (p < 0.01). Both narcolepsy type 1 and idiopathic hypersomnia showed a smaller melanopsin‐mediated pupil response, and narcolepsy type 1, unlike idiopathic hypersomnia, also displayed a smaller basal pupil diameter. Importantly, we found that the basal pupil size permitted to well discriminate idiopathic hypersomnia from narcolepsy type 1 with a specificity = 66.67% and a sensitivity = 72.22%. Pupillometry may aid to multi‐feature differentiation of central hypersomnia subtypes. [ABSTRACT FROM AUTHOR]

Evaluation of hypersomnolence disorders ideally includes an assessment of vigilance using the short Sustained Attention to Response Task (SART). We evaluated whether this task can differentiate between hypersomnolence disorders, whether it correlates with subjective and objective sleepiness, whether it is affected by the time of day, and symptoms of anxiety and depression. We analyzed diagnostic data of 306 individuals with hypersomnolence complaints diagnosed with narcolepsy type 1 (n=100), narcolepsy type 2 (n=20), idiopathic hypersomnia (n=49), obstructive sleep apnea (n=27) and other causes or without explanatory diagnosis (n=110). We included the Multiple Sleep Latency Test (MSLT), polysomnography, Epworth Sleepiness Scale (ESS), Hospital Anxiety and Depression Scale and SART, which were administered five times during the day (outcomes: reaction time, total, commission and omission errors). The SART outcomes did not differ between groups when adjusted for relevant covariates. Higher ESS scores were associated with longer reaction times and more commission errors (p<.01). The main outcome, total errors, did not differ between times of the day. Reaction times and omission errors were impacted (p<.05). The SART quantifies disturbed vigilance, an important dimension of disorders of hypersomnolence. Results do not suggest that depressive symptoms influence SART outcomes. A practice session is advised. Testing time should be taken into account when interpreting results. We conclude that the SART does not differentiate between central disorders of hypersomnolence. It may be a helpful addition to the standard diagnostic workup and monitoring of these disorders. • Vigilance is under-assessed in disorders of hypersomnolence. • Vigilance and daytime sleepiness are distinct key aspects of these disorders. • The Sustained Attention to Response Task (SART) is a short, low-cost vigilance test. • The SART may be a helpful addition to the diagnostic workup of these disorders. [ABSTRACT FROM AUTHOR]