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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]

• Synchrony between chronotype and time of day is largely associated with subjective mood and driving speed. • Driving behavior and mood constantly impair with time-on-task while driving under sleepiness. • Under sleep inertia, driving behavior and mood stay rather constant on a low level. • Performance and mood are differentially affected by the time of day under sleepiness versus sleep inertia. Sleep is a desired use case in highly automated driving and promises drivers relief from sleepiness. Benefits of sleeping on subjective mood and performance in the driving task may be opposed by sleep inertia, the post-sleep grogginess and performance impairment. The magnitude of both, sleepiness and sleep inertia may depend on sleep-homeostatic and circadian factors. We therefore investigated how the effects of sleep inertia are affected by the time of day a nap is taken during automated driving and the role of individual chronotypes both in comparison to the effects of sleepiness. In the presented driving simulator study, 10 distinct morningness and 10 eveningness chronotypes were invited to two test sessions, one in the early morning (starting at 6 a.m.) and one in the late evening (starting at 9 p.m.). Participants slept during an automated drive and were requested to drive manually before and after an instructed nap. We examined the time course of the subjective state, driving behavior and vigilance in dependence of time of day and individual chronotype under sleepiness and sleep inertia. Effects of both, sleepiness and sleep inertia on subjective arousal, wellbeing, motivation, and driving speed were stronger when the time of day did not fit the individual chronotype. This counts particularly for morningness types. Subjective arousal, wellbeing, and motivation were more impaired after the instructed nap in the evening than in the morning. Analogously, driving speed was slower and take-over times were longer after napping in the evening compared to in the morning. Compared to sleepiness, lane keeping and reaction times were not significantly impaired under sleep inertia, probably because the task induced workload could be compensated by reducing speed and prolonging take-over times. Under sleepiness, driving was characterized by distinct time-on-task effects, which caused mood, lane keeping, and vigilance to deteriorate with driving time. In contrast, the investigated measures were more stable with time on task under sleep inertia, possibly due to a compensation by speed reduction and a balance between beneficial and detrimental effects of the intermediate sleep. [ABSTRACT FROM AUTHOR]

• Positive effects of napping in automated driving emerge only after a phase of negative effects. • Stable sleep, deep sleep and, to a lesser extent, light sleep result in considerable sleep inertia. • Sleep architecture predicts sleep inertia better than nap duration. • Transferring the strategic NASA nap paradigm to automated driving is not the ideal solution. At higher levels of driving automation, drivers can nap during parts of the trip but must take over control in others. Awakening from a nap is marked by sleep inertia which is tackled by the NASA nap paradigm in aviation: Strategic on-flight naps are restricted to 40 min to avoid deep sleep and therefore sleep inertia. For future automated driving, there are currently no such strategies for addressing sleep inertia. Given the disparate requirements, it is uncertain whether the strategies derived from aviation can be readily applied to automated driving. Therefore, our study aimed to compare the effects of restricting the duration of nap opportunities following the NASA nap paradigm to the effects of sleep architecture on sleep inertia in takeover scenarios in automated driving. In our driving simulator study, 24 participants were invited to sleep during three automated drives. They were awakened after 20, 40, or 60 min and asked to manually complete an urban drive. We assessed how napping duration, last sleep stage before takeover, and varying proportions of light, stable, and deep sleep influenced self-reported sleepiness, takeover times, and the number of driving errors. Takeover times increased with nap duration, but sleepiness and driving errors did not. Instead, all measures were significantly influenced by sleep architecture. Sleepiness increased after awakening from light and stable sleep, and takeover times after awakening from light sleep. Takeover times also increased with higher proportions of stable sleep. The number of driving errors was significantly increased with the proportion of deep sleep and after awakenings from stable and deep sleep. These results suggest that sleep architecture, not nap duration, is crucial for predicting sleep inertia. Therefore, the NASA nap paradigm is not suitable for driving contexts. Future driver monitoring systems should assess the sleep architecture to predict and prevent sleep inertia. [ABSTRACT FROM AUTHOR]

• Differential effects of alertness, sleepiness and post-sleep inertia on driving behavior are compared in a simulated 10-min driving task. • Lane- and speed-keeping is unstable for drivers under the state of sleepiness and sleep inertia. • After napping, lane-keeping performance recovers rapidly while no recovery is evident under the state of sleepiness. • Under the state of sleep inertia, drivers compensate for impairments by reducing driving speed. No such compensation is evident for drivers under the state of sleepiness. • Performance decrements after awakening have to be taken into account when designing automated driving technology. Driver sleepiness is one of the major safety issues in conventional driving and sleep inertia emerges as a driver state in automated driving. The aim of the present study was to assess the differential impacts of sleepiness and sleep inertia on driving behavior. 61 participants completed a 10-min manual driving task during an otherwise automated drive. They completed the task (a) under an alert state, (b) under a sleepy state, and (c) after EEG-confirmed sleep. Driving performance was assessed with the parameters lane-keeping, speed choice, and speed-keeping. The eye-blink-based sleepiness measure PERCLOS (the proportion of time with eyes closed) was compared for the three driver states. Lane- and speed-keeping performance were impaired under the sleepy state and after sleep, relative to the alert state. After sleep, lane-keeping behavior recovered rapidly and speed-keeping recovered by trend. Under the sleepy state, performance deteriorated. After sleep, the mean speed was lower than in the sleepy state and in the alert state. PERCLOS was increased after sleep and under the sleepy state, relative to the alert state. Although sleep inertia had detrimental effects on driving parameters similar to sleepiness, this effect rapidly vanished. Hence, while brief naps might be suitable to restore alertness in general, the minimal time needed to regain full capacity after napping should be a focus of future research. [ABSTRACT FROM AUTHOR]

Sleep inertia refers to the transient physiological state of hypoarousal upon awakening, associated with various degrees of impaired neurobehavioral performance, confusion, a desire to return to sleep and often a negative emotional state. Scalp and intracranial electro-encephalography as well as functional imaging studies have provided evidence that the sleep inertia phenomenon is underpinned by an heterogenous cerebral state mixing local sleep and local wake patterns of activity, at the neuronal and network levels. Sleep inertia is modulated by homeostasis and circadian processes, sleep stage upon awakening, and individual factors; this translates into a huge variability in its intensity even under physiological conditions. In sleep disorders, especially in hypersomnolence disorders such as idiopathic hypersomnia, sleep inertia may be a daily, serious and long-lasting symptom leading to severe impairment. To date, few tools have been developed to assess sleep inertia in clinical practice. They include mainly questionnaires and behavioral tests such as the psychomotor vigilance task. Only one neurophysiological protocol has been evaluated in hypersomnia, the forced awakening test which is based on an event-related potentials paradigm upon awakening. This contrasts with the major functional consequences of sleep inertia and its potentially dangerous consequences in subjects required to perform safety-critical tasks soon after awakening. There is a great need to identify reproducible biomarkers correlated with sleep inertia-associated cognitive and behavioral impairment. These biomarkers will aim at better understanding and measuring sleep inertia in physiological and pathological conditions, as well as objectively evaluating wake-promoting treatments or non-pharmacological countermeasures to reduce this phenomenon. [ABSTRACT FROM AUTHOR]

Introduction: Idiopathic hypersomnia (IH) is a rare orphan disease characterized by excessive daytime sleepiness, frequently accompanied by prolonged nocturnal sleep and difficulties awakening, termed sleep inertia or sleep drunkenness. Severe sleepiness usually causes a greater handicap than manifestations of narcolepsy.Methods: Forty-three IH patients (17 male, mean age 42.8 ± SD 12.2 years, range 20-67), diagnosed in the past 20 years according to ICSD-2 or ICSD-3 criteria were invited for clinical examination to evaluate the course, manifestations and severity of the disease, as well as clinical comorbidities. The patients completed a set of questionnaires scoring sleepiness, sleep inertia, fatigue, depression, anxiety, circadian preference, and quality of life.Results: IH patients were divided according to the duration of nocturnal sleep at the time of their diagnosis into two cohorts: (1) with normal sleep duration (n = 25, 58.1%) and (2) with long sleep duration (n = 18, 41.9%). The mean duration of ad libitum sleep per 22 h in the second cohort was 732.0 ± 115.4 min (range 603-1100), and women markedly prevailed (n = 14, 77.8%). Age at disease onset was younger in the group with long sleep duration (21.2 ± 11.4 years versus 28.1 ± 13.6 years, p = 0.028), their MSLT latency was longer (7.2 ± 3.7 min versus 5.1 ± 1.7 min, p = 0.005), a history of sleep inertia prevailed (p = 0.005), and daily naps were mostly non-refreshing (p = 0.014). Additionally, questionnaires in the group with long sleep duration showed more severe sleep inertia (p = 0.007), fatigue (p = 0.004), and a tendency towards evening chronotype (p = 0.001).Conclusions: IH patients with long sleep duration differ clinically as well as by objective measures at the time of diagnosis and in long-term follow up from IH patients without long 24-h sleep time. In our opinion they represent an independent clinical entity to be considered in the revised ICSD-3 criteria. [ABSTRACT FROM AUTHOR]

Abstract Background Caffeine increases alertness when consumed in single servings of various products including coffee, tea, soft drinks, and energy drinks. Although not a nutrient, caffeine is consumed by 90% of the adult population in the United States. Objective This study examined the daily pattern of caffeine intake and its relationship to multiple demographic variables. Methods Data from the National Health and Nutrition Examination Survey (NHANES) 2007–2012 (adults aged 19+ years; n=16,173) were used to determine the time of day at which caffeine is consumed and demographic factors associated with intake. Regression analyses characterized factors associated with caffeine intake including sex, age, ethnicity, education, smoking status, physical activity, employment status, total work hours, alcohol, and energy intake. Results Mean adult per capita caffeine intake was 169±4 mg/d (mean±standard error). Most caffeine (70%) was consumed before noon, often at breakfast, and intake decreased progressively over the day, with little consumed after 9:00 pm. Intake was associated with age, ethnicity, smoking status, total calorie intake, and work hours (P <0.01) but not physical activity, economic status, education level, or employment status. Variables with the largest associations with intake were, respectively, ethnicity and age. Non-Hispanic black individuals consumed the smallest amounts (80±2 mg/d), non-Hispanic white individuals consumed the greatest amounts (194±3 mg/d), and Asian individuals (126±7 mg/d) and Hispanic individuals consumed intermediate amounts (127±3 mg/d). Middle-aged individuals (aged 50 to 54 years) consumed more caffeine (211±6 mg/d) than younger (107±4 mg/d, aged 20 to 24 years) and older individuals (153±4 mg/d, aged 75 to 79 years). Conclusion Most caffeine is consumed in the morning, when alertness is lowest, and very little in the evening before sleep. Ethnicity and age were the variables most strongly associated with intake; work hours, occupation, energy and alcohol intake, and smoking were also associated with intake. Because caffeine increases alertness, it is not surprising that its pattern of consumption and factors associated with its intake vary from those of most other food constituents. [ABSTRACT FROM AUTHOR]

Idiopathic hypersomnia (IH) is a chronic neurologic disorder with unknown mechanisms that result in long night-time sleep, daytime sleepiness, long non-refreshing naps, and difficult awakening presenting as sleep drunkenness. IH patients are typically diagnosed by shorter sleep latency on multiple sleep latency test (MSLT) along with long sleep time. Only symptomatic drug treatments are currently available for IH and no animal model to study it. Sleepy mice carry a splicing mutation in the Sik3 gene, leading to increased sleep time and sleep need. Here we used a mouse version of MSLT and a decay analysis of wake EEG delta power to validate the Sleepy mutant mouse as an animal model for IH. Sleepy mice had shorter sleep latency in the dark (active) phase than wild-type mice. They also showed lower decay of EEG delta density during wakefulness, possibly reflecting increased sleep inertia. These data indicate that the Sleepy mouse may have partial face validity as a mouse model for idiopathic hypersomnia. We then investigated the effect of orexin-A and the orexin receptor 2-selective agonist YNT-185 on the sleepiness symptoms of the Sleepy mouse. Intracerebroventricular orexin-A promoted wakefulness for 3 h and decreased wake EEG delta density after injection in Sleepy mice and wild-type mice. Moreover, Sleepy mice but not wild-type mice showed a sleep rebound after the orexin-A-induced wakefulness. Intraperitoneal YNT-185 promoted wakefulness for 3 h after injection in Sleepy mice, indicating the potential of using orexin agonists to treat not only orexin deficiency but hypersomnolence of various etiologies. [ABSTRACT FROM AUTHOR]

Idiopathic hypersomnia is a central hypersomnolence disorder of unknown origin characterized by excessive daytime sleepiness despite normal or long sleep time, and frequent severe sleep inertia. Management strategies have been largely derived from expert consensus, due to a lack of disease-specific assessments and reliance on case series and rare randomized controlled studies. Guidelines recommend treatment with off-label medications. Modafinil, which was approved for idiopathic hypersomnia until 2011 in Europe, is the most commonly used treatment and improved sleepiness in two recent randomized placebo-controlled trials. In 2021, low-sodium oxybate (LXB) was approved in the United States for idiopathic hypersomnia. In a placebo-controlled, double-blind, randomized withdrawal study, LXB reduced daytime sleepiness and sleep inertia, and improved daily functioning. Here, treatment options are reviewed considering the authors' professional experience, current guidelines, and the latest research developments. The choice of pharmacotherapy should be guided by symptom profile, age, comorbidities (eg, depressive symptoms, cardiovascular problems), and concomitant medications (eg, oral contraceptives). Nonpharmacologic approaches have a role in management. An instrument (idiopathic hypersomnia severity scale) has been validated in idiopathic hypersomnia specifically, opening a path to better assessment of symptoms, impact, and response to treatment. Continued research on idiopathic hypersomnia is needed to support treatment algorithms. [ABSTRACT FROM AUTHOR]

The transition from sleep to wake is marked by sleep inertia, a distinct state that is measurably different from wakefulness and manifests as performance impairments and sleepiness. Although the precise substrate of sleep inertia is unknown, electroencephalographic, evoked potential, and neuroimaging studies suggest the persistence of some features of sleep beyond the point of awakening. Forced desynchrony studies have demonstrated that sleep inertia impacts cognition differently than do homeostatic and circadian drives and that sleep inertia is most intense during awakenings from the biological night. Recovery sleep after sleep deprivation also amplifies sleep inertia, although the effects of deep sleep vary based on task and timing. In patients with hypersomnolence disorders, especially but not exclusively idiopathic hypersomnia, a more pronounced period of confusion and sleepiness upon awakening, known as "sleep drunkenness", is common and problematic. Optimal treatment of sleep drunkenness is unknown, although several medications have been used with benefit in small case series. Difficulty with awakening is also commonly endorsed by individuals with mood disorders, disproportionately to the general population. This may represent an important treatment target, but evidence-based treatment guidance is not yet available. [ABSTRACT FROM AUTHOR]

Idiopathic hypersomnia is a sleep disorder of neurologic origin characterized by excessive daytime sleepiness, with sleep inertia, long, unrefreshing naps, and prolonged nighttime sleep being key symptoms in many patients. Idiopathic hypersomnia is described in the International Classification of Sleep Disorders, 3rd Edition as a central disorder of hypersomnolence with distinct clinical features and diagnostic criteria; however, confirming the diagnosis of idiopathic hypersomnia is often challenging. Diagnosis of idiopathic hypersomnia is based on objective sleep testing and the presence of associated clinical features but may be difficult for clinicians to recognize and correctly diagnose because of its low prevalence, clinical heterogeneity, and symptoms, which are similar to those of other sleep disorders. The testing required for diagnosis of idiopathic hypersomnia also presents logistical barriers, and reliability of objective sleep measures is suboptimal. The pathophysiology of idiopathic hypersomnia remains unknown. In this review, clinical considerations related to the pathogenesis, diagnosis, and management of idiopathic hypersomnia will be discussed, including perspectives from the European Union and United States. [ABSTRACT FROM AUTHOR]

Responding to an emergency alarm poses a significant risk to firefighters’ health and safety, particularly to cardiovascular health, physical and psychological stress, and fatigue. These risks have been largely categorised for salaried firefighters working ‘on station’. Less is known about the factors that contribute to these risks for the vast number of non-salaried personnel who serve in retained roles, often deploying from home. The present study investigated the alarm response procedure for Australian metropolitan fire fighters, identifying common and divergent sources of risk for salaried and retained staff. There were significant differences in procedure between the two workgroups and this resulted in differences in risk profile between groups. Sleep and fatigue, actual response to the alarm stimulus, work-life balance and trauma emerged as sources of risk experienced differently by salaried and retained firefighters. Key findings included reports of fatigue in both groups, but particularly in the case of retained firefighters who manage primary employment as well as their retained position. This also translated into a poor sense of work-life balance. Both groups reported light sleep, insufficient sleep or fragmented sleep as a result of alarm response. In the case of salaried firefighters, this was associated with being woken on station when other appliances are called. There were risks from physical and psychological responses to the alarm stimulus, and reports of sleep inertia when driving soon after waking. The findings of this study highlight the common and divergent risks for these workgroups, and could be used in the ongoing management of firefighters’ health and safety. [ABSTRACT FROM AUTHOR]

Background: Few stimulants have been evaluated for the treatment of idiopathic hypersomnia (IH). Sodium oxybate (indicated in narcolepsy type 1, NT1) has not been tested in IH patients.Objective: The aim of this study is to retrospectively evaluate the benefit/risk ratio of sodium oxybate in IH versus NT1 using a chart review.Methods: We reviewed the files of 46 patients with IH (35.7 ± 12.6 years old, 78% women) and 47 patients with NT1 (44.1 ± 18 years old, 47% women) and evaluated the benefits of sodium oxybate using the Epworth sleepiness scale (ESS) and a four-point scale assessing the global benefit, sleep inertia, sleepiness, sleep duration, and sleep onset latency. The spontaneously reported side effects were collected.Results: Sodium oxybate was prescribed at a lower dose in IH than in NT1 (4.3 ± 2.2 vs. 6.6 ± 2.8 g/night, p <0.0001) patients after having tried more (3.2 ± 1.4 vs. 2.2 ± 1, p <0.0001) stimulants, but it produced a similar ESS change (-3.5 ± 4.5 vs. -3.2 ± 4.2 points) in the IH and NT1 groups. Severe morning inertia was improved in 24/34 (71%) patients with IH. During the follow-up period (15.8 months in IH vs. 35 months in NT1 groups), 53% IH and 68% NT1 patients dropped out. The side effects were as frequent in the IH group as in the NT1 group (67% vs. 52%), but nausea (40% vs. 13%) and dizziness (34.3% vs. 4.3%) were more frequent in the IH group.Conclusion: The benefit/risk ratio of sodium oxybate in IH- was similar to NT1-associated sleepiness, with additional benefits on severe morning inertia, despite using smaller doses in more refractory patients. [ABSTRACT FROM AUTHOR]

Objective Behavioral and physiological indexes of high sleep inertia (SI) characterize the awakening from recovery (REC) sleep after prolonged wakefulness, but the associated electroencephalogram (EEG) topography has never been investigated. Here, we compare the EEG topography following the awakening from baseline (BSL) and REC sleep. Methods We have recorded the EEG waking activity of 26 healthy subjects immediately after the awakening from BSL sleep and from REC sleep following 40 h of prolonged wakefulness. In both BSL and REC conditions, 12 subjects were awakened from stage 2 sleep, and 14 subjects from rapid eye movement (REM) sleep. The full-scalp waking EEG (eyes closed) was recorded after all awakenings. Results Subjects awakened from REC sleep showed a reduction of fronto-central alpha and beta-1 activities, while no significant effects of the sleep stage of awakening have been observed. Positive correlations between pre- and post-awakening EEG modifications following REC sleep have been found in the posterior and lateral cortices in the frequency ranges from theta to beta-2 and (only for REM awakenings) extending to the fronto-central regions in the beta-1 band, and in the midline central and parietal derivations for the alpha and delta bands, respectively. Conclusions These findings suggest that the higher SI after REC sleep may be due to the fronto-central decrease of alpha and beta-1 activity and to the persistence of the sleep EEG features after awakening in the posterior, lateral, and fronto-central cortices, without influences of the sleep stage of awakening. [ABSTRACT FROM AUTHOR]

Summary: Introduction: Sleep inertia refers to the inability to attain full alertness following awakening from sleep and is a major component of hypersomnia. As event-related potentials (ERPs) are correlated to the degree of consciousness, they allow exploring information processing in transitional states of vigilance. Their modifications during forced awakening (FA) context have been shown to reflect sleep inertia. Objectives: To assess the diagnostic value of a FA test using an oddball stimulation protocol during a nap in a representative sample of patients with excessive daytime sleepiness (EDS). Methods: One hundred and seventy three patients [30 narcolepsy, 62 idiopathic hypersomnia, 33 sleep apnoea syndrome, and 48 other (mainly psychiatric) hypersomnia] performed an auditory target detection stimulation task during pre-, post-nap wakefulness, and during two successive intra-nap FA while the EEG was simultaneously recorded. Both the accuracy of target detection and the ERPs were evaluated. ERPs during forced awakening test were considered to reflect sleep inertia if they presented with a P300 delay and/or sleep negativities (N350/N550). Results: Pre-nap behavior and ERPs were normal in all patients. Behavioral results were significantly worse during FA than during wakefulness for all groups of patients. P300 latencies were significantly delayed on FA conditions in each group of patients except the psychiatric group. Sensitivity and specificity for detection of sleep inertia were 64% and 94%, respectively, with predictive values of 96% (positive) and 50% (negative). Conclusions: Our results suggest that the FA test could be helpful as a diagnostic procedure for discriminating neurological from psychiatric hypersomnia. [Copyright &y& Elsevier]

Abstract: Sleep inertia (SI) denotes a period of hypovigilance, confusion and impaired cognitive and behavioral performance that immediately follows awakening. Based on the observation that the reactivation of some cortical areas is faster than other upon awakening, here we examined regional differences between presleep and postsleep waking period. Moreover, we also compared rapid eye movements (REM) and stage 2 non-rapid eye movements (NREM) awakenings in a within-subject design. Presleep and postsleep waking electroencephalogram (EEG; 5 min with eyes-closed and 5 min with eyes-open) of 18 healthy subjects (12 males, mean age=23.8±2.3 years) were recorded from 19 derivations. Participants slept for two consecutive nights in the laboratory. In one night they were awakened from stage 2 NREM, while in the other from REM sleep. EEG power spectra were calculated across the following bands: delta (1–4 Hz), theta (5–7 Hz), alpha (8–12 Hz), beta-1 (13–16 Hz) and beta-2 (17–24 Hz). Moreover, a detailed hertz-by-hertz analysis has been repeated in the 2–4 Hz frequency range. Postsleep wakefulness, compared to presleep, is characterized by a generalized decrease of higher beta-1 and beta-2 EEG power over almost all scalp locations. A detailed analysis of topographical modifications in the low-frequency range showed that postsleep wakefulness is characterized by an increased delta activity in the posterior scalp locations, and by a concomitant frontal decrease compared to presleep. Moreover, it was found a prevalence of EEG power in the high frequency ranges (beta-1 and beta-2) upon awakening from stage 2 compared to REM awakenings over the left anterior derivations. Altogether these findings support the hypothesis that a generalized reduction in beta activity and increased delta activity in more posterior areas upon awakening may represent the EEG substratum of the sleep inertia phenomenon. [Copyright &y& Elsevier]

Abstract: In most healthy people morning awakening is associated with a burst of cortisol secretion: the cortisol awakening response (CAR). It is argued that the CAR is subject to a range physiological regulatory influences that facilitate this rapid increase in cortisol secretion. Evidence is presented for reduced adrenal sensitivity to rising levels of ACTH in the pre-awakening period, mediated by an extra-pituitary pathway to the adrenal from the suprachiasmatic nucleus (SCN). A role for the hippocampus in this pre-awakening regulation of cortisol secretion is considered. Attainment of consciousness is associated with ‘flip-flop’ switching of regional brain activation, which, it is argued, initiates a combination of processes: (1) activation of the hypothalamic pituitary adrenal (HPA) axis; (2) release of pre-awakening reduced adrenal sensitivity to ACTH; (3) increased post-awakening adrenal sensitivity to ACTH in response to light, mediated by a SCN extra-pituitary pathway. An association between the CAR and the ending of sleep inertia is discussed. [ABSTRACT FROM AUTHOR]

Abstract: The present study examined the effects of self-awakening on sleep inertia after nocturnal sleep. Ten undergraduate and graduate students participated in the study. Their polysomnograms were recorded for five consecutive nights; the first, second, and third to fifth nights were adaptation, forced-awakening, and self-awakening nights, respectively. Participants rated sleepiness, fatigue, comfort, and work motivation, and these ratings were followed by switching (7min) and auditory reaction time tasks (6min), both before bedtime (15min) and immediately after awakening (4min×15min). Although reaction times on the auditory were task prolonged, and participants complained of feeling uncomfortable immediately after forced-awakening, reaction times were shortened after self-awakening, and the participants did not complain of feeling uncomfortable on these nights. The results of this study suggest that sleep inertia occurs after forced-awakening and that it can be prevented by self-awakening. [Copyright &y& Elsevier]

• Exercise may reduce sleep inertia by targeting key physiological processes on waking. • Exercise (30 s) on waking improved subjective sleepiness but not cognitive performance. • High intensity exercise led to a greater cortisol awakening response than no exercise. • Core body temperature was not affected by exercise on waking. • Combining exercise with other countermeasures (e.g., caffeine) should be examined. Determine whether 30 s (s) of exercise performed upon waking can reduce sleep inertia and accelerate an increase in the cortisol awakening response (CAR) and core body temperature (CBT), compared to when sedentary. Fifteen participants (mean age ± SD, 25.9 ± 5.9 years; six females) completed a counterbalanced, repeated measures, in-laboratory study involving three single experimental nights, each separated by a four-night recovery period. Participants were woken following a 2-h nap (2400–0200) and completed a cycling bout of high-intensity (30-s sprint), low-intensity (30 s at 60% maximum heart rate), or no exercise (sedentary). Sleep inertia testing (eight batteries, 15-min intervals) began immediately following and included measures of subjective sleepiness (Karolinska Sleepiness Scale) and cognitive performance tasks (psychomotor vigilance, serial addition and subtraction, and spatial configuration). CBT was measured continuously via an ingestible telemetric capsule. The CAR was determined using salivary cortisol samples collected at 0, 30 and 45 min post-waking. Data were analysed using mixed effects analysis of variance. There was no difference in cognitive performance or CBT between conditions. Participants felt less sleepy in the high-intensity condition, followed by the low-intensity and sedentary conditions (p =.003). The CAR was greatest in the high-intensity condition, followed by the sedentary condition, and low-intensity condition (p < 0.001), with no differences between the low-intensity and sedentary conditions. Those who exercise upon waking should be aware that while they may feel more alert, they may not be performing better than if they had not exercised. Future research should investigate whether exercise of different duration or timing may impact sleep inertia. [ABSTRACT FROM AUTHOR]

Abstract: The aim of the present study was to characterize the regional electroencephalographic substratum of the awakening process by means of a Hz-by-Hz EEG spectral power analysis. For this purpose, we recorded a group of 25 female subjects who slept for at least two consecutive nights in the laboratory. The postsleep waking EEG was compared to the one recorded during the presleep wakefulness from four midline derivations (Fz–A1, Cz–A1, Pz–A1, Oz–A1). Results indicated that the first 10min after awakening are characterized by an increase of EEG power in the low-frequency range (1–9Hz) compared to the corresponding presleep waking period, and by a significant decrease of EEG power in the beta range (18–24Hz). As regards topographic differences, the increase of EEG power upon awakening in the delta–theta range showed a parieto-occipital prevalence. Moreover, the occipital derivation showed a larger decrease of power in the beta range as compared to the other derivations. In conclusion, the EEG substratum of the sleep offset period is characterized by a pattern of increased EEG power in the delta–theta and low-alpha bands, and of decreased power in the beta range. This pattern could be considered as the spectral EEG signature of the sleep inertia phenomenon. The state of postsleep EEG hypoarousal does not subside in the first 10-min period after awakening considered in the present analysis. Finally, according to our results, the more posterior scalp locations show stronger EEG signs of sleep inertia, and could be the last ones to properly wake up. [Copyright &y& Elsevier]

Abstract: Sleep inertia (SI) is a transient period occurring immediately after awakening, usually characterized by performance decrement. When sleep is sufficient, SI is moderate, and produces few or no deficit. When it is associated with prior sleep deprivation, SI shows dose-dependent negative effects on cognitive performance, especially when subjects have been awaken in slow wave sleep (SWS). In the present study, spectral analysis was applied during the last 10 min before and the first 10 min after awakening, and during 1 h after awakening while subjects performed the Stroop test. Seventeen subjects were divided into a Control group who slept 8 h, and a Sleep Deprived group who slept only 2 h. The results show that performance was normal in the Control group, whereas reaction time was increased during the first half hour and error level during the second half hour in the Sleep Deprived group. Spectral analysis applied on the waking EEG during the whole test session showed that alpha activity was increased in both groups, but theta power only in the Sleep Deprived group. There was a high positive correlation in sleep deprived subjects between delta power during the last 10 min of sleep and subsequent performance decrement in speed and accuracy. Comparison of individual records showed a high positive correlation between spectral power before and after awakening in the Control group (generally in the sense of an increased frequency band), but no correlation was found in the Sleep Deprived group who exhibited a rather disorganized pattern. We discuss these results in terms of incoherence in the EEG continuity during sleep offset after prior sleep loss, which could partly account for the performance decrement observed during SI in sleep deprived subjects. [Copyright &y& Elsevier]

Abstract: Napping benefits and sustains subsequent performance. Prophylactic naps have been recommended as a means to maintain performance during extended wakefulness, as required during shiftwork. However, napping may cause short-term performance impairments, because awakening from sleep is followed by sleep inertia, a period of hypovigilance and impaired cognitive and behavioral performance. We investigated sleep inertia after an afternoon nap. Healthy 18–28 year-olds (n=50, not sleep deprived) were assigned to sleep, active wake or rest groups for a 2-h experimental phase with polysomnography starting either at 14:00 or 16:00 for half of each group. Before (baseline, 12:30 or 14:30) and in five sessions during the hour after the experimental phase (16:00–17:00 or 18:00–19:00), subjects completed an addition task, an auditory reaction time task, and the Stanford Sleepiness Scale. In session one, addition speed in the sleep group was reduced compared with baseline and with active wake controls, whereas calculation accuracy did not change. Addition speed in the sleep and rest groups increased substantially from session one to session two and reached a level similar to that of the active wake group by the fifth session. In the first session, auditory reaction speed of the sleep group was reduced compared with baseline and with rest controls but did not differ from the active wake group. The slowest reaction times showed significant recovery after 20 min. The groups reported similar increases in subjective sleepiness after the experimental period. These findings provide evidence for performance slowing and recovery during the hour following a 2-h nap opportunity. They highlight the importance of employing multiple control groups and various objective and subjective measures to assess sleep inertia. [Copyright &y& Elsevier]

Objective: The present study examined whether the combination of a short daytime nap with caffeine, bright light and face washing was effective against mid-afternoon sleepiness.Methods: Ten young healthy adults participated in 5 experimental conditions; those experiments were—Nap only: taking a 20 min nap; Caffeine+Nap: taking 200 mg of caffeine followed by a nap; Nap+Bright-light: being exposed to 2000 lx of bright light for 1 min immediately after napping; Nap+Face-washing: washing their faces immediately after napping; and No-Nap: taking a rest without sleep. These naps were taken at 12:40 hours. The subjects engaged in computer tasks for 15 min before napping and for 1 h after napping.Results: Caffeine+Nap was the most effective for subjective sleepiness and performance level; its effects lasted throughout 1 h after napping. Nap+Bright-light was comparable with Caffeine+Nap, except for performance level. Nap+Face-washing showed mild and transient effects, however, it suppressed subjective sleepiness immediately after napping.Conclusions: The effects of a short nap against mid-afternoon sleepiness could be enhanced by combining caffeine intake, exposure to bright light, or face washing.Significance: The present study would provide effective countermeasures against mid-afternoon sleepiness and sleepiness related accidents. [Copyright &y& Elsevier]

Objectives: This study examined whether anticipatory changes exist in heart rate prior to awakening from a nap by means of self-awakening. The effects of self-awakening on sleepiness after the short nap were also studied.Method: Nine students participated in 3 experimental conditions: (1) the control condition, in which participants watched television instead of taking a short nap; (2) the self-awakening condition, in which participants tried to wake up approximately 15 min after ‘lights off’ (criterion range: 15±5 min) and (3) the forced-awakening condition, in which participants were instructed to sleep for 30 min, but were awoken by the experimenter after 15 min.Results: In the self-awakening condition, heart rate gradually increased approximately 3 min before awakening. The error response ratio of the auditory-oddball task and the duration of doze time during the task were less after both types of nap conditions than in the control condition. Subjective sleepiness, which is measured after awakening, was lowest in the self-awakening condition.Conclusions: The results of this experiment suggest that self-awakening prepares autonomic activation that facilitates a more smooth transition from sleep to awakening, and reduces sleepiness after naps. [Copyright &y& Elsevier]

Objectives: To assess auditory evoked potentials (AEPs) before sleep and upon 3 awakenings during an undisturbed baseline night and to compare them to AEPs during a night characterized by a recuperative increase in the amount of slow-wave sleep (SWS) as a consequence of two consecutive nights of selective SWS deprivation.Methods: Ten male subjects slept in the laboratory for 6 consecutive nights. The first 2 nights were undisturbed. The 3rd night was considered as baseline. During the 4th and 5th nights, selective SWS deprivation was obtained by means of acoustic stimulation. The 6th night was a recovery. The data reported here were collected during the baseline and the recovery night. Subjects were awakened 3 times: after 2 h, 5 h (nocturnal awakenings) and 7.5 h (final morning awakening) of sleep, respectively. All the awakenings were carried out from stage 2. The AEP recordings were carried out in bed, while subjects were performing a simple auditory reaction time task.Results: The amplitude of the N1-P2 complex decreased upon the first awakening of the baseline night as compared to pre-sleep wakefulness levels; during the recovery night, the decrease of N1-P2 amplitude was present also upon the second and final awakening. N1 latency increased upon the two nocturnal awakenings regardless of the night, while P2 latency was not affected. Moreover, the N1-P2 amplitude increased during recovery at the frontal midline derivation as compared to baseline, while it decreased at Pz and Oz.Conclusions: The N1-P2 amplitude and, to a lesser extent, the N1 latency, are sensitive in showing a state of brain deactivation during the sleep-wake transition. The decrease of N1-P2 amplitude at the parieto-occipital locations during recovery is coherent with the hypothesis of a functional link between SWS amount and cortical hypoarousal upon awakening. The unexpected increase of the same variable at Fz can be interpreted as the effect of a compensatory effort of the frontal areas for the increased homeostatic drive for sleep during the recovery night. [ABSTRACT FROM AUTHOR]

Women who wake from sleep during sexual assault commonly report confusion and disorientation. Confusion and disorientation, with impaired decision making after waking, are symptoms of 'sleep inertia', and part of the normal transition from sleep to full wakefulness which is maximal in the minutes after wakening and can be prolonged. In this study of 305 adult females (median age 26, range 18-68), who presented for a sexual assault forensic medical examination, 38 (12%) (median age 27, range 18-51) woke to find sexual acts already in progress. For 25 of these women (25/38 for 66%), an act of penile-vaginal penetration was already occurring when the woman woke. Of the 38 women (12%) who woke during the sexual assault, several had factors known to enhance the impairment of sleep inertia including forced arousal (38/38, 100%) and age under 25 (15/38, 39%). 17 (17/38 for 45%) of these women who woke had consumed varying amounts of alcohol prior to sleep and these 17 woke fully during the assault and then stayed awake. A further 16 women, (16/38 for 42%) woke during the sexual assault but returned to sleep during or after the assault, and all these 16 gave a history of intoxication by drugs or alcohol prior to sleep. Importantly 5, (5/38 for 13%) of the women who woke during the assault had consumed no intoxicating substances. A further 68 (23%) of the 305 women, (median age 26, range 18-58) had no memory on waking of the alleged sexual assault despite having other reasons to believe that a sexual assault had occurred. Forensic medical examiners can assist both the justice process, and patient care, by considering the possibility of sleep inertia among victims who report disorientation and slow or confused decision making on waking during a sexual assault. [ABSTRACT FROM AUTHOR]

• Take-over performance and manual driving behavior are investigated in drivers after electroencephalography-confirmed stable sleep.. • After sleep, take-over performance is impaired yielding "driving errors" in the Take-Over Controllability-Rating. • Manual driving performance after sleep yields impairments in lane and speed keeping and drivers chose lower speeds. • Sleep inertia has a serious impact on driving behavior and has to be accounted for in the development of automated vehicles. Sleep is emerging as a new driver state in automated driving. Post-sleep performance impairments due to sleep inertia, the transitional phase from sleep to wakefulness that can take up to 30 min, are a potential safety issue. Take-over performance immediately after sleep is impaired and drivers perceive the take-over as critical. The aim of the presented study was to assess take-over behavior immediately after sleep and driving behavior during the 10 min after sleep. A study with N = 31 drivers was conducted in a high-fidelity driving simulator. Take-over performance and driving performance were assessed a) under alert baseline conditions and b) after awakening from electroencephalography-confirmed stable sleep. Take-over performance 15 s after awakening was impaired resulting in more driving errors compared to the alert baseline. Lane keeping was dramatically impaired in the first 3 min after sleep and recovered rapidly. Drivers drove slower after sleep and speed keeping was less stable for at least 10 min. The results suggest that human-machine interaction design should account for the drivers' impaired post-sleep driving performance. [ABSTRACT FROM AUTHOR]

Emergency services present a unique operational environment for the management of fatigue and sleep inertia. Communities request and often expect the provision of emergency services on a 24/7/365 basis. This can result in highly variable workloads and/or significant need for on-demand or on-call working time arrangements. In turn, the management of fatigue-related risk requires a different approach than in other more predictable shift working sectors (e.g., mining and manufacturing). The aim of this review is to provide a comprehensive overview of fatigue risk management that is accessible to regulators, policy makers and organisations in the emergency services sector. The review outlines the unique fatigue challenges in the emergency services sector, examines the current scientific and policy consensus around managing fatigue and sleep inertia, and finally discusses strategies that emergency services organisations can use to minimise the risks associated with fatigue and sleep inertia. [ABSTRACT FROM AUTHOR]

The aim of this European initiative is to facilitate a structured discussion to improve the next edition of the International Classification of Sleep Disorders (ICSD), particularly the chapter on central disorders of hypersomnolence. The ultimate goal for a sleep disorders classification is to be based on the underlying neurobiological causes of the disorders with clear implication for treatment or, ideally, prevention and or healing. The current ICSD classification, published in 2014, inevitably has important shortcomings, largely reflecting the lack of knowledge about the precise neurobiological mechanisms underlying the majority of sleep disorders we currently delineate. Despite a clear rationale for the present structure, there remain important limitations that make it difficult to apply in routine clinical practice. Moreover, there are indications that the current structure may even prevent us from gaining relevant new knowledge to better understand certain sleep disorders and their neurobiological causes. We suggest the creation of a new consistent, complaint driven, hierarchical classification for central disorders of hypersomnolence; containing levels of certainty, and giving diagnostic tests, particularly the MSLT, a weighting based on its specificity and sensitivity in the diagnostic context. We propose and define three diagnostic categories (with levels of certainty): 1/"Narcolepsy" 2/"Idiopathic hypersomnia", 3/"Idiopathic excessive sleepiness" (with subtypes). [ABSTRACT FROM AUTHOR]