Eyelid Closure Behavior of Patients with Idiopathic and Nonorganic Hypersomnia, Narcolepsy-Cataplexy, and Healthy Controls in the Maintenance of Wakefulness Test.

PURPOSE Differential diagnosis of central disorders of hypersomnolence remains challenging, particularly between idiopathic (IH) and nonorganic hypersomnia (NOH). We hypothesized that eyelid closure behavior in the maintenance of wakefulness test (MWT) could be a valuable biomarker. PATIENTS AND METHODS MWT recordings of patients with IH, NOH, narcolepsy-cataplexy (NC), and healthy sleep-deprived controls (H) were retrospectively analyzed (15 individuals per group). For each MWT trial, visual scoring of face videography for partial (50-80%) and full eyelid closure (≥80%) was performed from "lights off" to the first microsleep episode (≥3 s). RESULTS In all groups, the frequency and cumulative duration of periods with partial and full eyelid closure gradually increased toward the first microsleep episode. On the group level, significant differences occurred for the latency to the first microsleep episode (IH 21 min (18-33), NOH 23 min (17-35), NC 11 min (7-19), H 10 min (6-25); p = 0.009), the ratio between partial and full eyelid closure duration (IH 2.2 (0.9-3.1), NOH 0.5 (0-1.2), NC 2.8 (1.1-5), H 0.7 (0.4-3.3); p = 0.004), and the difference between full and partial eyelid closure duration in the five minutes prior to the first microsleep episode (∆full - partial eyelid closure duration: IH -16 s (-35 to 28); NOH 46 s (9-82); NC -6 s (-26 to 5); H 10 s (-4 to 18); p = 0.007). IH and NOH significantly differed comparing the ratio between partial and full eyelid closure (p = 0.005) and the difference between ∆full - partial eyelid closure duration in the five minutes prior to the first microsleep episode (p = 0.006). CONCLUSION In the MWT, eyelid closure behavior (∆full - partial) in the period prior to the first microsleep episode could be of value for discriminating NOH from other etiologies of excessive daytime sleepiness, particularly IH

Eyelid Closure Behavior of Patients with Idiopathic and Nonorganic Hypersomnia, Narcolepsy-Cataplexy, and Healthy Controls in the Maintenance of Wakefulness Test

Annelies Santschi,1,* David R Schreier,1,* Anneke Hertig-Godeschalk,1 Samuel EJ Knobel,1 Uli S Herrmann,1 Jelena Skorucak,2 Wolfgang J Schmitt,3 Johannes Mathis1,4 1Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; 2University Children’s Hospital Zurich, Zurich, Switzerland; 3University Hospital of Psychiatry, University of Bern, Bern, Switzerland; 4Sleep Medicine, Neurozentrum Bern, Bern, Switzerland*These authors contributed equally to this workCorrespondence: David R Schreier, Department of Neurology, Inselspital, Bern University Hospital, Freiburgstrasse 16, Bern, CH-3010, Switzerland, Tel +41 31 632 21 11, Email [email protected]: Differential diagnosis of central disorders of hypersomnolence remains challenging, particularly between idiopathic (IH) and nonorganic hypersomnia (NOH). We hypothesized that eyelid closure behavior in the maintenance of wakefulness test (MWT) could be a valuable biomarker.Patients and Methods: MWT recordings of patients with IH, NOH, narcolepsy-cataplexy (NC), and healthy sleep-deprived controls (H) were retrospectively analyzed (15 individuals per group). For each MWT trial, visual scoring of face videography for partial (50– 80%) and full eyelid closure (≥ 80%) was performed from “lights off” to the first microsleep episode (≥ 3 s).Results: In all groups, the frequency and cumulative duration of periods with partial and full eyelid closure gradually increased toward the first microsleep episode. On the group level, significant differences occurred for the latency to the first microsleep episode (IH 21 min (18– 33), NOH 23 min (17– 35), NC 11 min (7– 19), H 10 min (6– 25); p = 0.009), the ratio between partial and full eyelid closure duration (IH 2.2 (0.9– 3.1), NOH 0.5 (0– 1.2), NC 2.8 (1.1– 5), H 0.7 (0.4– 3.3); p = 0.004), and the difference between full and partial eyelid closure duration in the five minutes prior to the first microsleep episode (∆full – partial eyelid closure duration: IH − 16 s (− 35 to 28); NOH 46 s (9– 82); NC − 6 s (− 26 to 5); H 10 s (− 4 to 18); p = 0.007). IH and NOH significantly differed comparing the ratio between partial and full eyelid closure (p = 0.005) and the difference between ∆full – partial eyelid closure duration in the five minutes prior to the first microsleep episode (p = 0.006).Conclusion: In the MWT, eyelid closure behavior (∆full – partial) in the period prior to the first microsleep episode could be of value for discriminating NOH from other etiologies of excessive daytime sleepiness, particularly IH.Keywords: hypersomnia, hypersomnia associated with psychiatric disorders, excessive daytime sleepiness, vigilance test, central disorders of hypersomnolence, microslee

WAKE: a behind-the-ear wearable system for microsleep detection

Microsleep, caused by sleep deprivation, sleep apnea, and narcolepsy, costs the U.S.'s economy more than $411 billion/year because of work performance reduction, injuries, and traffic accidents. Mitigating microsleep's consequences require an unobtrusive, reliable, and socially acceptable microsleep detection solution throughout the day, every day. Unfortunately, existing solutions do not meet these requirements. In this paper, we propose a novel behind-the-ear wearable device for microsleep detection, called WAKE. WAKE detects microsleep by monitoring biosignals from the brain, eye movements, facial muscle contractions, and sweat gland activities from behind the user's ears. In particular, we introduce a Three-fold Cascaded Amplifying (3CA) technique to tame the motion artifacts and environmental noises for capturing high fidelity signals. The behind-the-ear form factor is motivated by the fact that bone-conductance headphones, which are worn around the ear, are becoming widely used. This technology trend gives us an opportunity to enable a wide range of cognitive monitoring and improvement applications by integrating more sensing and actuating functionality into the ear-phone, making it a smarter one. Through our prototyping, we show that WAKE can suppress motion and environmental noise in real-time by 9.74-19.47 dB while walking, driving, or staying in different environments ensuring that the biosignals are captured reliably. We evaluated WAKE against gold-standard devices on 19 sleep-deprived and narcoleptic subjects. The Leave-One-Subject-Out Cross-Validation results show the feasibility of WAKE in microsleep detection on an unseen subject with average precision and recall of 76% and 85%, respectively

WAKE: a behind-the-ear wearable system for microsleep detection

Microsleep, caused by sleep deprivation, sleep apnea, and narcolepsy, costs the U.S.'s economy more than $411 billion/year because of work performance reduction, injuries, and traffic accidents. Mitigating microsleep's consequences require an unobtrusive, reliable, and socially acceptable microsleep detection solution throughout the day, every day. Unfortunately, existing solutions do not meet these requirements. In this paper, we propose a novel behind-the-ear wearable device for microsleep detection, called WAKE. WAKE detects microsleep by monitoring biosignals from the brain, eye movements, facial muscle contractions, and sweat gland activities from behind the user's ears. In particular, we introduce a Three-fold Cascaded Amplifying (3CA) technique to tame the motion artifacts and environmental noises for capturing high fidelity signals. The behind-the-ear form factor is motivated by the fact that bone-conductance headphones, which are worn around the ear, are becoming widely used. This technology trend gives us an opportunity to enable a wide range of cognitive monitoring and improvement applications by integrating more sensing and actuating functionality into the ear-phone, making it a smarter one. Through our prototyping, we show that WAKE can suppress motion and environmental noise in real-time by 9.74-19.47 dB while walking, driving, or staying in different environments ensuring that the biosignals are captured reliably. We evaluated WAKE against gold-standard devices on 19 sleep-deprived and narcoleptic subjects. The Leave-One-Subject-Out Cross-Validation results show the feasibility of WAKE in microsleep detection on an unseen subject with average precision and recall of 76% and 85%, respectively.</p

Sleep Physiology, Circadian Rhythms, Waking Performance and the Development of Sleep-Wake Therapeutics

Disturbances of the sleep-wake cycle are highly prevalent and diverse. The aetiology of some sleep disorders, such as circadian rhythm sleep-wake disorders, is understood at the conceptual level of the circadian and homeostatic regulation of sleep and in part at a mechanistic level. Other disorders such as insomnia are more difficult to relate to sleep regulatory mechanisms or sleep physiology. To further our understanding of sleep-wake disorders and the potential of novel therapeutics, we discuss recent findings on the neurobiology of sleep regulation and circadian rhythmicity and its relation with the subjective experience of sleep and the quality of wakefulness. Sleep continuity and to some extent REM sleep emerge as determinants of subjective sleep quality and waking performance. The effects of insufficient sleep primarily concern subjective and objective sleepiness as well as vigilant attention, whereas performance on higher cognitive functions appears to be better preserved albeit at the cost of increased effort. We discuss age-related, sex and other trait-like differences in sleep physiology and sleep need and compare the effects of existing pharmacological and non-pharmacological sleep- and wake-promoting treatments. Successful non-pharmacological approaches such as sleep restriction for insomnia and light and melatonin treatment for circadian rhythm sleep disorders target processes such as sleep homeostasis or circadian rhythmicity. Most pharmacological treatments of sleep disorders target specific signalling pathways with no well-established role in either sleep homeostasis or circadian rhythmicity. Pharmacological sleep therapeutics induce changes in sleep structure and the sleep EEG which are specific to the mechanism of action of the drug. Sleep- and wake-promoting therapeutics often induce residual effects on waking performance and sleep, respectively. The need for novel therapeutic approaches continues not at least because of the societal demand to sleep and be awake out of synchrony with the natural light-dark cycle, the high prevalence of sleep-wake disturbances in mental health disorders and in neurodegeneration. Novel approaches, which will provide a more comprehensive description of sleep and allow for large-scale sleep and circadian physiology studies in the home environment, hold promise for continued improvement of therapeutics for disturbances of sleep, circadian rhythms and waking performance