Relevant bibliographies by topics / Sleep onset latency

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Sleep onset latency'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Sleep onset latency"

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Babson, Kimberly A., Casey D. Trainor, Liviu Bunaciu, and Matthew T. Feldner. "An Examination of Anxiety Sensitivity as a Moderator of the Relation Between Sleep Anticipatory Anxiety and Sleep Onset Latency." Journal of Cognitive Psychotherapy 22, no. 3 (2008): 258–70. http://dx.doi.org/10.1891/0889-8391.22.3.258.

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Evidence suggests that advancing currently limited knowledge about self-reported sleep onset latency is important for better understanding insomnia. Relatively little research has been conducted to understand factors that affect sleep onset latency. The current study tested a hypothesized role of factors of the global anxiety sensitivity (AS) construct as moderators of the relation between sleep onset latency and physical and cognitive components of sleep anticipatory anxiety. As hypothesized, AS-Physical Concerns moderated the relation between the physical component of sleep anticipatory anxiety and sleep onset latency, even after controlling for age, gender, negative affect, and substance use variables. However, in contrast to prediction, AS-Mental Incapacitation Concerns did not appear to moderate the relation between sleep onset latency and the cognitive component of sleep anticipatory anxiety. These findings are discussed in terms of extant research on sleep onset latency, and future directions for research to advance this body of knowledge are considered.
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Raymann, Roy J. E. M., Dick F. Swaab, and Eus J. W. Van Someren. "Cutaneous warming promotes sleep onset." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 6 (2005): R1589—R1597. http://dx.doi.org/10.1152/ajpregu.00492.2004.

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Sleep occurs in close relation to changes in body temperature. Both the monophasic sleep period in humans and the polyphasic sleep periods in rodents tend to be initiated when core body temperature is declining. This decline is mainly due to an increase in skin blood flow and consequently skin warming and heat loss. We have proposed that these intrinsically occurring changes in core and skin temperatures could modulate neuronal activity in sleep-regulating brain areas (Van Someren EJW, Chronobiol Int 17: 313–54, 2000). We here provide results compatible with this hypothesis. We obtained 144 sleep-onset latencies while directly manipulating core and skin temperatures within the comfortable range in eight healthy subjects under controlled conditions. The induction of a proximal skin temperature difference of only 0.78 ± 0.03°C (mean ± SE) around a mean of 35.13 ± 0.11°C changed sleep-onset latency by 26%, i.e., by 3.09 minutes [95% confidence interval (CI), 1.91 to 4.28] around a mean of 11.85 min (CI, 9.74 to 14.41), with faster sleep onsets when the proximal skin was warmed. The reduction in sleep-onset latency occurred despite a small but significant decrease in subjective comfort during proximal skin warming. The induction of changes in core temperature (δ = 0.20 ± 0.02°C) and distal skin temperature (δ = 0.74 ± 0.05°C) were ineffective. Previous studies have demonstrated correlations between skin temperature and sleep-onset latency. Also, sleep disruption by ambient temperatures that activate thermoregulatory defense mechanisms has been shown. The present study is the first to experimentally demonstrate a causal contribution to sleep-onset latency of skin temperature manipulations within the normal nocturnal fluctuation range. Circadian and sleep-appetitive behavior-induced variations in skin temperature might act as an input signal to sleep-regulating systems.
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Smith, Simon, and John Trinder. "The effect of arousals during sleep onset on estimates of sleep onset latency." Journal of Sleep Research 9, no. 2 (2000): 129–35. http://dx.doi.org/10.1046/j.1365-2869.2000.00194.x.

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Kim, Bowon, Eunjin Hwang, Youngsoo Kim, and Jee Hyun Choi. "Prolonged Sleep-Onset Latency during Chronic Sleep Restriction in Mice." Sleep Medicine Research 4, no. 1 (2013): 28–32. http://dx.doi.org/10.17241/smr.2013.4.1.28.

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Kräuchi, Kurt, Christian Cajochen, Esther Werth, and Anna Wirz-Justice. "Functional link between distal vasodilation and sleep-onset latency?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 3 (2000): R741—R748. http://dx.doi.org/10.1152/ajpregu.2000.278.3.r741.

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Thermoregulatory processes have long been implicated in initiation of human sleep. The purpose of this study was to evaluate the role of heat loss in sleep initiation, under the controlled conditions of a constant-routine protocol modified to permit nocturnal sleep. Heat loss was indirectly measured by means of the distal-to-proximal skin temperature gradient (DPG). A stepwise regression analysis revealed that the DPG was the best predictor variable for sleep-onset latency (compared with core body temperature or its rate of change, heart rate, melatonin onset, and subjective sleepiness ratings). This study provides evidence that selective vasodilation of distal skin regions (and hence heat loss) promotes the rapid onset of sleep.
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Milkins, Bronwyn, Lies Notebaert, Colin MacLeod, and Patrick J. F. Clarke. "The Potential Benefits of Targeted Attentional Bias Modification on Cognitive Arousal and Sleep Quality in Worry-Related Sleep Disturbance." Clinical Psychological Science 4, no. 6 (2016): 1015–27. http://dx.doi.org/10.1177/2167702615626898.

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Attentional bias for sleep-related negative information is believed to contribute to symptoms of insomnia by elevating arousal during the presleep period. In the present study, we examined whether the delivery of an attentional bias modification (ABM) procedure in the presleep period could produce transient benefits for sleep-disturbed individuals by reducing presleep cognitive arousal and improving ease of sleep onset. In a counterbalanced repeated A-B design, participants alternated completing an ABM training task and a nontraining control task across six nights and reported on presleep cognitive arousal and sleep onset latency. Significant reductions in presleep cognitive arousal and sleep onset latency were observed on nights where the ABM task was completed relative to nights where the control task was completed. These results suggest that delivery of ABM can attenuate cognitive arousal and sleep onset latency and highlights the possibility that targeted delivery of ABM could deliver real-world benefits for sleep-disturbed individuals.
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Cantero, Jose L., Mercedes Atienza, Robert Stickgold, and J. Allan Hobson. "Nightcap: A Reliable System for Determining Sleep Onset Latency." Sleep 25, no. 2 (2002): 238–45. http://dx.doi.org/10.1093/sleep/25.2.238.

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Patel, Kamal, and Bianca J. Lang. "1253 Multiple sleep onset REM episodes in middle age woman with excessive daytime sleepiness – Is this automatically assumed narcolepsy?" Sleep 43, Supplement_1 (2020): A477. http://dx.doi.org/10.1093/sleep/zsaa056.1247.

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Abstract Introduction Presence of sleep onset REM episodes often raises concerns of narcolepsy. However other conditions have shown to have presence of sleep on REM episodes which include but not limited to obstructive sleep apnea, sleep wake schedule disturbance, alcoholism, neurodegenerative disorders, depression and anxiety Report of Case Here we present a case of 30 year old female with history of asthma, patent foraman ovale, migraine headache, and anxiety who presented with daytime sleepiness, falling asleep while at work, occasional scheduled naps, non-restorative sleep, sleep paralysis, and hypnopompic hallucination. Pertinent physical exam included; mallampati score of 4/4, retrognathia, high arched hard palate, crowded posterior oropharynx. She had a score of 16 on Epworth sleepiness scale. Patient previously had multiple sleep latency test at outside facility which revealed 4/5 SOREM, with mean sleep onset latency of 11.5 minutes. She however was diagnosed with narcolepsy and tried on modafinil which she failed to tolerate. She was tried on sertraline as well which was discontinued due to lack of benefit. She had repeat multiple sleep latency test work up which revealed 2/5 SOREM, with mean sleep onset latency was 13.1 minutes. Her overnight polysomnogram prior to repeat MSLT showed SOREM with sleep onset latency of 10 minutes. Actigraphy showed consistent sleep pattern overall with sufficient sleep time but was taking hydroxyzine and herbal medication. Patient did not meet criteria for hypersomnolence disorder and sleep disordered breathing. Conclusion There is possibility her medication may have played pivotal role with her daytime symptoms. We also emphasize SOREMs can be present in other disorders such as anxiety in this case and not solely in narcolepsy
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WHITE, MARJORIE A., PHOEBE D. WILLIAMS, DORIS J. ALEXANDER, GAIL M. POWELL-COPE, and MICHAEL CONLON. "Sleep Onset Latency and Distress In Hospitalized Children." Nursing Research 39, no. 3 (1990): 134???139. http://dx.doi.org/10.1097/00006199-199005000-00002.

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MA, White, Williams PD, Alexander DJ, Powell-Cope CM, and Conlon M. "Sleep onset latency and distress in hospitalized children." Dimensions Of Critical Care Nursing 9, no. 5 (1990): 310. http://dx.doi.org/10.1097/00003465-199009000-00018.

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Dissertations / Theses on the topic "Sleep onset latency"

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Holmes, Alexandra L. "Melatonin and zopiclone reduce sleep onset latency and core body temperature /." Title page and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09SB/09sbh749.pdf.

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Pollard, Katherine A. "Daytime melatonin administration in elderly subjects : effects on core temperature and sleep onset latency /." Title page and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09SB/09sbp771.pdf.

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Hodges, Amanda E. "Objective Quantification of Daytime Sleepiness." Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/iph_theses/175.

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BACKGROUND: Sleep problems affect people of all ages, race, gender, and socioeconomic classifications. Undiagnosed sleep disorders significantly and adversely impact a person’s level of academic achievement, job performance, and subsequently, socioeconomic status. Undiagnosed sleep disorders also negatively impact both direct and indirect costs for employers, the national government, and the general public. Sleepiness has significant implications on quality of life by impacting occupational performance, driving ability, cognition, memory, and overall health. The purpose of this study is to describe the prevalence of daytime sleepiness, as well as other quantitative predictors of sleep continuity and quality. METHODS: Population data from the CDC program in fatigue surveillance were used for this secondary analysis seeking to characterize sleep quality and continuity variables. Each participant underwent a standard nocturnal polysomnography and a standard multiple sleep latency test (MSLT) on the subsequent day. Frequency and chi-square tests were used to describe the sample. One-Way Analysis of Variance (ANOVA) was used to compare sleep related variables of groups with sleep latencies of <5 >minutes, 5-10 minutes, and >10 minutes. Bivariate and multivariate logistic regression was used to examine the association of the sleep variables with sleep latency time. RESULTS: The mean (SD) sleep latency of the sample was 8.8 (4.9) minutes. Twenty-four individuals had ≥1 SOREM, and approximately 50% of participants (n = 100) met clinical criteria for a sleep disorder. Individuals with shorter sleep latencies, compared to those with longer latencies reported higher levels of subjective sleepiness, had higher sleep efficiency percentages, and longer sleep times. The Epworth Sleepiness Scale, sleep efficiency percentage, total sleep time, the presence of a sleep disorder, and limb movement index were positively associated with a mean sleep latency of <5 >minutes. CONCLUSIONS: The presence of a significant percentage of sleep disorders within our study sample validate prior suggestions that such disorders remain unrecognized, undiagnosed, and untreated. In addition, our findings confirm questionnaire-based surveys that suggest a significant number of the population is excessively sleepy, or hypersomnolent. Therefore, the high prevalence of sleep disorders and the negative public health effects of daytime sleepiness demand attention. Further studies are now required to better quantify levels daytime sleepiness, within a population based sample, to better understand their impact upon morbidity and mortality. This will not only expand on our current understanding of daytime sleepiness, but it will also raise awareness surrounding its significance and relation to public health.
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Fahlman, Emma. "The benefits of power up the phone while wiring down the mind : Decreasing sleep onset latency through smartphone interaction." Thesis, Umeå universitet, Institutionen för tillämpad fysik och elektronik, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-151977.

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To be able to sleep is vital for our existence. During the process of falling asleep, many people are struggling and as an outcome, various mental health problems and sleep disorders are occurring among them. Previous studies are blaming the spreading health problems on the smartphone users for bringing their phone into their bedroom. Simultaneously, studies are showing that nocturnal smartphone usage is extremely common, with a huge spike in use during nighttime. Also, findings in studies with a different area of focus are showing that people suffering from sleep difficulties and insomnia benefits from visual stimulation and focused attention during sleep onset. This study aims to find beneficial smartphone interactions for people who are currently experiencing sleep problems. By gathering information from literature and previous studies done in the fields of insomnia, mental health problems, smartphone usage, human-computer interaction and sleep in general, the theoretical foundation of this study is laid out. To verify the previous findings and find out more about nocturnal smartphone usage, interviews and exercises with both subjective good and bad sleepers are performed. Ideas are generated and extracted through a workshop together with the collaboration partners. Visualization of the possible solution is made as a hi-fi prototype, which is later tested upon the target group of bad sleepers for three nights. In combination, the solution concept is tested together with a secondary concept through the Wizard of Oz method. The evaluation of the concepts is collected as an online form through their smartphones and the feedback from the participants is leading to a final design suggestion. This study is presenting solutions for designing for nocturnal usage, which through this study has been proven decreasing the subjective sleep onset latency among the users and in the long run will improve the user's digital well being.
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Azevedo, Cármina Augusta Pereira. "On the improvement of sleep onset latency detection and sleep-wake classification using cardiorespiratory features." Master's thesis, 2016. http://hdl.handle.net/1822/49391.

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Dissertação de mestrado integrado em Engenharia Biomédica (área de especialização em Informática Médica)<br>This document describes an investigation performed at Philips Research (Eindhoven, The Netherlands) which aimed at improving the performance of Philips current sleep/wake classification methods using portable devices based on unobtrusive cardiorespiratory signal modalities. Particularly, this research focused on improving the detection of the Sleep Onset Latency (SOL) parameter. Using a data set with recordings of healthy subjects, several alternative classification models were built, evaluated and compared to the current classifier. It was found that the performance of the current classifier, regarding SOL detection, decreases with increasing SOL, leading to an underestimation of this parameter, and possibly undervaluation of symptoms of sleep disruptions or even sleep disorders, during medical diagnosis. The main issue associated to this fault is that the current classifier is trained with examples from the entire night and therefore, for subjects with extended SOL periods, fails to capture the characteristics of wake before the initiation of sleep. In this report a new method of distinguishing sleep from wake, to be applied with recordings of subjects with SOL over 30 minutes, is proposed. The new method comprises two steps: one specially dedicated to identify wake before the initiation of sleep (and more accurately detect the moment of Sleep Onset (SO)), and the other one to distinguish wake after SOL. Hence, it requires the use of two classifiers which differ regarding techniques for feature selection and are trained with examples of different periods of the night recordings.<br>O presente documento descreve uma investigação desenvolvida na instituição Philips Research (Eindhoven, The Netherlands). O objetivo deste trabalho é melhorar o desempenho de atuais métodos Philips de classificação sleep/wake que utilizam dispositivos portáteis baseados na aquisição de sinais cardiorrespiratórios. Em particular, este trabalho foca o melhoramento do desempenho desta tecnologia na deteção do período de latência de sono. Utilizando um dataset que inclui registos de gravações noturnas de sujeitos saudáveis, vários modelos de classificação foram construídos, avaliados e comparados com o modelo atual. Verificou-se que o desempenho do classificador atual, no que diz respeito à deteção do período de latência de sono, é inferior para sujeitos com dificuldade em adormecer (com latência de sono superior a 30 minutos [1]) o que conduz a uma subestimação deste parâmetro e, possivelmente, à subestimação de sintomas de distúrbios associados com o sono, aquando do diagnóstico médico. Esta falha no desempenho está relacionada com o facto de o modelo de classificação atual ser treinado com exemplos de gravações noturnas completas, fazendo com que, para sujeitos com períodos de latência de sono prolongados, as caraterísticas da classe wake antes da iniciação do sono, não sejam bem capturadas. Nesta dissertação é proposto um novo método para a deteção sleep/wake destinado a pessoas com latência de sono superior a 30 minutos. Este método inclui dois passos: o primeiro destinado especificamente à identificação da classe wake durante o período de latência de sono (detetando-o a sua duração com maior eficácia) e o segundo com o objectivo de distinguir wake durante o restante tempo da noite de sono. Assim, torna-se necessária a utilização de dois classificadores que diferem relativamente às técnicas utilizadas para a seleção de features e utilizam diferentes exemplos de treino, isto é, períodos distintos das gravações noturnas.
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Nguyen, Anh Kiet Danny. "Le nombre de symptômes de type autistique : quelle est leur place dans le processus de développement ?" Thèse, 2018. http://hdl.handle.net/1866/21760.

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Books on the topic "Sleep onset latency"

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Pizza, Fabio, and Carlo Cipolli. Other sleep laboratory procedures (MSLT, MWT, and actigraphy). Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0009.

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Sleep medicine practice requires different objective procedures apart from nocturnal polysomnography (PSG) to quantify sleep patterns and daytime sleepiness. Two approaches are available to measure daytime sleep propensity and vigilance: the multiple sleep latency test (MSLT) and the maintenance of wakefulness test (MWT). Both tests require multiple nap opportunities under online dynamic PSG monitoring; however, in the MSLT, the subject is asked to try to fall asleep (and sleep 15 minutes to document sleep onset REM periods), but in the MWT to remain awake. The MSLT is the gold standard test for the differential diagnosis of central disorders of hypersomnolence after careful clinical assessment, while the MWT is useful to document vigilance levels for safety reasons. Rest–activity patterns can be documented for prolonged periods by actigraphy to measure circadian sleep distribution. Actigraphy is therefore a useful objective tool for insomnia, circadian rhythm, and sleepiness assessment and to track treatment response.
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Book chapters on the topic "Sleep onset latency"

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Lynch, Gordon S., David G. Harrison, Hanjoong Jo, et al. "Sleep Onset Latency." In Encyclopedia of Exercise Medicine in Health and Disease. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3043.

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Naitoh, Paul, and Tamsin L. Kelly. "Modification of the multiple sleep latency test." In Sleep onset: Normal and abnormal processes. American Psychological Association, 1994. http://dx.doi.org/10.1037/10166-019.

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Bonnet, Michael H., and Donna A. Arand. "Impact of the level of physiological arousal on estimates of sleep latency." In Sleep onset: Normal and abnormal processes. American Psychological Association, 1994. http://dx.doi.org/10.1037/10166-008.

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Jurić, Mislav, Maksym Gaiduk, and Ralf Seepold. "Influence of Illuminance on Sleep Onset Latency in IoT Based Lighting System Environment." In Bioinformatics and Biomedical Engineering. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-17938-0_38.

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Rohrs, Bruce, Benjamen Gangewere, Alicia Kaplan, and Amit Chopra. "Anxiety, Obsessive-Compulsive, and Related Disorders." In Management of Sleep Disorders in Psychiatry, edited by Amit Chopra, Piyush Das, and Karl Doghramji. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190929671.003.0019.

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Despite its common comorbidity, sleep disturbance is often underrecognized and undertreated in individuals with anxiety disorders. Compared to mood disorders, sleep disturbance in this population is less well studied except for panic disorder and generalized anxiety disorder. Some evidence suggests a bidirectional link between anxiety disorders and sleep disturbance. Polysomnography findings point to some commonalities across anxiety disorders, including longer sleep onset latency, reduced total sleep time, and reduced sleep efficiency. The underlying biological mechanisms linking anxiety disorders and sleep disturbance are still unclear. However, there is limited evidence suggesting a connection between impaired executive functioning due to sleep problems and failure to inhibit anxiety related thoughts and feelings. Cortisol irregularities and disruption in the serotonergic system may also play a role. Evidence suggests that anxiety sensitivity is a transdiagnostic factor that contributes to both anxiety disorders and sleep disturbance. Further research is warranted to elucidate common biological and psychological factors underlying sleep disturbances and anxiety disorders. There is an imminent need to systematically assess the impact of sleep disturbance on symptom severity and treatment outcomes in anxiety, obsessive-compulsive, and related disorders. Limited evidence is available for medications and targeted psychotherapeutic interventions for management of sleep disturbance thus warranting the development of robust sleep interventions to achieve optimal clinical outcomes in this patient population.
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Wong, Agnes. "Disorders of Neuromuscular Transmission." In Eye Movement Disorders. Oxford University Press, 2008. http://dx.doi.org/10.1093/oso/9780195324266.003.0022.

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Myasthenia gravis is the most common disorder affecting the neuromuscular junction (incidence: 5 per 100,000). Ocular involvement accounts for initial complaints in 75% of patients. Of patients presenting with ocular myasthenia, 50–80% eventually develop generalized myasthenia, usually within two years of onset. Myasthenia gravis is an autoimmune disease caused by the presence of antibodies against acetylcholine receptors, which leads to decreased number of available receptors (usually less than one-third that of normal). It is associated with other autoimmune diseases, including thymoma, dysthyroidism, sarcoidosis, pernicious anemia, aplastic anemia, and collagen vascular diseases (e.g., rheumatoid arthritis, lupus, ankylosing spondylitis, ulcerative colitis, Sjögren’s syndrome). ■ Side effects: cholinergic (e.g., bradycardia, angina, bronchospasm) ■ Steps for performing Tensilon test: 1. Prepare 10 mg/mL Tensilon in a tuberculin syringe, 0.6 mg atropine in a tuberculin syringe, and 10 mL normal saline. 2. Establish intravenous access using butterfly needle; flush with 1 mL normal saline. 3. Inject 0.2 mL Tensilon, flush with 1 ml normal saline, and wait 1 min for possible side effects. 4. Inject 0.6 mL Tensilon, flush with 1 mL normal saline, then attach atropine syringe. 5. Wait 3 min; improvement of ptosis or diplopia constitutes a positive test. Improvement of ptosis after application of ice for 2 min on the ptotic eyelid constitutes a positive test. The ice test is especially useful for very young, elderly, or ill patients. Improvement of ptosis or ocular alignment after 30–45 min of sleep constitutes a positive test. ■ Repetitive nerve stimulation with supramaximal stimuli delivered at 2–3 Hz: Rapid decrement of the amplitude of compound muscle action potentials (CMAPs) ≥10–15% confirms the diagnosis in 95% of cases. ■ Single-fiber electromyography (EMG; e.g., frontalis muscle) is highly sensitive (88–99% sensitivity). A positive test consists of increased jitter (increased latency between nerve stimulation and action potential of muscle fibers) and increased blockage (response failure). Acetylcholine receptor antibody is not detectable in about 15% of patients. Muscle-specific kinase is detected in 20% patients who have no acetylcholine receptor antibody and is usually detected in patients with generalized myasthenia gravis.
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Conference papers on the topic "Sleep onset latency"

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Nano, Marina-Marinela, Pedro Fonseca, Sebastiaan Overeem, Rik Vullings, and Ronald M. Aarts. "Autonomic cardiac activity in adults with short and long sleep onset latency." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8512534.

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Zavrel, Erik A., and Matthew R. Ebben. "An Active Distal Limb Warming Device for Insomnia Treatment." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3469.

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The defining characteristics of insomnia are widely recognized as difficulty falling asleep, difficulty staying asleep, and sleep that is non-restorative [1]. Insomnia is among the most common health complaints: about 10% of the adult population complains of a chronic insomnia problem [2]. With aging, increasingly disturbed sleep and less satisfaction with sleep quality are reported [3]. This common problem has wide ranging physiological, cognitive, and behavioral consequences including higher healthcare utilization [4–6]. Current major treatment options for insomnia (hypnotic medications and non-pharmacological behavioral interventions) suffer side effects and shortcomings. Thermoregulation plays a key role in promoting and maintaining sleep. At night, core body temperature (CBT) drops while distal skin temperature (DST) increases. It was previously believed that the nighttime drop in CBT was the most important promoter of sleep. However, recent research has shown that it is in fact the increase in DST (with net body heat loss owing to the large distal skin surface area) which is associated with an increase in sleepiness, whereas a decrease in DST (with resulting net body heat retention) is associated with a decrease in sleepiness [7]. The amount of distal vasodilation, as measured by the distal-proximal skin temperature gradient (DPG), is more predictive of sleep onset than subjective sleepiness ratings, CBT, or dim light melatonin onset. In fact, “the degree of dilation of blood vessels in the skin of the hands and feet, which increases heat loss at these extremities, is the best physiological predictor for the rapid onset of sleep” [8]. The link between distal skin warming and sleep propensity is further strengthened by the fact that warm water immersion of hands and feet has been found to decrease sleep onset latency (SOL) and pre-sleep warm baths have long been prescribed as an insomnia treatment. In a recent study, we used a multiple sleep latency test (MSLT) to perform multiple nap trials throughout the day, with the participants’ hands and feet immersed in warm water prior to each nap. We found that both mild and moderate warming of the hands and feet prior to a nap significantly reduced SOL compared to a baseline MSLT without warming [9]. We also previously conducted a trial of temperature biofeedback for insomnia treatment in which we demonstrated SOL reduction using muscle relaxation techniques to induce distal vasodilation, increase blood flow to the extremities, and modulate temperature of hands and feet [10]. Additionally, it has been shown that regardless of circadian variation throughout the day, finger temperature shows a rapid increase immediately before sleep onset [11]. Lastly, people with primary vascular dysregulation (a condition caused by abnormal vasoconstriction that results in cold hands and feet) exhibit significantly increased SOL and greater difficulty falling asleep following nocturnal arousal [12]. Thus, some presentations of insomnia may be secondary to distal vasodilation failure. The motivation for an active distal limb warming device as a treatment for insomnia is based on the established functional link between distal vasodilation and sleep induction [13]. Somewhat counterintuitively then, heating of hands and feet can induce distal vasodilation, promote net body heat loss, and facilitate sleep onset [14, 15].
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Sun, He, Xin'an Wang, Tianxia Zhao, Hao Ma, and Zhong Liu. "A Study of Gridding Scatter Plot for Heart Rate Variability in the Sleep Onset Latency." In the 2019 4th International Conference. ACM Press, 2019. http://dx.doi.org/10.1145/3325730.3325770.

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Kahanowitch, R., H. M. Aguilar, M. Weiss, et al. "Sleep Architecture in Trisomy 21 Is Characterized by a Longer Rapid Eye Movement (REM) Sleep Onset Latency Independent of Age and Sleep Disordered Breathing." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3365.

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Da Woon Jung, Gih Sung Chung, Su Hwan Hwang, and Kwang Suk Park. "Estimation of sleep onset latency based on the correlation between blood pressure and heart beat interval." In 2012 IEEE-EMBS International Conference on Biomedical and Health Informatics (BHI). IEEE, 2012. http://dx.doi.org/10.1109/bhi.2012.6211733.

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Zavrel, Erik A., and Matthew R. Ebben. "A Novel Two-Degree-of-Freedom Mechatronic Bed for Insomnia Treatment." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3534.

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The population prevalence of insomnia has been surveyed numerous times and is among the most common medical complaints. This common problem has wide ranging psychological and physiological health consequences. Ample anecdotal evidence exists that motion promotes sleep: automobile and train passengers are routinely observed becoming drowsy and falling asleep [1]. The sleep-inducing effect of motion has long been appreciated in the scientific community as well. For example, rocking effectively produces sleep in infants [2]. Sleepiness is also a primary symptom of motion sickness and in some cases may be its sole manifestation [3]. To date, three studies have attempted to determine whether vestibular stimulation promotes sleepiness in adults. Two of these studies involved rocking beds. In one study, investigators found that regular, periodic motion achieved using a rocking bed reduced sleep onset latency (SOL) and increased REM in normal sleepers [4]. In another study, normal sleepers napped in a swinging bed of the same design. The study showed that rocking motion promotes sleep onset and transition to deeper, more restful stages of sleep [5]. In another study, investigators employed electrical stimulation of the inner ear in an attempt to decrease SOL, finding a significant reduction in a subset of participants whose SOL was elevated at baseline [6]. This illustrates that insomniacs may be particularly responsive to vestibular stimulation. The non-pharmacological promotion of sleep is an active commercial pursuit with numerous related patents filed and commercial products introduced in recent years; however, existing devices suffer serious shortcomings. Previous experimental and current commercial designs intended for adults function(ed) as a pendulum, requiring a custom bed (and associated custom linens) along with a special overarching scaffolding installation to suspend the bed [7]. An advanced robotic infant seat [8], while elegantly designed, utilizes active load support, severely limiting the maximum weight capacity and excluding the possibility that a similar implementation could be used for adults. Phillips Respironics developed the SleepWave, a non-invasive (clip-on) device to electrically stimulate the vestibular nerve to generate the sensation of motion, which has undergone promising clinical trials but is not yet commercially available [9]. The motivation for a mechatronic bed as a treatment for insomnia is based on the demonstrated link between motion-induced vestibular stimulation and sleep induction. To date, no design has been proposed that is practical to implement or capable of being incorporated into existing beds: cost, necessary dedicated physical space, and convenience represent substantial barriers to acceptance.
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