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Journal articles on the topic 'Sleep deprivation'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 August 2024

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1

Handayani, Fani Tuti, Pratiwi Nur Widyaningsih, and Fitranto Arjadi. "EFFECT OF DIFFERENT TYPES OF SLEEP DEPRIVATION AND SLEEP RECOVERY ON SALIVARY PH." Journal of Vocational Health Studies 4, no. 3 (March 31, 2021): 95. http://dx.doi.org/10.20473/jvhs.v4.i3.2021.95-99.

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Background: Salivary pH can rise or fall influenced by intrinsic and extrinsic factors. Sleep deprivation is one example of intrinsic factors. Sleep deprivation causes a reduction in sleep time at a certain time. Purpose: Analyze the effect of different types of sleep deprivations and sleep recovery on salivary pH. Method: This study was experimental research with a post-test only with a control group design. Thirty white Wistar strain rats were randomly divided into 5 groups: healthy control group (KI), partial sleep deprivation (PSD/KII), total sleep deprivation (TSD/KIII), partial sleep deprivation, and continued sleep recovery (PSD+SR/KIV) and total sleep deprivation and continued sleep recovery (TSD+SR/KV). The treatment is carried out on a single platform method. Salivary pH was measured with the help of color-coded pH strips that were given grading after the completion of sleep deprivation induction. Result: The mean decrease in salivary pH was highest in the TSD group. One Way ANOVA test showed significant differences (p <0.05) in the control group with PSD and TSD, the PSD group with PSD+SR, TSD group with PSD+SR and TSD+SR. Conclusion: Sleep deprivation is proven to reduce the pH of Saliva. Total sleep deprivation is a chronic condition that has the most influence on decreasing salivary pH. The effect of decreasing salivary pH due to sleep deprivation is proven to be overcome by sleep recovery.

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Ocampo-Garcés, Adrián, Enrique Molina, Alberto Rodríguez, and Ennio A. Vivaldi. "Homeostasis of REM Sleep After Total and Selective Sleep Deprivation in the Rat." Journal of Neurophysiology 84, no. 5 (November 1, 2000): 2699–702. http://dx.doi.org/10.1152/jn.2000.84.5.2699.

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During specific rapid eye movement (REM) sleep deprivation its homeostatic regulation is expressed by progressively more frequent attempts to enter REM and by a compensatory rebound after the deprivation ends. The buildup of pressure to enter REM may be hypothesized to depend just on the time elapsed without REM or to be differentially related to non-REM (NREM) and wakefulness. This problem bears direct implications on the issue of the function of REM and its relation to NREM. We compared three protocols that combined REM-specific and total sleep deprivation so that animals underwent similar 3-h REM deprivations but different concomitant NREM deprivations for the first 2 (2T1R), 1 (1T2R), or 0 (3R) hours. Deprivation periods started at hour 6 after lights on. Twenty-two chronically implanted rats were recorded. The median amount of REM during all three protocols was ∼1 min. The deficits of median amount of NREM in minutes within the 3-h deprivation periods as compared with their baselines were, respectively for 2T1R, 1T2R, and 3R, 35 (43%), 25 (25%), and 7 (7%). Medians of REM rebound in the three succeeding hours, in minutes above baseline, were, respectively, 8 (44%), 9 (53%), and 9 (50%), showing no significant differences among protocols. Attempted transitions to REM showed a rising trend during REM deprivations reaching a final value that did not differ significantly among the three protocols. These results support the hypothesis that the build up of REM pressure and its subsequent rebound is primarily related to REM absence independent of the presence of NREM.

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Aguirre, Claudia C. "Sleep deprivation." Current Opinion in Pulmonary Medicine 22, no. 6 (November 2016): 583–88. http://dx.doi.org/10.1097/mcp.0000000000000323.

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4

Malik, Syed W., and Joseph Kaplan. "Sleep Deprivation." Primary Care: Clinics in Office Practice 32, no. 2 (June 2005): 475–90. http://dx.doi.org/10.1016/j.pop.2005.02.011.

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5

Abrams, Robert M. "Sleep Deprivation." Obstetrics and Gynecology Clinics of North America 42, no. 3 (September 2015): 493–506. http://dx.doi.org/10.1016/j.ogc.2015.05.013.

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Hill, Joal. "Sleep deprivation." Lancet 363, no. 9413 (March 2004): 996. http://dx.doi.org/10.1016/s0140-6736(04)15810-8.

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7

Lim, Julian, and David Dinges. "Sleep deprivation." Scholarpedia 2, no. 8 (2007): 2433. http://dx.doi.org/10.4249/scholarpedia.2433.

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CULLEN, TOM, GAVIN THOMAS, and ALEX J. WADLEY. "Sleep Deprivation." Medicine & Science in Sports & Exercise 52, no. 4 (April 2020): 909–18. http://dx.doi.org/10.1249/mss.0000000000002207.

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9

Hampton, Tracy. "Sleep Deprivation." JAMA 299, no. 5 (February 6, 2008): 513. http://dx.doi.org/10.1001/jama.299.5.513-c.

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10

Zieneldien, Tarek, and Janice Kim. "Sleep deprivation." Canadian Medical Education Journal 15, no. 3 (July 13, 2024): 128. http://dx.doi.org/10.36834/cmej.79534.

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11

Fernandes, G. L., P. Araujo, S. Tufik, and M. Andersen. "0270 Somnolence Profiles in Mice Submitted to Acute and Chronic Sleep Deprivation." Sleep 43, Supplement_1 (April 2020): A103. http://dx.doi.org/10.1093/sleep/zsaa056.268.

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Abstract Introduction Sleepiness is a behavioral marker of homeostatic sleep regulation and is related to several negative outcomes with interindividual variation, which may amount to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by acute and chronic sleep deprivation. Thus, the study objective was to investigate the development of sleepiness in sleep deprived mice. Methods C57BL/6J male mice (n=340) were distributed in 5 sleep deprivation groups, 5 sleep rebound groups and 10 control groups. Animals underwent acute total sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had the opportunity to sleep for 1, 2, 3, 4 hours after acute sleep deprivation or 24 hours after chronic sleep deprivation. During the protocol, sleep attempts were counted as a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results Using the average group sleep attempts, it was possible to differentiate between sleepy (mean>group average) and resistant to sleepiness animals (mean<group average). Frequency of resistant mice was 65%, 56%, 56% and 53% for 3, 6, 9 and 12 hours of acute sleep deprivation, respectively, and 74% in chronic sleep deprivation. 52% of the sleepiness variance might be explained by individual variation during chronic sleep deprivation and 68% of sleepiness variance during acute sleep deprivation was attributed to extended wakefulness. A normal corticosterone zenith was observed at the start of the dark phase, independent of sleep deprivation. Conclusion Different degrees of sleepiness in sleep deprived mice were verified. Sleep deprivation per se was the main factor explaining sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant. Support This work was financially supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (#2017/18455-5), Coordenação de Aperfeiçoamento de Pessoal Nível Superior (CAPES) - grant code 001, ConselhoNacional de Desenvolvimento Científico e Tecnológico (CNPq) (#169040/2017–8)and Associação Fundo de Incentivo à Pesquisa (AFIP).

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Fernandes, Guilherme, Paula Araujo, Sergio Tufik, and Monica Andersen. "0009 Interindividual variation and extended wakefulness in sleepiness after acute and chronic sleep deprivation." Sleep 45, Supplement_1 (May 25, 2022): A4. http://dx.doi.org/10.1093/sleep/zsac079.008.

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Abstract Introduction Sleepiness is a behavioural consequence of sleep pressure and is associated with negative outcomes with interindividual variation, possibly related to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by total acute and chronic sleep deprivation. Thus, the objective of the study was to investigate the development of sleepiness in sleep deprived mice. Methods Male C57BL/6J mice were distributed in sleep deprivation, sleep rebound and control groups. Animals underwent acute sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had a sleep opportunity for 1, 2, 3, or 4 hours after acute sleep deprivation or 24 hours after chronic sleep deprivation. During the protocols, sleep attempts were counted to calculate a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results Using the average of group sleep attempts, it was possible to differentiate between sleepy (mean>group average) and resistant animals (mean<group average). Resistant mice were more frequent in all settings. Individual variation accounted for 52% of sleepiness variance during chronic sleep deprivation and extended wakefulness explained 68% of sleepiness variance during acute sleep deprivation. A normal corticosterone peak was observed at the start of the dark phase, independent of sleep deprivation. Conclusion Different profiles of sleepiness emerged in sleep deprived mice. Sleep deprivation was the main factor for sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant. Support (If Any) Our studies are supported by the following funding agencies: AFIP (Associação Fundo de Incentivo à Pesquisa), São Paulo Research Foundation (FAPESP #2017/18455-5 to GLF), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES - Finance Code 001 to GLF), and CNPq (fellowships to MLA and ST; #169040/2017-8, and #141445/2021-1 to GLF). This study received indirect funding from AFIP and CNPq, which support the department in which the project was conducted.

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13

Everson, Carol A., Bernard M. Bergmann, and Allan Rechtschaffen. "Sleep Deprivation in the Rat: III. Total Sleep Deprivation." Sleep 12, no. 1 (January 1989): 13–21. http://dx.doi.org/10.1093/sleep/12.1.13.

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Kushida, Clete A., Bernard M. Bergmann, and Allan Rechtschaffen. "Sleep Deprivation in the Rat: IV. Paradoxical Sleep Deprivation." Sleep 12, no. 1 (January 1989): 22–30. http://dx.doi.org/10.1093/sleep/12.1.22.

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15

Parkes, J. "Epilepsy, Sleep and Sleep Deprivation." Journal of Neurology, Neurosurgery & Psychiatry 48, no. 2 (February 1, 1985): 197. http://dx.doi.org/10.1136/jnnp.48.2.197.

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16

Yusan, Rizak Tiara, and Synta Haqqul Fadlilah. "REVIEW SLEEP AND SLEEP DEPRIVATION." Medical and Health Journal 2, no. 1 (January 19, 2023): 148. http://dx.doi.org/10.20884/1.mhj.2022.2.1.7820.

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Sleep is a sedentary mental and physical condition. Sleep is necessary for emotional, physical, and cognitive well-being and accounts for approximately one-third of a person's life. Sleep happens in cycles in which the body alternates between two modes: REM sleep and non-REM sleep. Behavioural observation, physiological monitoring, or a mix of the two can be used for the assessment of sleep and wake. Current clinical recommendations for scoring PSGs describe three phases of progressively. The majority of hormones in plasma show strong 24-hour cycles, highlighting the significance of the circadian clock and sleep-related impacts on hormone release and/or metabolism. Lack of sufficient sleep for duration or quality might affect one's ability to function normally and maintain good health. The typical adult requires seven or more hours of sleep each night to be healthy. This report will inform the current state of the science of sleep and sleep deprivation.

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Jung, C. M., E. L. Melanson, E. J. Frydendall, L. Perreault, R. H. Eckel, and K. P. Wright. "Energy expenditure during sleep, sleep deprivation and sleep following sleep deprivation in adult humans." Journal of Physiology 589, no. 1 (November 8, 2010): 235–44. http://dx.doi.org/10.1113/jphysiol.2010.197517.

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18

Xu, Lin, Tao Song, Ziyi Peng, Cimin Dai, Letong Wang, Yongcong Shao, Lanxiang Wang, Xiechuan Weng, and Mengfei Han. "Acute Sleep Deprivation Impairs Motor Inhibition in Table Tennis Athletes: An ERP Study." Brain Sciences 12, no. 6 (June 7, 2022): 746. http://dx.doi.org/10.3390/brainsci12060746.

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Excellent response inhibition is the basis for outstanding competitive athletic performance, and sleep may be an important factor affecting athletes’ response inhibition. This study investigates the effect of sleep deprivation on athletes’ response inhibition, and its differentiating effect on non-athlete controls’ performance, with the aim of helping athletes effectively improve their response inhibition ability through sleep pattern manipulation. Behavioral and event-related potential (ERP) data were collected from 36 participants (16 table tennis athletes and 20 general college students) after 36 h of sleep deprivation using ERP techniques and a stop-signal task. Sleep deprivation’s different effects on response inhibition in the two groups were explored through repeated-measures ANOVA. Behavioral data showed that in a baseline state, stop-signal response time was significantly faster in table tennis athletes than in non-athlete controls, and appeared significantly longer after sleep deprivation in both groups. ERP results showed that at baseline state, N2, ERN, and P3 amplitudes were lower in table tennis athletes than in non-athlete controls, and corresponding significant decreases were observed in non-athlete controls after 36 h of sleep deprivation. Table tennis athletes showed a decrease in P3 amplitude and no significant difference in N2 and ERN amplitudes, after 36 h of sleep deprivation compared to the baseline state. Compared to non-athlete controls, table tennis athletes had better response inhibition, and the adverse effects of sleep deprivation on response inhibition occurred mainly in the later top-down motor inhibition process rather than in earlier automated conflict detection and monitoring.

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Dharia, Sonali, Adam Zeman, and Royal Devon. "SLEEP-DEPRIVATION AMNESIA." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 9 (August 13, 2015): e3.41-e3. http://dx.doi.org/10.1136/jnnp-2015-311750.46.

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MUNSON, BECKY LIEN. "…About sleep deprivation." Nursing 30, no. 7 (July 2000): 77. http://dx.doi.org/10.1097/00152193-200030070-00035.

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21

Blau, JN. "Sleep Deprivation Headache." Cephalalgia 10, no. 4 (August 1990): 157–60. http://dx.doi.org/10.1046/j.1468-2982.1990.1004157.x.

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Headaches due to insufficient or interrupted sleep are generally labelled “tension headaches” of psychogenic origin. In 25 healthy subjects, variable amounts of sleep loss (1–3 h for 1–3 nights) caused headaches lasting from 1 h to all day. The headache was most frequently a dull ache, a heaviness or a pressure sensation felt in the forehead and/or at the vertex. Simple analgesics, purchaseable without a doctor's prescription, completely or markedly reduced the head pain in 20–60 min. Headaches due to insufficient sleep differ from tension headaches in their site, duration and response to analgesics. Assuming that pain implies a regional dysfunction, headaches caused by sleep loss provide support for the notion that sleep has a restorative function in the brain.

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22

Kuhs, H., and R. Tölle. "Sleep deprivation therapy." Biological Psychiatry 29, no. 11 (June 1991): 1129–48. http://dx.doi.org/10.1016/0006-3223(91)90255-k.

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Karia, Sagar, Mansi Shah, Mihir Pathak, and Avinash De Sousa. "Sleep deprivation delirium." Telangana Journal of Psychiatry 9, no. 1 (2023): 58. http://dx.doi.org/10.4103/tjp.tjp_44_22.

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Matsubara, Akira, Gang Deng, Lili Gong, Eileen Chew, Masutaka Furue, Ying Xu, Bin Fang, and Tomohiro Hakozaki. "Sleep Deprivation Increases Facial Skin Yellowness." Journal of Clinical Medicine 12, no. 2 (January 12, 2023): 615. http://dx.doi.org/10.3390/jcm12020615.

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Sleep shortage is a major concern in modern life and induces various psycho-physical disorders, including skin problems. In cosmeceutics, females are aware that sleep deprivation worsens their facial skin tone. Here, we measured the effects of sleep deprivation on facial skin yellowness and examined yellow chromophores, such as bilirubin and carotenoids, in blood serum as potential causes of yellowness. Total sleep deprivation (0 h sleep overnight, N = 28) and repeated partial sleep deprivation (4 h sleep for 5 consecutive days, N = 10) induced significant increases in facial skin yellowness. The higher yellowness was sustained even after both sleep deprivation types stopped. However, circulating levels of yellow chromophores were unchanged in the total sleep deprivation study. Neither circulating interleukin-6 nor urinary biopyrrin levels were affected by total sleep deprivation, suggesting that apparent oxidative stress in the body was not detected in the present total deprivation protocol. Facial redness was affected by neither total nor repeated partial sleep deprivation. Therefore, blood circulation may play a limited role in elevated yellowness. In conclusion, facial skin yellowness was indeed increased by sleep deprivation in our clinical studies. Local in situ skin-derived factors, rather than systemic chromophore change, may contribute to the sleep deprivation-induced elevation of facial skin yellowness.

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Khan, Aesha, Catharine Trice, Daniel Holt, and Jeff Dyche. "0294 Voluntary Alcohol Consumption and Sleep Deprivation in Rats." Sleep 45, Supplement_1 (May 25, 2022): A132—A133. http://dx.doi.org/10.1093/sleep/zsac079.292.

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Abstract Introduction Alcohol is one of the most common psychoactive drugs that has depressant effects on the central nervous system. The vast majority of research on alcohol and sleep indicates chronic alcohol consumption has a detrimental impact on sleep architecture and homeostasis. However, less research has explored the effects of sleep deprivation on alcohol consumption; that is, the relationship in the opposite direction. Previous animal studies have explored a potential bi-directional relationship between sleep and alcohol with promising results. However, there was concern that the potential relationship may be a result of stress as a by-product of the sleep deprivation method. The present study examines the effect of sleep deprivation on voluntary alcohol consumption using two sleep deprivation methods in the rat, forced exercise wheels and the automated sleep deprivation system. Methods Twelve male Sprague-Dawley rats had ad libitum access to a 7% alcohol solution and water. Alcohol and water consumption was measured daily at 0900. Baseline consumption levels were recorded in the home cage prior to introduction to the sleep deprivation equipment. Following baseline, rats were placed in the stationary equipment for the first sleep deprivation environment control. Rats were then subjected to 6hr/day of sleep deprivation for five consecutive days in either the forced exercise wheel (n=6) or the automated sleep deprivation system (n=6). After sleep deprivation, rats were placed back in the stationary equipment as a second control measure. In total, there were four conditions, home cage baseline, first sleep deprivation environment control, sleep deprivation, second environment control. Results Data indicates that rats consumed significantly more alcohol in the sleep deprivation condition and the second sleep deprivation control. There was no difference between the two sleep deprivation methods. The mean alcohol consumption (g/kg) significantly increased from the sleep deprivation condition to the second environment control indicating a cumulative effect. Conclusion The increase in alcohol consumption in the final condition rejects the hypothesis of a bi-directional relationship. Instead, the data suggests potential receptor downregulation due to alcohol exposure over time and a conditioned compensatory effect of the sleep deprivation environment. Research methodology issues also may have confounded results. Support (If Any)

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Schwärzler, F., C. Bernecker, M. Schweinsberg, and H. Giedke. "Therapeutic sleep deprivation in depression: total sleep deprivation versus late partial sleep deprivation, a review of the literature." European Psychiatry 17 (May 2002): 129. http://dx.doi.org/10.1016/s0924-9338(02)80570-3.

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Dijk, D. J. "Circadian regulation of sleep propensity, sleep structure and alertness: A symphony of paradoxes." Acta Neuropsychiatrica 7, no. 2 (June 1995): 24–26. http://dx.doi.org/10.1017/s0924270800037467.

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The adult human typically exhibits a monophasic sleep-wake cycle, i.e., remains awake and alert for approximately 16 hours and then sleeps for 8 hours. Recent experiments have provided new insights in the role of the endogenous circadian pacemaker in this consolidation of sleep and wakefulness.Sleep deprivation studies had shown previously that sleepiness and alertness are co-determined by a process which keeps track of the history of sleep and wakefulness and the circadian pacemaker, which keeps track of time. During every day life and during sleep deprivation both processes change simultaneously and their relative contribution to alertness and sleep propensity cannot be assessed under these conditions.

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Gilliland, Marcia A., Bernard M. Bergmann, and Allan Rechtschaffen. "Sleep Deprivation in the Rat: VIII. High EEG Amplitude Sleep Deprivation." Sleep 12, no. 1 (January 1989): 53–59. http://dx.doi.org/10.1093/sleep/12.1.53.

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Stepanski, Edward J. "Sleep Fragmentation, Sleep Deprivation, or Both." Journal of Clinical Sleep Medicine 02, no. 04 (October 15, 2006): 479. http://dx.doi.org/10.5664/jcsm.26668.

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30

Persson, Hans E., and Eva Svanborg. "Sleep Deprivation Worsens Obstructive Sleep Apnea." Chest 109, no. 3 (March 1996): 645–50. http://dx.doi.org/10.1378/chest.109.3.645.

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Ajjimaporn, Amornpan, Papatsorn Ramyarangsi, and Vorasith Siripornpanich. "Effects of a 20-min Nap after Sleep Deprivation on Brain Activity and Soccer Performance." International Journal of Sports Medicine 41, no. 14 (July 6, 2020): 1009–16. http://dx.doi.org/10.1055/a-1192-6187.

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AbstractWe examined effects of a 20-min nap following 3 h of sleep deprivation on brain wave activity, auditory reaction time, the running-based anaerobic sprint test, leg muscle strength and the rating of perceived exertion in male college soccer players. Eleven players underwent three sleep conditions; normal sleep, sleep deprivation and 20-min nap after sleep deprivation. The sleep deprivation demonstrated an increase in the mean power of delta waves over the frontal area and a decrease in the mean power of alpha waves over the parietal area compared to the normal sleep. The nap and the sleep deprivation showed an increase in auditory reaction time compared with those in the normal sleep. The sleep deprivation demonstrated a decrease in the running-based anaerobic sprint test compared to the normal sleep, whereas the nap has partially reversed only minimal power and average power of the running-based anaerobic sprint test. The nap showed a recovery effect on leg muscle strength, but not on the rating of perceived exertion compared with the sleep deprivation. Thus, a 20-min nap after sleep deprivation did not completely return brain activity back to active state and did not entirely reverse the negative impact of sleep deprivation on soccer performance in soccer players.

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Chernyshev, Oleg Y. "Sleep Deprivation and Its Consequences." CONTINUUM: Lifelong Learning in Neurology 29, no. 4 (August 2023): 1234–52. http://dx.doi.org/10.1212/con.0000000000001323.

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ABSTRACT OBJECTIVE This article reviews the clinical, cognitive, behavioral, and physiologic consequences of sleep deprivation in relation to general neurology practice. LATEST DEVELOPMENTS Despite being one of the most common sleep problems in modern society, the role of sleep deprivation is underrecognized and underestimated in clinical medicine and general neurology practice. The recognition, diagnosis, and management of sleep deprivation in neurologic practice have only recently received close attention. The consequences of sleep deprivation involve all aspects of general neurology practice, including individuals with neurologic disease, neurologists, communities, and health care systems. The identification and timely management of sleep deprivation symptoms may help to improve symptoms of underlying primary neurologic disorders. ESSENTIAL POINTS This article emphasizes complexities related to the identification and evaluation of sleep deprivation in general neurology practice and describes the consequences of sleep deprivation. By recognizing sleep deprivation in patients with neurologic conditions, the neurologist can provide comprehensive care and contribute to improved clinical and neurologic outcomes.

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Brückner, T. U., and M. H. Wiegand. "Motor activity in depressed patients during therapeutic sleep deprivation." European Psychiatry 25, no. 8 (December 2010): 465–67. http://dx.doi.org/10.1016/j.eurpsy.2009.11.004.

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AbstractProblemBoth sleep and motor activity have a bidirectional relationship with depression. The existing literature on motor activity during therapeutic sleep deprivation in depressed patients is inconsistent and fragmentary. In the present study we measured motor activity continuously during 40 hours of sleep deprivation in depressed patients.MethodThirty-four inpatients suffering from a major depression (DSM-IV) underwent sleep deprivation with a continuous waking period of 40 hours. Motor activity of the patients was continuously recorded using an actigraph on the non-dominant wrist. The effect of sleep deprivation was assessed by the Hamilton Depression Scale (six-item version), thus separating the group into responders and non-responders to sleep deprivation.ResultsWe found no significant differences in motor activity between responders and non-responders on the day before sleep deprivation. During the night, responders to sleep deprivation exhibited a higher motor activity and less periods of rest. On the day after sleep deprivation, responders exhibited a higher activity, too.ConclusionsMotor activity levels differ between the two groups, thus giving more insight into possible mechanisms of action of the therapeutic sleep deprivation. We suggest that higher motor activity during the night prevents naps and leads to better response to sleep deprivation.

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Neculicioiu, Vlad Sever, Ioana Alina Colosi, Carmen Costache, Dan Alexandru Toc, Alexandra Sevastre-Berghian, Horațiu Alexandru Colosi, and Simona Clichici. "Sleep Deprivation-Induced Oxidative Stress in Rat Models: A Scoping Systematic Review." Antioxidants 12, no. 8 (August 11, 2023): 1600. http://dx.doi.org/10.3390/antiox12081600.

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Sleep deprivation is highly prevalent in the modern world, possibly reaching epidemic proportions. While multiple theories regarding the roles of sleep exist (inactivity, energy conservation, restoration, brain plasticity and antioxidant), multiple unknowns still remain regarding the proposed antioxidant roles of sleep. The existing experimental evidence is often contradicting, with studies pointing both toward and against the presence of oxidative stress after sleep deprivation. The main goals of this review were to analyze the existing experimental data regarding the relationship between sleep deprivation and oxidative stress, to attempt to further clarify multiple aspects surrounding this relationship and to identify current knowledge gaps. Systematic searches were conducted in three major online databases for experimental studies performed on rat models with oxidative stress measurements, published between 2015 and 2022. A total of 54 studies were included in the review. Most results seem to point to changes in oxidative stress parameters after sleep deprivation, further suggesting an antioxidant role of sleep. Alterations in these parameters were observed in both paradoxical and total sleep deprivation protocols and in multiple rat strains. Furthermore, the effects of sleep deprivation seem to extend beyond the central nervous system, affecting multiple other body sites in the periphery. Sleep recovery seems to be characterized by an increased variability, with the presence of both normalizations in some parameters and long-lasting changes after sleep deprivation. Surprisingly, most studies revealed the presence of a stress response following sleep deprivation. However, the origin and the impact of the stress response during sleep deprivation remain somewhat unclear. While a definitive exclusion of the influence of the sleep deprivation protocol on the stress response is not possible, the available data seem to suggest that the observed stress response may be determined by sleep deprivation itself as opposed to the experimental conditions. Due to this fact, the observed oxidative changes could be attributed directly to sleep deprivation.

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Lim, Sung Chul. "0193 The Effect of Sleep Deprivation on Pain Perception in Awake Rats." SLEEP 47, Supplement_1 (April 20, 2024): A82—A83. http://dx.doi.org/10.1093/sleep/zsae067.0193.

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Abstract Introduction This study was conducted to determine how sleep deprivation affects headache perception and brain structure in an animal model of headache. Methods The effect of sleep deprivation on mechanical pain threshold was assessed in two groups of animals: (i) NSD-C group and (ii) SD group. The VFMF thresholds were assessed every day during 96 hours of sleep deprivation. After 96 hours sleep deprivation, the brain of each groups were analyzed with immunohistochemistry staining. The effect of sleep deprivation in supradural capsicin infusion were assessed in two groups. The VFMF threshold was performed during sleep deprivation and 4 weeks of recovery phase. Results 1) The effect of sleep deprivation on mechanical pain threshold. In comparison between SD and NSD-C group, the significant difference appeared after 1 day of sleep deprivation and lasted 4 days. 2) The effect of sleep deprivation on FOS reactivity. In hyptothalamus, the number of Fos-positive cells in PoHT increased significantly in SD group compared NSD-C group. In PAG, the number of Fos-positive cells in VLPAG increased significantly in SD group compared NSD-C group. The number of Fos-positive cells of supf C in TCC increased significantly in SD group compared NSD-C group. 3) The effect of sleep deprivation on mechanical pain threshold in supradural capsicin infusion. SD-Capsicin showed the tendency of lower VFMF threshold compared to NSD-Capsicin, which reach to statistical significant 3rd days of capsicin infusion period. During the recovery phase, the reduced VFMF threshold of NSD-Capsicin group was persisted 1 week after sleep deprivation and returned to baseline thereafter. In SD-Capsicin group, the reduced VFMF threshold was persisted 3 week after sleep deprivation. Conclusion In this study, pain lasted for 1 week after 4 days of continuous infusion of capsicin without sleep deprivation, but lasted for more than 3 weeks when combined with sleep deprivation, confirming the possibility that sleep deprivation contributes to the chronicity of headache. The chronicity and persistence of headache is associated with the centralization of pain. The findings of this study that sleep deprivation results in changes in TNC activity, which plays an important role in centralization, support this possibility. Support (if any)

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Li, Wenyi. "Lack of Sleep among College Students Can Lead to Negative Emotions and Affect Memory." Lecture Notes in Education Psychology and Public Media 45, no. 1 (April 19, 2024): 16–22. http://dx.doi.org/10.54254/2753-7048/45/20230227.

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Sleep deprivation is associated with various disorders in most body systems. College students are one of the most significantly affected groups by sleep deprivation. However, the impact of sleep deprivation on emotions and memory has been fully demonstrated. No researchers have studied whether sleep deprivation causes social anxiety and affects college students' ability to remember words. This study aims to explore the effects of sleep deprivation on emotional control and memory abilities in adolescents. Thirty-four participants were investigated online to collect and evaluate sleep quality, Social anxiety, and vocabulary memory. The questionnaire included the Pittsburgh Sleep Quality Index (PSQI), Self Review Anxiety Scale (SAS), and vocabulary memory time under different sleep qualities. Correlation and regression analyses of sleep quality, Social anxiety, and memory foreword ability. There was no significant correlation between sleep deprivation, anxiety, and vocabulary memory. Research has shown that sleep deprivation does not cause stress or affect vocabulary memory. To improve the reliability of current research, future work can increase the sample size.

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Lumbantoruan, Septa Meriana, Juhdeliena Juhdeliena, and Agustina Saputri. "Sleep deprivation in patients with heart failure: A literature review." Malahayati International Journal of Nursing and Health Science 7, no. 2 (April 28, 2024): 231–41. http://dx.doi.org/10.33024/minh.v7i2.210.

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Background: Sleep deprivation in patients with heart failure can negatively deteriorate its condition. Purpose: Identify the sleep deprivation in patients with heart failure (HF) and related factors, and the impact of sleep deprivation. Method: literature review of quantitative studies. The search strategy employs terms relevant to the research question: HF, sleep deprivation on HF patients. Inclusion criteria papers had to be published in English after 2013 to 2023. 3 databases were searched (Pubmed, Ovid, Ebscohost). Results: 12 studies were identified (cross-sectional (9 studies) secondary from longitudinal observational (2 studies), randomized controlled trial (1 study). Total patients with HF in all studies are 2359 samples.The most questionnaire to measure sleep deprivation used over the papers are Pittsburgh Sleep Quality Index (PSQI).PSQI mean score range from 5.04 (2.80) to 12.29 (3.91). The prevalence of sleep deprivation ranges from 36.5% to 98.8%. The related factors with sleep deprivation including older age, women, living in urban, lower employment, smoking, high BMI, HF condition, sleep factors, anxious, depressive, and stress. The consequences of sleep deprivation such as lower self-care behavior, self-confidence, attention, increasing pain, shorter cardiac event-free survival, functional outcome, prognosis, quality of life, increase unplanned hospitalization risks, poorer perfomance in cognitive in adults and worse perfomance on cognitive. Conclusion: Sleep deprivation in HF is higher and related with demographic, HF related factors, lifestyle, sleep factors, and psychosocial. The consequences of sleep deprivation have adverse effects on psychosocial and cognitive.

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Liu, Shuailing, Xiya Wang, Qian Zheng, Lanyue Gao, and Qi Sun. "Sleep Deprivation and Central Appetite Regulation." Nutrients 14, no. 24 (December 7, 2022): 5196. http://dx.doi.org/10.3390/nu14245196.

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Research shows that reduced sleep duration is related to an increased risk of obesity. The relationship between sleep deprivation and obesity, type 2 diabetes, and other chronic diseases may be related to the imbalance of appetite regulation. To comprehensively illustrate the specific relationship between sleep deprivation and appetite regulation, this review introduces the pathophysiology of sleep deprivation, the research cutting edge of animal models, and the central regulatory mechanism of appetite under sleep deprivation. This paper summarizes the changes in appetite-related hormones orexin, ghrelin, leptin, and insulin secretion caused by long-term sleep deprivation based on the epidemiology data and animal studies that have established sleep deprivation models. Moreover, this review analyzes the potential mechanism of associations between appetite regulation and sleep deprivation, providing more clues on further studies and new strategies to access obesity and metabolic disease.

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Pal, Dinesh, William J. Lipinski, Amanda J. Walker, Ashley M. Turner, and George A. Mashour. "State-specific Effects of Sevoflurane Anesthesia on Sleep Homeostasis." Anesthesiology 114, no. 2 (February 1, 2011): 302–10. http://dx.doi.org/10.1097/aln.0b013e318204e064.

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Background Prolonged propofol administration does not result in signs of sleep deprivation, and propofol anesthesia appears to satisfy the homeostatic need for both rapid eye movement (REM) and non-REM (NREM) sleep. In the current study, the effects of sevoflurane on recovery from total sleep deprivation were investigated. Methods Ten male rats were instrumented for electrophysiologic recordings under three conditions: (1) 36-h ad libitum sleep; (2) 12-h sleep deprivation followed by 24-h ad libitum sleep; and (3) 12-h sleep deprivation, followed by 6-h sevoflurane exposure, followed by 18-h ad libitum sleep. The percentage of waking, NREM sleep, and REM sleep, as well as NREM sleep δ power, were calculated and compared for all three conditions. Results Total sleep deprivation resulted in significantly increased NREM and REM sleep for 12-h postdeprivation. Sevoflurane exposure after deprivation eliminated the homeostatic increase in NREM sleep and produced a significant decrease in the NREM sleep δ power during the postanesthetic period, indicating a complete recovery from the effects of deprivation. However, sevoflurane did not affect the time course of REM sleep recovery, which required 12 h after deprivation and anesthetic exposure. Conclusion Unlike propofol, sevoflurane anesthesia has differential effects on NREM and REM sleep homeostasis. These data confirm the previous hypothesis that inhalational agents do not satisfy the homeostatic need for REM sleep, and that the relationship between sleep and anesthesia is likely to be agent and state specific.

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Aryashree L, Prashant Verma, Aditya Thakur, Jagmohan Singh Dhakar, and Rajesh Tiwari. "Screening for sleep deprivation and mood states among staff nurses of tertiary care hospital in central India." Asian Journal of Medical Sciences 14, no. 12 (December 1, 2023): 67–72. http://dx.doi.org/10.3126/ajms.v14i12.57117.

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Background: A Nurse’s fatigue raises significant concerns for individual and patient safety. The impact of sleep deprivation on the quality of patient care is an important consideration in today’s health-care environment. Aims and Objectives: The aim of this study was to find the proportion of sleep deprivation among nurses in a tertiary care hospital and to find the association between sleep deprivation and mood states among staff nurses. Materials and Methods: It was a cross-sectional design done in a duration of 2 months from September to October 2022. The study group consisted of nurses working in a tertiary care hospital located in Jabalpur district. A sample size of 70 nurses was calculated through the statistical formula. The questionnaire has three sections: Demographics (nine questions), Epworth sleep scale (eight questions), and Profile of mood states (65 questions). The collected data were tabulated and analyzed using MS Office Excel and SPSS version 21. Results: Interviews were conducted with 70 nurses and 8.6% of them were found to be excessively sleepy and should seek medical attention. Significant results have been obtained for the association with tension, depression, anger, fatigue, and confusion with sleep deprivation. Conclusion: The findings suggest that sleep deprivation exists in a considerable state. Some workplace interventions need to be done to make the efforts of nurses worthwhile and to increase their vigor and positive mood.

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Xu, YaHui, BinBin Qu, FengJuan Liu, ZhiHua Gong, Yi Zhang, and DeXiang Xu. "Sleep Deprivation and Heart Rate Variability in Healthy Volunteers: Effects of REM and SWS Sleep Deprivation." Computational and Mathematical Methods in Medicine 2023 (July 11, 2023): 1–5. http://dx.doi.org/10.1155/2023/7121295.

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Objective. Using PSG-guided acute selective REM/SWS sleep deprivation in volunteers, this study examined the effects of sleep deprivation on the cardiovascular and autonomic nervous systems, as well as the relationship between cardiac neuromodulation homeostasis and cardiovascular disease. Methods. An experiment was conducted using 30 healthy volunteers ( male : female = 1 : 1 , aged 26.33 ± 4.5 years) divided into groups for sleep deprivation of SWS and REM sleep, and then, each group was crossed over for normal sleep (2 days) and repeated sleep deprivation (1 day, 3 times). During the study period, PSG and ELECTRO ECG monitoring were conducted, and five-minute frequency domain parameters and blood pressure values were measured before and after sleep deprivation. Results. Changes in VLF, LFnu, LF/HF, HF, and HFnu after SWS sleep deprivation were statistically significant ( P < 0.05 ), but not LF ( P = 0.063 ). Changes in VLF, LF, HF, LF/HF, LFnu, and HFnu after REM sleep deprivation were not statistically significant ( P > 0.05 ). Conclusions. An increase in sympathetic nerve activity results from sleep deprivation and sudden awakening from SWS sleep is associated with a greater risk of cardiovascular disease.

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Harrison, Yvonne, and James A. Horne. "Sleep Deprivation Affects Speech." Sleep 20, no. 10 (October 1997): 871–77. http://dx.doi.org/10.1093/sleep/20.10.871.

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Shen, Bingyao, Zhiqiang Tian, Jiajia Li, Yu Sun, Yi Xiao, and Rixin Tang. "Sleep Deprivation Influences Trial-to-Trial Transfer but Not Task Performance." Journal of Clinical Medicine 11, no. 19 (September 20, 2022): 5513. http://dx.doi.org/10.3390/jcm11195513.

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Previous research has shown that sleep deprivation can affect emotions and some cognitive functions. However, research on how sleep deprivation influences the visuomotor memory have rarely been reported. In the current study, a Fitts’ Law task was used to investigate how movement and the visuomotor memory are affected under the condition of sleep deprivation. Experiment 1 had 36 participants (15 males, mean age = 21.61 years) complete the same Fitts’ Law task 10 days apart under standard conditions. Experiment 2 had five participants (three males, mean age = 27.2 years) complete the task after 7 days of sleep deprivation, then complete it again after 10 days without sleep deprivation. Experiment 1 demonstrated the stability of the trial-to-trial effects. Experiment 2 showed that the previous trial (n) exerted no effect on the current trial (n + 1) under the conditions of sleep deprivation (p = 0.672). However, the effect was observed after 10 days without sleep deprivation (p = 0.013). This suggests that sleep deprivation did not affect task performance but influenced the transfer of the trial history. Future studies are required to investigate the effect of sleep deprivation with more participants.

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Wright, J. B. D. "Mania Following Sleep Deprivation." British Journal of Psychiatry 163, no. 5 (November 1993): 679–80. http://dx.doi.org/10.1192/bjp.163.5.679.

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A first episode of mania is described in a previously healthy man who was partially sleep deprived for four nights. The sleep deprivation preceded the psychosis. During the psychotic episode he believed that he was the Messiah. This case is discussed in the light of reports exploring the relationship between psychosis and sleep deprivation.

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Thoret, Etienne, Thomas Andrillon, Caroline Gauriau, Damien Léger, and Daniel Pressnitzer. "Sleep deprivation detected by voice analysis." PLOS Computational Biology 20, no. 2 (February 5, 2024): e1011849. http://dx.doi.org/10.1371/journal.pcbi.1011849.

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Sleep deprivation has an ever-increasing impact on individuals and societies. Yet, to date, there is no quick and objective test for sleep deprivation. Here, we used automated acoustic analyses of the voice to detect sleep deprivation. Building on current machine-learning approaches, we focused on interpretability by introducing two novel ideas: the use of a fully generic auditory representation as input feature space, combined with an interpretation technique based on reverse correlation. The auditory representation consisted of a spectro-temporal modulation analysis derived from neurophysiology. The interpretation method aimed to reveal the regions of the auditory representation that supported the classifiers’ decisions. Results showed that generic auditory features could be used to detect sleep deprivation successfully, with an accuracy comparable to state-of-the-art speech features. Furthermore, the interpretation revealed two distinct effects of sleep deprivation on the voice: changes in slow temporal modulations related to prosody and changes in spectral features related to voice quality. Importantly, the relative balance of the two effects varied widely across individuals, even though the amount of sleep deprivation was controlled, thus confirming the need to characterize sleep deprivation at the individual level. Moreover, while the prosody factor correlated with subjective sleepiness reports, the voice quality factor did not, consistent with the presence of both explicit and implicit consequences of sleep deprivation. Overall, the findings show that individual effects of sleep deprivation may be observed in vocal biomarkers. Future investigations correlating such markers with objective physiological measures of sleep deprivation could enable “sleep stethoscopes” for the cost-effective diagnosis of the individual effects of sleep deprivation.

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Şahin, Leyla. "Akut REM Uyku Yoksunluğu Oluşturulan Sıçanlarda Uzun dönem Ilımlı Egzersizin Depresif/Anksiyete Benzeri Davranış Üzerine Etkisi." Turkish Journal of Agriculture - Food Science and Technology 6, no. 11 (October 29, 2018): 1640. http://dx.doi.org/10.24925/turjaf.v6i11.1640-1646.2161.

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Sleep is a physiological process that influenced by internal and external factors and brain is as active as waking in certain periods. REM sleep is demonstrated in the literature that provides psychological relaxation due to more frequent occurrence of psychiatric disorders in sleep deprivation and causes depression / anxiety-like situations. There are studies in the literature indicate that physical exercise may be useful on depressive / anxiety. However, the duration and physical severity of the physical exercise and sleep deprivation affects the results. For this reason, we investigated the effect of long-term exercise on depression / anxiety behavior on acute REM sleep deprived rats. Rats were divided into control (C), exercise (E), REM sleep deprivation (SD) and exercise + REM sleep deprivation (E + SD) (n = 7). For developing REM sleep deprivation, rats were kept in a sleep deprivation tank during a 48-hour period. Exercise was performed with treadmill for 15, 30, 45 and 60 minutes for 4 weeks. Depressive / anxiety behaviors were assessed with open field and elevated plus maze tests. It has been shown that the sleep deprivation group takes less distance in the open field test. It was observed that in the elevated plus maze test, the rats in the sleep deprivation group spent less time on the open-arm compared to the other groups, and the number of entries and exits in this group also decreased. Behavioral test findings show that depressive / anxiety-like effects of sleep deprivation are reduced by moderate treadmill exercise.

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Kundermann, Bernd, Jürgen-Christian Krieg, Wolfgang Schreiber, and Stefan Lautenbacher. "The Effects of Sleep Deprivation on Pain." Pain Research and Management 9, no. 1 (2004): 25–32. http://dx.doi.org/10.1155/2004/949187.

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Chronic pain syndromes are associated with alterations in sleep continuity and sleep architecture. One perspective of this relationship, which has not received much attention to date, is that disturbances of sleep affect pain. To fathom this direction of cause, experimental human and animal studies on the effects of sleep deprivation on pain processing were reviewed. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can counteract analgesic effects of pharmacological treatments involving opioidergic and serotoninergic mechanisms of action. The heterogeneity of the human data and the exclusive interest in rapid eye movement sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity. The significance of opioidergic and serotoninergic processes as mediating mechanisms of the hyperalgesic changes produced by sleep deprivation are discussed.

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Hairston, Ilana S., Christelle Peyron, Daniel P. Denning, Norman F. Ruby, Judith Flores, Robert M. Sapolsky, H. Craig Heller, and Bruce F. O'Hara. "Sleep Deprivation Effects on Growth Factor Expression in Neonatal Rats: A Potential Role for BDNF in the Mediation of Delta Power." Journal of Neurophysiology 91, no. 4 (April 2004): 1586–95. http://dx.doi.org/10.1152/jn.00894.2003.

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The sleeping brain differs from the waking brain in its electrophysiological and molecular properties, including the expression of growth factors and immediate early genes (IEG). Sleep architecture and homeostatic regulation of sleep in neonates is distinct from that of adults. Hence, the present study addressed the question whether the unique homeostatic response to sleep deprivation in neonates is reflected in mRNA expression of the IEG cFos, brain-derived nerve growth factor (BDNF), and basic fibroblast growth factor (FGF2) in the cortex. As sleep deprivation is stressful to developing rats, we also investigated whether the increased levels of corticosterone would affect the expression of growth factors in the hippocampus, known to be sensitive to glucocorticoid levels. At postnatal days 16, 20, and 24, rats were subjected to sleep deprivation, maternal separation without sleep deprivation, sleep deprivation with 2 h recovery sleep, or no intervention. mRNA expression was quantified in the cortex and hippocampus. cFos was increased after sleep deprivation and was similar to control level after 2 h recovery sleep irrespective of age or brain region. BDNF was increased by sleep deprivation in the cortex at P20 and P24 and only at P24 in the hippocampus. FGF2 increased during recovery sleep at all ages in both brain regions. We conclude that cortical BDNF expression reflects the onset of adult sleep-homeostatic response, whereas the profile of expression of both growth factors suggests a trophic effect of mild sleep deprivation.

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Haslam, Diana R. "Sleep deprivation and naps." Behavior Research Methods, Instruments, & Computers 17, no. 1 (January 1985): 46–54. http://dx.doi.org/10.3758/bf03200896.

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Brown, Lee K. "Physicians and sleep deprivation." Current Opinion in Pulmonary Medicine 14, no. 6 (November 2008): 507–11. http://dx.doi.org/10.1097/mcp.0b013e3283165e81.

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