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Quelques observations experimentales sur l'influence de l'insomnie absolue
... Хотя прямой и однозначный ответ на этот вопрос был получен еще в конце ХIХ века, благодаря экспериментам М.М. Манасеиной [8,9], предложившей лишать животных сна с целью выяснения его предназначения посредством наблюдения. Последствия оказались чрезвычайно наглядными. ...
... Но этот ясный вывод сделан не был, поскольку, как и большинство их современников, и М.М. Манасеина [8,9], и итальянские исследователи M. Daddi [10] и G. Tarozzi [11], вскоре повторившие ее эксперименты, считали, что сон в первую очередь необходим для обеспечения работы мозга. В результате они ожидали увидеть последствия депривации сна в его структурных изменениях. ...
... Причем, М.М. Манасеина [9] и итальянские физиологи [10,11] действительно описали такие изменения в морфологии некоторых клеток коры больших полушарий. Однако сегодня уровень морфометрии и использованные методологические подходы того времени позволяют усомниться в достоверности сделанных описаний. ...
It was proposed that historical analysis of ideas concerning the function of sleep will help to evaluate the tendencies in this field of science and will show the probable direction for further approach to understanding of this problem. We reviewed ideas of Ivan Pavlov and his Russian forerunners (Ivan Tarkhanoff and Maria Manaceine) and followers (Nikolay Rozjanskiy and Konstantin Bykov) on the functional role of sleep. This analysis led to the conclusion that state of sleep have been connected with realization of such functional operations, which have not been considered in the past and are not under consideration in the present neuroscience. Thus, one can expect that real understanding of sleep function will come only with new neurophysiologic paradigm.
... Her research, which laid the foundation for somnology as an independent branch of physiological science, was described in detail by V Kovalzon 6 and M Bentivoglio. 7 Experiments of Maria Manaseina-The first direct demonstration of the functional role of sleep As already mentioned, for many researchers, the function of sleep still remains a mystery, in spite of the fact that a direct and definite answer to this question was given by Manaseina 8,9 at the end of the 19th century. She deprived animals (puppies) of sleep to find out the consequences of sleep loss. ...
... In essence, their work was a repetition of the experiments of M Manaseina. 9 However, the study, on adult dogs, in the laboratory of K Bykov was carried out using new methods. Five dogs were used in this study. ...
We reviewed the ideas of Ivan Pavlov and his Russian forerunners (Ivan Tarkhanov and Maria Manaseina) and followers (Nikolai Rozjanskiy and Konstantin Bykov) on the functional role of sleep. This analysis led to the conclusion that the state of sleep is connected with functional operations that have not been considered in the past and are also not being investigated in present neuroscience. Thus, a real understanding of the function of sleep may only come with a new neurophysiological paradigm.
... Tarkhanov had been interested in sleep problems, which led to early studies to determine effects of sleep loss. Manàsseina kept 10 puppies constantly active, and after fourfive days without sleep, they died (Manàsseina, 1894). Observations during sleep deprivation and post-mortem analyses revealed that body temperatures dropped 4-6 • C even though the puppies were kept active, locomotor activity was impaired, red blood cell numbers were reduced, there were local brain hemorrhages, and cerebral ganglion were impaired. ...
This narrative traces the historical discoveries that formed the basis of our current understanding of sleep - immune interactions.
... In recent years, a main focus of sleep research has been on the relationship between sleep and synaptic plasticity (Stickgold and Walker, 2013;Dissel et al., 2015a;Dissel and Shaw, 2017;Seibt and Frank, 2019;Tononi and Cirelli, 2020;Frank, 2021). Nevertheless, it is important to note that thermoregulation has been implicated in sleep regulation and function from the earliest days of research in the field (De Manaceine, 1894;Kleitman and Doktorsky, 1933;Bentivoglio and Grassi-Zucconi, 1997). Indeed, decades of research have firmly established that sleep and thermoregulation are inextricably intertwined on many levels (Glotzbach and Heller, 1976;Parmeggiani et al., 1983;Szymusiak and McGinty, 1990). ...
Despite the fact that sleep deprivation substantially affects the way animals regulate their body temperature, the specific mechanisms behind this phenomenon are not well understood. In both mammals and flies, neural circuits regulating sleep and thermoregulation overlap, suggesting an interdependence that may be relevant for sleep function. To investigate this relationship further, we exposed flies to 12 h of sleep deprivation, or 48 h of sleep fragmentation and evaluated temperature preference in a thermal gradient. Flies exposed to 12 h of sleep deprivation chose warmer temperatures after sleep deprivation. Importantly, sleep fragmentation, which prevents flies from entering deeper stages of sleep, but does not activate sleep homeostatic mechanisms nor induce impairments in short-term memory also resulted in flies choosing warmer temperatures. To identify the underlying neuronal circuits, we used RNAi to knock down the receptor for Pigment dispersing factor, a peptide that influences circadian rhythms, temperature preference and sleep. Expressing UAS-PdfrRNAi in subsets of clock neurons prevented sleep fragmentation from increasing temperature preference. Finally, we evaluated temperature preference after flies had undergone a social jet lag protocol which is known to disrupt clock neurons. In this protocol, flies experience a 3 h light phase delay on Friday followed by a 3 h light advance on Sunday evening. Flies exposed to social jet lag exhibited an increase in temperature preference which persisted for several days. Our findings identify specific clock neurons that are modulated by sleep disruption to increase temperature preference. Moreover, our data indicate that temperature preference may be a more sensitive indicator of sleep disruption than learning and memory.
... In what is widely considered the first experiment into biological rhythms, eighteenth-century French astronomer Jean-Jacques d'Ortous de Mairan (Mairan, 1729) placed a mimosa plant in a box to see if it would still open and close its leaves without exposure to the light-dark cycle. Scientific interest in rhythms picked up pace in the late nineteenth century with physiological and medical research into body temperature and sleep deprivation in humans, and diurnal movements and activity patterns in plants, insects and animals (Allbutt, 1870;Darwin & Darwin, 1880;Laycock, 1860;Manacéïne, 1894). By the middle part of the twentieth century, researchers were increasingly focused on unravelling whether these rhythms were a response to environmental conditions or independent from them. ...
In the middle of the twentieth century, physiologists interested in human biological rhythms undertook a series of field experiments in natural spaces that they believed could closely approximate conditions of biological timelessness. With the field of rhythms research was still largely on the fringes of the life sciences, natural spaces seemed to offer unique research opportunities beyond what was available to physiologists in laboratory spaces. In particular, subterranean caves and the High Arctic became archetypal 'natural laboratories' for the study of human circadian (daily) rhythms. This paper is explores the field experiments which occurred in these 'timeless spaces'. It considers how scientists understood these natural spaces as suitably 'timeless' for studying circadian rhythms and what their experimental practices can tell us about contemporary physiological notions of biological time, especially its relationship to 'environmentality' (Formosinho et al. in Stud History Philos Sci 91:148-158, 2022). In so doing, this paper adds to a growing literature on the interrelationship of field sites by demonstrating the ways that caves and the Arctic were connected by rhythms scientists. Finally, it will explore how the use of these particular spaces were not just scientific but also political - leveraging growing Cold War anxieties about nuclear fallout and the space race to bring greater prestige and funding to the study of circadian rhythms in its early years.
... In recent years, a main focus of sleep research has been on the relationship between sleep and synaptic plasticity (Stickgold and Walker, 2013;Dissel et al., 2015a;Dissel and Shaw, 2017;Seibt and Frank, 2019;Tononi and Cirelli, 2020;Frank, 2021). Nevertheless, it is important to note that thermoregulation has been implicated in sleep regulation and function from the earliest days of research in the field (De Manaceine, 1894;Kleitman and Doktorsky, 1933;Bentivoglio and Grassi-Zucconi, 1997). Indeed, decades of research have firmly established that sleep and thermoregulation are inextricably intertwined on many levels (Glotzbach and Heller, 1976;Parmeggiani et al., 1983;Szymusiak and McGinty, 1990). ...
Despite the fact that sleep deprivation substantially affects the way animals regulate their body temperature, the specific mechanisms behind this phenomenon are not well understood. In both mammals and flies, neural circuits regulating sleep and thermoregulation overlap, suggesting an interdependence that may be relevant for sleep function. To investigate this relationship further, we exposed flies to 12 h of sleep deprivation, or 48 h of sleep fragmentation and evaluated temperature preference in a thermal gradient. Flies exposed to 12 h of sleep deprivation chose warmer temperatures after sleep deprivation. Importantly, sleep fragmentation, which prevents flies from entering deeper stages of sleep, but does not activate sleep homeostatic mechanisms nor induce impairments in short-term memory also resulted in flies choosing warmer temperatures. To identify the underlying neuronal circuits, we used RNAi to knock down the receptor for Pigment dispersing factor , a peptide that influences circadian rhythms, temperature preference and sleep. Expressing UAS- Pdfr RNAi in subsets of clock neurons prevented sleep fragmentation from increasing temperature preference. Finally, we evaluated temperature preference after flies had undergone a social jet lag protocol which is known to disrupt clock neurons. In this protocol, flies experience a 3 h light phase delay on Friday followed by a 3 h light advance on Sunday evening. Flies exposed to social jet lag exhibited an increase in temperature preference which persisted for several days. Our findings identify specific clock neurons that are modulated by sleep disruption to increase temperature preference. Moreover, our data indicate that temperature preference may be a more sensitive indicator of sleep disruption than learning and memory.
... A number of pioneering experimental sleep studies were performed in the 19 th century. 1 In 1894, the Russian physician Marie de Manaceine submitted dogs to continuous stimulation to evaluate the effects of sleep deprivation (SD). 2 The results revealed a fascinating discoverysleep absence caused the puppies' deaths. Four years later, Lambert Daddi and Giulio Tarozzi kept dogs awake by walking them until they died, which occurred after 9 to 17 days of SD. 3 Interestingly, both studies revealed that SD provoked alterations in body temperature and blood cells combined with fatigue and small hemorrhages in the brain. ...
... In four of the five tested animal species, sleep deprivation experiments eventually terminated with the premature death of the animals, but the underlying cause of lethality still remains unknown. In rats and dog pups, death is associated with a severe systemic syndrome bearing important metabolic changes and clear signs of suffering, making it difficult to ultimately conclude whether lethality is caused by the mere removal of sleep or rather by the very invasive and stressful procedures used to keep the animals awake (7,12,13). In the cockroach Diploptera punctata, sleep deprivation was achieved by continuously startling the animals (9), without, however, accounting for exhaustion-induced stress, a known lethal factor for other species of cockroaches (14)(15)(16). ...
Sleep appears to be a universally conserved phenomenon among the animal kingdom, but whether this notable evolutionary conservation underlies a basic vital function is still an open question. Using a machine learning–based video-tracking technology, we conducted a detailed high-throughput analysis of sleep in the fruit fly Drosophila melanogaster , coupled with a lifelong chronic and specific sleep restriction. Our results show that some wild-type flies are virtually sleepless in baseline conditions and that complete, forced sleep restriction is not necessarily a lethal treatment in wild-type D. melanogaster . We also show that circadian drive, and not homeostatic regulation, is the main contributor to sleep pressure in flies. These results offer a new perspective on the biological role of sleep in Drosophila and, potentially, in other species.
... These changes were very different from those Manasseina had observed in animals that died of starvation, in which the brain was remarkably spared. She concluded that findings provided a proof of the great importance of sleep for the organic life of animals equipped with a cerebral system, and also entitles to consider a bad paradox the strange opinion regarding sleep as a useless, stupid and even noxious habit [8]. ...
This article is dedicated to two outstanding scientists of the nineteenth century, Ivan Tarchanoff (Ivane Tarkhnishvili) and Maria Manasseina, Russian physiologists worked at the St. Petersburg Medico-Surgical Academy. Among the numerous contributions of Tarchanoff was the discovery of the skin galvanic reflex and of the influence of X-rays on physiological systems and functions, among them the central nervous system and animal behavior, the heart and circulation, and embryonic development. Maria Manasseina, one of the first Russian women-doctor great contributed in biochemistry and both scientists are founders of experimental sleep research by their original discoveries. Tarchanoff and Manasseina presented their interesting findings in experimental studies on sleep at the International Congress of Medicine in Rome in 1894 and published their papers in Archives Italiennes de Biologie in the same year.
... Total sleep deprivation refers to depriving an individual of at least one full night of sleep. As early as the late 19 th century, it was shown that prolonged total sleep loss in animals could lead to death [120]. The impact of experimentally induced sleep loss in humans varies between individuals, being dependent upon a multitude of circadian, sleep, arousal, individual and experimental factors [121]. ...
Sleep is a vital component of good health, and sleep loss is associated with impaired cognition, decreased psychomotor performance, cardiovascular disease, adverse effects on endocrine and metabolic function, negative mood, impaired memory, and more. A growing burden of freight transportation on global railway networks will likely lead to an increase in nocturnal vibration and noise at nearby dwellings. However, there is currently limited knowledge on how railway freight vibration and noise may disrupt sleep.
Over a series of laboratory studies in young healthy adults, the effect of vi-bration and noise from railway freight was investigated. Objective sleep was recorded with polysomnography, cardiac activity was recorded with elec-trocardiography and subjective sleep quality and disturbance was recorded with questionnaires. Increased cardiac activation occurred at vibration amplitudes only slightly above wakeful perceptual detection thresholds. Arousals, awakenings and alterations of sleep structure began to manifest at only slightly higher vibration amplitudes. With increasing vibration ampli-tude, heart rate and the probability of event-related cortical response in-creased in a dose-dependent manner, with accompanying adverse effects on perceived sleep quality and sleep disturbance. Perceived disturbance was more pronounced among noise-sensitive individuals, although no significant physiologic differences were found relative to non-sensitive counterparts. Rather than affecting overall sleep architecture, vibration and noise interfered with the normal rhythms of sleep, although the impact of this on long-term physical and mental health is currently unclear. Cardiac response persisted with increasing number of events, indicating an absence of habituation. Vibration and noise were additive regarding their effect on cortical arousal and sleep stage change, demonstrating that both exposures differentially contribute to sleep fragmentation. From a public health perspective, interventions to protect the sleep of populations near railway lines should therefore consider both exposure types.
... In today's modern lifestyle, sleep deprivation (SD) is a common phenomenon which can seriously affect the abilities of the subjected individuals (6). The pioneering study on SD was performed on puppies at the end of the 19th century (7) followed by other reports on experimental animal insomnia, mainly in dogs (8) and formal human SD research. In the following years, the dog as animal model for SD was replaced by cat and later by rodents, with the rat being the animal of choice to date (9). ...
Sleep deprivation (SD) is known to result in a range of neurological, cognitive and physical consequences in chronically-afflicted subjects. The respiratory nuclei of brain-stem tend to play a pivotal part in the regulating sleep function, hence hypothesized to be affected in various types of sleep-related dysfunctions. The purpose of this methodological report is to explain the techniques of REM sleep deprivation and stereology which can be used to consider changes of the quantitative properties of the respiratory nuclei in sleep-deprived rats.
... This belief in the concept of, "sleep for the brain", was not shaken even by the unexpected results obtained in studies of the consequences of sleep deprivation. These experiments, which were first done in 19th century ( [55]; Tarozzi [88]), demonstrated the fatal outcome of prolonged sleep deprivation in dogs. A review of pioneering studies, which had used the method of sleep deprivation for investigation of sleep function, is given in a special work (Bentivoglio & Grassi-Zucconi [11]). ...
It was noticed long ago that sleep disorders or interruptions to the normal sleep pattern were associated with various gastrointestinal disorders. We review the studies which established the causal link between these disorders and sleep impairment. However, the mechanism of interactions between the quality of sleep and gastrointestinal pathophysiology remained unclear. Recently, the visceral theory of sleep was formulated. This theory proposes that the same brain structures, and particularly the same cortical sensory areas, which in wakefulness are involved in processing of the exteroceptive information, switch during sleep to the processing of information coming from various visceral systems.We review the studies which demonstrated that neurons of the various cortical areas (occipital, parietal, frontal) during sleep began to fire in response to activation coming from the stomach and small intestine. These data demonstrate that, during sleep, the computational power of the central nervous system, including all cortical areas, is engaged in restoration of visceral systems. Thus, the general mechanism of the interaction between quality of sleep and health became clear.
... One of the first published studies of total sleep loss in puppies dates back to 1894 (Manaceine, 1894) and for humans a couple of years later (Patrick and Gilbert, 1896). Manaceine's observations indicated that sleep loss when prolonged in animals is fatal; this concept was dismissed until recent findings. ...
... A remoção parcial ou supressão do sono em um organismo é conhecida como privação de sono (6) . Historicamente, estudos sobre a privação de sono tiveram início em 1894 com os experimentos de De Manacéine (7) , onde foi demonstrado que, filhotes e cães adultos, morriam após alguns dias de privação de sono, e que essa privação causava severas lesões no sistema nervoso central desses animais (8) . ...
Sleep deprivation can be defined as total or partial suppress of sleep and is associated with alterations in endocrine, metabolic, physical, cognitive functions and modifications of the sleep patterns that compromise health and quality of life. Physical exercise is associated with improvement of cardiovascular, respiratory, muscular, endocrine and nervous system, and a better sleep quality. However, the association of these two conditions is unclear, partly due to the difficulty to obtain volunteers to participate in this type of protocol with no financial compensation. The majority of the studies which investigate the association between physical exercises and sleep deprivation focus on aerobic performance and verify little or no effect of this parameter. Concerning anaerobic power and strength, significant alterations have not been found; however, for prolonged events there may be an interaction between these two factors, which suggests a protection mechanism. Nevertheless, it is important to consider that one of the main alterations caused by sleep deprivation the increase of the subjective perception, which presents a factor to decrease and compromise the physical performance per se, and may represent a masking element of the deleterious effects of sleep deprivation. Thus, the aim of present review is to discuss the different aspects of relationship between physical exercise and sleep deprivation, showing their effects and consequences in physical performance.
... The first reported experimental study on SD was conducted on puppies at the end of the 19th century (de Manaceine, 1894), followed by other pioneering reports on experimental animal insomnia, mainly in dogs (for a review see Bentivoglio and Grassi-Zucconi, 1997), and by the first formal human SD study (Patrick and Gilbert, 1896). In the following decades, the dog as animal model for SD was progressively replaced by the cat and later on by rodents, with the rat being the animal of choice up to this day. ...
Paradigms of sleep deprivation (SD) and memory testing in rodents (laboratory rats and mice) are here reviewed. The vast majority of these studies have been aimed at understanding the contribution of sleep to cognition, and in particular to memory. Relatively little attention, instead, has been devoted to SD as a challenge to induce a transient memory impairment, and therefore as a tool to test cognitive enhancers in drug discovery. Studies that have accurately described methodological aspects of the SD protocol are first reviewed, followed by procedures to investigate SD-induced impairment of learning and memory consolidation in order to propose SD protocols that could be employed as cognitive challenge. Thus, a platform of knowledge is provided for laboratory protocols that could be used to assess the efficacy of drugs designed to improve memory performance in rodents, including rodent models of neurodegenerative diseases that cause cognitive deficits, and Alzheimer's disease in particular. Issues in the interpretation of such preclinical data and their predictive value for clinical translation are also discussed.
... Since the early empirical observations of De Manacéine [87], it is well known that sleep loss has degrading effects on alertness and performance. If sleep is a behavioral state in which the body recovers physical and mental energies, the lack of sleep can jeopardize the execution of neurocognitive, psychological, and behavioral processes [88]. ...
There is a general consensus that sleep is strictly linked to memory, learning, and, in general, to the mechanisms of neural plasticity, and that this link may directly affect recovery processes. In fact, a coherent pattern of empirical findings points to beneficial effect of sleep on learning and plastic processes, and changes in synaptic plasticity during wakefulness induce coherent modifications in EEG slow wave cortical topography during subsequent sleep. However, the specific nature of the relation between sleep and synaptic plasticity is not clear yet. We reported findings in line with two models conflicting with respect to the underlying mechanisms, that is, the "synaptic homeostasis hypothesis" and the "consolidation" hypothesis, and some recent results that may reconcile them. Independently from the specific mechanisms involved, sleep loss is associated with detrimental effects on plastic processes at a molecular and electrophysiological level. Finally, we reviewed growing evidence supporting the notion that plasticity-dependent recovery could be improved managing sleep quality, while monitoring EEG during sleep may help to explain how specific rehabilitative paradigms work. We conclude that a better understanding of the sleep-plasticity link could be crucial from a rehabilitative point of view.
... the rest of Patrick and Gilbert's other work. Finally, unlike another famous sleep deprivation study of the time (de Manacéïne, 1894), Patrick and Gilbert did not inspire any further work for many years to come. Although sleep research in the late 19 th century already had a scientific basis grounded in medicine and physiology, the study of the effects of enforced wakefulness did not make an appearance before the early 1890's. ...
Document formatted into pages; contains viii, 173 p. : ill. Thesis (Ph.D.)--Bowling Green State University, 2006. Includes bibliographical references. Mode of access: World Wide Web. System requirements: Adobe Acrobat Reader.
... Chronic sleep deprivation has produced symptoms ranging from mild behavioral changes to cerebral hemorrhage and disrupted thermoregulation [1][2][3]. In early studies, deprivation was often not long enough to distinguish between homeostatically regulated increases in sleep tendency and biological deficits. ...
Sleep deprived rats undergo a predictable sequence of physiological changes, including changes in skin condition, increased energy expenditure, and altered thermoregulation. Amino-cupric-silver staining was used to identify sleep deprivation related changes in the brain. A significant increase in staining was observed in the supraoptic nucleus (SON) of the hypothalamus of rats with high sleep loss (>45 h) vs. their yoked controls. Follow-up experiments showed that staining was not significantly different in rats sleep deprived for less than 45 h, suggesting that injurious sleep deprivation-related processes occur above a threshold quantity of sleep loss. These anatomical changes suggest that the effects of sleep deprivation may be related to protein metabolism in certain brain regions.
Sleep neuroimaging is a subfield of sleep science that goes beyond polysomnography by combining neuroimaging techniques with validated sleep research methods to characterize sleep-wake states and investigate sleep-related processes across the 24-hour day. In this article, we review the historical advancements and applications that grew out of somnography leading to current sleep neuroimaging methods. We highlight the power of somnoimages to help visualize sleep research results and communicate complex information about sleep processes. We also suggest several ways in which applying neuroimaging during sleep has opened new avenues to more fully capture the nature of sleep, uncovered mechanisms of sleep-wake regulation, and increased understanding of sleep-related processes. Current applications and future directions of sleep neuroimaging are also discussed.
How much sleep does one need?’ is a critical question that has been difficult to answer. The long history of sleep research has culminated in population‐derived normative values of 7 to 9 h of sleep per night to avoid dysfunction. Such a wide range is sufficiently large that one cannot know what is required for any given individual. ‘Sleep need’ cannot currently be directly measured, might not be represented by one number (given the multiple functions that sleep subserves), and likely varies from individual‐to‐individual and from day‐to‐day. This said, the concept should be embraced and can be considered alongside more easily operationalised and routinely measured constructs of ‘sleep opportunity’ (e.g., time in bed) and ‘sleep ability’ (i.e., the obtained sleep, such as sleep duration). Considering the dynamics of all three constructs together may drive greater understanding about sleep health, sleep insufficiency, and sleep disorder pathology. In this article, we describe a new theory called Sleep Opportunity, Need, and Ability and provide a rationale for why this theory has both theoretical and clinical value.
The influence of sleep and circadian rhythms on daytime functioning has long been noted. Psychologists and psychology-oriented researchers were among the first to investigate the role of sleep and circadian rhythms in motivation, emotion, cognition, and performance. At the dawn of modern sleep science, psychological fellow, F. B. Dresslar found that telegram tapping speed varied according to time of day providing the first clues to the role of circadian rhythms on performance (Dresslar 1892). Marie de Manacéïne was the first to experimentally demonstrate that sleep was critical to life and that the brain and behaviour were adversely impacted by sleep loss (de Manacéïne 1894) Patrick and Gilbert elaborated on the role of sleep on psychological functioning and were the first to experimentally study the impact of sleep loss in humans (Patrick and Gilbert 1896). The past century has seen an explosion of interest in understanding which aspects of sleep and circadian rhythms relate to which aspects of daytime psychological functioning.
We present a historical review of the concepts of Russian researchers regarding the mechanisms and functional roles of sleep – I. P. Pavlov and his predecessors (I. R. Tarkhanov and M. M. Manaseina) and students (N. A. Rozhanskii and K. M. Bykov). This analysis leads to the conclusion that sleep is linked with the realization of functional operations not previously associated with sleep and not addressed by current neuroscience. Thus, a real understanding of sleep functions can be expected to come only with a new neurophysiological paradigm.
Chronic insomnia is a widespread and therapy resistant sleep disorder associated with multiple diseases and worsening of its course. Cognitive-behavior therapy of insomnia (CBT-I) is a pathogenetically based method of chronic insomnia treatment. 42 patients (male 14, female 28, age from 29 to 80) matched ICSD-3 criteria of chronic insomnia participated in the crossover study including 2-week courses of treatment by CBT-I and Zopiclone. All participants underwent polysomnography. Effectiveness of treatment was evaluated by questionnaires: Insomnia severity index (ISI), Pittsburgh sleep quality index, Beck depression inventory, Disfunctional beliefs about sleep, Sleep hygiene index. Treatment with CBT-I and zopiclone produced simular improvement of sleep quality with Insomnia severity index decreased to 3,6 (from 17,7±5,3 to 12,8±5,1) and 4,9 (from 16,5±5,8 to 12,9±6,2) respectively (р<0,05) while after two weeks of stopping treatment the significant difference remained only for CBT-I comparing with zopiclone treatment (12,9±6,2 and 15,5±4,6 points by ISI respectively) (p<0,05). The use of CBT-I leads to decrease of level of depression from 11,8±6,9 to 8,5±7, Sleep hygiene index decreases from 26,9±7,5 to 23,9±5,7 and disfunctional beliefs about sleep level drops from 104,9±29,7 to 84,4±34,2 (all these differences were significant at p<0,05). Analysis of the characteristics of responders and nonresponders has shown that the mean age of the first ones was younger comparing with nonresponders (40,5±12,9 and 57,2±11,7, p<0,05 respectively) that allows us to consider young age as predictor of CBT-I effectiveness. Treatment of chronic insomnia by CBT-I has simular efficacy as pharmacotherapy, but additionally it leads to the emprovement of emotional state and its therapeutistic effects after discontinuation lasts longer.
Sleep deprivation (SD) is known to result in a range of neurological, cognitive and physical consequences in chronically-afflicted subjects. The respiratory nuclei of brain-stem tend to play a pivotal part in the regulating sleep function, hence hypothesized to be affected in various types of sleep-related dysfunctions. The purpose of this methodological report is to explain the techniques of REM sleep deprivation and stereology which can be used to consider changes of the quantitative properties of the respiratory nuclei in sleep-deprived rats.
The discovery of electricity and artificial extension of light phase resulted in reduction in the sleep time to maximize the work or leisure time. Schedules where work has to be done during the nighttime by sleeping in the daytime also result in reduced sleep time invariably. Thus the twenty-first-century social lifestyle is composed of less sleep in our daily routine than what we typically require resulting in a state of chronic sleep deprivation. Sleep deprivation has become a major global public health concern due to its detrimental effects on cognitive functioning, road safety, workplace errors, and metabolic and endocrine function. Increasingly, sleep deprivation is being linked to life expectancy also. A recent study by Zhang et al. showed that sleep deprivation results in the degeneration of neurons in the locus ceruleus. Hublin et al. reported that short sleep (less than 7 h) increased the risk of mortality by 26 % in men and 21 % in women compared to individuals with an average length of sleep time of 7–8 h.
The International Classification of Sleep Disorders Third Edition (ICSD-3) lists five major types of sleep-related breathing disorders (SRBDs), including obstructive sleep apnea (OSA) disorders, central sleep apnea (CSA) syndromes, sleep-related hypoventilation (SRHV) disorders, sleep-related hypoxemia (SRHO) disorders, and isolated symptoms and normal variants. Positive airway pressure (PAP) treatment-emergent CSA, also known as complex sleep apnea, has been classified under CSA syndromes while mixed sleep apnea (both obstructive and central apneas occurring during the diagnostic study) has not yet been listed in the ICSD-3. Although excessive daytime sleepiness is a well-known consequence of SRBDs, insomnia occurs in 40–60 % of patients with OSA syndrome. Although there are no population-based estimates of the prevalence of the different subtypes of SRBDs, the vast majority (>90 %) of cases seen in clinical practice are due to OSA syndrome. Although habitual snoring and catathrenia (sleep groaning) can be disruptive to other household members’ sleep, these isolated symptoms, in the absence of neurocognitive symptoms and polysomnographically diagnosed sleep apnea, are not associated with adverse cardiovascular outcomes.
Spanning over half a century of investigation into Rapid Eye Movement (REM) sleep, this volume provides comprehensive coverage of a broad range of topics in REM sleep biology. World renowned researchers and experts are brought together to discuss past and current research and to set the foundation for future developments. Key topics are covered in six sections from fundamental topics (historical context and general biology) to cutting-edge research on neuronal regulation, neuroanatomy and neurochemistry, functional significance and disturbance in the REM sleep generating mechanism. A reference source for all aspects of REM sleep research, it also incorporates chapters on neural modelling, findings from non-human species and interactions between brain regions. This is an invaluable resource, essential reading for all involved in sleep research and clinical practice.
The time from 1800 to mid-twentieth century is a transitional epoch for understanding of sleep and its disorders. With the rise of physiology, organic chemistry, and finally psychology, sleep became an object of experimental study. At the same time, the development of clinical science, especially neurology, fueled an interest in questions of consciousness, motor and reflex activity, and sleep–wake control by the brain. The increasing understanding of pathological and psychopathological processes led to an improved classification of sleep disorders. At the same time, the development of organic chemistry resulted in the development of new treatment options for various sleep disorders. Finally, the rise of electrophysiology, in the first half of the twentieth century, enabled to study the activity of the sleeping brain on a time scale from seconds to hours. The resulting new understanding of sleep as a complex and highly regulated process allowed a better understanding of the pathophysiology of sleep disorders, and thus, became the basis for the development of sleep medicine as a medical subspeciality toward the end of the twentieth century. Finally, living and working conditions, which have changed dramatically during the period under discussion, led to a new appraisal of the role of sleep and its disorders.
During the twentieth century, only two researchers published world famous, encyclopedic monographs related to sleep. The first of these works appeared in 1913, when Henri Piéron published "Le probléme physiologique du sommeil", which is still a standard reference today. Although multiple researchers and clinicians, such as Economo (1917, 1928), Berger (1929), Hess (1931), Bremer (1935, 1936), Loomis et al. (1937) and Ranson (1939), subsequently published highly important findings on sleep-waking processes, the next fundamental phase was marked by the publication of the first edition of Sleep and Wakefulness, by Nathaniel Kleitman in 1939. Later, following his discovery of rapid eye movement (REM) dreaming sleep stage in 1953, Kleitman published the masterful second edition of this work in 1963. Later on, several researchers published highly important reviews (Jouvet 1962, 1972, Moruzzi 1963, 1972, Hobson 1988, Steriade and McCarley 1990), although they were directed to more limited topics. The book provides an overview of Piéron's and Kleitman's sleep-related papers, placed in their proper historical context.
The definition of what sleep
is depends on the method that is applied to record sleep. Behavioral and (electro)-physiological measures of sleep clearly overlap in mammals
and birds
, but it is often unclear how these two relate in other vertebrates and invertebrates. Homeostatic regulation of sleep, where the amount of sleep depends on the amount of previous waking, can be observed in physiology and behavior in all animals this was tested in. In mammals and birds, sleep is generally subdivided into two states, non-rapid eye movement (NREM) sleep
and REM sleep
. In mammals the combination of behavioral sleep and the changes in the slow-wave range of the NREM sleep electroencephalogram
(EEG) can explain and predict the occurrence and depth of sleep in great detail. For REM sleep this is far less clear. Finally, the discovery that slow-waves in the NREM sleep EEG are influenced locally on the cortex depending on prior waking behavior is an interesting new development that asks for an adaptation of the concept of homeostatic regulation
of sleep. Incorporating local sleep into models of sleep regulation is needed to obtain a comprehensive picture.
A privação do sono é a remoção ou supressão parcial do sono, e esta condição pode causar diversas alterações: endócrinas, metabólicas, físicas, cognitivas, neurais e modificações na arquitetura do sono, que em conjunto comprometem a saúde e a qualidade de vida do sujeito nestas condições. Já o exercício físico praticado regularmente promove benefícios como melhora do aparato cardiovascular, respiratório, endócrino, muscular e humoral, além disso, pode melhorar a qualidade do sono. Entretanto, a associação desses dois parâmetros não tem sido bem explorada, em parte pela dificuldade conseguir voluntários que se submetam a essa condição principalmente sem nenhum tipo de compensação financeira. A maioria dos estudos que investigaram o binômio exercício físico e privação de sono focou os efeitos no desempenho aeróbio. Embora ainda haja controvérsias, os estudos apontam para pequena ou nenhuma alteração desse parâmetro quando as duas situações se fazem presentes. Em relação à potência anaeróbia e força não tem sido encontrados alterações significativas, mas para eventos prolongados, parece haver uma interação entre a privação de sono e o exercício físico, o que sugere um mecanismo de proteção. Entretanto, é importante considerar que uma das alterações mais importantes causadas pela privação do sono é o aumento na percepção subjetiva, que por si só já representa um fator para diminuição e comprometimento do desempenho físico e pode representar um elemento de "mascaramento" dos efeitos deletérios da privação. Assim, o objetivo da presente revisão é o de discutir os diferentes aspectos da relação entre o exercício físico e a privação de sono, evidenciando seus efeitos e reflexos no desempenho físico.
1.1. Selective deprivation of paradoxical sleep (PS) had been carried out in cats with chronically implanted electrodes for 1–26 days by different methods (swimming pool or electric shocks). Total deprivation of sleep was also carried out for 24–48 h under EEG control.2.2. During sleep PS deprivation, a need for PS appears, requiring an increasing number of awakenings on successive days in order to prevent it.3.3. After PS deprivation longer than 8 days some discrete behavioural disturbances may appear: mostly drowsiness, muscular hypotonia and hypersexuality. There is also a constant tachycardia. Behaviour suggesting hallucinations was not seen.4.4. In sleep during recovery, after selective PS deprivation, a selective rebound of PS appears. Its characteristics are emphasized: it is associated with an increase of the phasic phenomena of PS; it is always periodically interrupted by slow sleep and its duration is equal to half the duration of PS deprivation. The return to a normal heart rate closely follows the return to a normal amount of PS. Finally, there is never complete recovery of the debt of PS which is accumulated during deprivation.5.5. One cat died on the 5th day of recovery, after a 26 day PS deprivation, after numerous episodes of narcolepsy during which waking was directly followed by PS, without an intermediate episode of slow sleep.6.6. Deprivation of both slow and paradoxical sleep is not followed by a PS rebound but on the contrary by an increase of slow sleep.7.7. These results are discussed in the light of a neuro-humoral theory of PS.
Electrical lighting and increasing capital intensiveness have helped undermine the importance that society previously placed on obtaining adequate sleep. Even modest amounts of daily sleep loss accumulate as sleep debt. Sleep debt manifests in a myriad of ways, the most common being an increasing tendency to fall asleep, increased risk of accidental injury, impaired mood, and reduced psychomotor performance. Sleep debt can have far reaching consequences, both to an individual in terms of increased cardiovascular risk and to society at large, because of sleepiness-related fatigue and errors. Sleep specialists need to further their understanding of the physiologic and behavioral consequences of total, partial, and selective sleep stage deprivation, because they affect many organ systems. Studies of selective sleep stage deprivation also provide insights into the function of sleep. Evaluating the effects of sleep deprivation must take into account the following factors: (1) the duration of prior sleep, (2) circadian time frame, (3) arousal influences, and (4) subject and test characteristics. Sleep deprivation has been extensively studied in the acute experimental setting. Under extreme conditions, sleep deprivation is associated with mortality in laboratory animals. In the natural human environment, the behavioral consequence of chronic sleep debt in shift work intolerance is well described. The link between electrophysiological sleep disturbance and pathogenesis of disease is less well understood in both acute and chronic states. Additional investigation into the relationship between sleep deprivation and disease mechanisms, such as impaired glucose tolerance, hormonal dysregulation, and cytokine imbalance, will enhance our comprehension of this link.
We report an attempted replication of G. T. W. Patrick and J. A. Gilbert’s pioneering sleep deprivation experiment ‘Studies
from the psychological laboratory of the University of Iowa. On the effects of loss of sleep’, conducted in 1895/96. Patrick
and Gilbert’s study was the first sleep deprivation experiment of its kind, performed by some of the first formally trained
psychologists. We attempted to recreate the original experience in two subjects, using similar apparatus and methodology,
and drawing direct comparisons to the original study whenever possible. We argue for a strong influence of an ‘Americanized’
Wundtian psychology on Patrick and Gilbert, a claim supported biographically by their education and by their experimental
methods. The replication thus opens interesting new perspectives, which are unlikely to be generated by any other historical
approach.
Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health.
Experimental studies of the extraction of substances from the brain capable of inducing normal sleep, until its establishment in the 1980s, are reviewed. Although it is believed that Legendre and Pieron induced sleep in dogs by injecting substances extracted from the brains of sleep-deprived dogs (1910–1913) and that Pappenheimer et al. (1975) extracted a sleep-inducing powder from the brains of sleep-deprived goats, the first person to actually attempt the extraction of sleep-inducing substances from the brain of sleep-deprived dogs was Kuniomi Ishimori, a Japanese physiologist. He reported his experimental results in 1909. The contents of his data and an outline of his study are introduced briefly. His original paper has been translated into English and is given in an Appendix.
A short note about the life and personality of Maria Manasseina (also known as Marie von Manassein, Marie de Manaceine), a Russian woman-doctor of the second half of the nineteenth century, a pioneer in biochemistry and experimental somnology.
A series of experiments compared sleep deprivation of rats by sleep contingent shock and by non punitive procedures. Sleep overrode shock in approximately 24 hours. Animals were kept awake by non punitive procedures for 12 and 15 days. Recovery measures were higher for the non punitive procedures.
In order to investigate whether sleep deprivation activates the photoconvulsive response 35 patients were investigated electroencephalographically after 24–36 h of waking. In 34 cases with sleep deprivation photostimulation showed a clear photosensitivity which was not present before sleep deprivation. This pathological response to photostimulation was unchanged after the short sleep period, in some even potentiated. Long-term anticonvulsive therapy could not suppress the positive photic reaction after sleep deprivation. No correlation between the blood glucose level and photosensibility could be determined. In summary it can be stated that sleep deprivation appears to have a activating effect on photosensitivity. The clinical employment and the neurophysiological mechanisms are discussed.Copyright © 1974 S. Karger AG, Basel
The experimental studies on sleep deprivation were initiated by the Russian physician and scientist, Marie de Manacéine, who studied sleep-deprived puppies kept in constant activity. She reported in 1894 that the complete absence of sleep was fatal in a few days, pointing out that the most severe lesions occurred in the brain. In 1898, the Italian physiologists Lamberto Daddi and Giulio Tarozzi also kept dogs awake by walking them; the animals died after 9-17 days, and their survival was unrelated to food consumption. In the histological study performed by Daddi, degenerative alterations, mainly represented by chromatolytic changes, were observed in neurons of the spinal ganglia, Purkinje cells of the cerebellum, and neurons of the frontal cortex. Daddi ascribed these changes to a state of autointoxication of the brain during insomnia. In 1898, the psychiatrist Cesare Agostini, interested in the psychic phenomena caused by prolonged insomnia in humans, sleep deprived dogs by keeping them in a metallic cage in order to avoid fatigue. The dogs survived about 2 weeks, and degenerative changes were observed in their brains. In these experimental paradigms, the effect of sleep loss was confounded by motor exhaustion and/or intense sensory stimulation. In spite of the absence of adequate controls, the pioneering studies performed at the end of the 19th century represented the first experimental attempts to relate sleep with neural centers and suggested that sleep is a vital function and that the brain may be affected by insomnia.
Since the closing decades of the nineteenth century, women have been contributing in a significant way to the neurosciences. This article looks at the contributions of some of the leading women pioneers in this field. It also deals with women who have written on the history of the neurosciences and the representation of women in the International Society for the History of the Neurosciences, the largest neuroscience history organization. Trends suggest that books and articles from and about women in the history of the neurosciences will increase markedly in the future.
The occurrence of chronic sleep deprivation in the population is commonplace. Both duration and quality of sleep are important to assess when evaluating a patient who has sleep complaints. Excessive sleepiness and decreased psychomotor performance have been demonstrated after sleep deprivation. Sleep loss may impact mood, autonomic function, and the immune system. Sleep-deprived adults may have impaired job performance and are prone to motor vehicle accidents. Simple interventions to ensure adequate sleep can help avoid these hazards.
Changes of cortical and corticospinal excitability as a function of sleep deprivation have been studied, using EEG power maps and several TMS measures in 33 normal subjects before and after a 40-h sleep deprivation (SD). The effects of SD were independently assessed by subjective and EEG measures of sleepiness, the latter being represented in terms of cortical maps for different frequency bands. Short intracortical facilitation (SICF) and inhibition (SICI) were measured by the paired-pulse TMS technique with different inter-stimulus intervals. Besides standardized motor threshold (MT), lower threshold (LT) and upper threshold (UT) were also determined. Subjective sleepiness severely increased as a consequence of SD, paralleled by a drastic decrease of alertness. EEG topography showed large increases in delta and theta activity, mainly evident at fronto-central areas. Standard MTs, as well as LTs and UTs, all increased as a consequence of SD. SICF also showed a significant increase as compared to pre-deprivation values, but only in females. The increase of theta activity was strongly associated in the left frontal and prefrontal cortex to a smaller decrease of corticospinal excitability, expressed by MTs, and a larger increase of intracortical facilitation, expressed by SICF. TMS and EEG measures converge in indicating that SD has severe effects on both cortical and corticospinal excitability, as shown respectively by the increases of slow-frequency EEG power and MTs. The SICF enhancement in females and the results of the combined topographical analysis of EEG and TMS changes are coherent with the hypothesis that cortical TMS-evoked responses are higher as a consequence of a longer wakefulness. However, the lack of an increase in cortical excitability after prolonged wakefulness in males suggests some caution in the generalization of these effects, that deserve further investigation.
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