Tesi sul tema "Sleep architecture"
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Dingwall, Kylie. "Effects of medication on the sleep architecture of patients with obstructive sleep apnea syndrome (OSAS) /". [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19264.pdf.
Testo completo
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Ajwad, Asma'a A. "SLEEP AND THERMOREGULATION: A STUDY OF THE EFFECT OF AMBIENT TEMPERATURE MANIPULATION ON MOUSE SLEEP ARCHITECTURE". UKnowledge, 2018. https://uknowledge.uky.edu/cbme_etds/54.
Testo completoAbstract (sommario):
Good quality sleep is essential for mental and physical health. Inadequate sleep impacts memory consolidation, learning and cognition, immune function, autonomic regulation, physical performance, and other vital functions. In many neurological disorders that are associated with sleep problems such as epilepsy and Alzheimer’s disease, changes in brain circuitry affect sleep-wake regulation mechanisms; this is reflected in anomalous sleep-wake architecture and usually accompanied by poor sleep depth. Thus, over many years, many approaches have been tried in humans and animal models with the goal of improving sleep quality. Unfortunately, each of those approaches comes with limitations or side effects. Thus, there is a need for a natural, safe, and low cost approach that overcomes many limitations to improve sleep and eventually the lives of individuals with sleep problems.
Environmental temperature is one of the most important factors that affect sleep in humans and other animals. Studies have shown that the part of the brain governing thermoregulation is also involved in sleep-wake regulation. Even a mild change in environmental temperature can produce a significant effect on sleep. Thus, a better understanding of the sleep-thermoregulation interaction could lead to novel ways for treating many sleep disorders. As a first step on the translational pathway, experiments in animal models of disease conditions with disordered sleep are needed for investigating sleep–thermoregulation interactions and for devising and validating related approaches to enhance sleep quality before conducting them on humans.
This dissertation explores and assesses the effect of changes in ambient temperature on sleep-wake architecture in control mice and epileptic mice, the latter from a model of temporal lobe epilepsy as an example of a disease model with disordered sleep. Then, based on the results of temperature effects on sleep in control and epileptic mice, different strategies are proposed and tested to modulate sleep through ambient temperature regulation in closed loop to improve sleep depth and regulate the timing of the sleep-wake cycle.
The results presented in this dissertation demonstrate the feasibility of sleep enhancement and regulation of its timing and duration through manipulation of ambient temperature using closed-loop control systems. Similar approaches could foreseeably be used as more natural means for enhancing deep sleep in patients with epilepsy, Alzheimer’s, or Parkinson’s disease in which poor sleep is common and associated with adverse outcomes.
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Kallushi, Abi Elena. "Healing Architecture for Troubled Nightowls: Restoring Natural Rhythms in Nocturnal U Street". Thesis, Virginia Tech, 2016. http://hdl.handle.net/10919/73776.
Testo completoAbstract (sommario):
This thesis is an exploration of architecture as an active participant in human life, not just as a stage. When architecture is considered a participant it contributes to the improvement of our quality of life as well as aiding the healing process when we fall ill. As more people are diagnosed with anxiety and sleep disorders, the thesis considered questions of how the places in which we carry out our day-to-day lives improve the prognosis and, further, can architecture be used as a powerful tool for healing? It is possible that our disconnection from nature is partially responsible for our disrupted sleep patterns and misplaced anxieties. Perhaps natural elements and rhythms are too absent in our daily urban lives. But as more of us move into cities and our urban centers become denser, designers must find clever ways to help city owls reset their circadian rhythm. Architecture can help reestablish that bond with nature. This thesis explores an architecture of healing by proposing a program and design that follows the day and night circadian rhythm of our bodies, which in turn follow the sun and other natural phenomena. Located in a tricky triangular site in one of the busiest nighttime neighborhoods of Washington DC, a wellness center and sleep clinic would allow city dwellers to find a peaceful oasis for healing. In parallel, this thesis is also a study of collage as a design tool, as well as designing from details and the human scale.Master of Architecture
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Johnson, Pamela Lesley. "Sleep and Breathing at High Altitude". University of Sydney, 2008. http://hdl.handle.net/2123/3531.
Testo completoAbstract (sommario):
Doctor of Philosphy (PhD)This thesis describes the work carried out during four treks, each over 10-11 days, from 1400m to 5000m in the Nepal Himalaya and further work performed during several two-night sojourns at the Barcroft Laboratory at 3800m on White Mountain in California, USA. Nineteen volunteers were studied during the treks in Nepal and seven volunteers were studied at White Mountain. All subjects were normal, healthy individuals who had not travelled to altitudes higher than 1000m in the previous twelve months. The aims of this research were to examine the effects on sleep, and the ventilatory patterns during sleep, of incremental increases in altitude by employing portable polysomnography to measure and record physiological signals. A further aim of this research was to examine the relationship between the ventilatory responses to hypoxia and hypercapnia, measured at sea level, and the development of periodic breathing during sleep at high altitude. In the final part of this thesis the possibility of preventing and treating Acute Mountain Sickness with non-invasive positive pressure ventilation while sleeping at high altitude was tested. Chapter 1 describes the background information on sleep, and breathing during sleep, at high altitudes. Most of these studies were performed in hypobaric chambers to simulate various high altitudes. One study measured sleep at high altitude after trekking, but there are no studies which systematically measure sleep and breathing throughout the whole trek. Breathing during sleep at high altitude and the physiological elements of the control of breathing (under normal/sea level conditions and under the hypobaric, hypoxic conditions present at high altitude) are described in this Chapter. The occurrence of Acute Mountain Sickness (AMS) in subjects who travel form near sea level to altitudes above 3000m is common but its pathophysiology not well understood. The background research into AMS and its treatment and prevention are also covered in Chapter 1. Chapter 2 describes the equipment and methods used in this research, including the polysomnographic equipment used to record sleep and breathing at sea level and the high altitude locations, the portable blood gas analyser used in Nepal and the equipment and methodology used to measure each individual’s ventilatory response to hypoxia and hypercapnia at sea level before ascent to the high altitude locations. Chapter 3 reports the findings on the changes to sleep at high altitude, with particular focus on changes in the amounts of total sleep, the duration of each sleep stage and its percentage of total sleep, and the number and causes of arousals from sleep that occurred during sleep at increasing altitudes. The lightest stage of sleep, Stage 1 non-rapid eye movement (NREM) sleep, was increased, as expected with increases in altitude, while the deeper stages of sleep (Stages 3 and 4 NREM sleep, also called slow wave sleep), were decreased. The increase in Stage 1 NREM in this research is in agreement with all previous findings. However, slow wave sleep, although decreased, was present in most of our subjects at all altitudes in Nepal; this finding is in contrast to most previous work, which has found a very marked reduction, even absence, of slow wave sleep at high altitude. Surprisingly, unlike experimental animal studies of chronic hypoxia, REM sleep was well maintained at all altitudes. Stage 2 NREM and REM sleep, total sleep time, sleep efficiency and spontaneous arousals were maintained at near sea level values. The total arousal index was increased with increasing altitude and this was due to the increasing severity of periodic breathing as altitude increased. An interesting finding of this research was that fewer than half the periodic breathing apneas and hypopneas resulted in arousal from sleep. There was a minor degree of upper airway obstruction in some subjects at sea level but this was almost resolved by 3500m. Chapter 4 reports the findings on the effects on breathing during sleep of the progressive increase of altitude, in particular the occurrence of periodic breathing. This Chapter also reports the results of changes to arterial blood gases as subjects ascended to higher altitudes. As expected, arterial blood gases were markedly altered at even the lowest altitude in Nepal (1400m) and this change became more pronounced at each new, higher altitude. Most subjects developed periodic breathing at high altitude but there was a wide variability between subjects as well as variability in the degree of periodic breathing that individual subjects developed at different altitudes. Some subjects developed periodic breathing at even the lowest altitude and this increased with increasing altitude; other subjects developed periodic breathing at one or two altitudes, while four subjects did not develop periodic breathing at any altitude. Ventilatory responses to hypoxia and hypercapnia, measured at sea level before departure to high altitude, was not significantly related to the development of periodic breathing when the group was analysed as a whole. However, when the subjects were grouped according to the steepness of their ventilatory response slopes, there was a pattern of higher amounts of periodic breathing in subjects with steeper ventilatory responses. Chapter 5 reports the findings of an experimental study carried out in the University of California, San Diego, Barcroft Laboratory on White Mountain in California. Seven subjects drove from sea level to 3800m in one day and stayed at this altitude for two nights. On one of the nights the subjects slept using a non-invasive positive pressure device via a face mask and this was found to significantly improve the sleeping oxyhemoglobin saturation. The use of the device was also found to eliminate the symptoms of Acute Mountain Sickness, as measured by the Lake Louise scoring system. This finding appears to confirm the hypothesis that lower oxygen saturation, particularly during sleep, is strongly correlated to the development of Acute Mountain Sickness and may represent a new treatment and prevention strategy for this very common high altitude disorder.
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Sedgwick, Philip Martin. "Sleep in a naturalistic environment and the influence of the calendar week". Thesis, St George's, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313277.
Testo completo
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Krenzke, Shaun R. "Housing for empowerment : more than just a place to eat, sleep, and watch TV". Virtual Press, 2004. http://liblink.bsu.edu/uhtbin/catkey/1305456.
Testo completoAbstract (sommario):
I began this investigation by asking a question. What is a possible design solutionthat can enable people who live-in or seek-out affordable housing to inhabit a structure that is more than a shelter, but a place they are proud to return to, bring friends to, and live in?The first portion of this thesis documents the need for affordable housing in the United States. Franklin Roosevelt, in 1944 before United States Congress, listed one of the economic rights of every citizen to be, "the right of every family to a decent home." Less money is being spent building new affordable housing or maintaining existing housing than at any other time in our history. The need for affordable housing continues to grow while the amount of available units continues to decline. There will always be a need for affordable housing in the United States. Some people will move out, but there will be new people with a need. I believe housing should be more than merely shelter. The rundown big box affordable housing we are all familiar with does not empower the people who occupy it to live their lives or easily better themselves. They are isolated in location and by negative connotation. There are a growing number of architects who have taken on the challenge to help people to better themselves, when they are unable to themselves. The four architectural precedents that are documented in the second portion of this thesis have dedicated their lives and abilities to creating better affordable housing that aids in allowing citizens, reguardless of race, ethnicity, or income (economic status), to benefit from their physical environment. Examples of each architectural firm's work are presented. I examine the design and participatory processes that enabled the architects to empower the people who live in their well-designed affordable housing.The final portion of this thesis focuses on stating and justifying seventeen design principles to enable people to create decent affordable housing based on the research and interviews. These principles investigate the ideas of being human, giving the sense of ownership to the people who live in affordable housing, being contextually respectful to one's neighborhood and community, being environmentally friendly, being modifiable or changeable for the different people who live in it over time, and respecting each family's specific story and enabling them to express their life and lifestyle. This thesis expresses the design principles of housing for empowerment.Department of Architecture
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Stewart, Fiona Anne. "The evolution of shelter : ecology and ethology of chimpanzee nest building". Thesis, University of Cambridge, 2011. https://www.repository.cam.ac.uk/handle/1810/241033.
Testo completoAbstract (sommario):
Human beings of all cultures build some form of shelter, and the global distribution of Homo sapiens depends on this basic trait. All great apes (chimpanzee, bonobo, gorilla, and orangutan) build analogous structures (called nests or beds) at least once a day throughout their adult lives, which suggests that this elementary technology was present before the hominid lines separated. This thesis investigates the variability and function of specifically wild chimpanzee shelters. I compared characteristics of chimpanzee nests, nesting trees, nest shape, and architecture in two savanna-dwelling populations on opposite sides of Africa: Fongoli, Senegal, and Issa, Tanzania. Savanna habitats are the most extreme habitats in which chimpanzees survive today, and may represent a similar environment to that in which early hominins evolved in the Plio-Pleistocene (Chapter 2). Investigating variation in nest-building within and between these two extreme habitats made it possible to tackle hypotheses of the shelter function of nests (Chapter 3).The influence of environment, specifically the role of protection from disease vectors and fluctuating temperatures, was assessed through a novel experiment in which I slept overnight in arboreal chimpanzee nests and on the bare earth (Chapter 4). To assess whether or not nests serve as an anti-predation function, I compared nesting in Issa, where predators are abundant, to Fongoli, where they are absent (Chapter 5). I provided further support for the thermoregulatory function of nests by showing that chimpanzees build more insulating nests in adverse weather conditions (Chapter 6).Nest-building is a learned behaviour, but its ontogeny is little known. I investigated social sources of variation in nest building in Fongoli to examine whether sex and age differences exist in nest building duration, nest position, shape and architecture (Chapter 7). Finally, ecosystem engineering is a consequence of animal construction, from ants to humans. I investigated use-wear traces around nests to assess niche construction of nest- building. I showed that chimpanzees repeatedly re-used these specific nest-spots within trees, which are pre-fabricated for future building through repeated pruning and shaping of these structures (Chapter 8).Nest building in great apes may be the foundation of constructivity in hominids. This thesis describes proximate functions and influences on nest-building variation in wild chimpanzees that help to model the evolution of shelter in hominids.
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Buechel, Heather M. "CHANGES IN SLEEP ARCHITECTURE AND COGNITION WITH AGE AND PSYCHOSOCIAL STRESS: A STUDY IN FISCHER 344 RATS". UKnowledge, 2013. http://uknowledge.uky.edu/pharmacol_etds/4.
Testo completoAbstract (sommario):
Changes in both sleep architecture and cognition are common with age. Typically these changes have a negative connotation: sleep fragmentation, insomnia, and deep sleep loss as well as forgetfulness, lack of focus, and even dementia and Alzheimer’s disease. Research has shown that psychosocial stressors, such as isolation from family and friends or loss of a loved one can also have significant negative effects on sleep architecture and cognitive capabilities. This leaves the elderly in a particularly vulnerable situation: suffering from cognitive decline and sleep dysregulation already, and more likely to respond negatively to psychosocial stressors. Taking all of these factors into account, it’s surprising that little research has been done to elucidate the mechanisms behind aged subjects’ enhanced vulnerability to new onset psychosocial stress.
Our lab embarked on a series of studies to test the effects of age and psychosocial stress on sleep architecture and cognition. Our first study measured sleep stages in young adult and aged F344 rats during their resting and active periods. Animals were behaviorally characterized on the Morris water maze and gene expression profiles of their parietal cortices were taken. We confirmed previous studies that found impaired cognition and decreased resting deep sleep with age. However, it was increased active deep sleep that correlated best with poor cognitive performance. In the second study rats were subjected to immobilization (restraint stress) immediately preceding their final water maze task. Hippocampi were prepared for synaptic electrophysiology and trunk blood was taken for corticosterone measurement after post-stress sleep architecture data was collected. Young subjects responded to acute stress with decreased cognition, elevated CORT levels and altered sleep architecture. In contrast, stressed aged subjects were statistically indistinguishable from control aged subjects, suggesting that aged rats are less responsive to an acute psychosocial stress event. Together, these studies suggest that alleviating sleep dysregulation could therapeutically benefit cognition psychosocial stress resilience.
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Henry, Michelle. "Associations between sleep architecture, cortisol concentrations, cognitive performance, and quality of life in patients with Addison's disease". Doctoral thesis, Faculty of Humanities, 2019. http://hdl.handle.net/11427/30377.
Testo completoAbstract (sommario):
Recent literature in the neurosciences suggests that there are mechanistic relations between sleep disruption and cognitive (particularly memory) deficits, and that varying concentrations of the hormone cortisol may play a particularly important role in mediating those relations. Because patients with Addison’s disease (AD) experience consistent and predictable periods of sub- and supra-physiological cortisol concentrations (due to lifelong glucocorticoid replacement therapy), and because they frequently report disrupted sleep and poor memory, those presenting with that endocrinological disorder form an ideal population to use in studies testing hypotheses about the ways in which (a) disrupted sleep is related to impaired consolidation of previously learned material (and, hence, poor performance on tests assessing memory for that material), and (b) cortisol concentrations may mediate this relationship between sleep and memory. This dissertation presents four studies that, together, tested those hypotheses. Study 1 (n = 60 per group) found that patients with AD self-reported significantly more disturbed sleep and poorer cognition and quality of life compared to matched healthy controls. Importantly, our analyses suggested that disrupted sleep, and not AD per se, accounted most strongly for the reported cognitive impairment. Study 2 (n = 35 per group) found that patients had significantly poorer objectively-measured declarative memory performance compared to matched healthy controls, but that other domains of cognition were relatively unimpaired. Study 3 (n = 10 per group) suggested that matched healthy controls retained significantly more declarative information than patients. Importantly, while controls retained significantly more declarative information when a period of sleep, rather than waking, separated learning from recall, patients derived no such benefit. Study 4 (n = 7 per group) suggested that, relative to matched healthy controls, patients had different patterns of night-time cortisol secretion, accompanied by significantly reduced slow-wave sleep. Together, these four studies suggest that, despite being on replacement medication, patients with AD still experience disrupted sleep and memory deficits. These disruptions and deficits may be related to the failure of replacement regimens to restore a normal circadian rhythm of cortisol secretion. This pattern of results provides support for existing theoretical frameworks which posit that (in AD and other neuroendocrine, neurological, or psychiatric disorders) disrupted sleep is an important biological mechanism that underlies, at least partially, the memory impairments that patients frequently report experiencing. With specific regard to patients with AD, the findings presented here suggest that future initiatives aimed at improving patients’ cognitive performance (and, indeed, their overall quality of life) should prioritise optimizing sleep. More generally, this dissertation advances our understanding of sleep as a critical biological process essential for cognitive well-being.
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Facer-Childs, Elise Rose. "'Citius, Altius, Fortius' : the impact of circadian phenotype and sleep on the brain's intrinsic functional architecture, well-being & performance". Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8300/.
Testo completoAbstract (sommario):
A major challenge facing our rapidly developing ‘round the clock’ society is in understanding how disruptions to sleep and endogenously driven biological clocks influence many aspects of our lives. This thesis combines the fields of chronobiology, sleep and neuroimaging to investigate the impact of Circadian Phenotype and time of day on the brain’s intrinsic architecture (using functional MRI), well-being and performance. Brain function changes during wakefulness and sleep, as well as in a range of neurological and psychiatric disorders. The results show, for the first time, clear differences in intrinsic functional architecture between Early and Late Circadian Phenotypes (ECP/LCP), as well as variations depending on the time of day. In general, ECPs have higher functional connectivity than LCPs to the majority of regions identified, and these differences can predict better outcomes in cognitive and physical performance measures. Performance also shows significant diurnal variations within Circadian Phenotypes. A wider investigation in the LCP group showed that a phase advance in a real world setting using non-pharmacological interventions has a positive impact on mental well-being and performance. In summary, this thesis supports the need to consider both Circadian Phenotype and time of day in neuroimaging and performance research. It also highlights that chronic disruptions often associated with LCPs could have intrinsic neural origins. Furthermore, it provides a novel intervention strategy for LCPs to enhance well-being and performance during a societal constrained day. These findings could have significant implications in clinical, research and real world settings.
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Patchev, Stephanie Anna. "The architecture and limbic activity patterns of rapid eye movement sleep as symptomatic and prognostic factors in an animal model of post-traumatic stress disorder". Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-177784.
Testo completo
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Patchev, Stephanie Anna [Verfasser], e Carsten [Akademischer Betreuer] Wotjak. "The architecture and limbic activity patterns of rapid eye movement sleep as symptomatic and prognostic factors in an animal model of post-traumatic stress disorder / Stephanie Anna Patchev. Betreuer: Carsten Wotjak". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1065610548/34.
Testo completo
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Laniepce, Alice. "Modifications du sommeil associées à la consommation chronique et excessive d'alcool : liens avec les altérations cérébrales structurales et les troubles cognitifs Neuropsychological and neuroimaging examinations of self‐reported sleep quality in alcohol use disorder with and without Korsakoff's syndrome Sleep architecture and episodic memory performance in alcohol use disorder with and without Korsakoff syndrome The effect of alcohol withdrawal severity on sleep, brain and cognition Dissociating thalamic alterations in alcohol use disorder defines specificity of Korsakoff's syndrome Cerebellar hypermetabolism in alcohol use disorder: compensatory mechanism or maladaptive plasticity ? Alcohol use disorder : permanent and transient effects on the brain and neuropsychological functions Effects of sleep and age on prospective memory consolidation Troubles cognitifs dans l'alcoolodépendance Repérage des troubles cognitifs liés à l’alcool". Thesis, Normandie, 2019. http://www.theses.fr/2019NORMC039.
Testo completoAbstract (sommario):
En amont du développement de complications neurologiques sévères telles que le syndrome de Korsakoff (SK), les patients présentant un Trouble de l’Usage d’Alcool (TUAL) présentent des altérations cérébrales et cognitives de nature et de sévérité variables, ainsi que des troubles du sommeil. Bien qu’il soit clairement établi que le sommeil contribue au fonctionnement cérébral et cognitif, son implication comme facteur explicatif des atteintes cérébrales et cognitives dans le TUAL reste peu documentée. L’objectif de cette thèse était de préciser les modifications (subjectives et objectives) du sommeil chez les patients TUAL et SK, et leurs liens avec la structure cérébrale et le fonctionnement cognitif. Nos résultats montrent que la plainte de sommeil doit être interprétée au regard de la sévérité des atteintes cérébrales et cognitives chez les patients TUAL et SK. De plus, nous montrons qu’une proportion élevée de patients présentent des apnées du sommeil. Chez les patients SK, une atteinte spécifique du sommeil paradoxal est observée, associée à la sévérité des difficultés mnésiques. Enfin, chez les patients TUAL, nous montrons le rôle particulier de la sévérité du syndrome de sevrage dans l’atteinte du sommeil lent profond, et son impact sur le fonctionnement cérébral et cognitif. Ainsi, il semble exister des similarités et des différences dans l’architecture du sommeil de ces deux formes cliniques (TUAL et SK). Ces modifications de sommeil dépendraient de la sévérité du sevrage et seraient impliquées dans la physiopathologie des atteintes structurales et cognitives liées à l’alcool. Ces résultats soulignent la nécessité d’évaluer et de prendre charge à la fois le sevrage et les modifications du sommeil des patients TUAL afin d’améliorer le pronostic des patients à la sortie des services hospitaliersWell before the development of severe alcohol-related neurological complications such as Korsakoff’s syndrome (KS), patients with Alcohol Use Disorder (AUD) exhibit variable brain damage and cognitive deficits, as well as sleep disturbances. Although it is well established that sleep contributes to brain and cognitive functioning, its involvement in brain damage and cognitive deficits in AUD remains poorly understood. The objective of this thesis was to investigate subjective and objective sleep quality in AUD and KS patients, and its relationships with brain structure and function. Our results show that sleep complaint must be interpreted with regard to the severity of brain alterations and cognitive impairments in AUD and KS patients. Moreover, we showed a high prevalence of sleep apnea in these patients. REM sleep abnormalities are specifically observed in KS patients and related to the severity of memory deficits. Regarding AUD patients, we highlight the contribution of the severity of withdrawal syndrome in slow wave sleep decrease, and its effects on brain and cognitive functioning. Hence, similarities and differences of sleep architecture have been found in the two clinical forms (AUD and KS). These sleep modifications could depend on the severity of alcohol withdrawal and be involved in the pathophysiology of alcohol-related structural brain damage and cognitive impairment. These results encourage evaluating and managing both alcohol withdrawal and sleep modifications to improve patients’ prognosis at discharge from Addiction department
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Carvalho, Bruno Miguel Santos. "Effects of antiepileptic drugs on sleep architecture". Master's thesis, 2020. https://hdl.handle.net/10216/128194.
Testo completo
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Carvalho, Bruno Miguel Santos. "Effects of antiepileptic drugs on sleep architecture". Dissertação, 2020. https://hdl.handle.net/10216/128194.
Testo completo
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Mdluli, Dalingcebo Christopher. "The effect of carpal tunnel syndrome pain on sleep architecture". Thesis, 2013. http://hdl.handle.net/10539/12294.
Testo completoAbstract (sommario):
Carpal tunnel syndrome (CTS) is a neuropathic condition commonly caused by the
entrapment of the median nerve. The most common complaint presented by the CTS
patients is pricking sensation, numbness, pins and needles, burning sensation as well
as in the hand and sometimes the arm/s distribution of the affected side. The patients
with CTS usually complain of nocturnal periodic sleep disruption caused by the pain
discomfort. In my dissertation, I explore the extent to which the CTS pain influences
sleep architecture using neurophysiological measurements like an overnight
electroencephalogram (EEG), conduction tests as well as subjective questionnaires. I
initially conducted a pilot research study on 33 patients with CTS using subjective
questionnaires. The CTS patients reported sleep disturbance. I also demonstrated that
they (patients) had a minimal mood and psychological disturbance. I was prompted
therefore to investigate the influence of the CTS pain on the sleep architecture using
more objective empirical instruments like the polysomnogram as well as subjective
measurements such as Beck Depression Inventory, Profile of mood states, Visual
analogue scales as well as the McGill pain questionnaire to further investigate
changes. The patients were required to spend four nights in the sleep laboratory
divided into two nights before surgery and two nights at least two to six weeks
following the CTS surgery. The CTS surgery is commonly used to release the
compression of the median nerve at the wrist. The changes in subjective and objective
variables were compared before and after CTS surgery. The age and gender-matched
control group was introduced into the research study. The control group was required
to spend the same number of nights in the sleep laboratory as the CTS group. The
control group was also going to have a non-painful procedure of the same magnitude
as the experimental subjects. The conclusion I reached on this study was that the CTS
patients reported poor sleep quality. I also demonstrated that there were not many
changes in the polysomnogram and that there were minimum changes shown on the
nerve conduction studies variables as might have been expected based on the severity
of the carpal tunnel syndrome. Another important finding was that there was a
relationship between pain and depressive mood in CTS patients. The removal of pain
in CTS patients showed that there was a subsequent subjective improvement in mood
and psychological status and no significant improvement in subjective measurements.
There were no significant changes noted on the control subjects who were pain-free.
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Benoit, Andre. "General Sleep Parameters and Sleep Architecture in Children with Attention-Deficit/Hyperactivity Disorder and their Typically Developing Peers". 2012. http://hdl.handle.net/10222/15334.
Testo completoAbstract (sommario):
Polysomnography (PSG) sleep studies that compare the sleep of children with attention-deficit/hyperactivity disorder (ADHD) to their typically developing (TD) peers have historically been highly inconsistent. Not only has there been sporadic control over potential confounding variables (e.g., age, medication-status), but no studies have compared sleep between ADHD subtypes. Therefore, this thesis compared the sleep parameters (sleep onset, duration) and sleep architecture (e.g., REM latency, % of REM and NREM sleep]) between a medication-naïve sample of 25 children diagnosed with ADHD, to an age- and sex-matched sample of 25 of their TD peers. Statistical analyses revealed that the ADHD group took longer to fall asleep and slept less than the TD group. However, no significant sleep architecture differences were found between the ADHD and TD groups, or between the ADHD subtypes. Results suggest that ADHD does not relate to intrinsic differences in sleep architecture in children.
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BASKARAN, ANUSHA. "An Investigation of the Sleep Architecture in Ziprasidone-Treated Bipolar Depression". Thesis, 2011. http://hdl.handle.net/1974/6626.
Testo completoAbstract (sommario):
Objective: To primarily determine the effect of ziprasidone augmentation therapy on sleep architecture, specifically slow wave sleep (SWS) and rapid eye movement sleep (REM), in the treatment of bipolar depression. Secondarily, to determine the effect of ziprasidone augmentation treatment on clinical measures of subjective sleep quality and illness severity. Finally, to examine the correlation between change in sleep architecture and change in clinical measures.
Methods: This was a prospective, double-blind, randomized, placebo-controlled study. 14 patients with bipolar disorder currently experiencing a major depressive episode were included. Patients were on a stable medication regime for 4 weeks prior to study enrollment and throughout the study. Sleep architecture was measured by overnight, ambulatory polysomnography. Subjective sleep quality was assessed using the self-reported Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale and a visual analogue scale. Illness severity was determined using the 17 item Hamilton Depression Rating Scale (HAMD-17), the Montgomery Asberg Depression Rating Scale (MADRS), the Hamilton Anxiety Rating Scale (HAMA) and the Clinical Global Impression-Severity scale (CGI-S). Polysomnographs and clinical measures were administered at baseline, after 2-5 days and after 28-31 days of treatment.
Results: There was no significant difference between ziprasidone and placebo treated groups on age, gender, diagnosis, education level, employment or marital status and number of children. Duration of SWS, latency to REM, duration of stage 2 sleep, total sleep time, onset to sleep latency, sleep efficiency and number of awakenings significantly improved in ziprasidone treated participants over placebo, whereas duration of REM sleep did not. CGI-S and HAMA scores were significantly improved with ziprasidone treatment. No significant difference between treatment groups was seen on the HAMD-17 and MADRS or in self-reported sleep quality. Change in REM sleep significantly correlated to change in subjective sleep quality in the ziprasidone group.
Conclusion: Ziprasidone augmentation treatment in bipolar depression improves SWS duration, REM latency, and sleep continuity while also having a beneficial effect on overall illness severity and anxiety symptoms.Thesis (Master, Neuroscience Studies) -- Queen's University, 2011-08-02 17:39:05.883
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Jordan, JE. "The effects of body temperature and oxygen consumption on sleep architecture". Thesis, 1993. https://eprints.utas.edu.au/20284/1/whole_JordanJoanneElizabeth1994_thesis.pdf.
Testo completoAbstract (sommario):
Two related theories have had a substantial impact on our understanding of the nature and function of sleep. These are the energy conservation and restorative theories of sleep. Both theories predict an increase in both slow wave sleep (sws) and sleep duration following increased energy expenditure. These predictions form the background to the empirical work of this thesis, and it is the effect of wake-period metabolism on both sleep metabolism and architecture that holds the main research focus.
Three studies were designed to evaluate the effects of either metabolic rate (MR), body temperature (T\(_b\)), or both, on sleep architecture, in particular sws. The first and second studies imposed variations in waking activity in order to assess the effects of MR and T\(_b\) on sleep architecture. The first study actively increased MR by physical exercise, while the second study used passive heating in a warm bath. The third study compared T\(_b\), MR and sleep in endurance athletes and sedentary individuals.
In the first study, the first sleep cycle of 10 young fit subjects (mean age = 21.8 years) was assessed after a 19km run, either immediately before bedtime or a few hours before retirement. There were four conditions: a no exercise condition; a late afternoon exercise session with evening meal; a late afternoon exercise session without evening meal; and a late evening exercise session with an evening meal. The results showed no evidence of an exercise-induced sws effect, and found that exercise transiently increased wake-period MR which returned to control levels by bedtime. Furthermore, there was some evidence to suggest that a rise in wake-period energy expenditure may have a negative effect upon sleep properties.
The second study investigated the effect of passive heating on sleep architecture by using a method similar to that described by Horne and Staff (1983), Sewitch (1987) and Berger and Phillips (1988a,b).
It also tested the hypotheses that sws levels increase following heating due to either a compensatory drop in T\(_b\)at sleep onset (Sewitch, 1987), or a sustained elevation in absolute T\(_b\) at sleep onset, and during sleep (Berger & Phillips, 1988; Berger, Palca, Walker & Phillips, 1988). Five healthy young male subjects (mean age = 20.4 years) were passively heated in a 42-43°c warm bath to induce elevated T\(_b\) and MR. A repeated measures design with two conditions was employed. These conditions included a control (no passive heating), and a passive heating condition in the late afternoon. Rectal temperature (T\(_{re}\)) was monitored from the early afternoon until the awakening period on the following morning. Metabolic rate was recorded for 20 minutes prior to, and immediately after the passive heating, and then across the sleep period. Sleep recordings also were monitored over the night. Results showed that passive heating significantly increased T\(_{re}\), MR and sws levels. Rectal temperature increases were sustained into, and across the sleep period, whereas MR increases were only transient and did not continue into the sleep period. sws levels were significantly elevated in the first 150 minutes of sleep. The direct relationship of T\(_b\) to sws supported the theory proposed by Berger and Phillips (1988a,b).
The third and final study determined whether the characteristically higher sws levels and longer sleep durations of endurance athletes (Trinder, Paxton, Montgomery & Fraser, 1985) may be attributable to the effect of T\(_b\) on sleep. It was designed to assess the role of T\(_b\) on sleep by comparing the laboratory sleep of endurance athletes and sedentary individuals with T\(_b\) at sleep onset held constant between the two groups based upon evidence from another study (Hedges, 1989) that showed higher average Tres and earlier sleep onset times in athletes compared to sedentary individuals. It was thus considered that the higher T\(_{re}\)S reported for athletes in this study may have been a consequence of their earlier sleep onset times. In the final study eight male endurance athletes (mean age = 21.5 years) and eight male non-athletes (mean age = 22.6 years) were compared under conditions of no-exercise.
The results showed sws levels to be higher and sleep duration longer in the endurance athletes as compared to sedentary subjects, despite T\(_b\) at sleep onset being the same for the two groups, as a result of sleep onset being held constant. The results suggest elevated T\(_b\) at sleep onset may not be the mechanism causing particular sleep characteristics of endurance athletes. Rather it is proposed that the sleep properties of endurance athletes are due to a phase delay of the circadian oscillator, which in this group is achieved by an advance of the sleep-wake cycle (earlier usual sleep onset time).
In conclusion, it is argued that there is a relationship between metabolism and sleep architecture where sws can be facilitated by either (a) high metabolism during sleep onset and the early part of sleep; or (b) the phase angle in the circadian temperature rhythm at sleep onset, or both.
20
LAZOWSKI, LAUREN. "An Investigation of Sleep Architecture and Consequent Cognitive Changes in Olanzapine Treated Patients with Depression". Thesis, 2009. http://hdl.handle.net/1974/5147.
Testo completoAbstract (sommario):
Objective: Primarily, to determine the effect of olanzapine augmentation therapy on sleep architecture, specifically slow wave sleep (SWS), in the treatment of depression. Secondarily, to determine the effect of olanzapine augmentation therapy on illness severity and cognitive function. Finally, to examine the correlation between sleep architecture, illness severity and cognition. Methods: Prospective, double-blind, randomized, placebo-controlled study. Patients with major depressive disorder or bipolar disorder currently experiencing a major depressive episode were included. Patients were on a stable medication regime for 4 weeks prior and throughout the study. Sleep architecture was measured by overnight, ambulatory, polysomnography. Illness severity was determined using the Hamilton Depression Rating Scale (HDRS), Montgomery Asberg Depression Rating Scale (MADRS) and Hamilton Anxiety Rating Scale (HARS). Cognitive function was examined using Cambridge Neuropsychological Test Automated Battery (CANTAB): Spatial Working Memory (SWM), Spatial Span (SSP), and Reaction Time (RTI) tasks. Polysomnographs, clinical measures and cognitive test were administered at baseline, after 2-4 days of treatment and after 28-31 days of treatment. Results: Twenty-five patients participated in the study. There was no significant difference between olanzapine and placebo treated groups on age, gender, diagnosis, education level, employment or marital status and number of children. Latency to SWS, duration of SWS, sleep efficiency, total sleep time, total wake time and sleep latency significantly improved in olanzapine treated participants over placebo treated participants. Latency to and duration of rapid eye movement sleep was not significantly different between olanzapine and placebo treated participants. HDRS scores were significantly improved in olanzapine treated versus placebo treated participants. No significant difference between treatment groups was seen in MADRS, HARS, and subjective sleep quality scores. There was no significant difference between olanzapine and placebo treated participants in SWM, SSP or RTI tasks. Change in sleep architecture was not significantly correlated to clinical change or change in SWM, SSP or RTI. Clinical change was not significantly correlated to SWM or SSP. Clinical change, however, was significantly correlated to change in RTI, in the placebo treated group only. Conclusion: Olanzapine augmentation treatment improves SWS, sleep continuity and depressive symptoms.Thesis (Master, Neuroscience Studies) -- Queen's University, 2009-09-09 13:46:57.159
21
Siebert, Dyana. "The effect of hypertonic saline infusion on sleep architecture in humans". Thesis, 2010. http://hdl.handle.net/10539/8285.
Testo completoAbstract (sommario):
Many patients with chronic pain complain of sleep problems. However, the
relationship between sleep and pain in these patients is still not fully understood.
Experimental models are used to understand the interaction between pain and
sleep, but up until now all such models have been of short duration and assessed
different end-points of sleep disruption. The aim of the study is to develop a
longer-acting model to mimic the muscle pain seen in patients with chronic pain,
assess whether the end-point of sleep disruption is constant over subjects and
assess whether the disruption is dependent on length of stimulation and/or the
sleep stage involved. Twelve healthy male subjects participated in the study. They
were exposed to multiple hypertonic and isotonic saline infusions, for a duration
of ten minutes, both while awake and during all stages of sleep. The muscle pain
intensity and quality during wakefulness were assessed using the Visual Analogue
Scale (VAS) and McGill Pain Questionnaire. Polysomnographic signals were
recorded to score sleep changes during all sleep stages. During wakefulness
hypertonic saline infusions produce significantly greater VAS Scores than
isotonic saline infusions. Differences between the VAS scores from evening to
morning were non-significant, therefore implying that there was no overnight
hyperalgesia after any of the experimental stimulations. When compared to the
isotonic saline infusions, the noxious hypertonic saline infusions triggered
significantly more microarousals during REM (67% of subjects); more sleep stage
shifts in SWS (42% of subjects) and more full arousals during stage 2 (83% of
subjects), SWS (67% of subjects) and REM (67% of subjects) sleep. The data
suggests that pain during sleep triggers multiple different end-points of sleep disruption during sleep and the specific end-points may be determined by the
sleep stage involved. The sleep disturbances found in our model of experimental
pain may be similar to those found in patients with chronic muscle pain.
22
Croft, Tobias Daniel. "The effects of evening bright-light on human body temperature and sleep architecture". Thesis, 1996. https://eprints.utas.edu.au/19651/1/whole_CroftTobiasDaniel1996_thesis.pdf.
Testo completoAbstract (sommario):
A number of influential theories of sleep function argue for a close
relationship between body temperature and sleep architecture. The energy
conservation theory and thermoregulatory theories of sleep, including the central
nervous system restoration and protection theories, each predict increased Slow
Wave Sleep (SWS) following elevations in body temperature at sleep onset and
during sleep. It has recently become apparent that appropriately timed evening
bright-light (BL) (>2500 lux) may suppress melatonin, elevate core temperature,
and produce delays of the human Core Temperature Rhythm (CTR). While these
effects are being investigated for their potential within industry and to treat
various affective and sleep related disorders, the effects of evening BL on sleep
are unclear as the literature is small and differing results are reported. The effects
of BL on temperature suggest that enhanced SWS might follow evening BL, as
increased SWS has been empirically associated with elevations in temperature at
sleep onset and, to a lesser extent, with a phase-delay of the CTR. However, the
suppression of melatonin associated with evening BL suggests sleep might be
disrupted, as melatonin has been proposed to be a hypnotic agent.
In the present thesis three experiments are reported which were designed
to investigate the effects of evening BL on rectal temperature and sleep. In the
first experiment 11 male subjects were twice exposed to BL or Dim-Light (DL)
(normal room illumination) for 2hrs prior to habitual bedtime for two consecutive
nights in a crossover design. Rectal temperature was significantly elevated
during the first and second hours following BL, and significantly more Stage 3
sleep and SWS occurred with a trend for increased SWS in the fourth sleep cycle.
The second experiment was designed to assess the immediate effects of
evening BL on core temperature and sleep, independent from potential CTR
phase-shifting effects produced after multiple exposures to evening BL on consecutive evenings. 11 male subjects were run in two conditions. In the BL
condition Ss were exposed to BL for three consecutive evenings and to DL on the
fourth. In the dim-light condition Ss were exposed to DL on all four evenings. It
was anticipated that three consecutive exposures to evening BL would phasedelay
the CTR such that the effects of a temperature rhythm delay on sleep
could be assessed independent of BL itself on night 4. On night 1 no significant
elevation in rectal temperature was found but SWS was increased in the fourth
sleep cycle. On night 3 rectal temperature was significantly elevated during the
first two hours following BL, and SWS and Slow Wave Activity (SWA) (.25-3
Hz EEG activity) were significantly increased across the night, most noticeably in
the third sleep cycle. No differences in the position of the CTR were evident on
night 4, but temperature in the BL condition was significantly lower than in the
DL condition during the first and fifth hours following light exposure. In
addition, sleep onset latency (SOL) and amounts of Wake were increased in the
BL condition on this night. The results indicated that BL administered until
habitual bedtime over three consecutive nights may produce immediate effects on
core temperature without necessarily delaying the CTR. The SWS enhancing
effects of evening BL were found when, and only when, core temperature was
significantly elevated around the time of sleep onset. This experiment also
suggested that these effects are found more robustly following more than one
exposure to BL.
The third experiment was designed to test this hypothesis. A betweensubjects
design was utilised in which three groups of 12 male subjects were run
in three conditions. In the Dim-Dim (DD) condition subjects were exposed to
DL for two consecutive nights. In the Dim-Bright (DB) condition subjects were
exposed to DL on night 1 and BL on night 2 over consecutive nights. In the
Bright-Bright (BB) condition subjects were exposed to BL on both nights.
Rectal temperature during the first hour following light treatment was
significantly elevated in the BB condition and non-significantly elevated in the
, DB condition compared to the DD condition. SWA and Total EEG Power (TP)
(0.25 Hz to 50 Hz EEG activity) were enhanced in both the DB and BB conditions. In addition, significantly more SWS was found to occur in the fourth
sleep cycle in the DB and BB conditions compared with the DD condition. Thus,
evening BL elevated rectal temperature and enhanced SWS upon a single
exposure, but these effects were enhanced by exposure to the light on the
previous night.
Taken together these experiments indicate that evening bright light
elevates rectal temperature and SWS/SWA increases during subsequent sleep,
particularly late in the night. These results are consistent with other experimental
paradigms in which temperature is raised (e.g. exercise and passive heating) and
SWS is observed to increase. Interpreted this way the results add to the body of
evidence that suggests SWS and thermoregulation are intimately linked. Another
possible interpretation is that a rebound in melatonin following early suppression
by bright-light produced increased SWS later the same night. It is also possible
that both thermal and melatonin rebound effects occurred following evening
bright-light; the thermal effects maintained SWS levels under conditions of
melatonin suppression early in the sleep period while melatonin rebound later in the sleep period resulted in the most prominent increases in SWS. Further
research might examine this possibility by monitoring plasma melatonin levels,
temperature and SWS continuously following evening bright-light. The major
finding of this thesis is that bright-light administered until habitual bedtime
produces immediate elevations in temperature and increased SWS/SWA,
especially late in the night.
23
Seok, Bong Soo. "The Effects of Neuroligin-2 Absence on Sleep Architecture and EEG Activity in Mice". Thèse, 2017. http://hdl.handle.net/1866/20539.
Testo completo
24
(9790292), Michael Cvirn. "The effects of temperature, sleep restriction, and physical activity on the sleep architecture and cognitive performance of volunteer firefighters during various simulation wildland fireground tours". Thesis, 2018. https://figshare.com/articles/thesis/The_effects_of_temperature_sleep_restriction_and_physical_activity_on_the_sleep_architecture_and_cognitive_performance_of_volunteer_firefighters_during_various_simulation_wildland_fireground_tours/13447676.
Testo completoAbstract (sommario):
The overall aim of this thesis was to investigate the interactions between firefighters’ sleep, ambient temperature, hydration status, and cognitive performance during simulated single and multi-day wildfire suppressions. These exact aims are addressed through four studies:
1.To assess the effect of ambient heat during day-(33-35°C) and night-time (23-25°C) exposures on firefighters’ sleep quantity and quality during a simulated multi-day wildfire suppression compared to thermoneutral temperatures (18-20°C; Study 1 -Chapter 4).
2.To quantify the effect of sleep restriction in either ambient heat with day- (33-35°C) and night-time (23-25°C) exposures or thermoneutral conditions (18-20°C) on firefighters’ sleep architecture during a simulated multi-day wildfire suppression compared to a control condition with normal sleep in temperate conditions (18-20°C; Study 2 –Chapter 5).
3.To examine the association between firefighters’ hydration status and cognitive performance during a simulated prolonged wildfire suppression shift in the heat (33-35°C) compared to thermoneutral temperatures (18-20°C; Study 3 –Chapter 6).
4.To examine the effect on cognitive performance of sleep restriction in either ambient heat with day-(33-35°C) and night-time (18-20°C) temperature changes or temperate conditions (18-20°C) during a simulated multi-day wildfire suppression compared to a control condition with full sleep opportunities in thermoneutral temperatures (18-20°C; Study 4 –Chapter 7).
25
Chen, Chieh-Wen, e 陳玠文. "The Patterns of Autonomic Function and Sleep Architecture in SHRs with a Dipping or Non-Dipping Blood Pressure Profile". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/28064854545830379885.
Testo completoAbstract (sommario):
碩士國立陽明大學
腦科學研究所
102
Background: There is a 10-20% decline in blood pressure (BP) relative to daytime wakefulness during nocturnal sleep (BP dipping) in humans, but some does not have this BP change (BP non-dipping). It has been reported that the non-dipping profile is more prevalent among hypertensive populations, and is a risk factor for cardiovascular disease. However, little is known of the underlying mechanism. We have previously shown that the degree of BP dipping is associated with the sleep-wake cycle and autonomic functioning in normotensive Wistar-Kyoto rats (WKYs). Hypothesis: Spontaneously hypertensive rats (SHRs) with a non-dipping profile have an exaggerated disruption of both autonomic functioning and sleep than do WKYs with a non-dipping profile. Materials and Methods: Polysomnographic recording was performed by telemetry in WKYs and SHRs over 24 hours. We used spectral analysis of heart rate variability as autonomic nervous system activity and analyzed electroencephalogram and electromyogram parameters for sleep structure. BP dipping = systolic BP (SBP) during dark awake (AW) – SBP during light quiet sleep (QS) / SBP during dark AW x 100%. Results: According to the human definition of BP dipping (10%), 26% of WKYs were dippers (≥10% dip) and 74% were non-dippers (<10% dip), whereas in SHRs, 59% were dippers and 41% were non-dippers. Regarding autonomic functioning, both parasympathetic activity and baroreflex sensitivity in sleep during the light period were lower in SHR non-dippers than in WKY non-dippers. Regarding sleep structure, compared with WKY non-dippers, SHR non-dippers spent more time in wakefulness and less time in sleep during the light period and the opposite during the dark period; moreover, delta power% of QS was lower throughout the light-dark cycle. Correlation analysis revealed that vascular sympathetic activity during dark AW and baroreflex sensitivity during light QS were correlated with the BP dipping percentage in WKYs. However, cardiovascular variables did not appear to be related to BP dipping percentage in SHRs. Conclusions: SHR non-dippers have more severe degrees of poor sleep quality and impaired autonomic functioning than do WKY non-dippers, which may account for a higher cardiovascular risk in this population.
26
Bach, Normand. "L'analyse des effets de l'expansion palatine rapide assistée chirurgicalement chez les jeunes adultes tels qu'observés au laboratoire du sommeil". Thèse, 2008. http://hdl.handle.net/1866/8064.
Testo completo
27
Barbaux, Loic. "Étude du changement de l’architecture du sommeil chez la personne âgée après un sevrage aux benzodiazépines couplé à la thérapie cognitivo-comportementale pour insomnie". Thesis, 2020. http://hdl.handle.net/1866/25204.
Testo completoAbstract (sommario):
Contexte : Les benzodiazépines (BZD) et substances apparentées sont consommées de façon chronique par une large proportion de la population de personnes âgées souffrant d’insomnie chronique. Cet usage dans cette population est cependant critiqué, pour le risque d’effets indésirables associés. La thérapie cognitivo-comportementale pour insomnie (TCC-I) constitue le traitement de première ligne pour lutter contre l’insomnie, en raison de son efficacité et de son innocuité.
Objectif : L’objectif de ce projet de recherche est d’évaluer les changements de la qualité du sommeil, de la macroarchitecture et de la microarchitecture du sommeil après un sevrage de BZD chez la personne âgée souffrant d’insomnie chronique. Nous étudierons par la suite l’effet de la TCC-I couplé au sevrage sur les mêmes variables d’intérêts. Nous faisons l’hypothèse que le sevrage s’accompagnera d’une amélioration de la qualité subjective du sommeil (diminution de l’Index de Sévérité de l’Insomnie (ISI) et augmentation de l’efficacité de sommeil (SE)) et d’une modification de certaines variables distinctes : fuseau de sommeil et stade N3 (augmentation du pourcentage au stade N3 et diminution de la densité des fuseaux de sommeil). De plus, nous faisons l’hypothèse que ces changements seront plus prononcés avec la TCC-I couplée au sevrage.
Méthodes : 41 participants (âge moyen : 69.39±6.88 ans) ont été randomisés en 2 groupes, stratifiés pour l’âge, la durée et la dose de BZD et apparentés consommés : le groupe sevrage+TCC-I (N=23) et le groupe sevrage (N=18). L’ensemble des participants complètent un plan de sevrage avec suivi de 16 semaines, et dans le même temps, uniquement le groupe sevrage+TCC-I reçoit la TCC-I. L’acquisition des données est réalisée avant et après sevrage à partir de questionnaire (ISI), agenda de sommeil (SE) sur une période de 14 jours, et par enregistrements polysomnographiques (stade N3 et densité des fuseaux de sommeil).
Résultats : 60.98% des participants (groupe sevrage+TCC-I: 60.87% ; groupe sevrage: 61.11%) ont réussi une cessation complète de leurs médications après sevrage. Il a été constaté une diminution de l’ISI (F(1,40)=4.36, p=0.01) et de la densité des fuseaux de sommeil (F(1,36)=7.18, p=0.01) après sevrage. Enfin, la TCC-I couplée au sevrage a montré une augmentation plus importante de la SE (F(1,35)=6.75, p=0.01) par rapport au groupe sevrage.
Conclusion : Le plan de sevrage avec suivi permet d’obtenir un sevrage complet chez une majorité de participants, sans qu’il ne soit observé d’aggravations significatives de leur qualité de sommeil. L’ajout d’une TCC-I lors d’un sevrage de BZD et apparentés a permis une amélioration plus importante de la qualité du sommeil auto-rapportée (Agenda de sommeil : SE).Background: Benzodiazepines (BZD) and related drugs are consumed chronically by a large part of the elderly population with chronic insomnia. However, this use in this population is criticized for the risk of associated side effects. Cognitive behavioral therapy for insomnia (CBT-I) is the first-line treatment for insomnia because of its efficacy and safety. Objective: The objective of this project is to assess changes in sleep quality, macroarchitecture and sleep microarchitecture after withdrawal from BZD in the elderly with chronic insomnia. Then, we study the effect of CBT-I coupled with withdrawal on the same variables of interest. We hypothesize that weaning will be accompanied by an improvement in the subjective sleep quality (decrease in Insomnia Severity Index (ISI) and increase in sleep efficiency (SE)) and a modification of certain distinct variables: sleep spindle and stage N3 (increase in the percentage at stage N3 and decrease in the density of sleep spindles). In addition, we hypothesize that these changes will be more pronounced with CBT-I coupled with weaning. Methods: 41 participants (mean age: 69.39 ± 6.88 years) were randomized into 2 groups; stratified for age, duration and dose of BZD and relatives consumed: the weaning+CBT-I group (N = 23) and the weaning group (N = 18). All participants complete a 16-week weaning plan with follow-up, and at the same time, only the therapy group receives CBT-I. Data acquisition is carried out before and after weaning from questionnaire (ISI), sleep diary (SE) over a period of 14 days, and by polysomnographic recordings (stage N3 and density of sleep spindles). Results: 60.98% of participants (weaning+CBT-I group: 60.87%; weaning group: 61.11%) succeeded in completely stopping their medication after withdrawal. A decrease in ISI (F(1.40) = 4.36, p = 0.04) and in sleep spindle density (F(1.36) = 7.18, p = 0.01) was observed after weaning. Finally, CBT-I coupled with weaning showed a greater increase in SE (Sleep Diary; F(1.35) = 6.75, p = 0.01) compared to the control group. Conclusion: The weaning plan with follow-up makes it possible to obtain complete weaning in a majority of participants, without any significant worsening of their quality of sleep being observed. The addition of CBT-I during withdrawal from BZD and related products resulted in a greater improvement in self-reported sleep quality (Sleep Diary: SE).
28
CARTOCCI, GIULIA. "Investigation of Electrophysiological Patterns and Multiple Treatments in Tinnitus". Doctoral thesis, 2014. http://hdl.handle.net/11573/916761.
Testo completoAbstract (sommario):
Tinnitus is the most common auditory desorder, it is defined as a sound sensation in the absence of any external sound source. Sleep disturbances and depression are symptoms very often present in tinnitus patients. Starting from this observation, in the present thesis two electrophysiological approaches to tinnitus study are described: the former concerns sleep architecture pattern investigation in tinnitus patients, and the second concerns an index of serotonin activity in the auditory cortex the intensity dependence of auditory evoked potential (IDAP). Beyond electrophysiological studies we also investigated two tinnitus therapies,we focused on the study of the Mozart effect and of the mindfulness based stress reduction therapy, because sound therapy and treatments aiming at increasing patient's strategies to face tinnitus are among the most common tinnitus therapies.
29
Zieleniewska, Magdalena. "Resting-State EEG Activity in Disorders of Consciousness". Doctoral thesis, 2020. https://depotuw.ceon.pl/handle/item/3636.
Testo completoAbstract (sommario):
The following thesis presents the results of a systematic research on resting-state electroencephalographic (EEG) activity in disorders of consciousness. First of all, the thesis discusses the state-of-the-art knowledge of the methods currently used to assess the level of consciousness, focusing on the neuroimaging techniques used in the diagnosis of patients with impaired consciousness after a severe brain injury. Active and passive paradigms are discussed, along with the measures reflecting circadian activity and the structure of resting-state connectivity networks. In the experimental part, we present the data, including overnight EEG recordings from the pediatric patients with disorders of consciousness from The Alarm Clock Clinic, used to assess sleep architecture and resting-state connectivity patterns. The discriminating value of the proposed measures in differentiating the patients behaviorally diagnosed as unresponsive from those in the minimally conscious state was evaluated with machine learning techniques.W niniejszej pracy przedstawiono wyniki badań nad elektroencefalograficzną (EEG) aktywnością spoczynkową w zaburzeniach świadomości. Pierwsza część pracy zawiera opis metod neuroobrazowania stosowanych w diagnostyce pacjentów po ciężkich urazach mózgu znajdujących się w stanie zaburzeń świadomości. Dyskutowane są paradygmaty pasywne i aktywne, a także wskaźniki związane z cyklem okołodobowym oraz strukturą połączeń w mózgu. Część eksperymentalna zawiera opis danych, w tym całonocnych zapisów polisomnograficznych, pochodzących od pacjentów z kliniki "Budzik"', które w ramach niniejszej pracy analizowane były pod kątem potencjalnych zastosowań diagnostycznych w dwóch głównych podejściach -- poprzez badanie architektury snu oraz struktury połączeń w spoczynkowym EEG. Wartość diagnostyczną zaproponowanych wskaźników w różnicowaniu pacjentów sklasyfikowanych według oceny behawioralnej jako świadomych, od tych nie przejawiających oznak świadomości, zbadano przy pomocy technik uczenia maszynowego.
30
Lin, Yu-Zhe, e 林裕哲. "Detection and Prediction of Obstructive Sleep Apnea Based on Traditional Machine Learning and Recent Deep Learning Architectures". Thesis, 2018. http://ndltd.ncl.edu.tw/handle/f6kfmz.
Testo completoAbstract (sommario):
碩士國立中正大學
電機工程研究所
106
In this thesis, we proposed the identification and prediction methods of obstructive sleep apnea (OSA), using traditional machine learning and recent deep learning approaches. The human’s physiological signal Electrocardiogram (ECG) was used to identify and predict the occurrence of OSA. The differences of using different architectures were compared. This study is composed of three parts, the first part is the traditional machine learning (ML) identification. The architecture can be divided into signal processing, feature extraction, feature normalization and classification. The features include time domain, frequency domain, EDR (ECG-derived respiratory) waveform and other efficient features such as focusing on the spectra of the baseline wander. The support vector machine was employed in this study to be classifier. The effectiveness of different kinds of feature selector were discussed. The second part is to explore the use of deep learning (DL) architecture. Convolutional Neural Network (CNN) was employed in this study. Both ECG and its Fourier spectrum were used as inputs to and the effects were studied. Both architectures used the Leave-One-Person-Out (LOPO) cross-validation to testify the performance of the classifiers. The third part is about OSA prediction. The ECG signals within 1 to 4 minutes before the occurrence of OSA were analyzed the performance of OSA occurrence prediction by using different system architectures were compared. The Five-Fold cross-validation was employed to test the performance of the methods. The results show that the recognition rate of the first part (Traditional ML) can reach 87.27%, and the second part (Recent DL) which used the time and spectra signals achieved an accuracy of 90.14%. When the Traditional ML and the Recent DL were used in the third part, the best OSA occurrence prediction rate were 71.25% and 96.58% , respectively. Both traditional and deep learning architectures were published in the literatures to identify of sleep apnea and the recognition rate ranged from 82% to 89%. Very few papers were devoted to OSA prediction. Comparatively, this study proposed novel features and deep learning architectures to identify and predict the occurrence of OSA. More reliable cross validation methods were used to testify the performance of classifier. The results showed that the identification rate is significantly higher than the relevant papers and the prediction accuracy is high, which demonstrated the superiority of the proposed identification and prediction architectures in our study. With the impressive results in the identification and prediction of OSA, we ported the model trained by the deep learning frameworks into a real-time OSA detection system. The result demonstrate the possibility of using this approach for medical purpose which to assist the clinical professional in treating OSA an important auxiliary tool.