Sleep deprivation.

Mayo Sleep Disorders Center, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA.
Primary Care Clinics in Office Practice (Impact Factor: 0.83). 07/2005; 32(2):475-90. DOI: 10.1016/j.pop.2005.02.011
Source: PubMed

ABSTRACT 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.

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    • "Sleep deprivation or insomnia, an extremely common ailment in modern society, may affect numerous neurobehavioural and physiological functions, such as memory, cognitive ability, hormone secretion, glucose metabolism and immune function (Malik & Kaplan, 2005; Van Cauter et al. 2007; Zisapel, 2007). Numerous studies have implicated associations between sleep deprivation and inflammatory responses, although the pathophysiological mechanisms underlying these associations remain unclear (Irwin et al. 2006; Frey et al. 2007; Simpson & Dinges, 2007). "
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    ABSTRACT: Sleep deprivation has been shown to be associated with an increase in inflammation that is also involved in the development of neointimal hyperplasia (or restenosis). The purpose of this study was to investigate whether total sleep deprivation (TSD) would worsen neointimal formation by balloon injury. Sixteen rats were randomly allocated into the following four groups: group 1, balloon angioplasty alone; group 2, TSD prior to angioplasty; group 3, angioplasty before TSD; and group 4, TSD before and after angioplasty. Total sleep deprivation was induced by the disc-over-water method, and balloon angioplasty was performed in the carotid artery. Histopathological analysis and assay of cytokines were applied to evaluate the effects of TSD in this study. Total sleep deprivation significantly increased the ratio of postinjury neointima-to-media area in groups 2, 3 and 4 (all P < 0.01) compared with group 1. Additionally, in all groups with TSD administration the serum level of interleukin 10 was also markedly decreased on day 3 after angioplasty injury (P < 0.05 or P < 0.01). Our findings suggest that perioperative TSD can significantly augment neointimal hyperplasia of the carotid artery in rats, which may be partly caused by a TSD-induced effect in suppressing the serum level of the anti-inflammatory cytokine, interleukin 10.
    Experimental physiology 08/2011; 96(11):1239-47. DOI:10.1113/expphysiol.2011.059246 · 2.87 Impact Factor
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    • "Although best known as a movement disorder, HD involves a panoply of other symptoms that includes cognitive decline, psychiatric disorder (for references, see Bates et al., 2002), and sleep and circadian abnormalities (Arnulf et al., 2008; Morton et al., 2005; Pallier et al., 2007; Petersén et al., 2005). Regular sleep/ wake cycles are central to normal neurological function (Malik and Kaplan, 2005; Maquet, 1995; Roth and Ancoli-Israel, 1999; Zammit et al., 1999; Zisapel, 2007), and their disruption is deleterious to cognitive function (Cirelli, 2005; Durmer and Dinges, 2005; Harrison and Horne, 2000; Zammit et al., 1999). In HD patients, disrupted sleep may not only contribute to disease progression, it may also have a knock-on effect on the quality of sleep of the partner or carer (Gruffydd and Randle, 2006; Morton et al., 2005). "
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    ABSTRACT: Normally, mice sleep during the day and are active at night. In Huntington's disease mice (R6/2 line) this circadian pattern disintegrates progressively over the course of their illness. Cognitive decline and apathy in R6/2 mice can be improved with sleeping drugs, suggesting that sleep disruption contributes to their neurological decline. We wondered if wakefulness was equally important. Here, we used two drugs to manage sleep/wake cycles in R6/2 mice, Alprazolam (to put them to sleep) and Modafinil (to wake them up). We found that both drugs improved cognitive function and apathy, but had a stronger effect when used in combination. Remarkably, beneficial effects on cognitive performance were also seen in vehicle-treated cage-mates of Alprazolam/Modafinil-treated mice, suggesting that behavioral intervention to regularize sleep/wake activity might be therapeutically useful. We suggest that focused management of sleep and wakefulness will slow the progression of cognitive decline and apathy in neurological conditions where sleep is disordered.
    Brain research 06/2009; 1279:90-8. DOI:10.1016/j.brainres.2009.03.072 · 2.83 Impact Factor
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    • "Electroencephalographic and electromyographic data were recorded on a Grass model 78 polygraph (Grass- Telefactor, West Warwick, RI, USA) and relayed to a computer for digital recording. Data were divided into 30- s epochs and scored as waking, non-rapid eye movement, or rapid eye movement sleep using an automated scoring system previously validated against visual and behavioral methods (Bergmann et al. 1989). "
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    ABSTRACT: Sleep disorders are associated with an increased rate of various metabolic disturbances, which may be related to oxidative stress and consequent lipid peroxidation. Since hepatic phosphatidylcholine plays an important role in metabolic regulation, the aim of the present study was to determine phosphatidylcholine expression in the liver following total sleep deprivation. To determine the effects of total sleep deprivation, we used adult rats implanted for polygraphic recording. Phosphatidylcholine expression was examined molecularly by the use of time-of-flight secondary ion mass spectrometry, along with biochemical solid-phase extraction. The parameters of oxidative stress were investigated by evaluating the hepatic malondialdehyde levels as well as heat shock protein 25 immunoblotting and immunohistochemistry. In normal rats, the time-of-flight secondary ion mass spectrometry spectra revealed specific peaks (m/z 184 and 224) that could be identified as molecular ions for phosphatidylcholine. However, following total sleep deprivation, the signals for phosphatidylcholine were significantly reduced to nearly one-third of the normal values. The results of solid-phase extraction also revealed that the phosphatidylcholine concentration was noticeably decreased, from 15.7 micromol g-1 to 9.4 micromol g-1, after total sleep deprivation. By contrast, the biomarkers for oxidative stress were drastically up-regulated in the total sleep deprivation-treated rats as compared with the normal ones (4.03 vs. 1.58 nmol mg-1 for malondialdehyde levels, and 17.1 vs. 6.7 as well as 1.8 vs. 0.7 for heat shock protein 25 immunoblotting and immunoreactivity, respectively). Given that phosphatidylcholine is the most prominent component of all plasma lipoproteins, decreased expression of hepatic phosphatidylcholine following total sleep deprivation may be attributed to the enhanced oxidative stress and the subsequent lipid peroxidation, which would play an important role in the formation or progression of total sleep deprivation-induced metabolic diseases.
    Journal of Anatomy 04/2008; 212(3):295-305. DOI:10.1111/j.1469-7580.2008.00860.x · 2.23 Impact Factor
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