Tolerance of debility in elderly dependants by supporters at home: its significance for hospital practice.
(57/1273)
Some 12% of all geriatric admissions to University College Hospital and Whittington Hospital are for patients whose relatives or friends can no longer cope with them at home. The person principally involved with home support was interviewed in 50 such cases. The causes of inability to cope were identified on a quantitative and qualitative basis. The supporters were asked to assess which of the problems identified would have to be alleviated to restore a tolerable situation at home; 46 (92%) were able to do so. Identification of the "alleviation factors" forms a therapeutic and prognostic guideline in this type of admission and may have far-reaching social and economic implications. (+info)
Restless legs syndrome.
(58/1273)
BACKGROUND: Restless legs syndrome is a common but not well-recognized central nervous system disorder that leads to insomnia and daytime distress. METHODS: A MEDLINE search of the recent English language literature was undertaken with review of appropriate articles and references. RESULTS: A growing body of work has added to an understanding of the epidemiology, diagnostic criteria, appropriate evaluation, and effective management of restless legs syndrome. CONCLUSIONS: Restless legs syndrome occurs in about 6% of the adult population, more so in the elderly. Affected patients experience uncomfortable sensations in the legs with inactivity, more pronounced late in the day and at bedtime, which are temporarily relieved by moving the limbs. Affected patients can suffer from insomnia, disrupted sleep, daytime fatigue, and difficulty with sedentary activities. Most cases are idiopathic, although secondary causes, such as iron deficiency, should be excluded. Dopaminergic agents are highly effective in treating restless legs syndrome, but side effects can be problematic. Alternative medications include benzodiazepines, opioids, gabapentin, and clonidine. (+info)
Sleep, sleepiness, and alcohol use.
(59/1273)
The study of alcohol's effects on sleep dates back to the late 1930s. Since then, an extensive literature has described alcohol's effects on the sleep of healthy, nonalcoholic people. For example, studies found that in nonalcoholics who occasionally use alcohol, both high and low doses of alcohol initially improve sleep, although high alcohol doses can result in sleep disturbances during the second half of the nocturnal sleep period. Furthermore, people can rapidly develop tolerance to the sedative effects of alcohol. Researchers have investigated the interactive effects of alcohol with other determinants of daytime sleepiness. Such studies indicate that alcohol interacts with sleep deprivation and sleep restriction to exacerbate daytime sleepiness and alcohol-induced performance impairments. Alcohol's effects on other physiological functions during sleep have yet to be documented thoroughly and unequivocally. (+info)
Modulation of brain gene expression during sleep and wakefulness: a review of recent findings.
(60/1273)
The characterization of the molecular correlates of sleep and wakefulness is essential to understand the restorative processes occurring during sleep and the cellular mechanisms underlying sleep regulation. In order to determine what molecular changes occur during the sleep-waking cycle, we have recently performed a systematic screening of gene expression in the brain of sleeping, sleep deprived, and spontaneously awake rats. Out of the approximately 10,000 genes screened so far, a small minority ( approximately 0.5%) was differentially expressed in the cerebral cortex across behavioral states. Most genes were upregulated in wakefulness and sleep deprivation relative to sleep, while only a few were upregulated in sleep relative to wakefulness and sleep deprivation. Almost all the genes upregulated in sleep, and several genes upregulated in wakefulness and sleep deprivation, did not match any known sequence. Known genes expressed at higher levels in wakefulness and sleep deprivation could be grouped into functional categories: immediate early genes/transcription factors, genes related to energy metabolism, growth factors/adhesion molecules, chaperones/heat shock proteins, vesicle and synapse-related genes, neurotransmitter/hormone receptors, neurotransmitter transporters, enzymes, and others. Although the characterization of the molecular correlates of sleep, wakefulness, and sleep deprivation is still in progress, it is already apparent that the transition from sleep to waking can affect basic cellular functions such as RNA and protein synthesis, neural plasticity, neurotransmission, and metabolism. (+info)
Individual 'fingerprints' in human sleep EEG topography.
(61/1273)
The sleep EEG of eight healthy young men was recorded from 27 derivations during a baseline night and a recovery night after 40 h of waking. Individual power maps of the nonREM sleep EEG were calculated for the delta, theta, alpha, sigma and beta range. The comparison of the normalized individual maps for baseline and recovery sleep revealed very similar individual patterns within each frequency band. This high correspondence was quantified and statistically confirmed by calculating the Manhattan distance between all pairs of maps within and between individuals. Although prolonged waking enhanced power in the low-frequency range (0.75-10.5 Hz) and reduced power in the high-frequency range (13.25-25 Hz), only minor effects on the individual topography were observed. Nevertheless, statistical analysis revealed frequency-specific regional effects of sleep deprivation. The results demonstrate that the pattern of the EEG power distribution in nonREM sleep is characteristic for an individual and may reflect individual traits of functional anatomy. (+info)
The effects of total sleep deprivation on cerebral responses to cognitive performance.
(62/1273)
We review the findings from a study utilizing functional magnetic resonance imaging (FMRI) to examine the effects of total sleep deprivation (TSD) on verbal learning, arithmetic, and divided attention. For verbal learning and divided attention, TSD was associated with increased activation in the bilateral prefrontal cortex and parietal lobes. Increased sleepiness after TSD and lower levels of memory impairment were correlated with increased activation in specific regions of the prefrontal cortex and parietal lobes, respectively. The arithmetic task led to significantly decreased activation in the bilateral prefrontal cortex and parietal lobes. Based on this and other data, we hypothesize an adaptive cerebral response during cognitive performance following TSD with the specific pattern of adaptation depending on the specific cognitive processes performed. We discuss the need to test the hypothesis in a variety of ways. (+info)
Clinical neurochemical implications of sleep deprivation's effects on the anterior cingulate of depressed responders.
(63/1273)
The antidepressant and cerebral metabolic effects of total sleep deprivation (TSD) or partial sleep deprivation (PSD) for one night has been studied with functional neuroimaging in seven publications from five different groups. Despite the variations in methods and techniques, the over-all findings were relatively consistent. First, before sleep deprivation, responders have significantly elevated metabolism compared with non-responders and normal controls, in the orbital medial prefrontal cortex, and especially the ventral portions of the anterior cingulate cortex. Second, after sleep deprivation, these hyperactive areas normalize in the responders. One functional imaging study suggested that synaptic dopamine release was associated with the antidepressant effects of TSD. The neurochemical implications of these findings are explored. Possible dopaminergic and serotonergic mechanisms are discussed. (+info)
Sleep deprivation, EEG, and functional MRI in depression: preliminary results.
(64/1273)
One night of total or partial sleep deprivation (SD) produces temporary remissions in 40-60% of patients with major depression. Two unmedicated patients with major depression and a matched control received quantitative perfusion MR images at baseline and after one night of partial SD (PSD). A reduction > or =30% in the 17-item Hamilton Depression Rating Scale (omitting sleep and weight loss items) defined antidepressant response. Theory, techniques, strengths and weaknesses of quantitative perfusion MRI are described in detail. At baseline, the responder exhibited elevated perfusion covering ventral anterior cingulate/medial frontal cortex; the control's maximal perfusion area was markedly smaller. The nonresponder's perfusion was lowest of all, particularly ventrally. PSD decreased perfusion over much of the responder's hyperperfused area but did not change the nonresponder's scan. These preliminary findings are consistent with previous SD studies using PET and SPECT. (+info)