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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In case new diagnostic procedures for Alzheimer's dementia (AD) appear, Nuclear Medicine (NM) would like to be aware of them in order to evaluate its own contribution to diagnose AD by SPET and PET brain studies. Recently, sleep disturbances were studied in AD and tend to be diagnostic for early AD. In AD the actual time of night sleep was found to be 5.7 h, while awakeness time for the same night sleep increased to 2.7 h. Also in AD, the REM and the slow wave stage (SWS) during sleep are shorter and hypopnea and apnea phases are abundant. Internal body temperature during night sleep is only slightly increased in AD, while in temporofrontal dementia and in normal individuals this increase is significant. The circadian rhythm of melatonin is disturbed in AD. The normal duration of inspiration and expiration during daytime which is reversed during normal night sleep, has not been studied in patients with AD. However, this reverse condition favoring inspiration is expected to provide more oxygen to the brain. Chronic but not acute stress causes memory loss and is currently being studied by us as a possible causative factor for memory loss in AD. Tomographic SPET and PET brain studies can locate the site of brain damage in AD. This is important since memory has recently been classified into four categories, namely episodic, semantic, procedural and working memory. In early AD only procedural memory remains intact. This means that these patients may drive a car, do computer word processing and play some games at home or/and in the field. This memory is located in specific nuclei in the cerebellum and the occipital frontal area which do not relate to sites of other kinds of memory. This difference could be well identified by tomographic SPET or PET studies. Thus NM may also diagnose the early stage of AD. Another issue refers to the indications that the unified Medicare and Medicaid system in the USA has issued on September 15, 2004 for performing a PET (18)F-FDG study for AD. These indications are fully described in this editorial.
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PMID:[Alzheimer's dementia, sleep disorders and nuclear medicine]. 1588 44

Sleep architecture is often disturbed after a stressful event; nevertheless, little is known about the brain circuitry responsible for the sleep perturbations induced by stress. We exposed rats to a psychological stressor (cage exchange) that initially causes an acute stress response, but several hours later generates a pattern of sleep disturbances similar to that observed in stress-induced insomnia in humans: increased sleep latency, decreased non-REM (nREM) and REM sleep, increased fragmentation, and high-frequency EEG activity during nREM sleep. We examined the pattern of Fos expression to identify the brain circuitry activated, and found increased Fos in the cerebral cortex, limbic system, and parts of the arousal and autonomic systems. Surprisingly, there was simultaneous activation of the sleep-promoting areas, most likely driven by ongoing circadian and homeostatic pressure. The activity in the cerebral cortex and arousal system while sleeping generates a novel intermediate state characterized by EEG high-frequency activity, distinctive of waking, during nREM sleep. Inactivation of discrete limbic and arousal regions allowed the recovery of specific sleep components and altered the Fos pattern, suggesting a hierarchical organization of limbic areas that in turn activate the arousal system and subsequently the cerebral cortex, generating the high-frequency activity. This high-frequency activity during nREM was eliminated in the stressed rats after inactivating parts of the arousal system. These results suggest that shutting down the residual activity of the limbic-arousal system might be a better approach to treat stress-induced insomnia, rather than potentiation of the sleep system, which remains fully active.
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PMID:Neural circuitry of stress-induced insomnia in rats. 1882 74