Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nocturnal sleep was poligraphycally recorded in three male patients aged 54-67, with progressive supranuclear palsy (PSP). All patients suffered from insomnia. In case 1 REM sleep was markedly reduced and spindles were less numerous than in normal subjects. In cases 2 and 3, EEG patterns were not distinguishable from those observed when the patients were awake. Sleep, therefore, was recognized only by constant observation of the patients. As seen in the literature EEG changes during sleep can be correlated to the severity of the clinical picture and the stage of evolution of the disease. EEG patterns of sleep in PSP are similar to those reported in patients with presenile dementia.
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PMID:[Sleep in progressive supranuclear palsy]. 718 69

The purpose of this study was to evaluate the short- and intermediate-term (21 days) effectiveness, as well as the carryover and withdrawal effects of 7.5 mg of zopiclone, a new short-acting hypnotic agent. 6 patients with chronic insomnia, ranging in age from 33 to 57, participated in the study. Both EEG sleep recordings and subjective rating scales were used to evaluate the drug. Zopiclone increased the total sleep time throughout its 3-week administration period although only during the short-term period was this increase statistically above baseline. There was no carryover effect nor rebound insomnia upon drug withdrawal. The drug significantly increased the duration of stage 2 sleep, decreased stages 3 and 4 sleep, and had no effect on the duration of REM sleep. There were no reported side effects.
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PMID:Effects of zopiclone on the sleep of chronic insomniacs. 718 73

Polysomnographic studies of nocturnal sleep were performed on a 63-year-old women. Sleep-onset and sleep-maintenance insomnia dated back to a cerebral infarction at age 53, which resulted in bilateral cerebral injury. Two patterns of respiration were observed, and both were sleep-stage-dependent. Classic Cheyne-Stokes respiration predominated during slow-wave sleep and stages 1 and 2. REM sleep, in contrast, was associated almost exclusively with normal respiration. Recurrent brief arousals, temporally linked to the Cheyne-Stokes pattern of respiration, markedly disturbed sleep stages 1 and 2 and appeared related to the patient's subjective sleep complaints. During waking, REM, and NREM sleep, respiration is known to have different sensitivity to CNS and peripheral controls. The selective association of Cheyne-Stokes respiration with NREM sleep in this patient supports the view that anatomically separate CNS mechanisms regulate respiration in REM and NREM sleep.
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PMID:Sleep-stage-dependent Cheyne-Stokes respiration after cerebral infarct: a case study. 720 Nov 14

1 This study was performed because dose-related effects of heroin on human sleep had not been described previously, and to discover if heroin produces a morphine-like insomnia. 2 After three adaptation nights, the sleep of seven male nondependent opiate addicts was studied following i.m. doses of heroin (3, 6, 12 mg/70 kg), morphine (10, 20 mg/70 kg) or placebo at weekly intervals in a randomized double-blind crossover design. 3 Heroin produces a dose-related increase in wakefulness, drowsiness episodes, muscle tension, and shifts in sleep-waking states. 4 Heroin produces a dose-related decrease in total sleep, sleep efficiency, delta sleep and REM sleep (REMS). 5 Heroin is about twice as potent as morphine in producing this type of insomnia. 6 'Morphine insomnia' appears to be a characteristic initial effect of several opioids, at least in nondependent opiate addicts, and might serve as a model insomnia for evaluation of hypnotics.
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PMID:Morphine-like insomnia from heroin in nondependent human addicts. 721 20

p-Bromomethamphetamine (V-111) was given as a single dose to one group of rats and for 28 days to another group and its influence was studied on the sleep-walking cycle. In a third group of rats the midbrain raphe nuclei was lesioned before administration of the drug. A single dose of 15 mg/kg s.c. V-111 produced total insomnia, the SWS returned 15-16 h, REM sleep 21-22 h after the injection. When the drug was given repeatedly the periods of insomnia were gradually shortened. At the end of third week the SWS returned in daytime after 3 h, at night after 6 h, REM sleep after 6 h and 8 h respectively. The destruction of the midbrain raphe nuclei failed to influence either the spontaneous sleep patterns or the insomnia elicited by V-111. In physiological conditions the integrity of 5-HT system is necessary for the regulation of sleep-waking cycle. After reduction of brain 5-HT, insomnia developed but the sleep-waking cycle could be restored while the brain 5-HT was decreased. The restored sleep mechanisms seem to be 5-HT dependent also.
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PMID:The effect of p-bromomethamphetamine (V-111) on sleep on the rat. 723 72

Scant attention has been paid to the objective evaluation of insomnia as a function of age, particularly with reference to increased drug sensitivity and resulting loss in balance performance. Therefore, the electroencephalographic sleep and the balance-board performance of 10 young and 12 geriatric insomniacs were studied under baseline and hypnotic drug (ketazolam) conditions. In terms of objectively measured sleep, the geriatric insomniacs had worse sleep on every dimension except sleep latency and percentage of stage-2 sleep. These differences between aged and young insomniacs, however, were no greater than might be expected as a function of normal aging. Drug-age interactions indicated that ketazolam differentially increased sleep efficiency, decreased the percentage of REM sleep, and eliminated any learning improvement on the balance board in geriatric versus young insomniacs. The findings indicate that the geriatric subjects were more sensitive to the hypnotic drug, in that their sleep improved to a greater extent. However, an important loss in balance performance was also observed.
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PMID:The interaction of age, performance and hypnotics in the sleep of insomniacs. 729 9

During nonentrained sleep--wake conditions in man, healthy adult subjects spontaneously develop "long" biological days (greater than 35 hr) in addition to the normal, approximately 25 hr day. The ratio of sleep to total time remains constant (approximately 0.30), with long sleep episodes occurring approximately 180 degrees out of phase with the short sleep episodes. The timing and amount of REM sleep advance to an earlier time within the sleep episode during free-running, whereas stage 3 + 4 sleep is related to the initiation and course of the sleep process itself. The REM--NREM cycle length does not change, comparing entrained and nonentrained conditions. The study of the chronophysiology of humans under nonentrained conditions may serve as a model of the chronopathology of sleep--wake changes which occur in sleep disorders associated with depression, narcolepsy--cataplexy, sleep--wake dyssomnias, delayed sleep phase insomnia, and aging.
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PMID:Timing of REM and stages 3 + 4 sleep during temporal isolation in man. 740 40

Twenty patients who had been insomniac since childhood were compared with 39 who had become insomniac during adult life. The childhood-onset insomniacs took longer to fall asleep, slept less, and showed excessive amounts of REM sleep without eye movements. Adult-onset insomniacs showed more restless sleep. No differences between childhood- and adult-onset groups were found on personality inventories, but those with childhood-onset insomnia reported more evidence of possible "soft" neurological impairment.
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PMID:Childhood-onset insomnia. 746 26

Magnocellular regions of the basal forebrain (BF) are recognized as important sites of sleep-wake regulation. Evidence is reviewed for the coexistence within the BF of mechanisms that regulate neocortical and limbic system arousal along with mechanisms that promote sleep. Arousal-related functions are mediated by a system of magnocellular cholinergic neurons. BF cholinergic neurons project monosynaptically to the entire neocortex and limbic telencephalon, exert excitatory effects on target cells and participate in the regulation of activated EEG patterns characteristic of waking and REM sleep. Evidence suggests that, within the waking state, the BF cholinergic system modulates processing of sensory information in the neocortex and is involved in cognitive processes. One or more noncholinergic cell types are responsible for the sleep-promoting functions of the BF. Neurons that display elevated discharge rates during transitions from waking to sleep and during nonREM sleep have been recorded in BF sites were electrical stimulation evokes sleep and experimental lesions cause insomnia. BF neurons function to promote sleep, in part, via descending inhibition of caudal hypothalamic and brainstem activating systems. GABAergic neurons located within magnocellular regions of the BF are hypothesized to mediate sleep-promoting actions. Afferents to the BF from hypothalamic and brainstem regions are functionally important for sleep-wake regulation. Thermosensitive inputs from the anterior hypothalamus modulate the activity of BF sleep- and arousal-related cell types. Excitatory effects of brainstem inputs to BF arousal-related cells have been documented. Additional evidence supports a critical role for GABAergic-cholinergic interactions, both within the magnocellular BF and at cortical and diencephalic sites, in the regulation of behavioral state.
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PMID:Magnocellular nuclei of the basal forebrain: substrates of sleep and arousal regulation. 748 20

The prevalence of sleep apnea, sleep apneic activity, nocturnal myoclonus, and nocturnal myoclonic activity was assessed in 375 outpatient insomniacs and 150 normal controls. Only a small percentage of insomniacs (n = 8, 2.3%) and normal controls (n = 2, 1.3%) presented > or = 30 apneic events per night. Only one of these subjects, an insomniac, met the laboratory and clinical criteria of sleep apnea sufficient to recommend treatment. A limited amount of sleep apneic activity per subject (only 3-29 apneic events per night) was evenly distributed between insomniacs (n = 52, 13.9%) and normal controls (n = 22, 14.7%). Also, small percentages of insomniacs (n = 43, 11.5%) and normal controls (n = 11, 8.5%) displayed nocturnal myoclonus (five or more leg movements per hour) or nocturnal myoclonic activity (less than five movements per hour). Thus, these results do not support the claim that sleep apnea or nocturnal myoclonus are common causes of insomnia. In addition, different cutoff points of REM latency (based on first-night recordings) were associated with very low sensitivity and moderately high specificity resulting in inadequate levels of diagnostic accuracy in differentiating depressed insomniacs from non-depressed insomniacs. Finally, empirically optimized values for REM variables were less successful than similarly optimized MMPI values in differentiating depressed insomniacs from nondepressed ones. In conclusion, with our current level of knowledge, polysomnography has limited clinical usefulness in the differential diagnosis of insomnia.
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PMID:Usefulness of polysomnographic studies in the differential diagnosis of insomnia. 759 15


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