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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep disturbances, which are a prominent symptom of depressive illness, were analyzed in endogenously depressed patients during depression and during full remission. These disturbances may be described at the level of sleep stages, at the level of the sleep profile, and at the level of consecutive sleep records. The scoring of sleep stages in sleep records of depressive patients provides difficulties, because the temporal coherence of different electrophysiological descriptors of sleep is weakened during depression. The sleep profile of depressed patients is characterized by alterations in the normal sequence of sleep stages and frequent stage changes. The disturbances in the sleep profile are unstable in that they show marked day to day fluctuations. It could be shown in some patients that there is a correlation between parameters of the first REM sleep and urinary free cortisol excretion in corresponding nights.
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PMID:The measurement of change in sleep during depression and remission. 68 64

Periodic sleep apnea may be due to repeated episodes of upper airway obstruction in patients who have a short thick neck and/or large jowls. Apnea due to complete cessation of breathing may occur to a lesser extent. Anaylsis of the sleep electroencephalogram shows that these patients rarely achieve deep sleep and have less stage 1-REM sleep than normal subjects of comparable age. They are chronically sleep-deprived, a manifestation expressed by daytime somnolence, chronic fatigue and often by personality disturbances marked by paranoia, agitated depression and hostility. The definitive diagnosis of this syndrome may be established by monitoring during sleep, the electroencephalogram, measuring abdominal excursions through a mercury-in-Silastic-strain gauge and recording air flow at the nose by means of a thermocouple. As demonstrated by other investigators, chronic hypoventilation during sleep leads to both pulmonary and systemic arterial hypertension, which may produce generalized cardiac enlargement and congestive heart failure. The abnormalities in the periodic sleep apnea syndrome are abolished by establishing a patent airway either through tracheostomy or weight reduction.
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PMID:Periodic sleep apnea: chronic sleep deprivation related to intermittent upper airway obstruction and central nervous system disturbance. 111 91

Very few epidemiological surveys have specifically studied relationships between sleep disturbances and psychiatric diseases. In this review, we preferred to use the classification proposed in 1979 by the Association of Sleep Disorders Centers. It includes four main categories: insomnias, excessive sleepiness, troubles of the wake/sleep schedule and parasomnias. Evaluating psychiatric disorders among general populations is easier owing to DSM III and DSM III-R criteria, but there are not equivalent criteria in evaluating sleep disorders. It is almost impossible to realize polysomnographic recordings in large samples, therefore sleep disorders are to be detected by questionnaires. It has been shown that there is a good correlation between self-reports and polysomnographic recordings among clinical and general samples. The prevalence of insomnia, defined as difficulties of initiating and maintaining sleep, is estimated between 9 and 31%. It is higher among women, elderly people, separated and divorced subjects, and low educational levels' groups. It has to be noticed that polysomnographic records of some subjective insomniacs are not different from those of good sleepers, sleep latency excepted. These subjective (and not objective) insomniacs have high scores in anxiety scale, depression scale, or psychologic distress. Insomnia is more frequently noted amongst subjects with psychiatric diagnoses, especially major depressive disorders and anxiety disorders. Depressive disorders are present in 21-40% of insomniacs versus 0-1% of non-insomniacs, and anxiety disorders in 13-24% of insomniacs versus 3-10% of non-insomniacs. In depressive disorders, sleep alterations are frequently noted: they are difficulties of initiating and maintaining sleep, decreasing proportion of slow-wave sleep, decreasing time of REM (rapid eye movement) sleep and REM sleep latency, and increasing density of REM sleep. Of these modifications, the last two ones seem to be specific for depression. The relationships between sleep, aging and depression are more complex than previously noted. For example, differences between depressed and non-depressed subjects depend on the age of the population. The prevalence of hypersomnia is lower than the insomnia's. It varies between 2 and 4%. It is more frequently noted among young people, and never married subjects. Two specific aetiologies must be looked for: sleep apnea syndrome and narcolepsy. These diagnoses are respectively found in 45% and 24% of hypersomniacs examined in American Sleep Centers. Hypersomnias are objectived by the Multiple Sleep Latency Test, which measures the physiologic sleep tendency.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Sleep disorders in psychiatric diseases. Epidemiological aspects]. 129 83

After REM sleep deprivation the time-course of the forced swimming was reorganized. As shown, reduction of rhythmical index of depression, such effect has an antidepressive nature. In this model potentiation of specific activity of antidepressant imipramine and attenuation of depressive properties of clonidine were observed. These results suggest that shifts in sleep phase structure may be a source of restriction of circadian desynchronosis, upon which depression is based.
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PMID:[The effect of the deprivation of the paradoxical sleep stage on the temporal dynamics of swimming in rats with antidepressive and depressant exposures]. 132 91

After REM sleep deprivation antidepressant shifts in forced swimming with increase of time of immobility and decrease of rhythmical index of depression were observed. Pinealectomy did not remove, but attenuated these behavioural changes.
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PMID:[The effect of the removal of the epiphysis on the antidepressive properties of paradoxical sleep deprivation in rats]. 133 93

Twenty years have passed since the discovery that a shorter REM latency was one of the most significant biological correlates of depression. Its diagnostic and clinical discriminant power have been challenged both in terms of sensitivity and specificity. The present paper is a review of the relevant literature of these years until the present time and has focused on (a) technical problems concerning the REM latency, (b) its diagnostic value, (c) the state or trait meaning, (d) the use of the cholinergic and aminergic challenge, (e) the effects of treatments. A summary of (f) the effects of age and (g) REM sleep propensity as a cycle phenomenon have been added. The conclusions tend toward considering REM sleep disorders as an expression of a multiple circadian cycle abnormality, globally seen as a trait, itself highly correlated with psychiatric pathology and especially with affective disorders.
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PMID:Is REM latency a dying concept? 134 29

The reciprocal interaction model of NonREM- and REM sleep regulation suggests that the cycling alternating pattern of Non-REM- and REM sleep is under the control of noradrenergic/serotonergic and cholinergic neuronal networks. This model was tested in healthy humans by administration of cholinergic agonists/antagonists and noradrenergic antagonists prior to or during sleep. Cholinomimetics like physostigmine, RS 86 and galanthamine provoked an earlier onset of REM sleep, whereas subchronic treatment with scopolamine, a cholinergic antagonist, only led to a heightening of REM density. Simultaneous administration of noradrenergic antagonists with a cholinergic agonist did not provoke a more pronounced REM sleep advance. Comparative studies with the cholinergic agonist RS 86 in depressed patients, schizophrenic patients and patients with other psychiatric disorders revealed the most pronounced REM sleep response in the depressed group. The REM sleep response to cholinergic stimulation in depression did however not predict the treatment response to a differential-therapeutic strategy.
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PMID:Cholinergic and noradrenergic neurotransmission: impact on REM sleep regulation in healthy subjects and depressed patients. 134 30

We present the pharmacological properties of two cyclopyrrolones, zopiclone as a hypnotic and suriclone as an anxiolytic, and examine their mechanism of action. The effects of zopiclone on the amount of time spent at each vigilance level have been studied in freely moving rats. Zopiclone from 2.5 mg/kg i.p. extends the duration of slow wave sleep (SWS), concomitantly shortening the periods awake. This SWS inducing effect of zopiclone was more potent after 10 mg/kg i.p.; moreover, zopiclone did not depress REM sleep and no rebound of activity in wakefulness or REM sleep were observed the day after zopiclone treatment. In rats, at the cortical level, zopiclone increases the spectral energy in the delta band (0.5 to 4 hertz). This rise in energy appears at doses starting from 1.25 mg/kg p.o. and can also reach the fast frequencies (beta band: 12 to 16 hertz). This power spectrum is characteristic of a compound having tranquilizing-hypnotic potential. Taken together these EEG results corroborate the clinical studies. In man, zopiclone increased SWS, decreased SWS latency and respected sleep architecture in both healthy volunteers and insomniacs. This respect of sleep structure and the relative short duration of action of zopiclone minimized the residual effects seen upon waking (drowsiness, impairment of psychomotor performance). In the Geller-Seifter test, an operant conflict procedure, the minimal effective dose (MED) of suriclone in reversing the conflict-induced inhibition of drinking behavior was 2.5 mg.kg-1 p.o. in rats. Depression of unpunished responding is only seen at higher doses (20 mg.kg-1 p.o.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological properties and mechanism of action of the cyclopyrrolones. 136 58

Twenty-three adolescents with DSM-III major depressive disorder (endogenous subtype) and 23 normal controls were studied polysomnographically (PSG). The depressed group showed significantly shortened REM latencies (P = 0.005) and longer sleep latencies (P = 0.04). No other PSG measures differentiated the two groups. The implications of these findings for adolescent depression are discussed.
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PMID:REM latency in endogenously depressed adolescents. 139 12

The microinjection of carbachol into the pons of acute decerebrate cats elicits a REM sleep-like atonia and a profound suppression of respiratory motoneuronal activity (J. Appl. Physiol., 69 (1990) 2280-2289). To assess whether this suppression is mediated by medullary neurons that provide respiratory drive to motoneurons of the respiratory pump muscles (diaphragm and intercostals), we studied the effect of pontine carbachol on the activity of neurons of the ventral respiratory group (VRG) in decerebrate, vagotomized, paralyzed and artificially ventilated cats. VRG neurons were recorded extracellularly along with the activity of phrenic and intercostal (external and internal) nerves. Both inspiratory (I) and expiratory (E) VRG neurons had incrementing, ramp-like bursts of activity during their firing periods and were not vagal motoneurons. Carbachol produced a depression of the peak firing rate in most (42/57) neurons studied. However, five cells showed no change and ten had an increase in activity in spite of consistent depression at the motoneuronal level. For the total population of cells (34 I and 23 E), the peak firing was reduced to 88.5% +/- 16.3 (S.D.) of control. The simultaneously recorded phrenic activity was reduced to 77.9% +/- 11.5, while inspiratory intercostal activity fell to 63.4% +/- 21.6 and expiratory to 23.2% +/- 21.2 of control. The carbachol-induced changes in peak firing of both I and E cells were quantitatively similar, and positively correlated to changes in peak phrenic activity. Analysis of this correlation suggested that phrenic and intercostal activities will be depressed to some degree by carbachol even when the average VRG cell activity remains unchanged. In addition, our data show that VRG cells may receive a combination of inhibitory and excitatory inputs during the carbachol-induced depression of respiratory motoneurons. Thus, although some disfacilitation from VRG cells may occur, there must be additional inhibitory or disfacilitatory pathways that mediate the decrease in activity of both phrenic and intercostal motoneurons that accompanies the REM sleep-like atonia.
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PMID:Behavior of VRG neurons during the atonia of REM sleep induced by pontine carbachol in decerebrate cats. 145 Sep 25


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