Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sleep electroencephalogram (EEG) of young, drug-free, recurrently depressed outpatients was analyzed for 2 nights and was compared to age-matched controls using a variety of standard and computerized measures of sleep activity. On the first night, young depressives showed significantly greater difficulty in falling asleep and decreased sleep efficiency. Sleep architecture differences between the young depressives and controls were highlighted by increased percentages of Stage 2 sleep and major decreases in Stages 3 and 4 (delta wave) sleep among the depressives, as indicated by either period analyses or spectral analysis. The greatest differences in delta wave activity during night 1 were found in the first two (non-rapid eye movement (NREM) periods as measured by period analysis (NREM period 1, p less than 0.04; NREM period 2, p less than 0.001--average delta wave count) or by spectral analysis for the first 100 min of sleep (0.5-2.0 Hz). In contrast to the NREM sleep findings, various REM variables, including REM latency did not significantly distinguish the two subject groups for either night 1 or 2. Stepwise discriminant analysis demonstrated that night 1 sleep latency and delta wave counts during the second NREM period correctly classified 100% of all 16 individuals studied. The only differences between the young depressed patients and controls that remained on night 2 were significant reductions in slow-wave sleep as quantified by the computerized methods. Taken together, these findings suggest that the EEG response of young outpatients to the first night's stay in a sleep laboratory may be a useful tool for the diagnosis of depression in this age group. In addition, the use of computerized methods in this study point to an underlying deficit in delta sleep waveforms as being a prominent feature of the sleep of young depressed subjects.
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PMID:EEG sleep in young depressives: first and second night effects. 291 11

Seven-hour sleep EEG recordings were obtained from rats (N = 15) given a single acute dose, and rats (N = 15) given 14 daily doses of zimelidine, 20 mg/kg IP. REM latency, REM sleep, number of REM episodes, and total sleep time were significantly affected by zimelidine administration when compared to controls, as well as to each animal's baseline sleep parameters. Sleep latency and slow-wave sleep were not significantly affected by zimelidine. The results are discussed in terms of the implications of the use of zimelidine as a clinical treatment for depression, as well as the implications for the use of REM changes as a diagnostic indicator of the efficacy of treatment with zimelidine.
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PMID:Effects of repeated zimelidine administration on sleep parameters in the rat. 293 99

Forty-five patients who met Research Diagnostic Criteria (RDC) for secondary depression were assessed by St. Louis criteria, and by demographic, illness history, REM latency and dexamethasone suppression test measures. Fully one-third of the RDC secondary sample met St. Louis criteria for primary depression; only age at onset and length of illness discriminated St. Louis primary from secondary depression. RDC depressed patients secondary to alcoholism were compared to those secondary to nonsubstance abuse disorders (excluding schizophrenia). The subgroup with a history of alcoholism reported less severe depression and were preponderantly male. Neither dexamethasone response nor REM latency differentiated the RDC secondary subtypes. Little support was found to validate separation of the RDC secondary subtypes studied.
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PMID:Secondary depression: a comparison among subtypes. 295 9

After one accommodation night, sleep EEG recordings were performed during three consecutive nights in ten drug-free inpatients presenting generalized anxiety disorder (GAD) with significant depression, compared with a age- and sex-matched group of patients with GAD and a group of primary major depressive disorder (MDD) patients. GAD patients with depression did not differ from GAD patients in any sleep variable. Patients with MDD showed more stage shifts and a greater number of awakenings than patients with GAD. REM latency was significantly shorter in MDD patients than in the other groups, and may thus help to differentiate anxious from depressed patients.
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PMID:Sleep EEG recordings in generalized anxiety disorder with significant depression. 297 80

Urinary cyclic adenosine monophosphate (AMP-c) was measured morning and evening in 35 patients with alcohol withdrawal syndrome (AWS). 65% of the patients revealed a higher night time than day time concentration of AMP-c in the urine, reflecting increased sympathetic adrenergic activity. The circadian rhythm was lost in 88.55% of the 35 patients. The pathogenic factors and mechanisms involved in AWS are discussed and the contribution of sympathetic adrenergic hyperactivity to the onset of the withdrawal syndrome with its concomitant depression of the cholinergic and GABAergic systems is emphasised. Finally it is suggested that insomnia and the loss of REM sleep may also contribute to the onset of the condition.
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PMID:[Changes in the circadian rhythm of urinary cyclic adenosine monophosphate during the alcoholic withdrawal syndrome and related neurobiological correlations]. 299 62

Beta adrenergic sites in rat brain are reduced after repeated treatment with antidepressant drugs, with REM sleep deprivation (REMSd) having the same effect. This paper reports the effects of REMSd in the production of 3H-cyclic AMP in frontal cortical slices by NE challenge. Data presented in this paper report a marked decrease in 3H-cyclic AMP synthesis after REMSd, which is in accordance with previous results showing adrenergic receptor down-regulation following REMSd. Results are discussed in view of possible interaction with dopaminergic systems and depression management.
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PMID:REM sleep deprivation induces a decrease in norepinephrine-stimulated 3H-cyclic AMP accumulation in slices from rat brain. 301 94

An examination was made of the effect of REM sleep deprivation (REMSD) on some forms of altered motor activity, such as akinesia and catalepsy, induced by intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of morphine in adult, male Wistar rats. Administration of morphine (25 mg/kg i.p.) induced an akinetic-cataleptic syndrome and decreased spontaneous vertical motor activity (SVMA) in animals allowed undisturbed sleep. REMSD decreased the morphine-induced akinesia and catalepsy that are known to be mediated by an inhibitory mu-opiate system. The locomotor depressant action of morphine was converted to excitation (manifested as increased SVMA and hopping behavior) by REMSD. Similarly, decreased motor activity following i.c.v. administration of morphine (25 micrograms) was replaced by excitation in the form of jumping behavior after REMSD. Naltrexone (1 mg/kg i.p.) blocked the akinetic and cataleptic effects, but not the excitatory effects, of morphine. It is suggested that REMSD is associated with a functional insufficiency of an inhibitory mu-opiate system, thus unmasking the excitatory morphine effects. The proposed insufficiency of an endogenous opioid system might explain an increase in neuronal excitation during REMSD and the therapeutic effect of REM deficiency in some types of depression.
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PMID:REM sleep deprivation antagonizes morphine-induced akinesia and catalepsy. 302 Jun 74

We observed that ventilation fell and end-tidal CO2 rose in the change from wakefulness to non-REM (NREM) sleep in 4 normal human subjects studied on two nights each. We hypothesized that the observed ventilatory depression was due to effects of sleep both upon the central respiratory neural output and upon the mechanical respiratory pump. Both the central controller response to CO2, as measured by diaphragmatic and intercostal EMG activity, and the ability of the respiratory pump in effecting ventilation in response to diaphragmatic or intercostal activation, as measured by the relationship between the EMG activities and minute ventilation, are reduced in NREM sleep. We describe a general method of apportioning the separate effects of sleep, or other factors, upon the central respiratory controller, the respiratory mechanical pump, and the metabolic rate, in determining the total observed increase in end-tidal CO2.
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PMID:Effects of non-REM sleep upon respiratory drive and the respiratory pump in humans. 308 91

We report on 2 children aged 13 and 14 months with congenital central alveolar sleep apnea which showed depression of respiratory drive during sleep resulting from dysfunction of central chemoreceptors. Hypoventilation was found to be more severe during NREM sleep (minimum of alveolar ventilation in stages 3/4) than during REM sleep. During NREM sleep arousal responses to hypoxia proved to be an important factor in influencing the level of alveolar ventilation and in preventing fatal asphyxia.
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PMID:[Regulation of respiration during sleep in congenital central sleep apnea]. 309 60

5 patients with endogenous depression of uni- and bipolar type, classified according to sleep characteristics as normo- (1), hypo- (3) and hypersomniacs (1), were treated for 3 weeks with a daily dose of 900 mg lithium carbonate. Polygraphic sleep recordings were taken in every patient in the course of 3 placebo nights, 3 nights during therapy and 2 registrations after lithium carbonate was discontinued. Before therapy, a prolonged sleep and a shortened REM latency were observed, which were changed in the course of the treatment especially in the normosomniac patient. In the other examined sleep parameters (total sleep time, sleep efficiency, percentage of REM sleep, slow wave sleep), discrepancies among hypo-, hyper- and normosomniac patients were present. From the clinical point of view all patients showed an improvement subjectively and objectively measured by means of Hamilton and Beck questionnaires for depression. This study emphasizes the necessity of administering daily lithium carbonate doses higher than 900 mg because of only a mild therapeutic effect.
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PMID:Effects of lithium carbonate on the clinical picture and the sleep of depressive patients. 309 37


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