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 effects of 400-600 mg trazodone on the sleep patterns of ten depressed in-patients treated for 5 weeks were studied during the initial (days 1-3) and terminal (days 26-28) treatment periods. The sleep parameters were compared to those obtained from three sleep recordings performed just prior to the initiation of the treatment and after 2 adaptation nights at the end of a 2-week drug-free period. At the same time, the clinical evolution of patients was evaluated weekly using MADRS and Hamilton-Anxiety scales for anxiety-depression symptomatology and Spiegel and Norris sleep scales. Weekly blood samples were collected to measure plasma levels of trazodone and, at the end of the study, the elimination half-life at steady state was calculated by repeated measurements of plasma levels. Clinical improvement, as assessed by a reduction of more than 60% in MADRS scale scores, was accompanied by evidence of the definitely beneficial effects of trazodone on the disturbed sleep of these depressed patients. From the beginning of treatment, there was a hypnotic-like effect (increase in total duration of sleep and stage II, decrease in sleep latency and intrasleep awakenings). In addition, records at the end of the study showed an increase in delta sleep and an increase in REM latency, an effect classically associated with an antidepressant action. These particularly valuable effects of trazodone on sleep would suggest that this drug should especially be given in cases of depression with major insomnia.
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PMID:Effects of trazodone on the sleep of depressed subjects--a polygraphic study. 313 13

This objectives of this study were three-fold: retrospectively evaluate anxiolytic/hypnotic consumption by psychiatric inpatients, identify the risk factors of prolonged intakes, and prospectively measure the impact of hospitalisation on the use of those drugs. Three hundred and seventy-six patients hospitalised in 11 psychiatric departments in the Paris region were studied using a structured interview for the anxiolytic/hypnotic treatments, DSM-III-R criteria, GHQ-12, HAD, Spiegel's questionnaire, COVI's anxiety scale and the CGI. Eighty-five per cent of the patients had taken one anxiolytic/hypnotic or more in the 3 months preceding hospitalisation. Hospitalisation induced little change in anxiolytic/hypnotic use: dosage frequency increased from 77% to 84% between the week preceding hospitalisation and that preceding discharge; 26% of consumers were taking at least two anxiolytics or two hypnotics in the first period vs. 23% in the second. The absence of withdrawal during hospitalisation was related to the high age and a diagnosis of depression rather than schizophrenia, to the existence of continuous intake over the 3 months preceding hospitalisation and to higher drug doses during the 7 days preceding hospitalisation. Prescription of treatment at the end of hospitalisation in previously non-user subjects was related to a higher HAD anxiety score at discharge.
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PMID:Anxiolytic and hypnotic use in 376 psychiatric inpatients. GERMED Neuropsychotropics Group. 1057 22

The aim of this study was to investigate for the effects of valpromide on heart rate circadian rhythm in remitted recurrent unipolar and bipolar disorders (DSM-III-R). It consisted of a comparative, randomized, double-blind, repeated cross-over study of valpromide versus placebo over four four-week periods. The primary evaluation criteria was heart rate (HR). Secondary criteria comprised motor activity (MA) and the Bech and Rafaelsen mania assessment scale, Horne and Ostberg questionnaire, Montgomery and Asberg depression rating scale, Spiegel questionnaire, a sleep diary, and Clinical Global Impression. Fifteen patients were included, giving 60 one-month periods (30 valpromide periods and 30 placebo periods). Cosinor analysis of HR and MA data revealed a difference in amplitude (P = 0.037, analysis of variance, one-tailed test). The clinical sleep study shows that the duration of sleep was greater with valpromide than with placebo (P = 0.007, one-tailed test). Similarly, evaluation of the quality of sleep by patients themselves showed valpromide to be superior to placebo (P = 0.045, one-tailed test). The results of analysis of the Spiegel questionnaire also confirm the superiority of valpromide over placebo. Safety and compliance were comparable for the active drug and the placebo. In conclusion, the relatively small sample size requires cautious interpretation of this study. Nevertheless, these initial results show a definite effect of valpromide on a biological rhythm that leads one to suppose that it may be effective through a 'synchronizing' effect.
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PMID:Valpromide increases amplitude of heart rate circadian rhythm in remitted bipolar and unipolar disorders. A placebo-controlled study. 1111 35

The effects of milnacipran (50 mg bid) on sleep patterns of eight depressed inpatients, treated for 4 weeks, were studied during the initial (days 1-3) and terminal (days 26-28) treatment periods and compared with those obtained from three sleep recordings performed just prior to the initiation of the treatment. The clinical evolution of patients was evaluated weekly using the MADRS depression scale and the Spiegel and Norris sleep scales. Clinical improvement, shown by a mean reduction of 58% in MADRS scale scores, was accompanied by an improvement of disturbed sleep parameters. From the beginning of treatment, there was an increase in the total duration of sleep and stage II sleep, a decrease in sleep latency and an increase in sleep efficiency. Total REM sleep was not modified although, since there was an increase in total sleep time, the percent REM sleep was significantly reduced. REM latency was increased early in the study, an effect classically associated with antidepressant treatment. This study suggests that milnacipran improves disturbed sleep parameters in depressed patients without any additional disturbance at the onset of treatment.
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PMID:Subjective and polysomnographic effects of milnacipran on sleep in depressed patients. 1525 22