Comparative effects of nefazodone and fluoxetine on sleep in outpatients with major depressive disorder

Rush, A. John; Armitage, Roseanne; Gillin, J. Christian; Yonkers, Kimberly A.; Winokur, Andrew; Moldofsky, Harvey; Vogel, Gerald W.; Kaplita, Stephen; Fleming, Jonathan B; Montplaisir, Jacques; Erman, Milton K.; Albala, Bruce J.; McQuade, Robert D.

doi:10.1016/s0006-3223(98)00092-4

Cited by 179 publications

(100 citation statements)

References 23 publications

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“…Substances with nonselective action on the serotoninergic system, for example, 5-HT reuptake inhibitors (SSRIs), often induce disturbed sleep as an increase in intermittent wakefulness, whereas SWS is largely unaffected by these substances (Saletu et al, 1991;Rush et al, 1998). No alterations of the spectral composition of sleep EEG were found during subchronic treatment with paroxetine in healthy subjects (Röschke et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

Schmid

Wichniak

Uhr

et al. 2005

Neuropsychopharmacol

143

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The noradrenergic and specific serotoninergic antidepressant mirtazapine improves sleep, modulates hormone secretion including blunting of hypothalamic-pituitary-adrenocortical (HPA) activity, and may prompt increased appetite and weight gain. The simultaneous investigation of sleep electroencephalogram (EEG) and hormone secretion during antidepressive treatment helps to further elucidate these effects. We examined sleep EEG (for later conventional and quantitative analyses) and the nocturnal concentrations of cortisol, adrenocorticotropin (ACTH), growth hormone (GH), prolactin, melatonin and the key factors of energy balance, ghrelin, and leptin before and after 28 days of treatment of depressed patients (seven women, three men, mean age 39.974.2 years) with mirtazapine. In addition, a sleep EEG was recorded at day 2 and the dexamethasone-corticotropin-releasing hormone (DEX-CRH) test was performed to assess HPA activity at days À3 and 26. Psychometry and mirtazapine plasma concentrations were measured weekly. Already at day 2, sleep continuity was improved. This effect persisted at day 28, when slow-wave sleep, low-delta, theta and alpha activity, leptin and (0300-0700) melatonin increased, and cortisol and ghrelin decreased. ACTH and prolactin remained unchanged. The first two specimens of GH collected after the start of quantitative EEG analysis were reduced at day 28. The DEX-CRH test showed, at day 26, a blunting of the overshoot of ACTH and cortisol found at day À3. The Hamilton Depression score decreased from 32.177.3 to 15.576.7 between days À1 and 28. A weight gain of approximately 3 kg was observed. This unique profile of changes is compatible with the action of mirtazapine at 5-HT-2 receptors, at presynaptic adrenergic alpha 2 receptors, at the HPA system, and on ghrelin and leptin.

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Section: Discussionmentioning

confidence: 99%

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

Schmid

Wichniak

Uhr

et al. 2005

Neuropsychopharmacol

143

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“…It should be noted, however, that some clinically effective antidepressants do not suppress REM sleep, e.g., trimipramine (Vogel et al 1990;Sonntag et al 1996;Wiegand and Berger 1989) and the postsynaptic serotonin antagonist and presynaptic serotonin and norepinephrine reuptake inhibitor nefazodone Armitage et al 1997;Rush et al 1998;Gillin et al 1997). Thus, REM latency changes may be associated with the mechanism of action of many antidepressants as previously suggested (Vogel 1983;Vogel et al 1975; this includes many SSRIs and specifically fluoxetine; cf.…”

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confidence: 90%

Fluoxetine and Sleep EEG Effects of a Single Dose, Subchronic Treatment, and Discontinuation in Healthy Subjects

Feige

2002

Neuropsychopharmacology

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In the last years, selective serotonin reuptake inhibitors (SSRIs) have increasingly replaced tricyclics in antidepressive treatment due to their more benign side effect profile. Still, compliance in long-term maintenance therapy often enough is insufficient, since many patients are reluctant to accept daily dosing of antidepressants and thus tend to omit medication sometimes. It is well known for most antidepressants that a discontinu-

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“…In support of an earlier study (43), 2 have shown increased wakefulness on this SSRI, either in the total number of awakenings or in decreased sleep efficiency (39,42). A large-scale, double-blind comparison between 2 antidepressants indicated that the 57 patients treated with fluoxetine showed significantly decreased sleep efficiency, an increase in the number and percentage of awakenings, decreased slow-wave sleep (stages 3 and 4), an increase in REM latency from 87 to 153 minutes, and a 3.5% decrease in total REM time, relative to baseline (44). Moreover, the sleep effects offluoxetine were similar in both responders and nonresponders.…”

Section: Selective Serotonin Reuptake Inhibitorsmentioning

confidence: 99%

“…Moreover, these data were part ofa multicentre trial and were subsequently included in a pooled analysis (44). The latter report included baseline to endpoint (last observation carried forward or at 8 weeks of treatment) sleep comparisons in 59 patients in the nefazodone arm of the protocol.…”

Section: Other Serotonergic Antidepressantsmentioning

confidence: 99%

The Effects of Antidepressants on Sleep in Patients with Depression

Armitage

2000

Can J Psychiatry

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As assessed by laboratory studies, sleep abnormalities in those with major depressive disorders can be classified as difficulties initiating and maintaining sleep, abnormal sleep architecture, and disruptions in the timing of rapid eye movement (REM) sleep. Sleep initiation and maintenance difficulties include prolonged sleep latency (sleep onset insomnia), intermittent wakefulness and sleep fragmentation during the night, early morning awakenings with an inability to return to sleep, reduced sleep efficiency, and decreased total sleep time. With regard to sleep architecture, abnormalities have been reported in the amounts and distribution of nonrapid eye movement (NREM) sleep stages across the night. These include increased light, stage 1 sleep and reductions in the amount ofdeep, slow-wave (stages 3 and 4) sleep. REM sleep disturbances in patients with depression include a short latency (65 minutes) to the first REM sleep, a prolonged first REM sleep period, and increased total REM sleep time, particularly in the first one-half of the night (1-3).Sleep disturbances are generally more prevalent among inpatients with depression (80%), whereas only 40% to 60% of outpatients show sleep abnormalities (4). A recent metaanalysis, however, indicated that no single sleep variable reliably distinguished patients with depression from healthy controls Manuscript

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Comparative effects of nefazodone and fluoxetine on sleep in outpatients with major depressive disorder

Cited by 179 publications

References 23 publications

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

Fluoxetine and Sleep EEG Effects of a Single Dose, Subchronic Treatment, and Discontinuation in Healthy Subjects

The Effects of Antidepressants on Sleep in Patients with Depression

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