Sleep and Sleep Electroencephalogram in Depressed Patients Treated With Phenelzine

Landolt, Hans‐Peter; Raimo, Eric B.; Schnierow, Bradley; Kelsoe, John R.; Rapaport, Mark Hyman; Gillin, J. Christian

doi:10.1001/archpsyc.58.3.268

Cited by 79 publications

(60 citation statements)

References 46 publications

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“…Within the frequency bands showing a significant Treatment effect, rANOVA identified four distinct bands with either a significant effect of Derivation and/or a significant Treatment X Derivation interaction. They were located in the ranges 2.0-3.25 Hz, Hz ( Table 2).As reported in our previous paper, phenelzine treatment was associated with increased tonic EMG activity during sleep (Landolt et al 2001). Spearman rank correlation analysis revealed that the treatment-induced increase of EEG power density in the 19.0-22.25 Hz band in fronto-central and centro-parietal derivations (Table 3) was significantly correlated with the increase of tonic EMG activity (r s ϭ 0.74 and 0.76, respectively, p Ͻ .04; n ϭ 8).…”

supporting

confidence: 69%

“…We have recently reported that delta power in non-REM sleep was not affected in a central EEG derivation in depressed patients when REM sleep was virtually abolished during treatment with phenelzine (Landolt et al 2001). In view of possible regional differences in sleep regulation, we have now investigated the effect of phenelzine on EEG topography in wakefulness and sleep.…”

Section: A Novel Approach To Investigate the Relationship Between Depmentioning

confidence: 99%

“…In other words, frontal parts of the cortex may be particularly susceptible to sleep loss and reflect the homeostatic process of sleep regulation more sensitively than other cortical regions. The monoamine oxidase inhibitor (MAOI) phenelzine is an effective "first generation" antidepressant capable of virtually abolishing REM sleep (Akindele et al 1970;Wyatt et al 1969Wyatt et al , 1971Dunleavy and Oswald 1973;Landolt et al 2001). Its antidepressant action has been proposed to be linked to the potent and long-lasting suppression of REM sleep (Vogel et al 1990).…”

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confidence: 99%

“…Studies in healthy subjects revealed that increased pressure for REM sleep, due to selective or preferential REM sleep deprivation by awakenings, inhibits delta activity in non-REM sleep (Beersma et al 1990;Brunner et al 1990). Similar changes may be expected to be associated with pharmacological REM sleep suppression.We have recently reported that delta power in non-REM sleep was not affected in a central EEG derivation in depressed patients when REM sleep was virtually abolished during treatment with phenelzine (Landolt et al 2001). In view of possible regional differences in sleep regulation, we have now investigated the effect of phenelzine on EEG topography in wakefulness and sleep.…”

mentioning

confidence: 99%

“…The signals were digitized and transmitted via fiber-optic cables to a notebook computer with a digital signal processor board. The detailed procedures of data recording and signal conditioning are described elsewhere (Landolt et al 2001). Briefly, EEG electrodes were placed bilaterally along the antero-posterior axes at the locations F3, F4, C3, C4, Cz, P3, P4, O1 and O2.…”

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confidence: 99%

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Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

Landolt

Gillin

2002

Neuropsychopharmacology

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A novel approach to investigate the relationship between depression and changes in sleep-wake regulatory mechanisms used the monoamine oxidase inhibitor (MAOI) phenelzine that is known to suppress rapid-eye-movement (REM) sleep. Sleep architecture and EEG topography during wakefulness and sleep were studied in eight depressed patients before and after five weeks of treatment with phenelzine (30-90 mg/day), which induced a significant alleviation of depressive symptoms. Theta power (4.75-7.5 Hz) during a 5-min wake EEG prior to sleep increased two-fold during administration of phenelzine. REM sleep was almost completely eliminated. This latter effect was compensated by increased duration of stage 2, whereas total sleep time was not shortened. In non-REM sleep (stages 2, 3, and 4), treatment slightly reduced EEG power between 2. Hz band increased. Activity in the delta band Mood and the regulation of sleep are closely related. This notion is supported by the presence of frequent sleep abnormalities in depressed patients, which may affect both rapid-eye-movement (REM) sleep and nonrapid-eye-movement (non-REM) sleep (Benca et al. 1992). A tight association between sleep and mood is further suggested by the beneficial action of total and partial sleep deprivation, as well as phase advance therapies of sleep in many patients with depression (Gillin and Borbély 1985; Wirz-Justice and Van den Hoofdakker 1999). Different theories have been proposed to account for the antidepressant effects of sleep manipulations. They include prolonged major suppression of REM sleep (Vogel 1975;Vogel et al. 1990), elevation of sleep propensity (Borbély and Wirz-Justice 1982), and reduction of non-REM sleep intensity (Beersma and Van den Hoofdakker 1992).The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus et al. 1981;Daan et al. 1984;Dijk et al. 1987;Achermann et al. 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness. Power in the theta band ( ‫ف‬ 5-8 Hz) of the wake EEG increases during sleep deprivation (Cajochen et al. 1995;Aeschbach et al. 1997;Finelli et al. 2000). The time constant of this increase is similar to that obtained for the wake-dependent rise of delta power as measured in non-REM sleep. Furthermore, topographical analyses of the EEG during prolonged wakefulness have shown that the increase of theta activity in waking and delta activity ( ‫ف‬ 1-4 Hz) in non-REM sleep are largest in frontal EEG derivations and positively correlated (Werth et al. 1998;Cajochen et al. 1999aCajochen et al. , 1999bFinelli et al. 2000). These findings suggest that sleep regulation may exhibit local features. In other words, frontal parts of the cortex may be particularly susceptible to sleep loss and reflect the homeostatic process of sleep regulation more sensitively than other cortical regions. The monoamine oxidase inhibitor...

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confidence: 69%

Section: A Novel Approach To Investigate the Relationship Between Depmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

Landolt

Gillin

2002

Neuropsychopharmacology

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Monoaminergic‐based Pharmacotherapy for Depression

Papakostas¹,

Fava²

2005

Biology of Depression

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Although recent advances in neuropharmacology, neuroendocrinology, molecular biology, and pharmacogenetics have been instrumental in bringing about potential treatments for depression which are fundamentally unrelated to their predecessors, including substance P antagonists, glutaminergic agents, and corticotropinreleasing factor (CRF) antagonists, nevertheless it was agents that influenced the function of monoamine receptors and transporters that were discovered initially by serendipity and then developed as treatments for depression. The development of such compounds also served as a framework for the understanding of depression as a medical illness affecting brain functioning. As a result of these efforts, our field has gained further understanding of the role of monoamines in depression. In previous chapters, the relevance of monoamines in the underlying pathophysiology of depression was reviewed. In the following chapter we will focus on describing the contemporary role of monoaminergic agents in the treatment of depression. 6.

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Current Awareness

2001

Human Psychopharmacology

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of human psychopharmacology. Each bibliography is divided into 18 sections: 1 Books, Reviews & Symposia; 2 General; 3 Psychotropic Drugs ‐ General; Antidepressive Agents: 4 Tricyclics; 5 Monoamine Oxidase Inhibitors; 6 Serotonergics; Euthymic Agents: 7 Lithium; Tranquillizing Agents: 8 Major; 9 Minor & Hypnotics; 10 Analeptic Agents; 11 Anticonvulsant Agents; 12 Drugs of Abuse; 13 Transmitters, Receptors, Metabolites & Modulating Agents; 14 Neuropeptides; 15 Psychoneuroendocrinology; 16 Psychoneuroimmunology; 17 Behavioural Genetics; 18 Others. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted.

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Sleep and Sleep Electroencephalogram in Depressed Patients Treated With Phenelzine

Abstract: Antidepressant response to phenelzine treatment does not depend on elimination of REM sleep or inhibition of SWA in non-REM sleep. In depressed patients, REM sleep is regulated independently from non-REM sleep and can be manipulated without altering the dynamics of SWA.

Cited by 79 publications

References 46 publications

Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

Monoaminergic‐based Pharmacotherapy for Depression

Current Awareness

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