Sleep and manipulations of the sleep–wake rhythm in depression

Berger, Thomas; Calker, Dietrich van; Riemann, Dieter

doi:10.1034/j.1600-0447.108.s418.17.x

Cited by 61 publications

(24 citation statements)

References 72 publications

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“…It is well known that depression might be successfully treated by sleep deprivation for a half or whole night, although the improvement after such type of wake therapy is usually shortlasting, with relapse after recovery sleep (Kuhs & Tö lle 1991;Wirz-Justice & van den Hoofdakker 1999;Berger et al 2003;Wirz-Justice et al 2005). More than 20 years ago, Kripke hypothesized that light might be an effective antidepressant during the procedure of sleep deprivation (Kripke 1981;Kripke et al 1983).…”

Section: Introductionmentioning

confidence: 97%

Antidepressant effects of combination of sleep deprivation and early evening treatment with melatonin or placebo for winter depression

Putilov¹,

Danilenko

2005

Biological Rhythm Research

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Patients with winter depression (seasonal affective disorder) respond beneficially to sleep deprivation and bright light, but the mechanisms of these responses remain unknown. The study was designed to test whether afternoon/evening melatonin can prevent further relapse after sleep deprivation (presumably due to a pharmacologically induced advance shift of circadian phase). Compared to phase advancing by alteration of sleep -wake schedule or by bright light exposure, the melatonin intake is a more tolerated treatment procedure, and it provides a possibility of blind comparison between chronotherapeutic and placebo treatments. The depression was scored in 16 female patients with winter depression and 17 age-matched female controls before and after total night sleep deprivation and after subsequent six-day administration of melatonin (0.5 mg) or placebo under double blind conditions. The melatonin intake was scheduled at 17:00 in order to produce a phase advance of circadian rhythms. Sleep deprivation resulted in 38% reduction of depression score in patients, but it did not reduce depression score in controls. After subsequent treatment with placebo or melatonin, slight but significant improvement of mood was found in controls. These treatments also stabilized the antidepressant response to sleep deprivation in patients. However, neither differential effect of melatonin and placebo on depression score nor alteration of habitual sleep timing was found in patients and controls. Thus, the study results do not provide evidence for the antidepressant potential of melatonin in patients with winter depression under realistic clinical conditions. The finding of stabilization of mood in patients with placebo points to the contribution of psychological factors to the therapeutic action of this and other types of innovative treatments for winter depression. To include psychosocial aspects in the theoretical framework of seasonal depression, we conceptualized depression as an evolved feature of emotional response to psychosocial rather than physical environment. The seasonality of depression might be explained by cumulative effects of aperiodical psychosocial factors and periodical physical factors on one of the mechanisms of brain neurotransmission.

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Section: Introductionmentioning

confidence: 97%

Antidepressant effects of combination of sleep deprivation and early evening treatment with melatonin or placebo for winter depression

Putilov¹,

Danilenko

2005

Biological Rhythm Research

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“…For example, patients who have MDD show persistent shortening of rapid eye movement (REM) latency (10), increased REM density, and decreases in total sleep time and sleep efficiency (11). In addition, chronotherapeutic interventions can often alleviate depressive symptoms (9,12,13).…”

mentioning

confidence: 99%

Circadian patterns of gene expression in the human brain and disruption in major depressive disorder

Li¹,

Bunney

Meng

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

513

405

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A cardinal symptom of major depressive disorder (MDD) is the disruption of circadian patterns. However, to date, there is no direct evidence of circadian clock dysregulation in the brains of patients who have MDD. Circadian rhythmicity of gene expression has been observed in animals and peripheral human tissues, but its presence and variability in the human brain were difficult to characterize. Here, we applied time-of-death analysis to gene expression data from high-quality postmortem brains, examining 24-h cyclic patterns in six cortical and limbic regions of 55 subjects with no history of psychiatric or neurological illnesses (“controls”) and 34 patients with MDD. Our dataset covered ∼12,000 transcripts in the dorsolateral prefrontal cortex, anterior cingulate cortex, hippocampus, amygdala, nucleus accumbens, and cerebellum. Several hundred transcripts in each region showed 24-h cyclic patterns in controls, and >100 transcripts exhibited consistent rhythmicity and phase synchrony across regions. Among the top-ranked rhythmic genes were the canonical clock genes BMAL1(ARNTL), PER1-2-3, NR1D1(REV-ERBa), DBP, BHLHE40 (DEC1) , and BHLHE41(DEC2) . The phasing of known circadian genes was consistent with data derived from other diurnal mammals. Cyclic patterns were much weaker in the brains of patients with MDD due to shifted peak timing and potentially disrupted phase relationships between individual circadian genes. This transcriptome-wide analysis of the human brain demonstrates a rhythmic rise and fall of gene expression in regions outside of the suprachiasmatic nucleus in control subjects. The description of its breakdown in MDD suggests potentially important molecular targets for treatment of mood disorders.

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“…In contrast, wake therapy, whether administered over the whole night or restricted to the second half of the night, provides astonishing responses -within hours -in approximately 60 % of patients with major depression, independent of diagnostic subgroup (Wu & Bunney, 1990 ;Leibenluft & Wehr, 1992;Wirz-Justice & Van den Hoofdakker, 1999;Berger et al 2003). Wake therapy has been extensively studied since it was first reported more than 30 years ago, yet it has suffered a fate similar to that of orphan drugs (Wirz-Justice, 1998).…”

mentioning

confidence: 99%

Chronotherapeutics (light and wake therapy) in affective disorders

Wirz‐Justice¹,

Benedetti²,

Berger³

et al. 2005

Psychol. Med.

224

100

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The Committee on Chronotherapeutics was recently formed by the International Society for Affective Disorders (ISAD), which has asked us to provide a consensus review of chronotherapeutics (light and wake therapy) in affective disorders. We consider these non-pharmaceutical, biologically based therapies to be potentially powerful adjuvants ready for clinical application. We also stress the need for additional studies, both in-patient and out-patient, to broaden the evidence base for indications and efficacy.

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Sleep and manipulations of the sleep–wake rhythm in depression

Cited by 61 publications

References 72 publications

Antidepressant effects of combination of sleep deprivation and early evening treatment with melatonin or placebo for winter depression

Antidepressant effects of combination of sleep deprivation and early evening treatment with melatonin or placebo for winter depression

Circadian patterns of gene expression in the human brain and disruption in major depressive disorder

Chronotherapeutics (light and wake therapy) in affective disorders

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