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Review
. 2020 Jan;45(1):74-89.
doi: 10.1038/s41386-019-0411-y. Epub 2019 May 9.

Sleep, insomnia, and depression

Dieter Riemann  1 , Lukas B Krone  2   3 , Katharina Wulff  4   5 , Christoph Nissen  6
Affiliations
Review

Sleep, insomnia, and depression

Dieter Riemann et al. Neuropsychopharmacology. 2020 Jan.

Abstract

Since ancient times it is known that melancholia and sleep disturbances co-occur. The introduction of polysomnography into psychiatric research confirmed a disturbance of sleep continuity in patients with depression, revealing not only a decrease in Slow Wave Sleep, but also a disinhibition of REM (rapid eye movement) sleep, demonstrated as a shortening of REM latency, an increase of REM density, as well as total REM sleep time. Initial hopes that these abnormalities of REM sleep may serve as differential-diagnostic markers for subtypes of depression were not fulfilled. Almost all antidepressant agents suppress REM sleep and a time-and-dose-response relationship between total REM sleep suppression and therapeutic response to treatment seemed apparent. The so-called Cholinergic REM Induction Test revealed that REM sleep abnormalities can be mimicked by administration of cholinomimetic agents. Another important research avenue is the study of chrono-medical timing of sleep deprivation and light exposure for their positive effects on mood in depression. Present day research takes the view on insomnia, i.e., prolonged sleep latency, problems to maintain sleep, and early morning awakening, as a transdiagnostic symptom for many mental disorders, being most closely related to depression. Studying insomnia from different angles as a transdiagnostic phenotype has opened many new perspectives for research into mechanisms but also for clinical practice. Thus, the question is: can the early and adequate treatment of insomnia prevent depression? This article will link current understanding about sleep regulatory mechanisms with knowledge about changes in physiology due to depression. The review aims to draw the attention to current and future strategies in research and clinical practice to the benefits of sleep and depression therapeutics.

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Figures

Fig. 1
Fig. 1
Comparison of the polysomnographic (PSG) profile of a good sleeper (upper panel) and a patient hospitalized for severe depression according to DSM-IV criteria (lower panel). Both subjects have been free from intake of any psychotropic drug for at least 14 days. The y-axis lists arousal (micro-arousals), wake and sleep stages (REM, stage N1 to N3) and eye movements). The x-axis is the time axis. Sleep in depression is characterized by alterations of sleep continuity (prolonged sleep onset and sleep maintenance problems), a decrement of SWS (Slow Wave Sleep, also measurable as a decline in Delta-Power) and a disinhibition of REM sleep: this encompasses shortening of REM latency, prolongation of the first REM period and increase of REM density. Original data from Freiburg sleep lab, hitherto unpublished
Fig. 2
Fig. 2
a, b The Hobson/McCarley Model and the regulation of Non-REM and REM sleep in good sleepers and patients with depression. Experiments by Hobson and McCarley in cats especially in the brain stem were able to show that manipulation of cholinergic or aminergic cell groups is able to change sleep. In the case of good sleepers (a) the aminergic systems (dorsal raphe/locus coeruleus) are active during Non-REM sleep and cease their activity around the onset of REM sleep, where cholinergic activity becomes dominant. The reciprocal interaction between the aminergic and the cholinergic system determines the Non-REM-REM cycle. In depression (b), an overactive cholinergic system or a weakened aminergic system leads to an earlier onset of REM sleep. Based on refs [10, 18], permission granted
Fig. 3
Fig. 3
The Two-Process-Model is based on two components or factors, i.e., process C and process S. Process C reflects circadian rhythmicity, which is under control of the light–dark cycle. Process S reflects sleep or sleep pressure and can be measured as delta waves during night sleep. The interaction between C and S describes or determines the sleep-wake cycle in good sleepers (upper left panel). In contrast, in depression (lower right panel), process S is deficient, as reflected by low levels of slow wave sleep/delta power in the spectral analysis of the sleep EEG. Sleep deprivation may act antidepressive because it enhances process S, thus leading to an increased amount of slow wave sleep after sleep deprivation. Personal permission by A. Borbely
Fig. 4
Fig. 4
This figure displays the relationships between normal and insomniac sleep, spectral analysis of sleep EEG and neuroanatomical structures as delineated from the “flip-flop” switch model. a Upper panel—healthy sleeper; lower panel—insomniac sleeper: It is shown that there is no grossly disturbed macrostructure of Non-REM-REM sleep cycling in insomniac patients, but an altered microstructure with many brief awakenings and arousals in insomnia especially in REM sleep (see arrows). b Here shown are spectral analytic data from healthy good sleepers (HGS) and people with insomnia, reflecting a significant increase in fast waves especially in the sigma and beta range. c Anatomical structures and pathways involved in the regulation of wake (left), Non-REM (middle), and REM sleep (right) according to “flip-flop” switch model (see text). Panels a and b of the figure are taken from ref. [53]—permission granted. Panel c is based on refs [60, 76, 193]—permission granted
Fig. 5
Fig. 5
Comprehensive insomnia model (see text)—authors´ own conception
See this image and copyright information in PMC

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