Sleep and depression — results from psychobiological studies: an overview

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Abstract

Disturbances of sleep are typical for most depressed patients and belong to the core symptoms of the disorder. Polysomnographic sleep research has demonstrated that besides disturbances of sleep continuity, in depression sleep is characterized by a reduction of slow wave sleep and a disinhibition of REM sleep, with a shortening of REM latency, a prolongation of the first REM period and increased REM density. These findings have stimulated many sleep studies in depressive patients and patients with other psychiatric disorders. In the meantime, several theoretical models, originating from basic research, have been developed to explain sleep abnormalities of depression, like the two-process-model of sleep and sleep regulation, the GRF/CRF imbalance model and the reciprocal interaction model of non-REM and REM sleep regulation. Interestingly, most of the effective antidepressant agents suppress REM sleep. Furthermore, manipulations of the sleep–wake cycle, like sleep deprivation or a phase advance of the sleep period, alleviate depressive symptoms. These data indicate a strong bi-directional relationship between sleep, sleep alterations and depression.

Section snippets

Sleep disturbances and depression

The relationship between depression and insomniac symptoms is not a one-way street as it was formerly assumed. Recent epidemiological studies strongly suggest that not only is insomnia a typical symptom of depression but, vice versa, insomnia may be an independent risk factor for depression in the long run. The relation between insomnia and depression constitutes a situation with evidence supporting a strong bi-directional linkage.

More than 90% of depressed patients complain about impairments

Polysomnographic studies in depression

Systematic sleep EEG investigations in unmedicated depressed patients using formalized diagnostic criteria were initiated by the group of David Kupfer (Kupfer, 1976, Kupfer and Foster, 1972). Besides sleep continuity disturbances, sleep in depression was characterized by a reduction of slow wave sleep (SWS) and by a shortening of the interval between sleep onset and the occurrence of the first REM period (i.e. REM latency). Further abnormal features included an increased amount of REM sleep, a

Important confounding/intervening influences on sleep parameters

Prior to the discussion of pathophysiological models interrelating sleep abnormalities and depression, several important methodological issues have to be mentioned in order to outline limitations, constraints and problems of polysomnographic research in psychiatry, especially in depression.

How stable are sleep abnormalities in depressed individuals over time?

An important research strategy in psychobiological research is based on the question of whether a given abnormality that is present during the acute disease phase normalizes with remission (‘state’-marker), can still be detected when the disorder is no longer present (‘scar’), or was already present prior to the clinical onset of the disorder and persists throughout the life-span (‘trait’- or ‘vulnerability’-marker). Rush et al. (1986) found a persistence of REM sleep abnormalities in a sample

The impact of antidepressive therapies on sleep in depression

The type of research described under this heading aims at correlating changes of sleep seen during any kind of antidepressive therapy with concurrent or delayed changes of psychopathology. Also relevant is the relationship between pre-therapy sleep abnormality and therapeutic outcome.

Chronobiological models

The most influential model suggested to explain sleep abnormalities in depression based on chronobiological assumptions is the two-process model of Borbély and coworkers (Borbély, 1982, Borbély and Wirz-Justice, 1982). This model attempts to explain the effects of sleep deprivation on depression, REM sleep disinhibition, and reduced SWS. According to this model the so-called process ‘S’ is deficient in depression, which is reflected by a diminution of delta-activity and SWS (see Fig. 2).

Conclusion

After reviewing all theories on the pathophysiology of sleep alterations in depression, one has to conclude that there is still no entirely convincing model capable of explaining all typical changes in the sleep EEG of depressives. The initial hope that the investigation of sleep may be a valuable tool for differential-diagnosis in psychiatry has not been fulfilled. Numerous studies in different psychiatric populations have not conclusively demonstrated specificity in the relationship between

Acknowledgements

We thank Professor Dr Charles Reynolds for his comments and suggestions concerning an earlier version of this manuscript.

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