Sleep, depression and insomnia have manifold associations. Psychiatric sleep research in affective disorders has demonstrated that sleep in depression is characterized by an impairment of sleep continuity, deficits in slow wave sleep and a disinhibition of REM sleep (including shortened REM latency and increased REM density). Traditionally, insomnia, i.e. prolonged latency to fall asleep and increased frequency of nocturnal wake periods, was considered as an unspecific symptom of affective disorders. In the meantime, a shift in clinical and scientific focus has taken place viewing insomnia in addition as an independent diagnostic entity and as a clinical predictor of depression. Unfortunately, the neurobiological processes underlying the relationships between sleep, insomnia and depression have not been fully identified yet. It is clear that both insomnia and depression are characterized by alterations in the arousal system in the CNS presenting as hyperarousal. Moreover, insomniac patients display reduced and fragmented REM sleep periods, which might interfere negatively with basal processes of emotion regulation. The alterations in the arousal system and the interaction of it with the affect-regulatory system over the course of time might influence cognitive systems and hence lead to the clinical picture of depression. Given the suggestion of insomnia symptoms as possibly involved in the causation and the maintenance of psychopathology in general, this type of sequence might also be found in relation to other mental disorders.
Sleep, depression, and insomnia: A vicious circle? (In press.) / Baglioni, Chiara; K., Spiegelhalder; B., Feige; C., Nissen; M., Berger; D., Riemann. - In: CURRENT PSYCHIATRY REVIEWS. - ISSN 1573-4005. - STAMPA. - (2012), p. in stampa.
Sleep, depression, and insomnia: A vicious circle? (In press.)
BAGLIONI, CHIARA;
2012
Abstract
Sleep, depression and insomnia have manifold associations. Psychiatric sleep research in affective disorders has demonstrated that sleep in depression is characterized by an impairment of sleep continuity, deficits in slow wave sleep and a disinhibition of REM sleep (including shortened REM latency and increased REM density). Traditionally, insomnia, i.e. prolonged latency to fall asleep and increased frequency of nocturnal wake periods, was considered as an unspecific symptom of affective disorders. In the meantime, a shift in clinical and scientific focus has taken place viewing insomnia in addition as an independent diagnostic entity and as a clinical predictor of depression. Unfortunately, the neurobiological processes underlying the relationships between sleep, insomnia and depression have not been fully identified yet. It is clear that both insomnia and depression are characterized by alterations in the arousal system in the CNS presenting as hyperarousal. Moreover, insomniac patients display reduced and fragmented REM sleep periods, which might interfere negatively with basal processes of emotion regulation. The alterations in the arousal system and the interaction of it with the affect-regulatory system over the course of time might influence cognitive systems and hence lead to the clinical picture of depression. Given the suggestion of insomnia symptoms as possibly involved in the causation and the maintenance of psychopathology in general, this type of sequence might also be found in relation to other mental disorders.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.