Furthermore, polysomnographically measured sleep continuity was disturbed (i.e., long sleep latency and frequent awakenings throughout the sleep period) and Slow Wave Sleep (SWS) reduced. from Pittsburgh were among the first to suggest that changes of REM sleep, i.e., shortened REM sleep latency (shorter interval between sleep onset and the first occurrence of REM sleep), increased total REM sleep duration and increased REM density (higher phasic eyes movements during REM sleep), are typical sleep characteristics of patients with primary vs. The discovery of phases of REM during sleep in 1953 and the ensuing interest in sleep research led to the establishment of psychiatric sleep research utilizing polysomnography (PSG). By telling the story of an early success, a subsequent stagnation phase and new enthusiasm based on the integration of emerging neurobiological knowledge into the mechanistic overlap of sleep and depression disturbances, this review is paving a way for the integration of this knowledge into clinical practice. This review seamlessly ties in with and extends an earlier line of research of using sleep as a window into the brain’s neurobiological links between sleep processes and depression. The incidence of depression is steadily rising globally and present-day epidemiological data reveal that depression is now the third leading contribution to global disease burden and an estimated 25% of the population in industrialized countries will suffer from depression once in a lifetime. Before then, pharmacological agents like bromides, paraldehyde, scopolamine, or barbiturates were used to treat insomnia accompanying depression until these were replaced by benzodiazepine hypnotics and sedating antidepressants in the 1950/60s. Thus, the idea that the type of sleep disturbance in depressed individuals might support differential-diagnostic considerations was already born over a 100 years ago and experienced a renaissance in the 1970s with the discovery of shortened rapid eye movement (REM) sleep latencies in depressed individuals. He postulated that a certain type of sleep difficulty co-occurred with a certain depressive subtype, i.e., sleep onset problems with “neurotic” and sleep maintenance/early morning awakenings with “endogenous” depression. Emil Kraepelin, the founder of modern psychiatry, observed that mental symptoms fall mainly into two groups and he created the illness categories ‘manic-depression’’ and ‘dementia praecox’’, today clinically similar to ‘affective’’ and ‘psychotic’’ phenotypes. Treatment of difficulties with sleep in antique times consisted of listening to calm music, reading, or the use of opium or alcohol. Robert Burton, in his Anatomy of Melancholia remarked that ancient Greek physicians were well aware of the fact that melancholic individuals complained of difficulties falling asleep, maintaining sleep or of waking up too early in the morning. 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. 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. Studying insomnia from different angles as a transdiagnostic phenotype has opened many new perspectives for research into mechanisms but also for clinical practice. 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. 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. The so-called Cholinergic REM Induction Test revealed that REM sleep abnormalities can be mimicked by administration of cholinomimetic agents. 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. Initial hopes that these abnormalities of REM sleep may serve as differential-diagnostic markers for subtypes of depression were not fulfilled. 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. Since ancient times it is known that melancholia and sleep disturbances co-occur.
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