1,721,114 research outputs found
Is Chronic Insomnia a Precursor to Major Depression? Epidemiological and Biological Findings
No full textInsomnia has been found to be a clinical predictor of subsequent depression. Nevertheless the biological processes underlying this causal relationship are yet not fully understood. Both conditions share a common imbalance of the arousal system. Patients with insomnia present fragmented REM sleep, which probably interferes with basal processes of emotion regulation. The interaction between the arousal and the affective system with the persistence of the disorder could slowly alter also the cognitive system and lead to depression. Although preliminary results seem to support this hypothesis, data are still too few to make valid conclusions
Il ruolo dell'arousal nell'insonnia: una rassegna della letteratura.
Full text linkTutte le attuali teorie sull’eziologia dell’insonnia riconoscono all’arousal un ruolo chiave sia come
fattore predisponente, sia come fattore di mantenimento del disturbo. Nel sonno si fa riferimento a
due forme di arousal: l’arousal fisiologico (autonomo e corticale) e l’arousal mentale (cognitivo ed
emozionale). Gli studi classici (ad esempio, Monroe, 1967) hanno indagato in particolar modo il ruolo
dell’arousal fisiologico, mentre le teorie più recenti si sono focalizzate sul ruolo dell’arousal cognitivo
ed emozionale (ad esempio, Espie, 2002; Morin, 1993), considerandoli come i principali fattori di
mantenimento. Anche a livello clinico, infatti, la lamentela più frequentemente riportata dai pazienti è
di fare esperienza di una elevata attività cognitiva nella fase di addormentamento, spesso associata
a vissuti emotivi connotati negativamente. In questa rassegna è stato esaminato il ruolo attribuito all’arousal
(autonomo, corticale, cognitivo ed emozionale) dalle teorie attuali sull’eziologia dell’insonnia
e le evidenze empiriche di cui disponiamo a sostegno di tale ruolo
REM sleep alterations in primary insomnia
No full textObjectives: We previously (2008) found an association between
REM sleep duration and perceived wakefulness in 81 patients with primary insomnia (PI) in addition to a clearly increased arousal index in REM sleep. The current study aimed to replicate and extend the previous findings.
Methods: Polysomnogram (PSG) and subjective sleep quality
questionnaire (Schlaffragebogen A, SFA) data of PI patients and
matched good sleeper controls (GSC) were evaluated for group
differences.
Results: One hundred and fifty-six new PI patients could be
matched to the same number of GSC (GSC; 60M, 96F; Mean age PI: 42.6 ± 12.4 years, GSC: 42.2 ± 13.4 years). PI patients had a higher wake time within bed time as well as lower REM and sleep stage 2 time. The association between perceived wake time and REM sleep time could be replicated in this new and larger group, as well as a clearly increased arousal index in REM sleep, while the arousal index in NREM sleep was significantly but less strongly increased.
Conclusion: We postulate that the psychophysiological hyperarousal characteristic for primary insomnia is particularly expressed as a REM sleep alteration. REM sleep appears to be particularly vulnerable to pre-sleep worries, leading to increased retrospective recall of this time as wake time and a lower restorative sleep quality
Sympathetic arousal and arousability predicts subsequent sleep quality
No full textThe aim of this study was to evaluate whether individuals with primary insomnia, in comparison to normal sleepers, show consistently higher autonomic arousal levels or changes in autonomic arousal which is systematically associated to differences in the quality of their night-time-sleeping. To address this aim, skin conductance levels (SCL) and inter beat intervals (IBI) were monitored before and after five consecutive nights in two different experimental conditions: 3 min with the instruction to rest and 3 min while providing acoustic stimuli inducing an orienting reflex. Twenty-three participants were recruited for the study, twelve people with insomnia and eleven good sleepers. The selection of the participants consisted in a first screening phase followed by a clinical interview and two weeks of assessment through the use of sleep diaries. Groups were matched for gender and age. Physiological indices were recorded in the participants' own homes through portable devices for one week (weekends excluded), during which sleep–wake cycles were monitored through actigraphic recording and sleep diaries. Sleep Efficiency Index (SEI), obtained as the ratio between total time spent sleeping divided by the total time spent in bed after lights off, was computed for each night. The SEIs were ordered from the worst to the best. Due to technical problems, two participants only had recording for 4 nights. Consequently, one night was excluded for the whole sample. Results showed that the SEI was always higher in good sleepers as opposed to people with insomnia which, moreover, presented higher within subjects and within group variability than did the control group. Regarding the physiological measures, it was found that sympathetic arousal measured by SCLs predicted the quality of the sleep during the subsequent night. Specifically, both groups showed marginally high rest arousal and significantly high arousal in response to stimulation (arousability) linked to low SEI during the subsequent night. The existence of a relationship between sympathetic arousal and sleep quality is consistent with previous results (e.g. Broman, Hetta, 1994). With respect to IBIs results evidenced no systematic change across both groups and nights of different qualities. In summary, results demonstrated that the variability of sleep quality, which is a central feature of insomnia, is also related to varying levels of evening autonomic arousal and arousability. The same relationship was found also in good sleepers
Significance of REM sleep dysregulation in depression: State of the art (In press.)
No full textDisturbances of sleep are typical for most depressed patients and belong to the core symptoms of the disorder. Since the 1960ies polysomnographic sleep research has demonstrated that besides disturbances of sleep continuity, depression is associated with altered sleep architecture, i.e. a decrease in slow wave sleep (SWS) production and disturbed REM sleep regulation. Shortened REM latency (i.e. the interval between sleep onset and the occurrence of the first REM period), increased REM sleep duration and increased REM density (i.e. the frequency of rapid eye movements per REM period) have been considered as biological markers of depression which might predict relapse and recurrence. High risk studies including healthy relatives of patients with depression demonstrate that REM sleep alterations may precede the clinical expression of depression and may thus be useful in identifying subjects at high risk for the illness. Several models have been developed to explain REM sleep abnormalities in depression, like the cholinergic-aminergic imbalance model or chronobiologically inspired theories, which are reviewed in this overview. Moreover, REM sleep alterations have been recently considered not only as biological "scars" but as true endophenotypes of depression. This review discusses the genetic, neurochemical and neurobiological factors that have been implicated to play a role in the complex relationships between REM sleep and depression. We hypothesize on the one hand that REM sleep dysregulation in depression may be linked to a genetic predisposition/vulnerability to develop the illness; on the other hand it is conceivable that REM sleep disinhibition in itself is a part of a maladaptive stress reaction with increased allostatic load. We also discuss whether the REM sleep changes in depression may contribute themselves to the development of central symptoms of depression such as cognitive distortions including negative self-esteem and the overnight consolidation of negatively toned emotional memories
- …
