Search

Comorbid insomnia and poor sleep quality in Parkinson's disease (PD) are associated with a poor health-related quality of life (HRQoL). However, the relationship between HRQoL and sleep measures obtained using polysomnography (PSG) remains unclear. We aimed to examine the association between various sleep measures and HRQoL in PD patients.We retrospectively included patients with PD who underwent PSG and responded to self-administered questionnaires including the Pittsburgh Sleep Quality Index (PSQI) and Medical Outcomes Study 36-Item Short-Form Health Survey.The patients' (n = 120) mean age was 67.06 (SD = 8.77) years, and their mean Hoehn and Yahr stage was 2.25 (SD = 0.78). A higher PSQI score (worse subjective sleep quality) was correlated in PSG with shorter sleep latency, less N1 sleep, and more N2 sleep. Multiple regression analysis showed that the total PSQI score correlated with both physical and mental HRQoL (p 0.001 in both cases). However, neither type of HRQoL studied correlated with objective sleep measures, including indicators of sleep architecture, sleep-disordered breathing, and sleep related movement disorders.Despite the association between subjective sleep quality and HRQoL, the associations between objective measures and HRQoL were negligible. Objective sleep fragmentation may not be perceived as a sleep disturbance in patients with PD, and therefore may not adversely affect their subjective health, given the paradoxical correlation between PSQI score and sleep architecture.

Background:Nonrestorative sleep (NRS), defined as insufficiently rested or refreshed sleep, is considered to play an important role in the development of depression. The aim of this study is to investigate the predictive ability of insomnia-related symptoms, including NRS, for incident depressive symptoms (DEPs) in a longitudinal manner., Methods:We used data of 1196 samples aged 18–64 years who participated in both the Hispanic Community Health Study/Study of Latinos conducted in 2008–2010 and the follow-up study (Sueño Ancillary Study) conducted in 2010–2013. DEPs and insomnia-related symptoms (difficulty initiating sleep [DIS], difficulty maintaining sleep [DMS], early morning awakening [EMA], difficulty returning to sleep [DRS], and NRS) were evaluated by the 10-item Center for Epidemiologic Studies Depression Scale and the Women's Health Initiative Insomnia Rating Scale, respectively. A logistic regression analysis was used to evaluate the predictive ability of each insomnia-related symptom at baseline for incident DEPs in couple-years., Results:In the univariate logistic regression analysis, all insomnia-related symptoms had significant associations with incident DEPs (DIS, odds ratio [OR] = 1.6; DMS, OR = 1.6; EMA, OR = 1.5; DRS, OR = 1.9; NRS, OR = 2.5). After adjusting for sociodemographic factors and the confounding effects of other insomnia-related symptoms, only NRS (OR = 2.2, 95% confidence interval = 1.4–3.5, p = .001) was significantly associated with incident DEPs., Conclusions:NRS was a risk factor for incident DEPs, which includes a predictive ability for other insomnia-related symptoms. Our results suggest that focusing on NRS is an effective strategy for preventing depression in public health promotions.

A discrepancy in subjective and objective estimations of sleep duration, which often diverge, could have long-term adverse effects on health outcomes in older adults. Using data from 2674 older adult men (≥ 65 years of age) of the Osteoporotic Fractures in Men Sleep Study, we assessed the longitudinal association between misperception index (MI), calculated as MI = (objective sleep duration – subjective sleep duration)/objective sleep duration, and all-cause mortality. During the follow-up with a mean (standard deviation) of 10.8 (4.2) years, 1596 deaths were observed. As a continuous variable, MI showed a linear relationship with all-cause mortality after adjusting for multiple covariates, including polysomnography-measured objective sleep duration [fully adjusted hazard ratio (HR), 0.69; 95% confidence interval [CI], 0.56–0.84]. As a categorical variable, the lowest MI quartile (vs. the interquartile MI range) was associated with increased mortality (fully adjusted HR, 1.28; 95% CI, 1.12–1.46), whereas the highest MI quartile was not associated with mortality (fully adjusted HR, 0.97; 95% CI, 0.85–1.11). The subjective overestimation of sleep duration may be a risk factor for all-cause mortality in older men. Future studies should examine why subjective overestimation of sleep duration is associated with all-cause mortality from a physiological perspective.

This study aimed to determine whether both subjective sleep quality and sleep duration are directly associated with quality of life (QOL), as well as indirectly associated with QOL through insomnia symptoms. Individuals aged 20–69 years without mental illness (n = 9305) were enrolled in this web-based cross-sectional survey. The Short Form-8 was used to assess physical and mental QOL. We used the Pittsburgh Sleep Quality Index (PSQI) and extracted items related to subjective sleep quality and sleep duration. Insomnia symptoms were also extracted from the PSQI. The hypothesized models were tested using structural equation modeling. Worse sleep quality, but not shorter sleep duration, was related to worse physical QOL. Both worse sleep quality and shorter sleep duration were related to worse mental QOL. Insomnia symptoms mediated these relationships. Subgroup analyses revealed a U-shaped relationship between sleep duration and physical/mental QOL. However, the relationship between sleep quality and physical/mental QOL was consistent regardless of sleep duration. The results suggest that subjective sleep quality has a more coherent association with QOL than subjective sleep duration. Because of its high feasibility, a questionnaire on overall sleep quality could be a useful indicator in future epidemiological studies of strategies for improving QOL.

Associations of sleep duration with human health could differ depending on whether sleep is restorative. Using data from 5804 participants of the Sleep Heart Health Study, we examined the longitudinal association of sleep restfulness combined with polysomnography-measured total sleep time (TST) or time in bed (TIB), representing different sleeping behaviors, with all-cause mortality. Among middle-aged adults, compared with restful intermediate TST quartile, the lowest TST quartile with feeling unrested was associated with higher mortality (hazard ratio [HR], 1.54; 95% confidence interval [CI] 1.01–2.33); the highest TST quartile with feeling rested was associated with lower mortality (HR, 0.55; 95% CI 0.32–0.97). Among older adults, the highest TIB quartile with feeling unrested was associated with higher mortality, compared with restful intermediate TIB quartile (HR, 1.57; 95% CI 1.23–2.01). Results suggest a role of restorative sleep in differentiating the effects of sleep duration on health outcomes in midlife and beyond.

Cognitive behavioral therapy for insomnia (CBT-I) is a first-line therapy for insomnia disorders. We assessed changes in discrepancies between subjective and objective sleep measures and correlations between discrepancy changes and clinical insomnia severity for CBT-I in patients with primary insomnia METHODS: Fifty-two outpatients (mean age, 60.3 years; 26 women) with primary insomnia were treated by individual CBT-I (50 min, maximum six sessions, once every 1-2 weeks). One week before and after CBT-I, patients recorded a sleep log and wore an actigraphy device. Subjective and objective time in bed (TIB), total sleep time (TST), sleep-onset latency (SOL), wake time after sleep onset (WASO), and sleep efficiency (SE) were evaluated by averaging 1-week records. Relative values of sleep discrepancy in TIB, TST, SOL, WASO, and SE were calculated for estimating effects of CBT-I. The therapeutic effects were also evaluated using psychological scales before and after CBT-I.Subjective and objective discrepancies in sleep measures decreased by 36, 25, and 37 min in TST, SOL, and WASO, respectively, and 7% in SE (all P 0.001) after CBT-I. Seven patients transitioned from underestimating SE before CBT-I to overestimating SE after CBT-I. Although CBT-I improved relative values of discrepancy in WASO and SE, alongside ISI, the improvement in insomnia severity only correlated with SOL discrepancy.CBT-I may reduce the discrepancy between subjective and objective sleep measures in patients with primary insomnia. However, a greater therapeutic effect of CBT-I was observed in reducing the ISI, which was slightly influenced by improvements in sleep discrepancies.

Background To date, no previous studies have evaluated the relationship between sleep duration and quality of life (QOL) or depression in the general population after controlling for daytime sleepiness and sleep disturbances. Methods A web-based cross-sectional survey was conducted with 8698 subjects aged 20–69 years. We examined the relationships between weekday sleep duration and daytime sleepiness, sleep disturbance, QOL and depression, using the Epworth Sleepiness Scale, Pittsburgh Sleep Quality Index (without the item for sleep duration), 8-item Short Form and Center for Epidemiological Studies Depression Scale (CES-D). Results Daytime sleepiness tended to increase in proportion to shorter weekday sleep durations. Sleep disturbances, physical and mental QOL, and CES-D scores were worse in both the shorter and longer sleep groups compared with the group with 7–8 h of sleep. Hierarchical logistic regression analyses revealed that short sleep duration but not long sleep duration was significantly associated with reduction of both physical and mental QOL, even after controlling for the presence of daytime sleepiness and sleep disturbance. Both short and long sleep duration were independently and significantly correlated with depression after controlling for daytime sleepiness; however, there was no statistically significant association after adjusting for the effects of sleep disturbance. Conclusions The results suggested adverse effects of short sleep but not long sleep on both physical and mental QOL. In addition, the negative impact of specific types of sleep disturbance on depression may be greater than the impact of shortening of sleep duration.

The effectiveness of D-cycloserine (DCS), an N-methyl-D-aspartate glutamate receptor partial agonist, and valproic acid (VPA), a histone deacetylase inhibitor, in facilitating the extinction of fear-conditioned memory has been explored in humans and animals. Here, we confirmed whether DCS (100 mg) and VPA (400 mg) act in off-line learning processes during sleep or waking, for further clinical application to anxiety disorders and posttraumatic stress disorder (PTSD). We performed a randomized, blind, placebo-controlled clinical trial in 90 healthy adults. Visual cues and electric shocks were used as the conditioned stimulus (CS) and unconditioned stimulus (US), respectively. The extinction effect was observed not in simple recall after the extinction of coupled CS-US, but was observed in the post-re-exposure phase after unexpected re-exposure to reinstatement CS-US coupling. Newly acquired conditioned fear was also eliminated or habituated by DCS and VPA administration, in line with previous findings. Furthermore, VPA facilitated the off-line learning process of conditioned fear extinction and habituation during sleep, while DCS facilitated this process during waking. These novel findings suggest that DCS and VPA might enhance exposure-based cognitive therapy for anxiety disorders and PTSD by reducing the vulnerability to reinstatement and preventing relapses of fear-conditioned responses, and provide evidence for a peculiarity of the sleep-dependent off-line learning process for conditioned fear extinction. This article is part of a Special Issue entitled 'Cognitive Enhancers'.

Appropriate inhibitory response control is associated with goal-directed behavior. Sleep accelerates the offline consolidation of acquired motor skills that are explicitly predictable; however, the effect of sleep on implicit (unpredictable) motor skills remains controversial. We speculated that a key component of response inhibition skill differentiates between these skill consolidation properties because explicit prediction can minimize the inhibitory efforts in a motor skill. We explored the offline skill learning properties of response inhibition during sleep and wakefulness using auditory Go and Go/Nogo tasks. We attempted to discriminate the possible effects of time elapsed after training (12 or 24 h), post-training sleep/wake state (sleep or wakefulness) and time of day (nighttime or daytime) in 79 healthy human subjects divided into 6 groups that underwent various sleep regimens prior to training and retesting. We found that delayed response inhibition skill improvement was achieved via a simple passage of daytime, regardless of the participants’ alertness level. Our results suggest that sleep-independent neuroplasticity occurs during the daytime and facilitates a delayed learning of response inhibition skill.

Sleep deprivation immediately following an aversive event reduces fear by preventing memory consolidation during homeostatic sleep. This suggests that acute insomnia might act prophylactically against the development of posttraumatic stress disorder (PTSD) even though it is also a possible risk factor for PTSD. We examined total sleep deprivation and memory suppression to evaluate the effects of these interventions on subsequent aversive memory formation and fear conditioning. Active suppression of aversive memory impaired retention of event memory. However, although the remembered fear was more reduced in sleep-deprived than sleep-control subjects, suppressed fear increased and seemed to abandon the sleep-dependent plasticity of fear. Active memory suppression, which provides a psychological model for Freud's ego defense mechanism, enhances fear and casts doubt on the potential of acute insomnia as a prophylactic measure against PTSD. Our findings bring into question the role of sleep in aversive-memory consolidation in clinical PTSD pathophysiology.

Working memory (WM) capacity improvement is impacted by sleep, and possibly by N-methyl-D-aspartate (NMDA) agonists such as D-cycloserine (DCS), which also affects procedural skill performance. However, the mechanisms behind these relationships are not well understood. In order to investigate the neural basis underlying relationships between WM skill learning and sleep, DCS, and both sleep and DCS together, we evaluated training-retest performances in the n-back task among healthy subjects who were given either a placebo or DCS before the task training, and then followed task training sessions either with wakefulness or sleep. DCS facilitated WM capacity enhancement only occurring after a period of wakefulness, rather than sleep, indicating that WM capacity enhancement is affected by a cellular heterogeneity in synaptic plasticity between time spent awake and time spent asleep. These findings may contribute to development, anti-aging processes, and rehabilitation of higher cognition.