Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • 2024-05
  • 2024-06
  • 2024-07
  • The majority of studies conducted on sleep

    2018-11-01

    The majority of studies conducted on sleep and cognitive functioning have employed a total sleep deprivation protocol in which participants are typically deprived of one or more nights of sleep. An experimentally induced total sleep deprivation, however, may not accurately resemble the kind of sleep loss experienced by individuals in their daily life. To address this issue, some studies have examined the effects of chronic partial sleep deprivation [10], and showed a sleep dose-response effect on cognitive performance (e.g. behavioural alertness, working memory, and cognitive throughput). Other studies, adopting a similar chronic partial sleep deprivation protocol, revealed that restricting sleep to six hours or less per night, over a nitric oxide synthase inhibitor of two weeks, results in cognitive performance deficits that are comparable to deficits experienced after two days of total sleep deprivation [11]. Altogether, these findings confirmed that sleep loss resulting from either total or chronic partial sleep deprivation has similar detrimental effects on cognitive performance [10]. Although partial sleep restriction and sleep deprivation studies have provided insights into the relationship between sleep and cognition, it remains difficult to generalize findings to individuals with chronic sleep disorders since experimental manipulations cannot fully replicate the long-term changes in sleep patterns that characterize those individuals [12]. This is the case for insomnia, a heterogeneous sleep disorder characterized by subjective poor sleep quality [13], difficulties in initiating and maintaining sleep, and impaired daytime functioning [14]. To date, findings from studies examining the relationship between cognitive functioning and insomnia have been inconsistent [15,16]. One study reported that people with insomnia rate their subjective performance on semantic memory tasks lower than controls despite the fact that their performance does not differ from control [17]; whereas, in another study, it has been shown that people with insomnia experience deficits when trying to retrieve semantic memories relative to healthy controls [18]. Despite the equivocal findings, it is suggested that mild to moderate cognitive deficits occur in the presence of insomnia [12,16,19].
    Material and methods
    Discussion We collected multiple sleep measures in order to better characterize the quality of sleep of the individuals and to define our poor-sleep group. First, to place individuals in the poor-sleep group, we administered the Insomnia Severity Index (ISI), a measure that is designed to evaluate perceived day-time and night-time symptoms of insomnia [22]. We also asked participants to complete the PSQI. Although not specifically designed to diagnose insomnia, the PSQI is a widely accepted instrument that assesses sleep quality and disturbance over the course of the past month [21]. We found that participants experiencing insomnia-like symptoms also reported poorer sleep quality, as measured by the PSQI, compared to controls. Participants in the poor-sleep group also differed significantly from controls in subjective sleep quality as assessed by the CSD-E, a standardized tool assessing qualitative (e.g. sleep quality) and quantitative (e.g. sleep duration) aspects of sleep [20], which is consistent with previous studies suggesting that complaints of poor sleep quality are a defining feature of insomnia [13]. Overall, sleep quality (as measured by PSQI, ISI and items of the CSD-E) was consistently measured to be poorer in the poor-sleep group than in the control group, and Processed pseudogene was the distinguishing feature between our two sleep groups. In addition to subjective measures, sleep quality can be evaluated through the use of objective methods such as actigraphy or polysomnography (PSG). In our study, we used actigraphy to collect objective data characterizing the quality of sleep of our participants. Our analyses did not reveal any group differences using this approach. Coherently, the correlation analysis between subjective and objective measures of sleep in our sample revealed no relationship between these two different types of measurements. Though this may seem surprising at first, the inconsistency between objective and subjective measures characterizing sleep quality, is an issue that has been already raised to question the ability of actigraphy to detect periods of wakefulness in specific populations or people with specific sleep disorders [30]. In fact, actigraphy utilizes a piezoelectric accelerometer that measures motor activity [27], which is used to characterize wakefulness, but the technique cannot distinguish between sleep and lack of movement [28]. This is an important issue as some insomnia sufferers will often remain in bed motionless and awake for extended periods of time [30], which results in the technique to be unable to detected their wakefulness. This issue is well-known in the field, and it is the main reason for which objective parameters acquired through the actigraphy are often not routinely nitric oxide synthase inhibitor used in the clinical practice for evaluation and diagnosis of insomnia while PSG remains the gold standard. In our specific study, there may be two potential explanations for why we did not find any group differences in the actigraph measures. First, the sleep quality identified in our poor-sleep group may refer to insomnia-like symptoms representative of subjective paradoxical insomnia, which refers to individuals reporting poor sleep quality despite having relatively normal PSG and actigraphy recordings [31]. On the other hand, the lack of group differences could be attributed to the actigraphy\'s inability to detect motionless wakefulness in our poor-sleep group. Either way, our findings are in support of revaluing the use of subjective measures in clinical setting.