Administration of triazolam prior to recovery sleep: effects on sleep architecture, subsequent alertness and performance

1989 ◽  
Vol 99 (4) ◽  
pp. 526-531 ◽  
Author(s):  
Thomas J. Balkin ◽  
Vincent M. O'Donnell ◽  
Gary H. Kamimori ◽  
Daniel P. Redmond ◽  
Gregory Belenky
2020 ◽  
Author(s):  
Christopher Holton ◽  
Nicola Hanley ◽  
Elaine Shanks ◽  
Penny Oxley ◽  
Andrew McCarthy ◽  
...  

Abstract BACKGROUND: Disturbed sleep is associated with cognitive decline in neurodegenerative diseases such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD). The progressive sequence of how neurodegeneration affects aspects of sleep architecture in conjunction with behavioural changes is not well understood. METHODS: We investigated changes in sleep architecture, spectral power and circadian rhythmicity in the tet-off rTg4510 mouse overexpressing human P301L tau within the same subjects over time. Doxycycline-induced transgene-suppressed rTg4510 mice, tTa carriers and wild-type mice were used as comparators. Spectral power and sleep stages were measured from within the home cage environment using EEG electrodes. In addition, locomotor activity and performance during a T-maze task were measured. RESULTS: Spectral power in the delta and theta band showed a time-dependent decrease in rTg4510 mice compared to all other groups. After the initial changes in spectral power, wake during the dark period increased whereas NREM and number of REM sleep bouts decreased in rTg4510 compared to wild-type mice. Home cage locomotor activity in the dark phase significantly increased in rTg4510 compared to wild-type mice by 40 weeks of age. Peak-to-peak circadian rhythm amplitude and performance in the T-maze was impaired throughout the experiment independent of time. At 46 weeks rTG4510 mice had significant degeneration in the hippocampus and cortex whereas doxycycline treated rTG4510 mice were protected. Pathology significantly correlated with sleep and EEG outcomes, in addition to locomotor and cognitive measures. CONCLUSIONS: We show that reduced EEG spectral power precedes reductions in sleep and home-cage locomotor activity in a mouse model of tauopathy. The data shows increasing mutant tau changes sleep architecture, EEG properties, behaviour and cognition; which suggest tau related effects on sleep architecture in patients with neurodegenerative diseases.


2020 ◽  
Author(s):  
Christopher Holton ◽  
Nicola Hanley ◽  
Elaine Shanks ◽  
Penny Oxley ◽  
Andrew McCarthy ◽  
...  

Abstract BACKGROUND: Disturbed sleep is associated with cognitive decline in neurodegenerative diseases such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD). The progressive sequence of how neurodegeneration affects aspects of sleep architecture in conjunction with behavioural changes is not well understood. METHODS: We investigated changes in sleep architecture, spectral power and circadian rhythmicity in the tet-off rTg4510 mouse overexpressing human P301L tau within the same subjects over time. Doxycycline-induced transgene-suppressed rTg4510 mice, tTa carriers and wild-type mice were used as comparators. Spectral power and sleep stages were measured from within the home cage environment using EEG electrodes. In addition, locomotor activity and performance during a T-maze task were measured. RESULTS: Spectral power in the delta and theta band showed a time-dependent decrease in rTg4510 mice compared to all other groups. After the initial changes in spectral power, wake during the dark period increased whereas NREM and number of REM sleep bouts decreased in rTg4510 compared to wild-type mice. Home cage locomotor activity in the dark phase significantly increased in rTg4510 compared to wild-type mice by 40 weeks of age. Peak-to-peak circadian rhythm amplitude and performance in the T-maze was impaired throughout the experiment independent of time. At 46 weeks rTG4510 mice had significant degeneration in the hippocampus and cortex whereas doxycycline treated rTG4510 mice were protected. Pathology significantly correlated with sleep and EEG outcomes, in addition to locomotor and cognitive measures. CONCLUSIONS: We show that reduced EEG spectral power precedes reductions in sleep and home-cage locomotor activity in a mouse model of tauopathy. The data shows increasing mutant tau changes sleep architecture, EEG properties, behaviour and cognition; which suggest tau related effects on sleep architecture in patients with neurodegenerative diseases.


2013 ◽  
Vol 23 (2) ◽  
pp. 176-185 ◽  
Author(s):  
Stefana Albu ◽  
Christoph P. N. Romanowski ◽  
M. Letizia Curzi ◽  
Vladimira Jakubcakova ◽  
Cornelia Flachskamm ◽  
...  

2020 ◽  
Author(s):  
Christopher Holton ◽  
Nicola Hanley ◽  
Elaine Shanks ◽  
Penny Oxley ◽  
Andrew McCarthy ◽  
...  

Abstract Disturbed sleep is associated with cognitive decline in Alzheimer’s disease (AD) patients. The progressive sequence of how neurodegeneration affects aspects of sleep architecture in conjunction with behavioural changes is not well understood. We investigated changes in sleep architecture, spectral power and circadian rhythmicity in the tet-off rTg4510 mouse overexpressing human P301L tau within the same subject over time. Doxycycline-induced transgene-suppressed rTg4510 mice, tTa carriers and wild-type mice were used as comparators. Using EEG electrodes, spectral power and sleep stages were measured from within the home cage environment. In addition, locomotor activity and performance during a T-maze task were measured. Spectral power, primarily in the NREM delta band, showed a time-dependent decrease in rTg4510 mice compared to all other groups. After the initial changes in spectral power, wake during the dark period increased whereas NREM and number of REM sleep bouts decreased in rTg4510 compared to wild-type mice. Home cage locomotor activity significantly increased in rTg4510 compared to wild-type mice by 40 weeks of age. Peak-to-peak circadian rhythm amplitude and performance in the T-maze was impaired throughout the experiment independent of time. At 46 weeks brain histopathological changes were measured in all animals demonstrating significant degeneration in hippocampus and cortex, and protection with doxycycline. Pathology significantly correlated with sleep outcomes, in addition to locomotor and cognitive measures. In conclusion, we show that reduced EEG slow wave activity precedes reductions in sleep and home-cage locomotor activity in a mouse model of tauopathy. The data shows increasing mutant tau changes sleep architecture, EEG properties, behavior and cognition; which suggest tau related effects on sleep architecture in AD patients.


2012 ◽  
Vol 29 (5) ◽  
pp. 537-548 ◽  
Author(s):  
Sophie M. T. Wehrens ◽  
Shelagh M. Hampton ◽  
Myriam Kerkhofs ◽  
Debra J. Skene

2021 ◽  
Vol 7 (4) ◽  
pp. 257-266
Author(s):  
Brijesh Prajapat ◽  
Nitesh Gupta ◽  
Dhruva Chaudhry ◽  
Ario Santini ◽  
AS Sandhya

Abstract Background and objective The sleep architecture of critically ill patients being treated in Intensive Care Units (ICU) and High Dependency Units (HDU) is frequently unsettled and inadequate both qualitatively and quantitatively. The study aimed to investigate and elucidate factors influencing sleep architecture and quality in ICU and HDU in a limited resource setting with financial constraints, lacking human resources and technology for routine monitoring of noise, light and sleep promotion strategies in ICU. Methods The study was longitudinal, prospective, hospital-based, analytic, and observational. Insomnia Severity Index (ISI) and the Epworth Sleepiness Scale (ESS) pre hospitalisation scores were recorded. Patients underwent 24-hour polysomnography (PSG) with the simultaneous monitoring of noise and light in their environments. Patients stabilised in ICU were transferred to HDU, where the 24-hour PSG with the simultaneous monitoring of noise and light in their environments was repeated. Following PSG, the Richards-Campbell Sleep Questionnaire (RCSQ) was employed to rate patients’ sleep in both the ICU and HDU. Results Of 46 screened patients, 26 patients were treated in the ICU and then transferred to the HDU. The mean (SD) of the study population’s mean (SD) age was 35.96 (11.6) years with a predominantly male population (53.2% (n=14)). The mean (SD) of the ISI and ESS scores were 6.88 (2.58) and 4.92 (1.99), respectively. The comparative analysis of PSG data recording from the ICU and HDU showed a statistically significant reduction in N1, N2 and an increase in N3 stages of sleep (p<0.05). Mean (SD) of RCSQ in the ICU and the HDU were 54.65 (7.70) and 60.19 (10.85) (p-value = 0.04) respectively. The disease severity (APACHE II) has a weak correlation with the arousal index but failed to reach statistical significance (coeff= 0.347, p= 0.083). Conclusion Sleep in ICU is disturbed and persisting during the recovery period in critically ill. However, during recovery, sleep architecture shows signs of restoration.


1994 ◽  
Vol 37 (6) ◽  
pp. 539-543 ◽  
Author(s):  
MA Quera-Salva ◽  
C McCann ◽  
J Boudet ◽  
M Frisk ◽  
P Borderies ◽  
...  

2020 ◽  
Author(s):  
Jin-xiang Cheng ◽  
Xianchao Zhao ◽  
Jian Qiu ◽  
Yingcong Jiang ◽  
Jiafeng Ren ◽  
...  

Abstract Background: Previous studies have claimed that transcranial direct current stimulation (tDCS) on the left dorsolateral prefrontal cortex (dlPFC) improves cognition in patients, but few studies that have evaluated the effects of tDCS on cognition improvement during sleep deprivation. To determine whether tDCS (anodal on the left DLPFC and cathodal on the right DLPFC at 2mA current for 30 minutes) can be an effective fatigue countermeasure. Methods: Seven participants and 8 participants underwent active or sham tDCS on the time participants’ cognition declined, respectively. All participants completed the psychomotor vigilance task, the trail making test A and B, the digit cancellation test, the stroop color word test, the brief visuospatial memory test-revised and a procedural game every two hours during the sleep deprivation and after recovery sleep. Results: The active tDCS had beneficial effects on attention, memory, executive function, processing speed, and the ability to inhibit cognitive interference, as well as improvements of subjective drowsiness and fatigue during sleep deprivation. The lasting effect of single tDCS on cognition during sleep deprivation can extend to more than 2 hours. All participants after tDCS gained no disturbed recovery sleep and recovered to baseline cognitive level after the recovery sleep. Conclusions: The study indicated that tDCS is an effective fatigue countermeasure during sleep deprivation, and doesn’t disturb the recovery sleep and performance postrecovery sleep.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A284-A285
Author(s):  
G M Paech ◽  
S Pradeepan ◽  
B Suthers

Abstract Introduction There is some evidence suggesting that patients with hypersomnia have delayed circadian timing, which could explain, at least in part, the excessive sleepiness and impaired daytime performance experienced by these individuals. This study investigated the effects of bright light treatment on improving daytime alertness in patients with idiopathic hypersomnia. Methods Participants were scheduled to two in-laboratory sessions (baseline and treatment) consisting of overnight sleep monitoring (polysomnography) followed by maintenance of wakefulness tests (MWT) and performance testing (10-min psychomotor vigilance task (PVT)). MWTs were performed at 10:00, 12:00, 14:00 and 16:00 and PVTs were performed at 11:00, 13:00, 15:00 and 15:00. In-laboratory sessions were separated by a two-week at-home treatment period during which participants were instructed to use commercially available light devices for 30-60 min each morning. Participants also completed the Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS) at baseline and after treatment. Paired t-tests were performed to assess differences in sleep architecture, sleep quality, performance (lapses; reaction time &gt;500ms) and alertness (MWT mean sleep latency) between baseline and treatment. Results To date, three participants (2 male) aged 62.7±13.2 (mean±SD) years have completed the study. Lapses (baseline: 17.9±11.9; treatment: 6.3±5.4), ESS (baseline: 17.3±3.1; treatment 12.3±6.8) and PSQI (baseline: 7.7±3.8; treatment: 4.0±1.0) all improved with light treatment, although this did not reach statistical significance. There were no statistical differences between baseline and treatment with regards to sleep architecture or mean sleep latency. Conclusion Although preliminary, results suggest that bright light treatment may improve subjective sleepiness, subjective sleep quality and performance. There was some variability between individuals, indicating that this treatment may not offer the same benefits to all patients. Although ongoing, this study suggests that light therapy could be used as an alternative, non-pharmacological treatment option to improve waking functions and sleepiness in hypersomnia patients. Support This project is supported by a Hunter Medical Research Institute Research Project Grant


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