169,932 research outputs found
The impact of sleep pressure, circadian phase and an ADA-polymorphism on working memory: a behavioral, electrophysiological, neuroimaging approach
No full textThe need for sleep, the so-called sleep pressure, increases continuously during wakefulness and decreases during sleep again, in particular during intense deep sleep (Borbely, 1982). This sleep homeostatic process is mediated by the increase and degradation of adenosine in frontal brain structures (Porkka-Heiskanen, 2013). At the behavioural level, it is commonly mirrored in declines of performance under high sleep pressure (Cajochen, Blatter, & Wallach, 2004).
Adenosine is degraded by adenosine deaminase (ADA) (Landolt, 2008). Due to a polymorphism (rs73598374), ADA activity differs inter-individually. Lower ADA activity in G/A- compared to G/G-allele carriers (Battistuzzi, Iudicone, Santolamazza, & Petrucci, 1981)has been associated with a trait-like higher sleep pressure level, indicated by deeper sleep and worse vigilance performance (Bachmann et al., 2012).
However, the impact of sleep pressure on several sleep and waking functions depends on circadian phase (Dijk & Franken, 2005): It is potentiated during the night while counteracted during daytime by circadian wake promoting mechanisms. Also, the influence of sleep pressure on neuro-behavioral performance depends on cognitive domain (Van Dongen, Baynard, Maislin, & Dinges, 2004). Performance relying on the frontal lobes, such as executive aspects of working memory (WM), has been suggested to be particularly vulnerable to high sleep pressure (Harrison & Horne, 2000).
In a multi-methodological approach we compared thus circadian variations in sleep and in a set of waking functions according to the ADA-genotype. To capture both circadian variations and their interaction with sleep pressure, we compared two 40-h conditions, in which sleep pressure was either kept low by multiple napping (low sleep pressure) or accumulated during sleep deprivation (high sleep pressure). Nap sleep electroencephalographic (EEG) activity, vigilance, WM performance and underlying blood oxygen level-dependent (BOLD) activity was assessed in regular time intervals.
Vigilance and WM performance was worse during high as compared to low sleep pressure, particularly during the night. Specifically in executive aspects of WM, sleep pressure-dependent performance modulations were evident in G/A- but not in G/G-allele carriers (Reichert, Maire, Gabel, Viola, et al., 2014). WM performance of G/A-allele carriers benefited during napping in particular from rapid eye movement (REM) sleep duration (Reichert, Maire, Gabel, Hofstetter, et al., 2014). At times of high circadian wake promotion G/A-allele carriers showed a reduced sleep ability, indicating changes of circadian arousal promotion in response to lower ADA activity. Accordingly, we observed at a cerebral level during high circadian sleep promotion, that G/A-allele carriers showed more corti-cal compensatory mechanisms during WM performance to cope with high sleep pressure at night.
Overall, the data suggest that the impact of sleep pressure on performance, whether state- or trait-like, is modulated by circadian mechanisms. These mechanisms contribute to a differential resistance or vulnerability to sleep deprivation according to cognitive domain.
References
Bachmann, V., Klaus, F., Bodenmann, S., Schafer, N., Brugger, P., Huber, S., . . . Landolt, H. P. (2012). Cerebral Cortex, 22(4), 962-970. doi: bhr173 [pii]10.1093/cercor/bhr173
Borbely, A. A. (1982). A two process model of sleep regulation. Hum Neurobiol, 1(3), 195-204.
Cajochen, C., Blatter, K., & Wallach, D. (2004). Psychologica Belgica, 44(1/2), 59-80.
Dijk, D. J., & Franken, P. (2005). In R. T. Kryger MH, Dement WC (Ed.), Principles and Practice of Sleep Medicine (pp. 418-435). Philadelphia: Elsevier Saunders.
Harrison, Y., & Horne, J. A. (2000). J Exp Psychol Appl, 6(3), 236-249.
Landolt, H. P. (2008). Biochem Pharmacol, 75(11), 2070-2079. doi: 10.1016/j.bcp.2008.02.024S0006-2952(08)00104-4 [pii]
Porkka-Heiskanen, T. (2013). Curr Opin Neurobiol, 23(5), 799-805. doi: 10.1016/j.conb.2013.02.010
Reichert, C. F., Maire, M., Gabel, V., Hofstetter, M., Viola, A. U., Kolodyazhniy, V., . . . Schmidt, C. (2014). PLoS One, 9(12), e113734. doi: 10.1371/journal.pone.0113734
Reichert, C. F., Maire, M., Gabel, V., Viola, A. U., Kolodyazhniy, V., Strobel, W., . . . Schmidt, C. (2014). J Biol Rhythms, 92(2), 119-130.
Van Dongen, H. P., Baynard, M. D., Maislin, G., & Dinges, D. F. (2004). Sleep, 27(3), 423-433
Circadian and homeostatic sleep regulation in humans : effects of age and monochromatic light
No full textThe first part of this thesis deals with age-related modifications in the circadian and
homeostatic sleep regulation, whereas in the second part, the effects of an evening
exposure to monochromatic light on subsequent sleep architecture and sleep
electroencephalographic power spectra are described.
Age and sleep
Sleep in humans undergoes several age-related changes, resulting in less
consolidated sleep, reduced slow wave sleep, advanced sleep-wake timing and
shorter nocturnal sleep episodes. The first aim of this thesis was to gain
comprehensive information about the influence of age on circadian and homeostatic
aspects of sleep regulation. We compared the sleep electroencephalogram (EEG) of
healthy young with older volunteers under high and low sleep pressure conditions.
The study design consisted of two different protocols, both started with a baseline
and ended up with a recovery night. The 40-h episode between these two nights
comprised either an episode of total sleep deprivation (SD; high sleep pressure) or
10 sleep/wake cycles with 75 min of sleep followed by 150 min of wakefulness (low
sleep pressure). The recovery nights served to investigate the age-related influence
during enhanced and reduced sleep pressure conditions. The sleep episodes during
the nap protocol allowed comparing circadian modulation of sleep characteristics
between young and older subjects.
The response to high sleep pressure (i.e. after 40 hours of sleep deprivation)
revealed a significantly attenuated frontal predominance of spectral EEG delta power
in the sleep EEG of older participants, most pronounced at the beginning of the night
(Chapter 2). In addition, the dissipation of homeostatic sleep pressure, as indexed by
EEG delta power density, was shallower in the older than in the young group. This
implies either an age-related weaker homeostatic response to sleep deprivation,
predominantly in frontal brain areas, and/or altered cortical functions with an agerelated
higher vulnerability to sleep deprivation.
Under low sleep pressure (i.e. after multiple naps), older participants exhibited
an attenuated occipital decline in delta frequencies in the all-night EEG during
recovery sleep. This arose from an altered time course of EEG delta power density.
The reduction of EEG delta activity after sleep satiation was similar in both age
groups during the first sleep cycle. However, the EEG delta decrease to low sleep
pressure was not longer present during the second sleep cycle in the older study
group compared with the young (Chapter 4).
During the 40-h nap protocol (Chapter 3), we have quantitative evidence for a
weaker circadian arousal signal in the older volunteers. This is reflected in higher
subjective sleepiness levels during the late afternoon and evening (‘wake
maintenance zone’), with more sleep in the elderly during the naps at this time of day
(Chapter 3). The day-night differences in the EEG lower alpha and spindle range
were less pronounced in the older group. Furthermore, the amplitude of the circadian
modulation of REM sleep was attenuated in the elderly and the nocturnal melatonin
secretion was significantly reduced.
Taken together, our study revealed different responses to high and low sleep
pressure, as assessed by the sleep EEG, subjective sleepiness levels and melatonin
secretion, in older subjects when compared to the younger group. These results
emphasize both the attenuation of circadian amplitude and alterations in homeostatic
sleep regulation with age. We also gained insight into age-related differences in
responsiveness of regional and time-dependent aspects of sleep. These age-related
modifications are not uniformly spread over the brain and thus are likely to reflect
differences in recovery or reactivation processes during sleep.
Light and sleep
Beside rods and cones, there is an additional so-called non-image-forming
visual system (NIF) in the human retinal ganglion cells, with highest sensitivity in the
‘blue’ portion of visible light. The NIF is mediated by the photopigment melanopsin
and projects to the circadian pacemaker, located in the suprachiasmatic nuclei
(SCN). With efferents from the SCN to sleep- and wake-promoting brain regions, the
NIF influences the circadian regulation of sleep and wakefulness. We compared
sleep architecture and EEG spectra in young healthy men after evening exposure to
two different wavelengths of light (blue; 460 nm vs. green; 550 nm) or no light. The
time course of EEG slow-wave activity (SWA; 0.75-4.5 Hz) after blue light was
altered, with slightly lower SWA during the first and significantly higher SWA during
the third sleep cycle in parietal and occipital brain regions. These findings could be
interpreted either as the immediate induction of a circadian phase delay, or that the
acute alerting effects of blue light continue into the sleep episode and are followed by
an intra-sleep SWA rebound. Concomitantly, shorter REM sleep cycles after blue
light exposure were observed during these two cycles. Our results show that the
effects of light on human physiology including sleep not only depend on the duration
and intensity of light but also on its wavelength, and thus further emphasize the
critical role of the NIF in the regulation of sleep and circadian rhythms
Ultradian and circadian modulation of dream recall: EEG correlates and age effects
No full textpeer reviewe
Non-visual effects of light on human circadian physiology and neurobehavioral performance
No full textLight is of crucial importance for human circadian rhythms. In fact, light exposure allows for resetting individual biological rhythms to the 24-h day. Besides its synchronizing effects, light also acts on different behavioural and physiological variables. The overarching aim of this thesis was to investigate the effect of different light properties, such as intensity, wavelength, duration, timing and dynamics, on neurobehavioral performance and circadian physiology, and possible inter-individual differences.
In the first part, we investigated the effect of three morning light settings (dim light, DL < 8 lux; monochromatic blue light, mBL at 100 lux; and dawn simulation light, DsL increasing from 0 to 250 lux) in 17 young participants (20-35 years old), after two nights of 6-h sleep restriction, on alertness, well-being, melatonin and cortisol profiles and cognitive performance. We found that exposure to artificial morning DsL improved subjective perception of well-being and mood, as well as cognitive performance across the day compared to DL and mBL. Only morning mBL induced a phase advance of the circadian profile of melatonin, thus impacting on the circadian system.
In the second part, we compared the effect of three light settings (dim light, DL <8 lux; polychromatic white light, WL at 250 lux; and blue- enriched polychromatic white light, BL at 250 lux) on subjective sleepiness and physiological variables during a 40-h sleep deprivation protocol. Inter-individual differences were investigated with respect to (1) age, by enrolling a cohort of 26 young (20-35 years old) and 12 older participants (55-75 years old); and (2) genetic predisposition (polymorphism in clock gene Period3), by enrolling 8 young PER34/4 and 8 young PER35/5 participants. Accordingly, the age-related effects were such that exposure to BL and WL improved subjective sleepiness in both age groups, while melatonin suppression was only detectable in the young, with a more pronounced effect under BL, and not in the older. Only the blue-enriched light modified cortisol levels, with a decrease in the young and an increase in the older. Both lights had a contrary effect depending on the age of the participant in regard to skin temperature and motor activity. With respect to the genetic predisposition, exposure to BL and WL suppressed melatonin in both groups, with a stronger effect under BL in the PER35/5. However, we showed a significant alerting response, a better well-being, and a decrease in cortisol levels only in the short allele carriers (PER34/4). In contrast, cognitive performance was decreased only in PER35/5 under WL.
In conclusion, depending on the purpose to use non-visual effects of light, either DsL or mDL can be used to improve subjective mood and cognitive performance or to shift internal rhythms, respectively. In a broader perspective, the use of moderately bright light in night work and shift work settings, where constant light levels are very common, may differ across shift workers given their age and their genetic predisposition
Chronobiology, excessive daytime sleepiness and depression: Is there a link?
No full textThe complaint of excessive daytime sleepiness (EDS), commonly encountered in clinical practice, may arise from a variety of psychiatric disorders, most importantly depression. Even though EDS frequently leads depressed patients to seek medical assistance, it is commonly under-evaluated and under-diagnosed. Therefore, a comprehensive understanding and management of EDS is essential in the clinical assessment of depression. Within a theoretical framework, a chronobiological approach may shed new light on the complex interaction of EDS and depression. In this review, studies on EDS and depression are summarized and discussed within the context of circadian and sleep regulatory mechanisms. Furthermore, potential chronobiological therapeutic strategies are proposed to address some of the unmet needs in the treatment of EDS and depression
What keeps us awake? : the role of clocks and hourglasses, light, and melatonin
No full textWhat is it that keeps us awake? Our assumption is that we consciously control our daily activities including sleep-wake behavior, as indicated by our need to make use of an alarm clock to wake up in the morning in order to be at work on time. However, when we travel across multiple time zones or do shift work, we realize that our intentionally planned timings to rest and to remain active can interfere with an intrinsic regulation of sleep/wake cycles. This regulation is driven by a small region in the anterior hypothalamus of the brain, termed as the "circadian clock". This clock spontaneously synchronizes with the environmental light-dark cycle, thus enabling all organisms to adapt to and anticipate environmental changes. As a result, the circadian clock actively gates sleep and wakefulness to occur in synchrony with the light-dark cycles. Indeed, our internal clock is our best morning alarm clock, since it shuts off melatonin production and boosts cortisol secretion and heart rate 2-3h prior awakening from Morpheus arms. The main reason most of us still use artificial alarm clocks is that we habitually carry on a sleep depth and/or the sleep-wake timing is not ideally matched with our social/work schedule. This in turn can lead hourglass processes, as indexed by accumulated homeostatic sleep need over time, to strongly oppose the clock. To add to the complexity of our sleep and wakefulness behavior, light levels as well as exogenous melatonin can impinge on the clock, by means of their so-called zeitgeber (synchronizer) role or by acutely promoting sleep or wakefulness. Here we attempt to bring a holistic view on how light, melatonin, and the brain circuitry underlying circadian and homeostatic processes can modulate sleep and in particular alertness, by actively promoting awakening/arousal and sleep at certain times during the 24-h day
Circadian and ultradian NREM-REM sleep modulation of dream recall : effects of age and spectral activity
No full textThis thesis deals with the electrophysiological correlates of sleep prior to dream recall and the age-related effects on dream processing. The dual NREM/REM sleep cycle and the circadian modulation of REM sleep sum to generate dream processing. However, little is known about the age-related effects on dream recall during both NREM and REM sleep, which comprises the first aim of this thesis. To address this question, seventeen young (20-31 years) and 15 older (57-74 years) healthy volunteers underwent continuous polysomnography recording and hormonal assessments during a 40-h multiple nap protocol (150 minutes of wakefulness and 75 minutes of sleep; 10 naps in total) under constant routine conditions. The analysis of NREM/REM sleep prior to dream recall focused on the last 15 minutes of each nap prior to dream recall. Number of dreams, dream recall and the emotional aspect of dreaming was investigated using the sleep mentation questionnaire. The results indicate that older participants had less dream recall after both NREM and REM sleep, although no differences were observed between the age-groups with respect to the emotional domain of dreaming. Interestingly, older volunteers had fewer dreams after naps scheduled during the biological day (outside the time window of melatonin secretion), which was closely associated with the circadian rhythm of REM sleep. This implies that aging can be associated to decreased amplitude in the circadian modulation of REM sleep, with repercussions on dream recall.
Since dreaming crucially relies on the ultradian NREM/REM sleep, it is very likely that differences in the spectral composition of sleep prior to dreaming may pinpoint the cortical networks associated to dream generation. Surprisingly, frequency and regional specific differences in EEG activity prior to dreaming remains both controversial and with mixed results, due to the use of different sleep recordings and dream assessments. To answer this issue, NREM/REM sleep EEG power density associated with and without dream recall was investigated in young participants. NREM sleep was associated with lower EEG power density for dream recall in frontal delta and centro-parietal sigma activity, while REM sleep was associated with low frontal alpha activity, and with high occipital alpha and beta activity. Thus, specific EEG frequency- and topography changes can modulate differences between dream recall and no recall after NREM and REM sleep awakening.
In the next logical step, we investigated how age-related changes in sleep structure can impact on dream processing, an issue that remains largely unknown. During NREM sleep prior to dream recall, older participants had higher frontal EEG delta activity and higher centro-parietal sigma activity than the young volunteers. Contrariwise, before no recall, older participants had less frontal-central delta activity and less sigma activity in frontal, central and parietal derivations than the young participants. REM sleep was associated to age-related changes, such that older participants had less frontal-central alpha and beta activity, irrespective of dream recall and no recall. Taken together, age-related differences in dream recall seem to be directly associated to specific frequency and topography EEG activity patterns, particularly during NREM sleep. Thus, aging can result in specific changes for dream processing, most likely through its effects on sleep. The results in this thesis indicate that the circadian and ultradian NREM/REM sleep modulation on dream recall can help to better understand the mechanistic framework of this complex cognitive process
Can light make us bright? : Effects of light on cognition and sleep
No full textLight elicits robust nonvisual effects on numerous physiological and behavioral variables, such as the human sleep-wake cycle and cognitive performance. Light effects crucially rely on properties such as dose, duration, timing, and wavelength. Recently, the use of methods such as fMRI to assess light effects on nonvisual brain responses has revealed how light can optimize brain function during specific cognitive tasks, especially in tasks of sustained attention. In this chapter, we address two main issues: how light impinges on cognition via consolidation of human sleep-wake cycles; and how light directly impacts on sleep and cognition, in particular in tasks of sustained attention. A thorough understanding of how light affects sleep and cognitive performance may help to improve light settings at home and at the workplace in order to improve well-being
Circadian rhythm and epilepsy
No full textAdvances in diagnostic technology, including chronic intracranial EEG recordings, have confirmed the clinical observation of different temporal patterns of epileptic activity and seizure occurrence over a 24-h period. The rhythmic patterns in epileptic activity and seizure occurrence are probably related to vigilance states and circadian variation in excitatory and inhibitory balance. Core circadian genes BMAL1 and CLOCK, which code for transcription factors, have been shown to influence excitability and seizure threshold. Despite uncertainties about the relative contribution of vigilance states versus circadian rhythmicity, including circadian factors such as seizure timing improves sensitivity of seizure prediction algorithms in individual patients. Improved prediction of seizure occurrence opens the possibility for personalised antiepileptic drug-dosing regimens timed to particular phases of the circadian cycle to improve seizure control and to reduce side-effects and risks associated with seizures. Further studies are needed to clarify the pathways through which rhythmic patterns of epileptic activity are generated, because this might also inform future treatment options
Association of Intraocular Cataract Lens Replacement With Circadian Rhythms, Cognitive Function, and Sleep in Older Adults.
No full textImportance
Cataract is associated with a progressive decline in light transmission due to the clouding and yellowing of the natural crystalline lens. While the downstream effects of aging lenses include long-term disruption of circadian rhythms, cognitive function, and sleep regulation, it remains unknown whether there is an association of intraocular cataract lens (IOLs) replacement with circadian rhythms, cognition, and sleep.
Objective
To test whether IOL replacement (blue blocking [BB] or ultraviolet [UV] only blocking) in older patients with previous cataract is associated with the beneficial light effects on the circadian system, cognition, and sleep regulation.
Design, Setting, and Participants
Cross-sectional study at the Centre for Chronobiology, University of Basel in Switzerland from February 2012 to April 2014, analyzed between June 2012 and September 2018. Sixteen healthy older controls and 13 patients with previous cataract and IOL replacement participated without medication and no medical and sleep comorbidities.
Exposures
Three and a half hours of prior light control (dim-dark adaptation), followed by 2 hours of evening blue-enriched (6500 K) or non-blue-enriched light exposure (3000 K and 2500 K), 30 minutes in dim post-light exposure, 8 hours of sleep opportunity, and 2 hours of morning dim light following sleep.
Main Outcomes and Measures
Salivary melatonin, cognitive tests, and sleep structure and electroencephalographic activity to test the association of IOLs with markers of circadian rhythmicity, cognitive performance, and sleep regulation, respectively.
Results
The participants included 16 healthy older controls with a mean (standard error of the mean [SEM]) of 63.6 (5.6) years; 8 women and 13 patients with previous cataract (mean [SEM] age, 69.9 [5.2] years; 10 women); 5 patients had UV IOLs and 8 had BB IOLs. Patients with previous cataract and IOLs had an attenuated increase in melatonin levels during light exposure (mean [SEM] increase in the BB group: 23.3% [2.6%] and in the UV lens group: 19.1% [2.1%]) than controls (mean [SEM] increase, 48.8% [5.2%]) (difference between means, 27.7; 95% CI, 15.4%-41.7%; P < .001). Cognitive function, indexed by sustained attention performance, was improved in patients with UV lens (mean [SEM], 276.9 [11.1] milliseconds) compared with patients with BB lens (mean [SEM], 348.3 [17.8] milliseconds) (difference between means, 71.4; 95% CI, 29.5%-113.1%; P = .002) during light exposure and in the morning after sleep. Patients with UV lens had increased slow-wave sleep (mean [SEM] increase, 13% [3.4%]) compared with controls (mean [SEM] increase, 5.2% [0.8%]) (percentage of total sleep time; difference between means, 7.9; 95% CI, 2.4%-13.4%; P = .02) and frontal non-rapid eye movement slow-wave activity (0.75-4.5 Hz) during the first sleep cycle (mean [SEM], 79.9 [13.6] μV2/Hz) compared with patients with BB lens (mean [SEM], 53.2 [10.7] μV2/Hz) (difference between means, 26.7; 95% CI, 9.2-48.9; P = .03).
Conclusions and Relevance
These in-laboratory empirical findings suggest that optimizing the spectral lens transmission in patients with previous cataract may minimize the adverse age-related effects on circadian rhythms, cognition, and sleep
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