Interhemispheric asymmetry during NREM sleep in the dog

Functional hemispheric asymmetry was evidenced in many species during sleep. Dogs seem to show hemispheric asymmetry during wakefulness; however, their asymmetric neural activity during sleep was not yet explored. The present study investigated interhemispheric asymmetry in family dogs using non-invasive polysomnography. EEG recordings during 3-h-long afternoon naps were carried out (N = 19) on two occasions at the same location. Hemispheric asymmetry was assessed during NREM sleep, using bilateral EEG channels. To include periods with high homeostatic sleep pressure and to reduce the variance of the time spent in NREM sleep between dogs, the first two sleep cycles were analysed. Left hemispheric predominance of slow frequency range was detected in the first sleep cycle of sleep recording 1, compared to the baseline level of zero asymmetry as well as to the first sleep cycle of sleep recording 2. Regarding the strength of hemispheric asymmetry, we found greater absolute hemispheric asymmetry in the second sleep cycle of sleep recording 1 and 2 in the frequency ranges of alpha, sigma and beta, compared to the first sleep cycle. Differences between sleep recordings and consecutive sleep cycles might be indicative of adaptation-like processes, but do not closely resemble the results described in humans.

Relationships between cortical, cardiac, and arousal-motor activities in the genesis of rhythmic masticatory muscle activity across sleep cycles in primary sleep bruxism children

Study Objectives The present study aimed to clarify the physiological relationships between rhythmic masticatory muscle activity (RMMA) and cyclic changes in cortical, autonomic, and arousal-motor activities during sleep in sleep bruxism (SB) children. Methods Polysomnographic recordings were performed on fifteen SB children (9 boys, 6 girls, 10.3 ± 2.5 years) and eighteen control children (5 boys, 13 girls, 10.7 ± 3.1 years) free from sleep and developmental disorders. Sleep and RMMA were scored by the standard rules. Sleep cycle was divided into NREM and REM sleep segments and the frequency of RMMA, transient arousal and movement, and cortical and cardiac activities were then quantitatively analyzed in relation to sleep cycles. Results Neither sleep architecture nor sleep stage distribution of RMMA significantly differed between two groups. In sleep cycles, SB children showed more frequent RMMA in all segments than controls, while cyclic changes in cortical and autonomic activities did not significantly differ between two groups. In SB children, RMMA was the most frequent in the last NREM segment before REM sleep and was associated with increases in cortical beta activity and arousal; more than 70% of RMMA time-dependently occurred with cortical and motor arousals. Conclusions This is the first study to suggest that the potentiation of RMMA occurrence was associated with transient arousal under cyclic sleep processes in primary SB children.

Discrepancies in the Time Course of Sleep Stage Dynamics, Electroencephalographic Activity and Heart Rate Variability Over Sleep Cycles in the Adaptation Night in Healthy Young Adults

ObjectiveThe aim of the present study was to characterize the cyclic sleep processes of sleep-stage dynamics, cortical activity, and heart rate variability during sleep in the adaptation night in healthy young adults.MethodsSeventy-four healthy adults participated in polysomnographic recordings on two consecutive nights. Conventional sleep variables were assessed according to standard criteria. Sleep-stage continuity and dynamics were evaluated by sleep runs and transitions, respectively. These variables were compared between the two nights. Electroencephalographic and cardiac activities were subjected to frequency domain analyses. Cycle-by-cycle analysis was performed for the above variables in 34 subjects with four sleep cycles and compared between the two nights.ResultsConventional sleep variables reflected lower sleep quality in the adaptation night than in the experimental night. Bouts of stage N1 and stage N2 were shorter, and bouts of stage Wake were longer in the adaptation night than in the experimental night, but there was no difference in stage N3 or stage REM. The normalized transition probability from stage N2 to stage N1 was higher and that from stage N2 to N3 was lower in the adaptation night, whereas that from stage N3 to other stages did not differ between the nights. Cycle-by-cycle analysis revealed that sleep-stage distribution and cortical beta EEG power differed between the two nights in the first sleep cycle. However, the HF amplitude of the heart rate variability was lower over the four sleep cycles in the adaptation night than in the experimental night.ConclusionThe results suggest the distinct vulnerability of the autonomic adaptation processes within the central nervous system in young healthy subjects while sleeping in a sleep laboratory for the first time.

Through the Open Window: How Does the Brain Talk to the Body?

The brain controls the activities of the body, including food digestion, drinking, sleep cycles, temperature, blood pressure, and more. These functions are essential to keep the body in homeostasis, which is the state of being steady and balanced. To control homeostasis, the brain talks to the body with the help of chemical messengers called hormones. Hormones travel through the blood stream from the brain to the body and back. However, in order to protect the delicate brain cells from unwanted intrusions, the blood vessels of the brain are tightly sealed, preventing the passage of most molecules. How, then, does the brain bypass this barrier to communicate with the body? The answer is that, in certain parts of the brain, the blood vessels contain special window-like openings that allow passage of hormones. Scientists are investigating why and how some blood vessels open their windows while others remain sealed.

‘SleepCycles’ package for R - A free software tool for the detection of sleep cycles from sleep staging

The detection of sleep cycles in human sleep data (i.e. polysomnographically assessed sleep stages) enables fine-grained analyses of ultradian variations in sleep microstructure (e.g. sleep spindles, and arousals), or other amplitude- and frequency-specific electroencephalographic features during sleep. While many laboratories have software that is used internally, reproducibility requires the availability of open source software. Therefore, we here introduce the ‘SleepCycles’ package for R, an open-source software package that identifies sleep cycles and their respective (non-) rapid eye movement ([N]REM) periods from sleep staging data. Additionally, each (N)REM period is subdivided into parts of equal duration, which may be useful for further fine-grained analyses. The detection criteria are, with some adaptations, largely based on criteria originally proposed by Feinberg and Floyd (1979). The latest version of the package can be downloaded from the Comprehensive R Archives Network (CRAN).•The package ‘SleepCycles’ for R allows to identify sleep cycles and their respective NREM and REM from sleep staging results.•Besides the cycle detection, NREM and REM are also split into parts of equal duration (percentiles) thereby allowing for a better temporal resolution across the night and temporal alignment of sleep cycles with different durations among different night recordings.

Wake-sleep cycles are severely disrupted by diseases affecting cytoplasmic homeostasis

The circadian clock is based on a transcriptional feedback loop with an essential time delay before feedback inhibition. Previous work has shown that PERIOD (PER) proteins generate circadian time cues through rhythmic nuclear accumulation of the inhibitor complex and subsequent interaction with the activator complex in the feedback loop. Although this temporal manifestation of the feedback inhibition is the direct consequence of PER’s cytoplasmic trafficking before nuclear entry, how this spatial regulation of the pacemaker affects circadian timing has been largely unexplored. Here we show that circadian rhythms, including wake-sleep cycles, are lengthened and severely unstable if the cytoplasmic trafficking of PER is disrupted by any disease condition that leads to increased congestion in the cytoplasm. Furthermore, we found that the time delay and robustness in the circadian clock are seamlessly generated by delayed and collective phosphorylation of PER molecules, followed by synchronous nuclear entry. These results provide clear mechanistic insight into why circadian and sleep disorders arise in such clinical conditions as metabolic and neurodegenerative diseases and aging, in which the cytoplasm is congested.

1133 The Recovery of Sleep Oscillations in Acute to Chronic Traumatic Brain Injury

Introduction Slow waves and spindles are essential oscillations occurring during NREM sleep that may be disrupted by moderate to severe traumatic brain injury (TBI). We investigated these oscillations in the acute and chronic trauma stage. Methods Four groups were tested with whole-night polysomnography: hospitalized patients with acute TBI (n=10, 29.7±13.8y) or severe orthopedic injuries (n=15, 39.9±17.1y), chronic TBI including 9 returning from the acute TBI group (n=43, 31.9±13.5y), and healthy controls (n=36, 30.5±12.7y). Characteristics for slow waves (density, amplitude, slope, frequency, duration) and spindles (density, amplitude, frequency, duration) were quantified over N2 and N3 sleep for the first three sleep cycles, and groups were compared using one-way ANOVAs. Results One-way ANOVAs showed group effects only for slow wave density (F=4.11 to 6.04, p=0.009 to 0.0008)) and spindle density (F=3.3 to 8.8, p=0.02 to 0.00003). These effects were present for the 2nd and 3rd sleep cycles, but not the 1st. More specifically, slow wave density in acute TBI was higher than in controls, and returned to normal levels in the chronic stage. Conversely, spindle density in acute TBI was lower than in controls and returned to normal levels in the chronic stage. No group difference was observed for the orthopedic group. Conclusion Our results suggest that immediately after a severely disruptive event such as a TBI, the brain needs additional deeper sleep to recover, resulting in more slow waves but also in less spindles. These changes are only present in the 2nd and 3rd sleep cycles, reflecting an absence of the expected dissipation of slow waves, which may suggest increased homeostatic sleep pressure due to the brain injury. Limits to interpretation include the hospital environment and medication, but the absence of changes in the orthopedic group under similar conditions emphasizes the effect of the brain injury itself. Support Canadian Institutes of Health Research (CIHR) and Fonds de Recherche Québec-Santé (FRQS)