scholarly journals Sleep‐related hypermotor epilepsy and non‐rapid eye movement parasomnias: Differences in the periodic and aperiodic component of the electroencephalographic power spectra

2021 ◽  
Author(s):  
Sara M. Pani ◽  
Matteo Fraschini ◽  
Michela Figorilli ◽  
Ludovica Tamburrino ◽  
Raffaele Ferri ◽  
...  
1988 ◽  
Vol 255 (1) ◽  
pp. R27-R37 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely

Sleep states and power spectra of the electroencephalogram were determined for consecutive 4-s epochs during 24 h in rats that had been implanted with electrodes under deep pentobarbital anesthesia. The power spectra in non-rapid eye movement sleep (NREMS) showed marked trends: low-frequency activity (0.75-7.0 Hz) declined progressively throughout the 12-h light period (L) and remained low during most of the 12-h dark period (D); high-frequency activity (10.25-25.0 Hz) rose toward the end of L and reached a maximum at the beginning of D. Within a single NREMS episode (duration 0.5-5.0 min), slow-wave activity (0.75-4.0 Hz) increased progressively to a plateau level. The rise was approximated by a saturating exponential function: although the asymptote level of the function showed a prominent 24-h rhythm, the time constant remained relatively stable (approximately 40 s). After short interruptions of NREMS episodes, slow-wave activity rose more steeply than after long interruptions. The marked 24-h variation of maximum slow-wave activity within NREMS episodes may reflect the level of a homeostatic sleep process.


2008 ◽  
Vol 1213 ◽  
pp. 48-56 ◽  
Author(s):  
J.L. Shea ◽  
T. Mochizuki ◽  
V. Sagvaag ◽  
T. Aspevik ◽  
A.A. Bjorkum ◽  
...  

1994 ◽  
Vol 267 (4) ◽  
pp. R945-R952 ◽  
Author(s):  
R. J. Berger ◽  
N. H. Phillips

Sleep patterns and circadian rhythms of body temperature, activity, body weight, and electroencephalographic (EEG) power spectra of pigeons were compared among three photic conditions: a 12:12-h light-dark cycle (LD), followed successively by constant bright (LL) and dim light (DD) periods. LL suppressed non-rapid-eye-movement and rapid eye movement sleep and circadian rhythms of the measured variables without producing increased drowsiness or other physiological or behavioral changes. Sleep patterns after LL-DD transitions also showed no evidence of prior sleep deprivation during LL. Sleep latency after LL-DD transitions was 93 min longer than after L-D transitions in LD. Total sleep and EEG slow wave activity during the first 24 h in DD did not differ from D in LD. Free-running circadian rhythms subsequently reappeared in DD after LL.


1995 ◽  
Vol 268 (1) ◽  
pp. E107-E113 ◽  
Author(s):  
E. Friess ◽  
L. Trachsel ◽  
J. Guldner ◽  
T. Schier ◽  
A. Steiger ◽  
...  

Dehydroepi-androsterone (DHEA) exhibits various behavioral effects in mammals, at least one of which is enhancement of memory that appears to be mediated by an interaction with the gamma-aminobutyric acidA (GABAA) receptor complex. We investigated the effects of a single oral dose of DHEA (500 mg) on sleep stages, sleep stage-specific electroencephalogram (EEG) power spectra, and concurrent hormone secretion in 10 healthy young men. DHEA administration induced a significant (P < 0.05) increase in rapid eye movement (REM) sleep, whereas all other sleep variables remained unchanged compared with the placebo condition. Spectral analysis of five selected EEG bands revealed significantly (P < 0.05) enhanced EEG activity in the sigma frequency range during REM sleep in the first 2-h sleep period after DHEA administration. In contrast, the EEG power spectra of non-REM sleep were not affected, nor were the nocturnal time course curves of plasma cortisol, growth hormone, or testosterone concentration. The results suggest that DHEA administration has a mixed GABAA-agonistic/antagonistic effect, exerted either directly or through DHEA-induced changes in steroid metabolism. Because REM sleep has been implicated in memory storage, its augmentation in the present study suggests the potential clinical usefulness of DHEA in age-related dementia.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yukino Ogawa ◽  
Chika Miyoshi ◽  
Nozomu Obana ◽  
Kaho Yajima ◽  
Noriko Hotta-Hirashima ◽  
...  

Abstract Dysbiosis of the gut microbiota affects physiological processes, including brain functions, by altering the intestinal metabolism. Here we examined the effects of the gut microbiota on sleep/wake regulation. C57BL/6 male mice were treated with broad-spectrum antibiotics for 4 weeks to deplete their gut microbiota. Metabolome profiling of cecal contents in antibiotic-induced microbiota-depleted (AIMD) and control mice showed significant variations in the metabolism of amino acids and vitamins related to neurotransmission, including depletion of serotonin and vitamin B6, in the AIMD mice. Sleep analysis based on electroencephalogram and electromyogram recordings revealed that AIMD mice spent significantly less time in non-rapid eye movement sleep (NREMS) during the light phase while spending more time in NREMS and rapid eye movement sleep (REMS) during the dark phase. The number of REMS episodes seen in AIMD mice increased during both light and dark phases, and this was accompanied by frequent transitions from NREMS to REMS. In addition, the theta power density during REMS was lower in AIMD mice during the light phase compared with that in the controls. Consequently, the gut microbiota is suggested to affect the sleep/wake architecture by altering the intestinal balance of neurotransmitters.


2021 ◽  
Vol 15 ◽  
Author(s):  
Francesca M. Manzella ◽  
Bethany F. Gulvezan ◽  
Stefan Maksimovic ◽  
Nemanja Useinovic ◽  
Yogendra H. Raol ◽  
...  

General anesthetics are neurotoxic to the developing rodent and primate brains leading to neurocognitive and socio-affective impairment later in life. In addition, sleep patterns are important predictors of cognitive outcomes. Yet, little is known about how anesthetics affect sleep-wake behaviors and their corresponding oscillations. Here we examine how neonatal general anesthesia affects sleep and wake behavior and associated neuronal oscillations. We exposed male and female rat pups to either 6 h of continuous isoflurane or sham anesthesia (compressed air) at the peak of their brain development (postnatal day 7). One cohort of animals was used to examine neurotoxic insult 2 h post-anesthesia exposure. At weaning age, a second cohort of rats was implanted with cortical electroencephalogram electrodes and allowed to recover. During adolescence, we measured sleep architecture (divided into wake, non-rapid eye movement, and rapid eye movement sleep) and electroencephalogram power spectra over a 24 h period. We found that exposure to neonatal isoflurane caused extensive neurotoxicity but did not disrupt sleep architecture in adolescent rats. However, these animals had a small but significant reduction in beta oscillations, specifically in the 12–20 Hz beta 1 range, associated with wake behavior. Furthermore, beta oscillations play a critical role in cortical development, cognitive processing, and homeostatic sleep drive. We speculate that dysregulation of beta oscillations may be implicated in cognitive and socio-affective outcomes associated with neonatal anesthesia.


2006 ◽  
Vol 291 (2) ◽  
pp. R473-R480 ◽  
Author(s):  
E. Szentirmai ◽  
J. M. Krueger

Neuropeptide Y (NPY) is a well-characterized neuromodulator in the central nervous system, primarily implicated in the regulation of feeding. NPY, orexins, and ghrelin form a hypothalamic food intake regulatory circuit. Orexin and ghrelin are also implicated in sleep-wake regulation. In the present experiments, we studied the sleep-modulating effects of central administration of NPY in rats. Rats received intracerebroventricular injection of physiological saline or three different doses of NPY (0.4, 2, and 10 μg in a volume of 4 μl) at light onset. Another group of rats received bilateral microinjection of saline or 2 μg NPY in the lateral hypothalamus in a volume of 0.2 μl. Sleep-wake activity and motor activity were recorded for 23 h. Food intake after the control and treatment injections was also measured on separate days. Intracerebroventricular and lateral hypothalamic administration of NPY suppressed non-rapid-eye-movement sleep and rapid-eye-movement sleep in rats during the first hour after the injection and also induced changes in electroencephalogram delta power spectra. NPY stimulated food intake in the first hour after both routes of administration. Data are consistent with the hypothesis that NPY has a role in the integration of feeding, metabolism, and sleep regulation.


1991 ◽  
Vol 261 (1) ◽  
pp. R198-R208 ◽  
Author(s):  
P. Franken ◽  
D. J. Dijk ◽  
I. Tobler ◽  
A. A. Borbely

Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) of 10 rats were obtained during a baseline day, a 24-h sleep deprivation (SD) period, and 2 days of recovery (recoveries 1 and 2). EEG power density in waking gradually increased in most frequencies during the SD period. Non-rapid-eye-movement (NREM) sleep was enhanced on both recovery days, and rapid-eye-movement sleep was enhanced only on recovery 1. In the initial 4 h of recovery 1, EEG slow-wave activity (SWA; mean power density 0.75-4.0 Hz) in NREM sleep was elevated relative to baseline, and the number of brief awakenings (nBA) was reduced. In the dark period of recovery 1 and the light period of recovery 2, SWA was below baseline, and nBA was increased. During the entire recovery period, SWA and nBA, both expressed as deviation from baseline values, were negatively correlated. During the SD period, TCRT was above baseline, and in the initial 16 h of recovery 1 it was below baseline. Whereas TCRT was negatively correlated with NREM sleep, no significant correlation was found between TCRT and SWA within NREM sleep. It is concluded that SD causes a short-lasting intensification of sleep, as indicated by the enhanced SWA and the reduced nBA, and a long-lasting increase in sleep duration. The different time courses of SWA and TCRT suggest that variations in NREM sleep intensity are not directly related to changes in TCRT.


2020 ◽  
Vol 11 ◽  
Author(s):  
Daniela Dudysová ◽  
Karolina Janků ◽  
Michal Šmotek ◽  
Elizaveta Saifutdinova ◽  
Jana Kopřivová ◽  
...  

Serotonergic agonist psilocybin is a psychedelic with antidepressant potential. Sleep may interact with psilocybin’s antidepressant properties like other antidepressant drugs via induction of neuroplasticity. The main aim of the study was to evaluate the effect of psilocybin on sleep architecture on the night after psilocybin administration. Regarding the potential antidepressant properties, we hypothesized that psilocybin, similar to other classical antidepressants, would reduce rapid eye movement (REM) sleep and prolong REM sleep latency. Moreover, we also hypothesized that psilocybin would promote slow-wave activity (SWA) expression in the first sleep cycle, a marker of sleep-related neuroplasticity. Twenty healthy volunteers (10 women, age 28–53) underwent two drug administration sessions, psilocybin or placebo, in a randomized, double-blinded design. Changes in sleep macrostructure, SWA during the first sleep cycle, whole night EEG spectral power across frequencies in non-rapid eye movement (NREM) and REM sleep, and changes in subjective sleep measures were analyzed. The results revealed prolonged REM sleep latency after psilocybin administration and a trend toward a decrease in overall REM sleep duration. No changes in NREM sleep were observed. Psilocybin did not affect EEG power spectra in NREM or REM sleep when examined across the whole night. However, psilocybin suppressed SWA in the first sleep cycle. No evidence was found for sleep-related neuroplasticity, however, a different dosage, timing, effect on homeostatic regulation of sleep, or other mechanisms related to antidepressant effects may play a role. Overall, this study suggests that potential antidepressant properties of psilocybin might be related to changes in sleep.


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