Time course of EEG power density during long sleep in humans

1990 ◽  
Vol 258 (3) ◽  
pp. R650-R661 ◽  
Author(s):  
D. J. Dijk ◽  
D. P. Brunner ◽  
A. A. Borbely
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Electroencephalogram Eeg

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

Correlation between ventilation and brain blood flow during hypoxic sleep

1986 ◽  
Vol 60 (1) ◽  
pp. 295-298 ◽  
Author(s):  
T. V. Santiago ◽  
J. A. Neubauer ◽  
N. H. Edelman
Keyword(s):  
Blood Flow ◽  
Tidal Volume ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Maxillary Artery ◽  
Brain Blood Flow ◽  
Ventilatory Depression

Ventilation and brain blood flow (BBF) were simultaneously measured during carbon monoxide (CO) inhalation in awake and sleeping goats up to HbCO levels of 40%. Unilateral BBF, which was continuously measured with an electromagnetic flow probe placed around the internal maxillary artery, progressively increased with CO inhalation in the awake and both sleep stages. The increase in BBF with CO inhalation during rapid-eye-movement (REM) sleep (delta BBF/delta arterial O2 saturation = 1.34 +/- 0.27 ml X min-1 X %-1) was significantly greater than that manifested during wakefulness (0.87 +/- 0.14) or slow-wave sleep (0.92 +/- 0.13). Ventilation was depressed by CO inhalation during both sleep stages but was unchanged from base-line values in awake goats. In contrast to slow-wave (non-REM) sleep, the ventilatory depression of REM sleep was primarily due to a reduction in tidal volume. Since tidal volume is more closely linked to central chemoreceptor function, we believe that these data suggest a possible role of the increased cerebral perfusion during hypoxic REM sleep. Induction of relative tissue alkalosis at the vicinity of the medullary chemoreceptor may contribute to the ventilatory depression exhibited during this sleep period.

scholarly journals Blockade of endogenous growth hormone-releasing hormone receptors dissociates nocturnal growth hormone secretion and slow-wave sleep

2004 ◽  
pp. 561-566 ◽  
Author(s):  
SK Jessup ◽  
BA Malow ◽  
KV Symons ◽  
AL Barkan
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Hormone Receptors ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Nrem Sleep ◽  
Temporal Association ◽  
Sleep Stages ◽  
Sleep Study

OBJECTIVES: A temporal association between non-rapid eye movement (NREM) sleep stages 3 and 4 and nocturnal augmentation of GH release was found long ago, yet the precise mechanism for this association has not been identified. It has been shown, however that pulsatile GHRH administration increases both slow-wave sleep (SWS) and GH. Based on these data, a role for GHRH as an inducer of SWS was proposed. To test this hypothesis, we have performed the corollary experiment whereby the action of endogenous GHRH has been antagonized. DESIGN: Healthy men (20-33 years old) had an infusion of GHRH antagonist ((N-Ac-Tyr(1), D-Arg(2)) GHRH-29 (NH(2))) or saline for a 12-h period, between 2100 and 0900 h. An i.v. bolus of GHRH was given at 0700 h and GH samples were drawn from 0700 to 0900 h to document the efficacy of GH suppression by the GHRH antagonist. METHODS: A limited montage sleep study was recorded from 2300 to 0700 h during each admission. Plasma GH concentrations were analyzed by the use of a sensitive chemiluminometric assay. RESULTS: Effectiveness of the GHRH antagonist was validated in all subjects by demonstrating 93+/-1.8% (P=0.012) suppression of GH response to a GHRH bolus. Polysomnography demonstrated that the percentage of SWS was not different when saline and GHRH antagonist nights were compared (P=0.607); other quantifiable sleep parameters were also unchanged. CONCLUSIONS: We conclude that endogenous GHRH is indispensable for the nocturnal augmentation of GH secretion, but that it is unlikely to participate in the genesis of SWS.

Application of automated REM and slow wave sleep analysis: II. Testing the assumptions of the two-process model of sleep regulation in normal and depressed subjects

1984 ◽  
Vol 13 (4) ◽  
pp. 335-343 ◽  
Author(s):  
David J. Kupfer ◽  
Richard F. Ulrich ◽  
Patricia A. Coble ◽  
David B. Jarrett ◽  
Victoria Grochocinski ◽  
...  
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Slow Wave Sleep ◽  
Sleep Regulation ◽  
Sleep Analysis

scholarly journals Strong Coincidence Between Slow Wave Sleep and Low AHI is Explainable by the High Instability of Slow Wave Sleep to Obstructive Apnea Exposure

2019 ◽  
pp. 857-865
Author(s):  
I. PEREGRIM ◽  
S. GREŠOVÁ ◽  
J. ŠTIMMELOVÁ ◽  
I. BAČOVÁ ◽  
B. FULTON ◽  
...  
Keyword(s):  
Slow Wave ◽  
Supine Position ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Lateral Position ◽  
Sleep Stages ◽  
Upper Airways ◽  
Obstructive Apnea ◽  
Obstructive Sleep ◽  
High Instability

It is well known that in patients with obstructive sleep apnea syndrome (OSAS) the apnea-hypopnea index (AHI) is significantly decreased during slow wave sleep (SWS). It used to be explained by the ability of SWS to stabilize the upper airways against collapse. Another explanation, which is the focus of the current study, is that it is just a result of high instability of SWS to obstructive apnea exposure, i.e. high susceptibility of SWS to transition into lighter sleep stages during exposure to obstructive apneas. A retrospective chart review was performed on 560 males who underwent an overnight polysomnography. Two hundred and eighty-seven patients were eligible for the study. They were divided into 3 groups according to different AHI level. All three groups had a higher SWS occurrence in the lateral position than in the supine position. A special fourth group of patients was created with severe OSAS in the supine position but with very mild OSAS in the lateral position. This group had, in the lateral position, (A) higher AHI in NREM sleep (4.1±3.1/h vs. 0.7±1.2/h, p<0.001) as well as (B) higher SWS occurrence (27.7±15.0 % vs. 21.4±16.2 % of NREM sleep, p<0.05), than the group with the lowest AHI in the study, i.e. AHI<5/h in NREM sleep. These data suggest that strong coincidence between SWS and low AHI is the result of the high instability of SWS to obstructive apnea exposure. The data also support the presence of SWS-rebound in OSAS patients in the lateral body position.

129 Greater NREM Sleep Rebound in Response to Experimental Sleep Disturbance Associated with Higher Inflammatory Resolution in Humans

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A52-A53
Author(s):  
Larissa Engert ◽  
Marc Dubourdeau ◽  
Rammy Dang ◽  
Janet Mullington ◽  
Monika Haack
Keyword(s):  
Sleep Disturbance ◽  
Slow Wave ◽  
Rem Sleep ◽  
Sleep Disturbances ◽  
Slow Wave Sleep ◽  
Sleep Onset ◽  
Nrem Sleep ◽  
Low Grade ◽  
German Research Foundation ◽  
Recovery Sleep

Abstract Introduction Sleep disturbances deteriorate immune function by not only affecting pro-inflammatory pathways, but also inflammatory resolution pathways, which actively terminate inflammation. It is assumed that slow wave sleep (SWS) amount and slow wave activity (SWA) convey the immune-supportive functions of sleep. We investigated whether changes in SWS induced by experimental sleep disturbance followed by recovery sleep predict changes in inflammatory resolution mediators. Methods The randomized controlled within-subjects trial (N=24, 20-42 years, 12 women) consisted of two 19-day in-hospital protocols (experimental sleep disturbance/control). After three nights of baseline sleep (8h/night), participants in the experimental sleep disturbance condition were exposed to three cycles of three nights of disturbed sleep (delayed sleep-onset, hourly sleep disruption, advanced sleep-offset) followed by one night of 8h-recovery sleep. The protocol ended with three nights of recovery sleep. In the control condition, participants had uninterrupted sleep (8h/night). Sleep (PSG) and resolvin lipid mediators in plasma (1100h, LC-MS/MS) were assessed at baseline, during the last cycle of sleep disturbance, and during/after the first and third night of final recovery sleep. Data were analyzed using generalized linear mixed models and Pearson/Spearman correlations. Results As expected, SWS amount decreased during experimental sleep disturbance and increased during the first recovery sleep night (p&lt;.001). Similarly, resolvin (Rv) D2 and RvD3 decreased during sleep disturbance and RvD2 increased with subsequent recovery sleep (p&lt;.001). The SWS response did not correlate with the resolvin response to sleep disturbance or to recovery sleep. However, the NREM sleep response correlated with the resolvin response during the third recovery sleep night, i.e., a greater NREM response was associated with a greater RvD2 and RvD3 response (r=.68, p=.002; r=.58, p=.012). In contrast, a greater REM sleep response was associated with a lower resolvin response (r=−.63, p=.005; r=−.66, p=.003). Conclusion These data suggest that during recovery from sleep disturbance, NREM rather than REM sleep promotes inflammatory resolution, thereby acting as the sleep state that protects against low-grade systemic inflammation, which has been frequently observed as a consequence of sleep disturbances. Analysis whether SWA is related to inflammatory resolution is in progress. Support (if any) NIH/NINDS R01-NS091177; NIH/NCRR UL1-RR02758, M01-RR01032; German Research Foundation (DFG) EN1291/1-1.

Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽  
2021 ◽  
Author(s):  
Jelena Skorucak ◽  
Nathan Weber ◽  
Mary A Carskadon ◽  
Chelsea Reynolds ◽  
Scott Coussens ◽  
...  
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Animal Studies ◽  
Sleep Restriction ◽  
Sleep Regulation ◽  
Homeostatic Process ◽  
Sleep Homeostasis ◽  
High Prevalence ◽  
Homeostatic Response ◽  
Chronic Sleep

Abstract The high prevalence of chronic sleep restriction in adolescents underscores the importance of understanding how adolescent sleep is regulated under such conditions. One component of sleep regulation is a homeostatic process: if sleep is restricted, then sleep intensity increases. Our knowledge of this process is primarily informed by total sleep deprivation studies and has been incorporated in mathematical models of human sleep regulation. Several animal studies, however, suggest that adaptation occurs in chronic sleep restriction conditions, showing an attenuated or even decreased homeostatic response. We investigated the homeostatic response of adolescents to different sleep opportunities. Thirty-four participants were allocated to one of three groups with 5, 7.5 or 10 h of sleep opportunity per night for 5 nights. Each group underwent a protocol of 9 nights designed to mimic a school week between 2 weekends: 2 baseline nights (10 h sleep opportunity), 5 condition nights (5, 7.5 or 10 h), and two recovery nights (10 h). Measures of sleep homeostasis (slow-wave activity and slow-wave energy) were calculated from frontal and central EEG derivations and compared to predictions derived from simulations of the homeostatic process of the two-process model of sleep regulation. Only minor differences were found between empirical data and model predictions, indicating that sleep homeostasis is preserved under chronic sleep restriction in adolescents. These findings improve our understanding of effects of repetitive short sleep in adolescents.

scholarly journals Autonomic Modulation During Baseline and Recovery Sleep in Adult Sleepwalkers

2021 ◽  
Vol 12 ◽  
Author(s):  
Geneviève Scavone ◽  
Andrée-Ann Baril ◽  
Jacques Montplaisir ◽  
Julie Carrier ◽  
Alex Desautels ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Low Frequency ◽  
Medium Effect ◽  
Sleep Cycle ◽  
Autonomic Modulation ◽  
Decomposition Group ◽  
Recovery Sleep

Sleepwalking has been conceptualized as deregulation between slow-wave sleep and arousal, with its occurrence in predisposed patients increasing following sleep deprivation. Recent evidence showed autonomic changes before arousals and somnambulistic episodes, suggesting that autonomic dysfunctions may contribute to the pathophysiology of sleepwalking. We investigated cardiac autonomic modulation during slow-wave sleep in sleepwalkers and controls during normal and recovery sleep following sleep deprivation. Fourteen adult sleepwalkers (5M; 28.1 ± 5.8 years) and 14 sex- and age-matched normal controls were evaluated by video-polysomnography for one baseline night and during recovery sleep following 25 h of sleep deprivation. Autonomic modulation was investigated with heart rate variability during participants' slow-wave sleep in their first and second sleep cycles. 5-min electrocardiographic segments from slow-wave sleep were analyzed to investigate low-frequency (LF) and high-frequency (HF) components of heart rate spectral decomposition. Group (sleepwalkers, controls) X condition (baseline, recovery) ANOVAs were performed to compare LF and HF in absolute and normalized units (nLF and nHF), and LF/HF ratio. When compared to controls, sleepwalkers' recovery slow-wave sleep showed lower LF/HF ratio and higher nHF during the first sleep cycle. In fact, compared to baseline recordings, sleepwalkers, but not controls, showed a significant decrease in nLF and LF/HF ratio as well as increased nHF during recovery slow-wave sleep during the first cycle. Although non-significant, similar findings with medium effect sizes were observed for absolute values (LF, HF). Patterns of autonomic modulation during sleepwalkers' recovery slow-wave sleep suggest parasympathetic dominance as compared to baseline sleep values and to controls. This parasympathetic predominance may be a marker of abnormal neural mechanisms underlying, or interfere with, the arousal processes and contribute to the pathophysiology of sleepwalking.

nCPAP Treatment of Obstructive Sleep Apnea Increases Slow Wave Sleep in Prefrontal EEG

2007 ◽  
Vol 38 (3) ◽  
pp. 148-154 ◽  
Author(s):  
Veera Eskelinen ◽  
Toomas Uibu ◽  
Sari-Leena Himanen
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Treatment Period ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Sleep Eeg ◽  
Sleep Stages ◽  
Obstructive Sleep ◽  
Sleep Stage Scoring

According to standard sleep stage scoring, sleep EEG is studied from the central area of parietal lobes. However, slow wave sleep (SWS) has been found to be more powerful in frontal areas in healthy subjects. Obstructive sleep apnea syndrome (OSAS) patients often suffer from functional disturbances in prefrontal lobes. We studied the effects of nasal Continuous Positive Airway Pressure (nCPAP) treatment on sleep EEG, and especially on SWS, in left prefrontal and central locations in 12 mild to moderate OSAS patients. Sleep EEG was recorded by polysomnography before treatment and after a 3 month nCPAP treatment period. Recordings were classified into sleep stages. No difference was found in SWS by central sleep stage scoring after the nCPAP treatment period, but in the prefrontal lobe all night S3 sleep stage increased during treatment. Furthermore, prefrontal SWS increased in the second and decreased in the fourth NREM period. There was more SWS in prefrontal areas both before and after nCPAP treatment, and SWS increased significantly more in prefrontal than central areas during treatment. Regarding only central sleep stage scoring, nCPAP treatment did not increase SWS significantly. Frontopolar recording of sleep EEG is useful in addition to central recordings in order to better evaluate the results of nCPAP treatment.

scholarly journals Bidirectional Interaction of Hippocampal Ripples and Cortical Slow Waves Leads to Coordinated Spiking Activity During NREM Sleep

2020 ◽  
Vol 31 (1) ◽  
pp. 324-340
Author(s):  
Pavel Sanda ◽  
Paola Malerba ◽  
Xi Jiang ◽  
Giri P Krishnan ◽  
Jorge Gonzalez-Martinez ◽  
...  
Keyword(s):  
Slow Wave ◽  
Memory Consolidation ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Slow Waves ◽  
Slow Oscillation ◽  
Cortical Input ◽  
Sharp Wave ◽  
Up States ◽  
Intracranial Recordings

Abstract The dialogue between cortex and hippocampus is known to be crucial for sleep-dependent memory consolidation. During slow wave sleep, memory replay depends on slow oscillation (SO) and spindles in the (neo)cortex and sharp wave-ripples (SWRs) in the hippocampus. The mechanisms underlying interaction of these rhythms are poorly understood. We examined the interaction between cortical SO and hippocampal SWRs in a model of the hippocampo–cortico–thalamic network and compared the results with human intracranial recordings during sleep. We observed that ripple occurrence peaked following the onset of an Up-state of SO and that cortical input to hippocampus was crucial to maintain this relationship. A small fraction of ripples occurred during the Down-state and controlled initiation of the next Up-state. We observed that the effect of ripple depends on its precise timing, which supports the idea that ripples occurring at different phases of SO might serve different functions, particularly in the context of encoding the new and reactivation of the old memories during memory consolidation. The study revealed complex bidirectional interaction of SWRs and SO in which early hippocampal ripples influence transitions to Up-state, while cortical Up-states control occurrence of the later ripples, which in turn influence transition to Down-state.

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