scholarly journals Cerebral metabolic rate of oxygen during transition from wakefulness to sleep measured with high temporal resolution OxFlow MRI with concurrent EEG

2020 ◽  
pp. 0271678X2091928
Author(s):  
Alessandra Caporale ◽  
Hyunyeol Lee ◽  
Hui Lei ◽  
Hengyi Rao ◽  
Michael C Langham ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Cerebral Metabolism ◽  
Sleep Onset ◽  
High Temporal Resolution ◽  
Mean Values ◽  
Cerebral Metabolic Rate ◽  
Sleep Physiology ◽  
Concomitant Reduction

During slow-wave sleep, synaptic transmissions are reduced with a concomitant reduction in brain energy consumption. We used 3 Tesla MRI to noninvasively quantify changes in the cerebral metabolic rate of O2 (CMRO2) during wakefulness and sleep, leveraging the ‘OxFlow’ method, which provides venous O2 saturation (SvO2) along with cerebral blood flow (CBF). Twelve healthy subjects (31.3 ± 5.6 years, eight males) underwent 45–60 min of continuous scanning during wakefulness and sleep, yielding one image set every 3.4 s. Concurrent electroencephalography (EEG) data were available in eight subjects. Mean values of the metabolic parameters measured during wakefulness were stable, with coefficients of variation below 7% (average values: CMRO2 = 118 ± 12 µmol O2/min/100 g, SvO2 = 67.0 ± 3.7% HbO2, CBF = 50.6 ±4.3 ml/min/100 g). During sleep, on average, CMRO2 decreased 21% (range: 14%–32%; average nadir = 98 ± 16 µmol O2/min/100 g), while EEG slow-wave activity, expressed in terms of [Formula: see text]-power, increased commensurately. Following sleep onset, CMRO2 was found to correlate negatively with relative [Formula: see text]-power (r = −0.6 to −0.8, P < 0.005), and positively with heart rate (r = 0.5 to 0.8, P < 0.0005). The data demonstrate that OxFlow MRI can noninvasively measure dynamic changes in cerebral metabolism associated with sleep, which should open new opportunities to study sleep physiology in health and disease.

scholarly journals Excessive Fragmentary Myoclonus: Time of Night and Sleep Stage Distributions

1993 ◽  
Vol 20 (2) ◽  
pp. 142-146 ◽  
Author(s):  
Otavio Lins ◽  
Michelle Castonguay ◽  
Wayne Dunham ◽  
Sonya Nevsimalova ◽  
Roger Broughton
Keyword(s):  
Sleep Disorders ◽  
Patient Group ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Sleep Onset ◽  
Sleep Fragmentation ◽  
New Technique ◽  
A New Technique

ABSTRACT:Excessive fragmentary myoclonus during sleep consists of high amounts of brief twitch-like movements occurring asynchronously and asymmetrically in different body areas and has been reported to occur in association with a number of sleep disorders. It was analyzed using a new technique of quantification, the fragmentary myoclonus index (FMI). The FMI exhibited high rates in all stages of sleep but with a somewhat lower frequency in slow wave sleep explaining, as well, a significantly lower rate in the first hour after sleep onset compared to later hours. There was no evidence for greater sleep fragmentation or lighter sleep compared to a matched patient group in whom it had not been noted.

scholarly journals New Molecular Knowledge Towards the Trigemino-Cardiac Reflex as a Cerebral Oxygen-Conserving Reflex

2010 ◽  
Vol 10 ◽  
pp. 811-817 ◽  
Author(s):  
N. Sandu ◽  
T. Spiriev ◽  
F. Lemaitre ◽  
A. Filis ◽  
B. Schaller
Keyword(s):  
Metabolic Rate ◽  
Cerebral Metabolism ◽  
Sympathetic Neurons ◽  
Small Population ◽  
Molecular Organization ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Cerebral Metabolic Rate ◽  
External Stimuli ◽  
The Brain

The trigemino-cardiac reflex (TCR) represents the most powerful of the autonomous reflexes and is a subphenomenon in the group of the so-called “oxygen-conserving reflexes”. Within seconds after the initiation of such a reflex, there is a powerful and differentiated activation of the sympathetic system with subsequent elevation in regional cerebral blood flow (CBF), with no changes in the cerebral metabolic rate of oxygen (CMRO2) or in the cerebral metabolic rate of glucose (CMRglc). Such an increase in regional CBF without a change of CMRO2or CMRglcprovides the brain with oxygen rapidly and efficiently. Features of the reflex have been discovered during skull base surgery, mediating reflex protection projects via currently undefined pathways from the rostral ventrolateral medulla oblongata to the upper brainstem and/or thalamus, which finally engage a small population of neurons in the cortex. This cortical center appears to be dedicated to transduce a neuronal signal reflexively into cerebral vasodilatation and synchronization of electrocortical activity; a fact that seems to be unique among autonomous reflexes. Sympathetic excitation is mediated by cortical-spinal projection to spinal preganglionic sympathetic neurons, whereas bradycardia is mediated via projections to cardiovagal motor medullary neurons. The integrated reflex response serves to redistribute blood from viscera to the brain in response to a challenge to cerebral metabolism, but seems also to initiate a preconditioning mechanism. Previous studies showed a great variability in the human TCR response, in special to external stimuli and individual factors. The TCR gives, therefore, not only new insights into novel therapeutic options for a range of disorders characterized by neuronal death, but also into the cortical and molecular organization of the brain.

scholarly journals Seasonal covariation of the circadian phases of rectal temperature and slow wave sleep onset

1997 ◽  
Vol 6 (1) ◽  
pp. 19-25 ◽  
Author(s):  
HANS VAN DONGEN ◽  
GERARD KERKHOF ◽  
HEINZ‐BERND KLÖPPEL
Keyword(s):  
Slow Wave ◽  
Rectal Temperature ◽  
Slow Wave Sleep ◽  
Sleep Onset

scholarly journals Progesterone Prevents Sleep Disturbances and Modulates GH, TSH, and Melatonin Secretion in Postmenopausal Women

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1193-1193
Author(s):  
Anne Caufriez ◽  
Rachel Leproult ◽  
Mireille L'Hermite-Balériaux ◽  
Myriam Kerkhofs ◽  
Georges Copinschi
Keyword(s):  
Postmenopausal Women ◽  
Slow Wave ◽  
Sleep Disturbances ◽  
Slow Wave Sleep ◽  
Hormone Replacement ◽  
Sleep Onset ◽  
Blood Sampling ◽  
Controlled Study ◽  
Deep Sleep ◽  
Double Blind

Abstract Context: A number of neuroactive progesterone metabolites produce sedative-like effects. However, the effects of progesterone administration on sleep are not well characterized. Objective: To investigate the effects of a 3-wk progesterone administration on sleep architecture and multiple hormonal profiles. Subjects: Eight healthy postmenopausal women, 48–74 yr old, without sleep complaints or vasomotor symptoms. None was on hormone replacement therapy. They did not take any medication for ≥2 months. Design: Randomized, double-blind, placebo-controlled study. For 3 wk, subjects took daily at 2300 h a capsule of either 300 mg of progesterone or placebo. Sleep was polygraphically recorded during the last two nights, and blood samples were obtained at 15-min intervals for 24 h. Results: During the first night (no blood sampling), sleep was similar in both conditions. Under placebo, blood sampling procedure was associated with marked sleep disturbances, which were considerably reduced under progesterone treatment: mean duration of wake after sleep onset was 53% lower, slow-wave sleep duration almost 50% higher, and total slow-wave activity (reflecting duration and intensity of deep sleep) almost 45% higher under progesterone than under placebo (P ≤ 0.05). Nocturnal GH secretion was increased, and evening and nocturnal TSH levels were decreased under progesterone (P ≤ 0.05). Conclusions: Progesterone had no effect on undisturbed sleep but restored normal sleep when sleep was disturbed (while currently available hypnotics tend to inhibit deep sleep), acting as a “physiologic” regulator rather than as a hypnotic drug. Use of progesterone might provide novel therapeutic strategies for the treatment of sleep disturbances, in particular in aging where sleep is fragmented and of lower quality.

Correlations between body temperatures, metabolic rate and slow wave sleep in humans

1988 ◽  
Vol 86 (2) ◽  
pp. 230-234 ◽  
Author(s):  
R.J. Berger ◽  
J.W. Palca ◽  
J.M. Walker ◽  
N.H. Phillips
Keyword(s):  
Metabolic Rate ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Body Temperatures

Sleep-electroencephalography and the secretion of cortisol and growth hormone in normal controls

1987 ◽  
Vol 116 (1) ◽  
pp. 36-42 ◽  
Author(s):  
A. Steiger ◽  
T. Herth ◽  
F. Holsboer
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Onset ◽  
Cell Activity ◽  
Cortisol Concentration ◽  
Sleep Stages ◽  
Sleep Structure ◽  
Endocrine Activity ◽  
Normal Controls

Abstract. Sleep-electroencephalography, and the nocturnal secretion of cortisol and GH were investigated simultaneously in a sample of 25 male normal controls (27.1 ± 1.3 years) in order further to examine interaction between sleep structure and concurrent endocrine activity. Slow wave sleep activity was increased during the first part of the night, whereas cortisol concentration was low and GH output reached maximal levels. The second half of the night was characterized by a relative preponderance of REM-sleep, low GH-concentration, and an increase in cortisol. However, no distinct reciprocal interaction between cortisol and GH concentration was noted. In all subjects, a pronounced GH surge between 22.00 and 02.00 h was recorded which occurred independently of the presence of slow wave sleep. Six out of the 25 subjects showed nocturnal GH increases even before sleep onset. These data indicate that somatotropic cell activity during night is less dependent upon the sleeping state or specific conventially defined sleep stages than originally reported.

scholarly journals Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia

2011 ◽  
Vol 31 (7) ◽  
pp. 1504-1512 ◽  
Author(s):  
Varsha Jain ◽  
Michael C Langham ◽  
Thomas F Floyd ◽  
Gaurav Jain ◽  
Jeremy F Magland ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Consumption ◽  
Magnetic Resonance ◽  
Metabolic Rate ◽  
Vascular Reactivity ◽  
Cerebral Metabolism ◽  
Metabolic Effects ◽  
Cerebral Metabolic Rate ◽  
Rate Of Oxygen Consumption ◽  
End Tidal

The effect of hypercapnia on cerebral metabolic rate of oxygen consumption ( CMRO2) has been a subject of intensive investigation and debate. Most applications of hypercapnia are based on the assumption that a mild increase in partial pressure of carbon dioxide has negligible effect on cerebral metabolism. In this study, we sought to further investigate the vascular and metabolic effects of hypercapnia by simultaneously measuring global venous oxygen saturation ( Sv O2) and total cerebral blood flow ( tCBF), with a temporal resolution of 30 seconds using magnetic resonance susceptometry and phase-contrast techniques in 10 healthy awake adults. While significant increases in Sv O2 and tCBF were observed during hypercapnia ( P < 0.005), no change in CMRO2 was noted ( P > 0.05). Additionally, fractional changes in tCBF and end-tidal carbon dioxide ( R2 = 0.72, P < 0.005), as well as baseline Sv O2 and tCBF ( R2 = 0.72, P < 0.005), were found to be correlated. The data also suggested a correlation between cerebral vascular reactivity ( CVR) and baseline tCBF ( R2 = 0.44, P = 0.052). A CVR value of 6.1% ± 1.6%/mm Hg was determined using a linear-fit model. Additionally, an average undershoot of 6.7% ± 4% and 17.1% ± 7% was observed in Sv O2 and tCBF upon recovery from hypercapnia in six subjects.

scholarly journals 703 From in-lab to at-home: Measuring sleep and memory in the time of SARS-COVID-19

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A274-A275
Author(s):  
Anna Mullins ◽  
Ankit Parekh ◽  
Korey Kam ◽  
Reagan Schoenholz ◽  
Daphne Valencia ◽  
...  
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Severe Disease ◽  
Sleep Onset ◽  
Mean Difference ◽  
Older Individuals ◽  
Home Environments ◽  
Research Activities ◽  
Testing Environments ◽  
At Home

Abstract Introduction The SARS-COVID-19 pandemic restricted in-lab research activities especially in older individuals who are considered at-risk for severe disease. To continue longitudinal sleep research in this population we sought to test the feasibility of remotely conducting at-home sleep and memory research and to compare two ambulatory polysomnography (PSG) devices for ongoing home sleep testing. Methods 20 older (age=65.6±5.5 years) cognitively normal adults (65% female) who had previously undergone 2 nights in-lab sleep, memory and vigilance testing were delivered equipment for 2 nights at-home, technician-guided remote PSG set-up (1 night each for Somté [EEG: Fp1-M2, Cz-M1] and Sleep Profiler (SP) [EEG: Fp1-Fp2] devices- randomized presentation), and 6 timed trials on a 3D spatial maze navigation memory plus morning psychomotor vigilance testing (PVT). The night-to-night differences for devices and in-lab versus at-home testing environments were compared for sleep macro and EEG microarchitecture using paired Wilcoxon rank sum and t-tests where appropriate. First-night maze completion time (CT) and PVT reaction time and lapses were also compared. Results 19 people completed 2 nights at-home PSG, 18 completed PVT and 9 completed all 6 maze trials. Quality frontal EEG signals were obtained for 16 SP and 11 Somté recordings. There was no significant night to night differences (night 1–night 2) between in-lab and at-home environments for total sleep time (mean difference: in-lab= -0.27 vs at-home = 0.35 hours), wake after sleep onset (WASO) (median difference: in-lab= 3.0 vs at-home = 0.7 %WASO), or slow wave sleep (SWS) (mean difference: in-lab= -0.70 vs at-home = 2.3 %SWS). Relative frontal slow wave activity and spindle density were not significantly different between devices or environments. K-complex density (SP= 1.0 vs Somté =2.7/minNREM2, p=0.004) was significantly reduced with the SP device compared to Somté devices. There were no significant differences for maze CT and PVT measures between in-lab and at-home environments. Conclusion The night-to-night differences in sleep macroarchitecture do not appear to be influenced by environment or device however measures of EEG microstructure such as K-complexes, which are amplitude-dependent, may be underestimated with the Sleep Profiler device due to smaller EEG amplitude from a derivation with short inter-electrode distances. Support (if any) NIH (R01AG056031, R01AG056531, K24)

Effect of Night Exercise during 27-Hr. Total Sleep Deprivation on the Subsequent Sleep

1985 ◽  
Vol 60 (3) ◽  
pp. 915-924
Author(s):  
Kazuya Matsumoto ◽  
Yoshio Saito ◽  
Kouichi Furumi ◽  
Masao Abe
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Sleep Onset ◽  
Bicycle Ergometer ◽  
Night Sleep ◽  
Total Sleep Deprivation ◽  
Exercise Condition ◽  
Recovery Sleep

This study was designed to determine the effects from loading and nonloading of night physical exercise during 27-hr. total sleep deprivation on the subsequent sleep. Subjects were 6 healthy male students. They cycled on the bicycle ergometer at 50% of VO2 max for 10 min., and then rested for 20 min.; repeated this schedule 14 times during the night (00:00 to 08:00). The standard polysomnograms were recorded during day sleep after exercise and during the following recovery-night sleep. When night exercise was not imposed, the sleep recordings were made during the day sleep (day sleep after no exercise), after the 27-hr. total sleep deprivation and following recovery night sleep. Stage 3 and Stage 4 sleep latencies were significantly shortened in the exercise condition as compared with those on baseline night and the no-exercise condition. The mean amount of slow-wave sleep was in the order of baseline < no exercise < exercise, each increase being significant. Stage 2 sleep, however, significantly decreased. The rectal temperature during sleep was significantly higher in the early half of day sleep after exercise than in that without exercise. The self-rating of the sleep depth and rapidness of sleep onset were only significantly better for both conditions compared with that for baseline night. There were no significant differences on any sleep parameters between the exercise conditions after recovery sleep. Results suggest that the increase in slow-wave sleep during day sleep after night exercise may be ascribed to the effects of both the exercise and the total sleep deprivation. The results support the hypothesis that increase in slow-wave sleep was part of recovery from fatigue.

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