Log amplitude is a linear function of log frequency in NREM sleep EEG of young and elderly normal subjects

1984 ◽  
Vol 58 (2) ◽  
pp. 158-160 ◽  
Author(s):  
I Feinberg ◽  
J.D March ◽  
T.C Floyd ◽  
G Fein ◽  
M.J Aminoff
Keyword(s):  
Linear Function ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Sleep Eeg

scholarly journals 0327 NREM Sleep EEG in Typically Developing and Drug-Naïve ADHD Adolescents: Data from a Longitudinal Study

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A124-A124
Author(s):  
T Basishvili ◽  
M Eliozishvili ◽  
T Oniani ◽  
T Tchintcharauli ◽  
I Sakhelashvili ◽  
...  
Keyword(s):  
Longitudinal Study ◽  
Nrem Sleep ◽  
Sleep Eeg ◽  
Brain Maturation ◽  
Adhd Group ◽  
Typically Developing ◽  
Eeg Activity ◽  
Theta Power ◽  
Delta Power ◽  
Drug Naïve

Abstract Introduction Structural MRI studies suggest delayed brain maturation in children with attention deficit hyperactivity disorder (ADHD). The steep adolescent decline in sleep slow wave EEG activity provides an opportunity to investigate brain electrophysiological evidence for this maturational delay. Most ADHD sleep EEG studies have been cross-sectional. Here we present data from an ongoing longitudinal study of the maturational trajectories of sleep EEG in drug-naïve ADHD and typically developing adolescents. Methods Nine children diagnosed with ADHD (combined subtype, DSM-V criteria, mean age 12.39±0.61 years), and nine typically developing controls (12.07±0.35 years) were recruited. Subjects underwent an adaptation night and all night polysomnography twice yearly at the Laboratory. Sleep EEG was analyzed using fast Fourier transform. NREM delta and theta EEG activity were compared across first two recordings. Results Group effects (ADHD vs. control) on all night delta and theta energy, and delta power were not significant (p>0.2 for all). All night theta power was lower (p=0.035) for the ADHD group, and all night NREM sleep duration trended (p=0.060) toward being lower for the ADHD group. Controlling for sleep duration differences by examining only the first 5 h of NREM sleep showed no group effect on delta power (p=0.77) and a trend toward lower theta power (p=0.057) for the ADHD group. Conclusion At age 12 to 13 years, NREM sleep delta EEG did not differ between ADHD and control subjects. Theta power, which declines at a younger age than delta, was lower in control subjects. The two recordings thus far differ only by 6 months. The entire study will provide 5 semiannual recordings and allow us to determine if the higher theta power in the ADHD group will hold and if delta power will be greater as well, and thus provide electrophysiological support for the delayed brain maturation suggested by MRI findings. Support Shota Rustaveli National Science Foundation Grant FR17_94; Subjects Recruitment Support - Mental Health Service in Tbilisi “Kamara”.

Parasomnias

2018 ◽  
Author(s):  
KyoungBin Im
Keyword(s):  
Mental Disorders ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Rem Sleep Behavior Disorder ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Related Phenomenon ◽  
Sleep Behavior ◽  
Diagnostic And Statistical Manual

Parasomnias have long been recognized as part of sleep-related disorders or diseases in the mental disorders classification system such as Diagnostic and Statistical Manual of Mental Disorders. Nevertheless, many parasomnia symptoms are considered as a transient deviation from the norm in otherwise normal subjects due to disrupted status of consciousness. Sleep states are classified as rapid eye movement (REM) sleep and non-REM (NREM) sleep; similarly, parasomnias are classified as NREM-related parasomnias and REM-related parasomnias. NREM-related parasomnias share common pathophysiology of arousal-related phenomenon out of slow-wave sleep. Although listed as REM parasomnia disorders, nightmares and sleep paralysis are still considered comorbid symptoms or signs of other sleep disorders or mental disorders. Only REM sleep behavior disorder (RBD) is considered a relatively homogenous disease entity among all parasomnia diagnoses. Although RBD is the most newly added disorder entity in parasomnias, it is the most rigorously studied parasomnia such as RBD is strongly and clearly associated with concomitant or future developing neurodegenerative disease. This review contains 1 figure, 4 tables, and 18 references. Key Words: confusional arousals, dream enactment, pseudo-RBD, REM sleep behavior disorder, sleep-related eating, sleep terror, sleepwalking

scholarly journals Vagal feedback in the entrainment of respiration to mechanical ventilation in sleeping humans

2000 ◽  
Vol 89 (2) ◽  
pp. 760-769 ◽  
Author(s):  
Peggy M. Simon ◽  
Alfred M. Habel ◽  
J. Andrew Daubenspeck ◽  
J. C. Leiter
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Rate ◽  
Eye Movement ◽  
Lung Transplant ◽  
Respiratory Activity ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
The Other ◽  
Absolute Requirement ◽  
Striking Contrast

We studied the capacity of four “normal” and six lung transplant subjects to entrain neural respiratory activity to mechanical ventilation. Two transplant subjects were studied during wakefulness and demonstrated entrainment indistinguishable from that of normal awake subjects. We studied four normal subjects and four lung transplant subjects during non-rapid eye movement (NREM) sleep. Normal subjects entrained to mechanical ventilation over a range of ventilator frequencies that were within ±3–5 breaths of the spontaneous respiratory rate of each subject. After lung transplantation, during which the vagi were cut, subjects did demonstrate entrainment during NREM sleep; however, entrainment only occurred at ventilator frequencies at or above each subject's spontaneous respiratory rate, and entrainment was less effective. We conclude that there is no absolute requirement for vagal feedback to induce entrainment in subjects, which is in striking contrast to anesthetized animals in which vagotomy uniformly abolishes entrainment. On the other hand, vagal feedback clearly enhances the fidelity of entrainment and extends the range of mechanical frequencies over which entrainment can occur.

Arousal and breathing responses to airway occlusion in healthy sleeping adults

1983 ◽  
Vol 55 (4) ◽  
pp. 1113-1119 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Total Occlusion ◽  
Airway Occlusion ◽  
Constant Bias ◽  
Bias Flow ◽  
Shallow Breathing

The arousal and breathing responses to total airway occlusion during sleep were measured in 12 normal subjects (7 males and 5 females) aged 25-36 yr. Subjects slept while breathing through a specially designed nosemask, which was glued to the nose with medical-grade silicon rubber. The lips were sealed together with a thin layer of Silastic. The nosemask was attached to a wide-bore (20 mm ID) rigid tube to allow a constant-bias flow of room air from a blower. Total airway occlusion was achieved by simultaneously inflating two rubber balloons fixed in the inspiratory and expiratory pipes. A total of 39 tests were done in stage III/IV nonrapid-eye movement (NREM) sleep in 11 subjects and 10 tests in rapid-eye-movement (REM) sleep in 5 subjects. The duration of total occlusion tolerated before arousal from NREM sleep varied widely (range 0.9-67.0 s) with a mean duration of 20.4 +/- 2.3 (SE) s. The breathing response to occlusion in NREM sleep was characterised by a breath-by-breath progressive increase in suction pressure achieved by an increase in the rate of inspiratory pressure generation during inspiration. In contrast, during REM sleep, arousal invariably occurred after a short duration of airway occlusion (mean duration 6.2 +/- 1.2 s, maximum duration 11.8 s), and the occlusion induced a rapid shallow breathing pattern. Our results indicate that total nasal occlusion during sleep causes arousal with the response during REM sleep being more predictable and with a generally shorter latency than that in NREM sleep.

628 Longitudinal Association between NREM Sleep Depth and Arousability with ADHD and Internalizing Disorders in Adolescence

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A246-A247
Author(s):  
Anna Ricci ◽  
Julio Fernandez-Mendoza ◽  
Fan He ◽  
Susan Calhoun ◽  
Magdy Younes ◽  
...  
Keyword(s):  
Behavioral Disorders ◽  
Nrem Sleep ◽  
Internalizing Disorders ◽  
Developmental Trajectory ◽  
Sleep Eeg ◽  
Behavioral Disorder ◽  
Sleep Depth ◽  
Transition To Adolescence ◽  
Psychoactive Medications

Abstract Introduction Sleep depth decreases in the transition from childhood to adolescence, even in typically developing (TD) youth. However, it remains unknown whether this developmental trajectory in NREM sleep depth differs across adolescents with psychiatric/behavioral disorders. Methods We analyzed the sleep EEG of 392 subjects aged 5–12 at baseline and 12–22 at follow-up (45.2% female, 23.2% racial/ethnic minority), of whom 246 were TD adolescents (controls), 62 were diagnosed with a psychiatric/behavioral disorder and were taking stimulant, anti-depressant, anxiolytic, sedative and/or anti-psychotic medications, and 84 were un-medicated. NREM sleep depth was measured at both time points using the odds ratio product (ORP), which provides a standardized continuous EEG measure of NREM sleep depth/arousability (higher ORP reflects lighter NREM sleep). General linear models examined mean differences between groups on the percent change in ORP between baseline and follow-up (ΔORP) while adjusting for sex, race/ethnicity, age, BMI and AHI at follow-up, and PSG system, psychiatric/behavioral disorders, psychoactive medications and ORP at baseline as well as time-to-follow-up. Results Overall, medicated (80.4%, 95%CI=66.2–94.6) and un-medicated (66.1%, 95%CI=53.0–79.1) subjects showed a higher ΔORP compared to controls (52.2%, 95%CI=40.0–64.5, p<0.01 and p<0.05, respectively) but did not differ between each other (p=0.134). Specifically, un-medicated subjects with ADHD (n=56) showed a higher ΔORP (77.3%, 95%CI=62.4–92.1) compared to controls (p<0.01), while subjects with ADHD on stimulant medication (n=36) did not differ (66.1%, 95%CI=48.9–93.2) from controls (p=0.268) or from un-medicated ADHD subjects (p=0.303). Subjects with internalizing disorders on psychoactive medications (n=29) showed a higher ΔORP (104.9%, 95%CI=82.8–127.0) compared to controls (p<0.01) and to un-medicated subjects (n=27) with internalizing disorders (60.1%, 95%CI=36.8–83.3, p<0.01), who did not differ from controls (p=0.772). Conclusion The greater increase in ORP in the transition to adolescence in un-medicated youth with ADHD suggests that decreased NREM sleep depth may be a biomarker of the disorder. In contrast, the greater increase in ORP in medicated youth with internalizing disorders suggests that psychoactive medications impact NREM sleep depth in these children as they transition to adolescence. These data have important implications for sleep EEG studies that include medicated and un-medicated youth with comorbid psychiatric disorders. Support (if any) NIH Awards Number R01MH118308, R01HL136587, R01HL97165, R01HL63772, UL1TR000127

Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation

1983 ◽  
Vol 55 (3) ◽  
pp. 813-822 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Periodic Breathing ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Positive Pressure ◽  
Sleep State ◽  
Co2 Partial Pressure ◽  
Apnea Duration ◽  
O2 Concentration ◽  
End Tidal ◽  
End Tidal Co2

The effect of sleep state on ventilatory rhythmicity following graded hypocapnia was determined in two normal subjects and one patient with a chronic tracheostomy. Passive positive-pressure hyperventilation (PHV) was performed for 3 min awake and during nonrapid-eye-movement (NREM) sleep with hyperoxia [fractional inspired O2 concentration (FIO2) = 0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no immediate posthyperventilation apnea was noted following abrupt cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep levels and 1-2 Torr below the waking level. In hypoxia, PETCO2 increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr below NREM sleep levels and 1-2 Torr above awake levels. Apnea duration (5-45 s) was significantly correlated to the magnitude of hypocapnia (range 27-41 Torr). PHV caused no apnea when isocapnia was maintained via increased inspired CO2. Prolonged hypoxia caused periodic breathing, and the abrupt transition from short-term hypoxic-induced hyperventilation to acute hyperoxia caused apnea during NREM sleep when PETCO2 was lowered to or below the subject's apneic threshold as predetermined (passively) by PHV. We concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].

scholarly journals Differential modulation of NREM sleep regulation and EEG topography by chronic sleep restriction in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bowon Kim ◽  
Eunjin Hwang ◽  
Robert E. Strecker ◽  
Jee Hyun Choi ◽  
Youngsoo Kim
Keyword(s):  
Nrem Sleep ◽  
Brain Regions ◽  
Sleep Eeg ◽  
Sleep Restriction ◽  
Electrode Arrays ◽  
Sleep Regulation ◽  
Amplitude Analysis ◽  
Delta Power ◽  
Eeg Topography ◽  
Chronic Sleep

AbstractCompensatory elevation in NREM sleep EEG delta power has been typically observed following prolonged wakefulness and widely used as a sleep homeostasis indicator. However, recent evidence in human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta power is not progressively increased despite of accumulated sleep loss over days. In addition, there has been little progress in understanding how sleep EEG in different brain regions responds to CSR. Using novel high-density EEG electrode arrays in the mouse model of CSR where mice underwent 18-h sleep deprivation per day for 5 consecutive days, we performed an extensive analysis of topographical NREM sleep EEG responses to the CSR condition, including period-amplitude analysis of individual slow waves. As previously reported in our analysis of REM sleep responses, we found different patterns of changes: (i) progressive decrease in NREM sleep duration and consolidation, (ii) persistent enhancement in NREM delta power especially in the frontal and parietal regions, and (iii) progressive increases in individual slow wave slope and frontal fast oscillation power. These results suggest that multiple sleep-wake regulatory systems exist in a brain region-specific manner, which can be modulated independently, especially in the CSR condition.

Determinants of poststimulus potentiation in humans during NREM sleep

1992 ◽  
Vol 73 (5) ◽  
pp. 1958-1971 ◽  
Author(s):  
M. S. Badr ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Control Period ◽  
Periodic Breathing ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Central Apnea ◽  
Inhibitory Effects ◽  
Arterial Pco2 ◽  
End Tidal ◽  
Sustained Hypoxia

To test whether active hyperventilation activates the “afterdischarge” mechanism during non-rapid-eye-movement (NREM) sleep, we investigated the effect of abrupt termination of active hypoxia-induced hyperventilation in normal subjects during NREM sleep. Hypoxia was induced for 15 s, 30 s, 1 min, and 5 min. The last two durations were studied under both isocapnic and hypocapnic conditions. Hypoxia was abruptly terminated with 100% inspiratory O2 fraction. Several room air-to-hyperoxia transitions were performed to establish a control period for hyperoxia after hypoxia transitions. Transient hyperoxia alone was associated with decreased expired ventilation (VE) to 90 +/- 7% of room air. Hyperoxic termination of 1 min of isocapnic hypoxia [end-tidal PO2 (PETO2) 63 +/- 3 Torr] was associated with VE persistently above the hyperoxic control for four to six breaths. In contrast, termination of 30 s or 1 min of hypocapnic hypoxia [PETO2 49 +/- 3 and 48 +/- 2 Torr, respectively; end-tidal PCO2 (PETCO2) decreased by 2.5 or 3.8 Torr, respectively] resulted in hypoventilation for 45 s and prolongation of expiratory duration (TE) for 18 s. Termination of 5 min of isocapnic hypoxia (PETO2 63 +/- 3 Torr) was associated with central apnea (longest TE 200% of room air); VE remained below the hyperoxic control for 49 s. Termination of 5 min of hypocapnic hypoxia (PETO2 64 +/- 4 Torr, PETCO2 decreased by 2.6 Torr) was also associated with central apnea (longest TE 500% of room air). VE remained below the hyperoxic control for 88 s. We conclude that 1) poststimulus hyperpnea occurs in NREM sleep as long as hypoxia is brief and arterial PCO2 is maintained, suggesting the activation of the afterdischarge mechanism; 2) transient hypocapnia overrides the potentiating effects of afterdischarge, resulting in hypoventilation; and 3) sustained hypoxia abolishes the potentiating effects of after-discharge, resulting in central apnea. These data suggest that the inhibitory effects of sustained hypoxia and hypocapnia may interact to cause periodic breathing.

Hypercapnic cerebral vascular reactivity is decreased, in humans, during sleep compared with wakefulness

2003 ◽  
Vol 94 (6) ◽  
pp. 2197-2202 ◽  
Author(s):  
Guy E. Meadows ◽  
Helen M. A. Dunroy ◽  
Mary J. Morrell ◽  
Douglas R. Corfield
Keyword(s):  
Blood Flow ◽  
Vascular Reactivity ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Stage Iii ◽  
Left Middle Cerebral Artery ◽  
Cortical Blood Flow ◽  
Pulsed Doppler Ultrasound ◽  
End Tidal ◽  
Cerebral Vascular

During wakefulness, increases in the partial pressure of arterial CO2 result in marked rises in cortical blood flow. However, during stage III–IV, non-rapid eye movement (NREM) sleep, and despite a relative state of hypercapnia, cortical blood flow is reduced compared with wakefulness. In the present study, we tested the hypothesis that, in normal subjects, hypercapnic cerebral vascular reactivity is decreased during stage III–IV NREM sleep compared with wakefulness. A 2-MHz pulsed Doppler ultrasound system was used to measure the left middle cerebral artery velocity (MCAV; cm/s) in 12 healthy individuals while awake and during stage III–IV NREM sleep. The end-tidal Pco 2(Pet CO2 ) was elevated during the awake and sleep states by regulating the inspired CO2 load. The cerebral vascular reactivity to CO2 was calculated from the relationship between Pet CO2 and MCAV by using linear regression. From wakefulness to sleep, the Pet CO2 increased by 3.4 Torr ( P < 0.001) and the MCAV fell by 11.7% ( P < 0.001). A marked decrease in cerebral vascular reactivity was noted in all subjects, with an average fall of 70.1% ( P = 0.001). This decrease in hypercapnic cerebral vascular reactivity may, at least in part, explain the stage III–IV NREM sleep-related reduction in cortical blood flow.

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