Congenital Central Hypoventilation and Sleep State

PEDIATRICS ◽  
1980 ◽  
Vol 66 (3) ◽  
pp. 425-428
Author(s):  
Peter J. Fleming ◽  
Darlene Cade ◽  
M. Heather Bryan ◽  
A. Charles Bryan
Keyword(s):  
Metabolic Control ◽  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Rapid Eye Movement ◽  
Sleep State ◽  
Quiet Sleep ◽  
Awake State ◽  
Central Hypoventilation

Congenital central hypoventilation (Ondine's curse) is described in an infant with persistant symptoms throughout the first nine months of life. Respiratory control was most severely affected in quiet sleep, although abnormalities were present in rapid eye movement (REM) sleep and while awake. Failure of metabolic control in quiet sleep led to profound hypoventilation. Behavioral or "behavioral-like" inputs in the awake state and REM sleep increased ventilation, but not to expected normal levels. The ventilatory response to inhaled 4% CO2 was markedly depressed in all states.

Cholinergic reticular mechanisms influence state-dependent ventilatory response to hypercapnia

1991 ◽  
Vol 261 (3) ◽  
pp. R738-R746 ◽  
Author(s):  
R. Lydic ◽  
H. A. Baghdoyan ◽  
R. Wertz ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Nrem Sleep ◽  
Neural Mechanisms ◽  
Rapid Eye Movement ◽  
State Dependent ◽  
First Time

Breathing is impaired by the loss of wakefulness that accompanies sleep, certain comatose states, and anesthesia. Although state-dependent decrements in breathing and the ability to respond to hypercapnic stimuli are characteristic of most mammals, the neural mechanisms that cause state-dependent changes in respiratory control remain poorly understood. The present study examined the hypothesis that cholinergic mechanisms in the medial pontine reticular formation (mPRF) can cause state-dependent changes in breathing and in the hypercapnic ventilatory response (HCVR). Six cats were anesthetized with halothane and chronically instrumented for subsequent studies of breathing during wakefulness, non-rapid-eye-movement (NREM) sleep, rapid-eye-movement (REM) sleep, and during the REM sleep-like state caused by mPRF microinjections of carbachol or bethanechol. Minute ventilation was significantly decreased during the carbachol-induced REM sleep-like state (DCarb) compared with wakefulness. The HCVR in NREM, REM, DCarb, and after bethanechol was less than the waking HCVR. These results show for the first time that cholinoceptive regions in the mPRF can cause state-dependent reductions in normocapnic minute ventilation and in the ventilatory response to hypercapnia.

scholarly journals Time-of-day influences on respiratory sequelae following maximal electroshock-induced seizures in mice

2017 ◽  
Vol 118 (5) ◽  
pp. 2592-2600 ◽  
Author(s):  
Benton S. Purnell ◽  
Michael A. Hajek ◽  
Gordon F. Buchanan
Keyword(s):  
Eye Movement ◽  
Cause Of Death ◽  
Rem Sleep ◽  
Refractory Epilepsy ◽  
Time Of Day ◽  
Sudden Unexpected Death ◽  
Maximal Electroshock ◽  
Rapid Eye Movement ◽  
Unexpected Death ◽  
Sleep State

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in refractory epilepsy patients. Although specific mechanisms underlying SUDEP are not well understood, evidence suggests most SUDEP occurs due to seizure-induced respiratory arrest. SUDEP also tends to happen at night. Although this may be due to circumstances in which humans find themselves at night, such as being alone without supervision or sleeping prone, or to independent influences of sleep state, there are a number of reasons why the night (i.e., circadian influences) could be an independent risk factor for SUDEP. We explored this possibility. Adult male WT mice were instrumented for EEG, EMG, and EKG recording and subjected to maximal electroshock (MES) seizures during wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep during the nighttime/dark phase. These data were compared with data collected following seizures induced during the daytime/light phase. Seizures induced during the nighttime were similar in severity and duration to those induced during the daytime; however, seizures induced during the nighttime were associated with a lesser degree of respiratory dysregulation and postictal EEG suppression. Seizures induced during REM sleep during the nighttime were universally fatal, as is seen when seizures are induced during REM during the daytime. Taken together, these data implicate a role for time of day in influencing the physiological consequences of seizures that may contribute to seizure-induced death. NEW & NOTEWORTHY Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy. SUDEP frequently occurs during the night, which has been attributed to an effect of sleep. We have shown that sleep state does indeed influence survival following a seizure. That SUDEP occurs during the night could also implicate a circadian influence. In this study we found that time of day independently affects the physiological consequences of seizures.

Coronary and total peripheral resistance changes during sleep in a porcine model

1996 ◽  
Vol 270 (2) ◽  
pp. H723-H729 ◽  
Author(s):  
S. M. Zinkovska ◽  
E. K. Rodriguez ◽  
D. A. Kirby
Keyword(s):  
Heart Rate ◽  
Eye Movement ◽  
Rem Sleep ◽  
Total Peripheral Resistance ◽  
Sleep Stage ◽  
Peripheral Resistance ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Autonomic Tone ◽  
Awake State

Changes in autonomic tone in the vasculature during sleep may have important implications for silent ischemia and sudden cardiac death. Few models exist in which both cardiac output and coronary blood flow are continuously measured during natural sleep and autonomic mechanisms are assessed. Catheters were chronically implanted in the aorta to measure mean arterial pressure (MAP), and flow probes were placed on the ascending aorta and the circumflex coronary artery of 18 pigs. Electrodes determined sleep stage as either non-rapid eye movement (NREM) or rapid eye movement (REM) sleep. The MAP was 73 +/- 3 mmHg in the quiet awake state, did not change in NREM, and decreased to 64 +/- 2 mmHg in REM sleep (P < 0.05). In NREM sleep, heart rate did not change from awake state values of 136 +/- 8 beats/min but increased by 5 beats/min in REM sleep (P < 0.05). Coronary vascular resistance decreased from awake state values of 2.7 +/- 0.2 to 2.2 +/- 0.2 mmHg.ml-1.min in REM (P < 0.05); total peripheral resistance decreased from awake values of 0.061 +/- 0.004 mmHg.ml-1.min to 0.050 +/- 0.003 in REM sleep (P < 0.05). Those changes appear to have been mediated primarily by reduction of alpha-adrenergic activity. Spectral analysis of heart rate suggests that power in the high-frequency range (a presumed indicator of parasympathetic tone) was lower in REM sleep than NREM sleep.

Diaphragmatic muscle tone

1979 ◽  
Vol 47 (2) ◽  
pp. 279-284 ◽  
Author(s):  
N. Muller ◽  
G. Volgyesi ◽  
L. Becker ◽  
M. H. Bryan ◽  
A. C. Bryan
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Animal Studies ◽  
Muscle Tone ◽  
Muscle Spindles ◽  
Rapid Eye Movement ◽  
Tonic Activity ◽  
Halothane Anesthesia ◽  
Quiet Sleep ◽  
Diaphragmatic Muscle

It is generally believed that there is a scarcity of muscle spindles in the diaphragm and that there is no tonic activity at end expiration. This conclusion is based mainly on animal studies and the difficulty in differentiating tonic electromyogram activity from noise. We have, however, found a number of muscle spindles in the newborn human diagphragm, concentrated in the region of the central tendon. We also tried to detect tonic activity by decreasing it (by rapid-eye movement (REM) sleep or anesthesia) or increasing it (with abdominal loading). During REM sleep in five infants and five adults, using subcostal electrodes were observed a marked fall in tonic activity (P less than 0.001) compared to non-REM or quiet sleep. We also observed a reduction in diaphragmatic tonic activity with halothane anesthesia (P less than 0.001). With esophageal electrodes in adult subjects, there was a rise in tonic diaphragmatic activity proportional to the amount of abdomina load (P less than 0.001). We conclude that there are muscle spindles in the human diaphragm and that there is tonic activity at end expiration.

Maturation of ventilatory response to hypoxia in puppies during sleep

1982 ◽  
Vol 52 (2) ◽  
pp. 309-314 ◽  
Author(s):  
G. G. Haddad ◽  
M. R. Gandhi ◽  
R. B. Mellins
Keyword(s):  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Inspiratory Time ◽  
Sleep State ◽  
Quiet Sleep ◽  
Steady Level ◽  
The Mean ◽  
Ventilatory Response To Hypoxia

Using the barometric method, we studied the maturation of the ventilatory response to steady-level hypoxia (FIO2 = 15%O2) during sleep in 37 beagle puppies. In rapid-eye-movement (REM) sleep, instantaneous minute ventilation (VT/Ttot) and mean inspiratory time (VT/TI) increased, and inspiratory time (TI) and expiratory time (TE) were shortened in response to hypoxia at all the ages studied (14, 19, 24, 29 days). In quiet sleep, however, VT/Ttot decreased, and TE and Ttot were prolonged at 14 days in response to the same hypoxic stimulus. There was no change in VT/Ttot at 19 and 24 days of age, but VI/Ttot and VT/TI increased, and TI and TE were shortened at 29 days of age in response to hypoxia in the same sleep state. The mean arterial O2 tension (PaO2) dropped during hypoxia to about 45 Torr, and the mean arterial CO2 tension (PaCO2) decreased, and the mean pH increased at all ages in both REM and quiet sleep. We conclude that in beagles puppies 1) the ventilatory response to hypoxia matures at a slower rate in quiet than in REM sleep and depends primarily on timing rather than volume mechanisms: and 2) in response to hypoxia, the regulation of blood gases in REM sleep may be achieved differently from that in quiet sleep in early life.

Cluster headache shows no association with rapid eye movement sleep

Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 289-296 ◽  
Author(s):  
Sebastian Zaremba ◽  
Dagny Holle ◽  
Thomas E Wessendorf ◽  
Hans C Diener ◽  
Zaza Katsarava ◽  
...  
Keyword(s):  
Cluster Headache ◽  
Eye Movement ◽  
Rem Sleep ◽  
Sleep Stage ◽  
Sleep Time ◽  
Brain Regions ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Sleep State ◽  
Wake Time

Background: The connection of cluster headache (CH) attacks with rapid eye movement (REM) sleep has been suggested by various studies, while other authors challenge this assumption. We performed serial polysomnography to determine the association of nocturnal CH attacks and sleep. Methods: Five patients diagnosed with CH (two with the episodic and three with the chronic subtype) were included and studied over four consecutive nights to evaluate connections between attacks onset and sleep stage. Results: Twenty typical CH attacks were reported. Thirteen of these attacks arose from sleep. Seven attacks were reported after waking in the morning or shortly before going to sleep. The beginnings of sleep-related attacks were distributed arbitrarily between different non-REM sleep stages. No association of CH attacks with REM or sleep disordered breathing was observed. Increased heart rate temporally associated with transition from one sleep state to another was observed before patients awoke with headache. Total sleep time, total wake time, arousal index and distribution of non-REM sleep stages were different between chronic and episodic CH. Conclusion: CH attacks are not associated with REM sleep. Brain regions involved in sleep stage transition might be involved in pathophysiology of CH. Differences in sleep characteristics between subgroups might indicate adaptation processes or underlying pathophysiology.

scholarly journals Monotremes and the evolution of rapid eye movement sleep

1998 ◽  
Vol 353 (1372) ◽  
pp. 1147-1157 ◽  
Author(s):  
J. M. Siegel ◽  
P. R. Manger ◽  
R. Nienhuis ◽  
H. M. Fahringer ◽  
J. D. Pettigrew
Keyword(s):  
Eye Movement ◽  
High Voltage ◽  
Rem Sleep ◽  
Sleep Pattern ◽  
Rapid Eye Movement ◽  
Mammalian Evolution ◽  
Sleep State ◽  
Precursor State ◽  
Electroencephalogram Eeg ◽  
Head Twitching

Early studies of the echidna led to the conclusion that this monotreme did not have rapid eye movement (REM) sleep. Because the monotremes had diverged from the placental and marsupial lines very early in mammalian evolution, this finding was used to support the hypothesis that REM sleep evolved after the start of the mammalian line. The current paper summarizes our recent work on sleep in the echidna and platypus and leads to a very different interpretation. By using neuronal recording from mesopontine regions in the echidna, we found that despite the presence of a high–voltage cortical electroencephalogram (EEG), brainstem units fire in irregular bursts intermediate in intensity between the regular non–REM sleep pattern and the highly irregular REM sleep pattern seen in placentals. Thus the echidna displays brainstem activation during sleep with high–voltage cortical EEG. This work encouraged us to do the first study of sleep, to our knowledge, in the platypus. In the platypus we saw sleep with vigorous rapid eye, bill and head twitching, identical in behaviour to that which defines REM sleep in placental mammals. Recording of the EEG in the platypus during natural sleep and waking states revealed that it had moderate and high–voltage cortical EEGs during this REM sleep state. The platypus not only has REM sleep, but it had more of it than any other animal. The lack of EEG voltage reduction during REM sleep in the platypus, and during the REM sleep–like state of the echidna, has some similarity to the sleep seen in neonatal sleep in placentals. The very high amounts of REM sleep seen in the platypus also fit with the increased REM sleep duration seen in altricial mammals. Our findings suggest that REM sleep originated earlier in mammalian evolution than had previously been thought and is consistent with the hypothesis that REM sleep, or a precursor state with aspects of REM sleep, may have had its origin in reptilian species.

Effect of sinoaortic denervation on arousal responses to hypotension in newborn lambs

1989 ◽  
Vol 256 (2) ◽  
pp. H434-H440 ◽  
Author(s):  
R. S. Horne ◽  
P. J. Berger ◽  
G. Bowes ◽  
A. M. Walker
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Rapid Eye Movement ◽  
Arterial Oxygenation ◽  
Quiet Sleep ◽  
Arterial Baroreceptors ◽  
Significant Fall ◽  
Before And After ◽  
Acute Hypotension ◽  
Arousal Response

To examine whether hypotension reflexly initiates arousal from sleep and the mechanisms involved, we subjected sleeping lambs to hypotensive stimuli of 1-min duration, before and after sinoaortic denervation (SAD). In intact lambs, hypotension increased the probability of arousal from both quiet sleep (QS) and rapid-eye-movement (REM) sleep. Hypotension resulted in nonarousal in 42% (QS) and 47% (REM) of tests. Arousal time was significantly longer in REM (34.9 +/- 1.8 s, means +/- SE) than in QS (26.0 +/- 1.8 s). Arterial saturation of O2 (SO2) and PO2 measured at the point of arousal were unchanged from control values in those tests in which arousal occurred. In nonarousal tests, there was a significant fall in both SO2 (4.9 +/- 1.2%) and PO2 (21.6 +/- 4.2 mmHg). After SAD, hypotension did not increase the probability of arousal. Nonarousals significantly increased to 75% (QS and REM, P less than 0.02). We conclude that acute hypotension is a potent stimulus for arousal from sleep in newborn lambs. As the arousal response is abolished by SAD and is not correlated with arterial oxygenation, hypotensive arousal appears to be mediated via arterial baroreceptors.

Occlusion pressure and ventilation during sleep in normal humans

1986 ◽  
Vol 61 (4) ◽  
pp. 1279-1287 ◽  
Author(s):  
D. P. White
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Respiratory Drive ◽  
Rapid Eye Movement ◽  
System Sensitivity ◽  
Hypercapnic Ventilatory Response ◽  
Normal Humans

Previous investigation in normal humans has demonstrated reduced ventilation and ventilatory responses to chemical stimuli during sleep. Most have interpreted this to be a product of decreasing central nervous system sensitivity to the normal stimuli that maintain ventilation, whereas other factors such as increasing airflow resistance could also contribute to this reduction in respiration. To improve our understanding of these events, we measured ventilation and occlusion pressures (P0.1) during unstimulated ventilation and rebreathing-induced hypercapnia during wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. Eighteen subjects (10 males and 8 females) of whom seven were snorers (5 males and 2 females) were studied. Ventilation was reduced during both NREM and REM sleep (P less than 0.05), but this decrement in minute ventilation tended to be greater in snorers than nonsnorers. Unstimulated P0.1, on the other hand, was maintained or increased during sleep in all groups studied, with males and snorers showing the largest increase. The hypercapnic ventilatory response fell during both NREM and REM sleep and tended to be lower during REM than NREM sleep. However, the P0.1 response to hypercapnia during NREM sleep was well maintained at the waking level although the REM response was statistically reduced. These studies suggest that the mechanism of the reduction in ventilation and the hypercapnic ventilatory response seen during sleep, particularly NREM sleep, is likely to be multifactorial and not totally a product of decreasing central respiratory drive.

Loss of putative GABAergic neurons in the ventrolateral medulla in multiple system atrophy

SLEEP ◽  
2021 ◽  
Author(s):  
Ann M Schmeichel ◽  
Elizabeth A Coon ◽  
Joseph E Parisi ◽  
Wolfgang Singer ◽  
Phillip A Low ◽  
...  
Keyword(s):  
Multiple System Atrophy ◽  
Eye Movement ◽  
Rem Sleep ◽  
Respiratory Control ◽  
Gabaergic Neurons ◽  
Ventrolateral Medulla ◽  
Rapid Eye Movement ◽  
Control Subjects ◽  
Neuropathological Diagnosis

Abstract Study Objectives Multiple system atrophy (MSA) is associated with disturbances in cardiovascular, sleep and respiratory control. The lateral paragigantocellular nucleus (LPGi) in the ventrolateral medulla (VLM) contains GABAergic neurons that participate in control of rapid eye movement (REM) sleep and cardiovagal responses. We sought to determine whether there was loss of putative GABAergic neurons in the LPGi and adjacent regions in MSA. Methods Sections of the medulla were processed for GAD65/67 immunoreactivity in eight subjects with clinical and neuropathological diagnosis of MSA and in six control subjects. These putative GABAergic LPGi neurons were mapped based on their relationship to adjacent monoaminergic VLM groups. Results There were markedly decreased numbers of GAD-immunoreactive neurons in the LPGi and adjacent VLM regions in MSA. Conclusions There is loss of GABAergic neurons in the VLM, including the LPGi in patients with MSA. Whereas these findings provide a possible mechanistic substrate, given the few cases included, further studies are necessary to determine whether they contribute to REM sleep-related cardiovagal and possibly respiratory dysregulation in MSA.

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