Effect of Sleep State and Position on the Incidence of Obstructive and Central Apnea in Infants

PEDIATRICS ◽  
1985 ◽  
Vol 75 (5) ◽  
pp. 832-835
Author(s):  
William C. Orr ◽  
Monte L. Stahl ◽  
James Duke ◽  
Mary Anne McCaffree ◽  
Paul Toubas ◽  
...  

Sixty-four infants with a history of apnea were studied to determine the effects of sleeping position and sleep state (rapid eye movement [REM]) v (nonrapid eye movement [NREM]) on the occurrence of central and obstructive apneas. All-night polysomnographic studies were conducted on each infant, and the spontaneous occurrence of central and obstructive apneic events was determined in the prone, supine, and side positions. Sleeping position did not significantly affect the rate or duration of central or obstructive apneas. Furthermore, neither central nor obstructive apneic episodes were significantly altered by sleep state. These data suggest that, in spite of an ostensible predisposition to upper airway obstruction in the supine position and during rapid eye movement sleep, neither sleeping position nor sleep state appears to affect the rate of duration of apneic events.

1998 ◽  
Vol 84 (1) ◽  
pp. 269-276 ◽  
Author(s):  
Christine R. Wilson ◽  
Shalini Manchanda ◽  
David Crabtree ◽  
James B. Skatrud ◽  
Jerome A. Dempsey

Wilson, Christine R., Shalini Manchanda, David Crabtree, James B. Skatrud, and Jerome A. Dempsey. An induced blood pressure rise does not alter upper airway resistance in sleeping humans. J. Appl. Physiol. 84(1): 269–276, 1998.—Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-μg iv boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 ± 5 (mean ± SD) mmHg (range 12–37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 l/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20–25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non-rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.


1991 ◽  
Vol 70 (6) ◽  
pp. 2574-2581 ◽  
Author(s):  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White

We propose that a sleep-induced decrement in the activity of the tensor palatini (TP) muscle could induce airway narrowing in the area posterior to the soft palate and therefore lead to an increase in upper airway resistance in normal subjects. We investigated the TP to determine the influence of sleep on TP muscle activity and the relationship between changing TP activity and upper airway resistance over the entire night and during short sleep-awake transitions. Seven normal male subjects were studied on a single night with wire electrodes placed in both TP muscles. Sleep stage, inspiratory airflow, transpalatal pressure, and TP moving time average electromyogram (EMG) were continuously recorded. In addition, in two of the seven subjects the activity (EMG) of both the TP and the genioglossus muscle simultaneously was recorded throughout the night. Upper airway resistance increased progressively from wakefulness through the various non-rapid-eye-movement sleep stages, as has been previously described. The TP EMG did not commonly demonstrate phasic activity during wakefulness or sleep. However, the tonic EMG decreased progressively and significantly (P less than 0.05) from wakefulness through the non-rapid-eye-movement sleep stages [awake, 4.6 +/- 0.3 (SE) arbitrary units; stage 1, 2.6 +/- 0.3; stage 2, 1.7 +/- 0.5; stage 3/4, 1.5 +/- 0.8]. The mean correlation coefficient between TP EMG and upper airway resistance across all sleep states was (-0.46). This mean correlation improved over discrete sleep-awake transitions (-0.76). No sleep-induced decrement in the genioglossus activity was observed in the two subjects studied.(ABSTRACT TRUNCATED AT 250 WORDS)


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A324-A324
Author(s):  
Tuyet Pham ◽  
Sonal Malhotra

Abstract Introduction Parasomnias are abnormal sleep-related movements that can occur during non-rapid eye movement sleep, rapid eye movement sleep, or transition of sleep. The prevalence of parasomnias in young children ranges from 9–40% which may be underestimated as this relies on parental recall. There are multiple reported cases of pharmacologically-induced parasomnias. Quetiapine is an atypical antipsychotic medication associated with somnambulism and sleep-related eating disorder. Report of case(s) A 9-year-old female with a history of attention deficit hyperactivity disorder, post-traumatic-stress disorder, depression, and sexual abuse during childhood presented to the Sleep Medicine Clinic for two years of worsened sleepwalking and sleep eating. Her medications included Methylphenidate, Quetiapine, Clonidine, and Duloxetine. She has had parasomnias since she was 3-years-old, initially presenting as abnormal sleeping positions (standing or sitting). She was initiated on Seroquel at 4-years-old, but parasomnias worsened over the last two years when Quetiapine was increased from 50 mg to 200 mg for behavioral and mood issues. Her somnambulism began to occur nightly. The family was required to remove all items from her bedroom except for the bed to prevent major injuries. She also had significant changes to her eating habit: she would eat two to three times her normal quantity as well as eating while asleep. The family would find her eating ice cream, chips, grapes, cold tortillas, or anything she was able to access. Fortunately, she did not consume raw meat or other frozen foods. The child did not have any recollection of eating at night. Psychiatry worked with her to cross-taper Quetiapine and Topiramate. At the lower dose of Quetiapine, she had exacerbation of her mood symptoms, paranoia, and insomnia; therefore, Topiramate was discontinued and Quetiapine was titrated to 150 mg with improvement in mood symptoms, insomnia, and resolution of sleep-related eating disorder. She continues to have somnambulism. Conclusion This case illustrates that quetiapine-induced somnambulism and sleep-related eating disorder can be dose-dependent; thus, important for clinicians to educate patients and/or family members of adverse effects while titrating quetiapine. Support (if any):


1996 ◽  
Vol 271 (4) ◽  
pp. E763-E772 ◽  
Author(s):  
M. Lancel ◽  
J. Faulhaber ◽  
F. Holsboer ◽  
R. Rupprecht

There is much evidence that progesterone has hypnotic anesthetic properties. In this vehicle-controlled study, we examined the effects of three doses of progesterone (30, 90, and 180 mg/kg) administered intraperitoneally at light onset on sleep in rats. Progesterone dose dependently shortened non-rapid eye movement sleep (NREMS) latency, lengthened rapid eye movement sleep (REMS) latency, decreased the amount of wakefulness and REMS, and markedly increased pre-REMS, an intermediate state between NREMS and REMS. Progesterone also elicited dose-related changes in sleep state-specific electroencephalogram (EEG) power densities. Within NREMS, EEG activity was reduced in the lower frequencies (< or = 7 Hz) and was enhanced in the higher frequencies. Within REMS, EEG activity was markedly enhanced in the higher frequencies. The effects were maximal during the first postinjection hours. The concentrations of progesterone and the progesterone metabolites 3 alpha-hydroxy-5 alpha-pregnan-20-one and 3 alpha-hydroxy-5 beta-pregnan-20-one, both positive allosteric modulators of gamma-aminobutyric acid A (GABAA) receptors, were determined at different time intervals after vehicle and 30 or 90 mg/kg progesterone. Progesterone administration resulted in dose-dependent initially supraphysiological elevations of progesterone and its metabolites in the plasma and brain, which were most prominent during the first hour postinjection. The effects of progesterone on sleep closely resemble those of agonistic modulators of GABAA receptors such as benzodiazepines and correlate well with the increases in the levels of its GABAA agonistic metabolites. These observations suggest that the hypnotic effects of progesterone are mediated by the facilitating action of its neuroactive metabolites on GABAA receptor functioning.


1993 ◽  
Vol 148 (1) ◽  
pp. 185-194 ◽  
Author(s):  
Joan C. Hendricks ◽  
Basil J. Petrof ◽  
Karen Panckeri ◽  
Allan I. Pack

1993 ◽  
Vol 75 (5) ◽  
pp. 2117-2124 ◽  
Author(s):  
J. R. Wheatley ◽  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White

Increased retropalatal airway resistance may be caused by a sleep-induced loss of palatal muscle activity and a diminished ability of these muscles to respond to the increasing intrapharyngeal negative pressure that develops during sleep. To investigate these possibilities, in six normal subjects, we determined the effect of non-rapid-eye-movement sleep on 1) the tensor palatini (TP) electromyogram (EMG) response to rapid-onset negative-pressure generations (NPG) in the upper airway and 2) the collapsibility of the retropalatal airway during these NPGs. During wakefulness, the change in TP EMG from basal to peak levels (during NPG) was 19.8 +/- 3.2 arbitrary units (P < 0.005). This was markedly reduced during sleep (3.6 +/- 1.5 arbitrary units; P < 0.001). The latency of the TP EMG response was 48.5 +/- 5.6 ms during wakefulness but was prolonged during sleep (105.0 +/- 12.2 ms; P < 0.02). The peak transpalatal pressure during NPG (a measure of airway collapse) was 2.1 +/- 0.7 cmH2O during wakefulness and increased to 5.3 +/- 0.8 cmH2O during sleep (P < 0.05). We conclude that the brisk reflex response of the TP muscle to negative pressure during wakefulness is markedly reduced during non-rapid-eye-movement sleep, in association with a more collapsible retropalatal airway. We speculate that the reduction in this TP reflex response contributes to retropalatal airway narrowing during sleep in normal subjects.


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