Negative pressure-induced deformation of the upper airway causes central apnea in awake and sleeping dogs

1996 ◽  
Vol 80 (5) ◽  
pp. 1528-1539 ◽  
Author(s):  
C. A. Harms ◽  
Y. J. Zeng ◽  
C. A. Smith ◽  
E. H. Vidruk ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Negative Pressure ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Electromyographic Activity ◽  
Rapid Eye Movement ◽  
Topical Anesthetic ◽  
Control Value ◽  
States Of Consciousness

We investigated the effects of negative pressure (NP) in the isolated upper airway (UA) in three unanesthetized dogs. The UA was isolated, and the dogs breathed through an endotracheal tube while wearing a fitted fiberglass snout mask. NP (-2 to -32 cmH2O) was applied in a square wave below the larynx or at the snout at end expiration and was held until inspiratory effort during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep. During all states of consciousness, NP applied to the UA prolonged expiratory time (TE) 1) below a threshold of -8 to -10 cmH2O, which coincided with closure of the oro- and/or velopharynx; and 2) in a progressive fashion at more negative pressures than threshold, up to a mean apneic length of 324% of the control value (or 13.9 s) at -30 cmH2O. TE prolongation was less during REM sleep at a given NP (P < 0.05). Augmented tonic genioglossal electromyographic activity also occurred with the applied NP during wakefulness and NREM sleep but not with REM sleep. NP (-20 to -32 cmH2O) applied as a brief pulse (300-500 ms) during NREM sleep caused transient airway occlusion, terminated the breath during inspiration, and prolonged TE when applied at end expiration. Central apneas always persisted beyond the termination of the UA closure. TE prolongation in response to NP persisted in the presence of a topical anesthetic nebulized through the UA sufficient to abolish the laryngeal gag reflexes. We conclude that UA closure and deformation will cause significant TE prolongation during all states of consciousness and activation of the genioglossus muscle during wakefulness and NREM sleep but not during REM sleep.

scholarly journals Effect of upper airway negative pressure on inspiratory drive during sleep

1998 ◽  
Vol 84 (3) ◽  
pp. 1063-1075 ◽  
Author(s):  
P. R. Eastwood ◽  
A. K. Curran ◽  
C. A. Smith ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Negative Pressure ◽  
Upper Airway ◽  
Resistive Load ◽  
Rapid Eye Movement ◽  
Inhibitory Effects ◽  
Lung Inflation ◽  
Tracheal Occlusion ◽  
Tracheal Pressure

To determine the effect of upper airway (UA) negative pressure and collapse during inspiration on regulation of breathing, we studied four unanesthetized female dogs during wakefulness and sleep while they breathed via a fenestrated tracheostomy tube, which was sealed around the permanent tracheal stoma. The snout was sealed with an airtight mask, thereby isolating the UA when the fenestration (Fen) was closed and exposing the UA to intrathoracic pressure changes, but not to flow changes, when Fen was open. During tracheal occlusion with Fen closed, inspiratory time (Ti) increased during wakefulness, non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep (155 ± 8, 164 ± 11, and 161 ± 32%, respectively), reflecting the removal of inhibitory lung inflation reflexes. During tracheal occlusion with Fen open (vs. Fen closed): 1) the UA remained patent; 2) Ti further increased during wakefulness and NREM (215 ± 52 and 197 ± 28%, respectively) but nonsignificantly during REM sleep (196 ± 42%); 3) mean rate of rise of diaphragm EMG (EMGdi/Ti) and rate of fall of tracheal pressure (Ptr/Ti) were decreased, reflecting an additional inhibitory input from UA receptors; and 4) both EMGdi/Ti and Ptr/Ti were decreased proportionately more as inspiration proceeded, suggesting greater reflex inhibition later in the effort. Similar inhibitory effects of exposing the UA to negative pressure (via an open tracheal Fen) were seen when an inspiratory resistive load was applied over several breaths during wakefulness and sleep. These inhibitory effects persisted even in the face of rising chemical stimuli. This inhibition of inspiratory motor output is alinear within an inspiration and reflects the activation of UA pressure-sensitive receptors by UA distortion, with greater distortion possibly occurring later in the effort.

Upper airway closing pressures in obstructive sleep apnea

1984 ◽  
Vol 57 (2) ◽  
pp. 520-527 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Eye Movement ◽  
Rem Sleep ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Stage I ◽  
Stage Iii ◽  
Rapid Eye Movement ◽  
Obstructive Sleep

We studied 18 patients with obstructive sleep apnea (OSA). Each subject slept while breathing through the nose with a specially designed valveless breathing circuit. Low levels of continuous positive airway pressure (CPAP) applied through the nose (2.5–15.0 cmH2O) prevented OSA and allowed long periods of stable stage III/IV sleep and rapid-eye-movement (REM) sleep. Externally applied complete nasal occlusion while the upper airway was patent resulted in upper airway closure during inspiration which was identified by a sudden deviation of nasal pressure from tracheal or esophageal pressure. The level of upper airway closing pressure (UACP) did not change throughout the occlusion test, suggesting that upper airway dilator muscles do not respond to asphyxia during sleep. The upper airway was more collapsible during stage I/II non-rapid-eye-movement (NREM) and REM sleep compared with stage III/IV NREM sleep. The pooled mean UACP was 3.1 +/- 0.4 cmH2O in stage I/II NREM, 4.2 +/- 0.2 cmH2O in stage III/IV NREM, and 2.4 +/- 0.2 cmH2O in REM sleep. Nasal occlusion at successively higher levels of CPAP did not alter the level of UACP in stage I/II NREM and REM sleep but resulted in the upper airway becoming more stable in stage III/IV NREM sleep, suggesting a reflex which augments the tone of upper airway dilator muscles.

Alae nasi electromyographic activity and timing in obstructive sleep apnea

1985 ◽  
Vol 58 (4) ◽  
pp. 1252-1256 ◽  
Author(s):  
P. M. Suratt ◽  
R. McTier ◽  
S. C. Wilhoit
Keyword(s):  
Eye Movement ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Esophageal Pressure ◽  
Emg Activity ◽  
Electromyographic Activity ◽  
Rapid Eye Movement ◽  
Rib Cage ◽  
Dilator Muscle ◽  
Obstructive Sleep

The alae nasi is an accessible dilator muscle of the upper airway located in the nose. We measured electromyograms (EMG) of the alae nasi to determine the relationship between their activity and timing to contraction of the rib cage muscles and diaphragm during obstructive apnea in nine patients. Alae nasi EMG were measured with surface electrodes and processed to obtain a moving time average. Contraction of the rib cage and diaphragm during apneas was detected with esophageal pressure. During non-rapid-eye-movement (NREM) sleep, there was a significant correlation in each patient between alae nasi EMG activity and the change in esophageal pressure. During rapid-eye-movement (REM) sleep, correlations were significantly lower than during NREM sleep. As the duration of each apnea increased, the activation of alae nasi EMG occurred progressively earlier than the change in esophageal pressure. We conclude that during obstructive apneas in NREM sleep, activity of the alae nasi increases when diaphragm and rib cage muscle force increases and the activation occurs earlier as each apneic episode progresses.

Effects of rapid-eye-movement sleep on the apneic threshold in dogs

1993 ◽  
Vol 75 (3) ◽  
pp. 1129-1139 ◽  
Author(s):  
L. Xi ◽  
C. A. Smith ◽  
K. W. Saupe ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Breathing Pattern ◽  
Nrem Sleep ◽  
Inhibitory Response ◽  
Rapid Eye Movement ◽  
Central Apnea ◽  
Fourfold Increase ◽  
Control Value ◽  
End Tidal

We determined whether the apneic threshold after active hyperventilation was different in rapid-eye-movement (REM) vs. non-REM (NREM) sleep. Sleeping dogs were repeatedly exposed to 35–45 s of hypoxia of varying severity (end-tidal PO2 40–60 Torr) that was abruptly terminated with 100% O2. Changes in breathing pattern after brief hypoxia were compared with those after a normoxia-to-hyperoxia transition, i.e., control conditions. In NREM sleep, hypoxic hyperventilation was consistently followed by central apnea, the duration of which was linearly related to the corresponding hypocapnia and/or increase in tidal volume (VT) during hypoxia. After hypoxia, expiratory duration averaged 3.5 x control value at -5-Torr change in end-tidal PCO2 and twofold increase in VT; mean expiratory duration was 5 x control value at -10-Torr change in end-tidal PCO2 and fourfold increase in VT. In REM sleep, central apnea of varying duration did occur on occasion after brief hypoxic hyperventilation, but there was no systematic relationship with magnitude of hypocapnia or increase in VT. Breathing pattern during or after hypoxia in REM was not related to temporal changes in either eye movement density or electroencephalogram frequency. Thus, in contrast to NREM sleep, in REM sleep ("phasic" or "tonic") a posthyperventilation apneic threshold was not present. We attribute this effect of REM to 1) a reduced VT response to hypoxia that would minimize inhibitory "memory" effect from lung stretch and 2) attenuated inhibitory response to any given magnitude of hypocapnia or increased VT. Active hyperventilation-induced apneic threshold may be "masked" by actions of nonchemoreceptor and nonmechanoreceptor inputs affecting respiratory motor output in REM sleep. These data are consistent with the relative absence of central apnea and periodic breathing in humans in REM sleep.

Response of genioglossus muscle activity to nasal airway occlusion in normal sleeping adults

1988 ◽  
Vol 64 (1) ◽  
pp. 347-353 ◽  
Author(s):  
S. T. Kuna ◽  
J. Smickley
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Muscle Activity ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Mouth Breathing ◽  
Nasal Airway ◽  
Rapid Eye Movement ◽  
Genioglossus Muscle ◽  
Airway Occlusion

To determine the combined effect of increased subatmospheric upper airway pressure and withdrawal of phasic volume feedback from the lung on genioglossus muscle activity, the response of this muscle to intermittent nasal airway occlusion was studied in 12 normal adult males during sleep. Nasal occlusion at end expiration was achieved by inflating balloon-tipped catheters located within the portals of a nose mask. No seal was placed over the mouth. During nose breathing in non-rapid-eye-movement (NREM) sleep, nasal airway occlusion resulted in multiple respiratory efforts before arousal. Mouth breathing was not initiated until arousal. Phasic inspiratory genioglossus activity was present in eight subjects during NREM sleep. In these subjects, comparison of peak genioglossus inspiratory activity on the first three occluded efforts to the value just before occlusion showed an increase of 4.7, 16.1, and 28.0%, respectively. The relative increases in peak genioglossus activity were very similar to respective increases in peak diaphragm activity. Arousal was associated with a large burst in genioglossus activity. During airway occlusion in rapid-eye-movement (REM) sleep, mouth breathing could occur without a change in sleep state. In general, genioglossus responses to airway occlusion in REM sleep were similar in pattern to those in NREM sleep. A relatively small reflex activation of upper airway muscles associated with a sudden increase in subatmospheric pressure in the potentially collapsible segment of the upper airway may help compromise upper airway patency during sleep.

Effects of high-frequency oscillating pressures on upper airway muscles in humans

1993 ◽  
Vol 75 (2) ◽  
pp. 856-862 ◽  
Author(s):  
K. G. Henke ◽  
C. E. Sullivan
Keyword(s):  
Sleep Apnea ◽  
Eye Movement ◽  
Rem Sleep ◽  
High Frequency ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Low Pressure ◽  
Rapid Eye Movement ◽  
Pressure Oscillations

We examined the effects of high-frequency- (30-Hz) low-pressure oscillations (< 1 cmH2O) applied to the upper airway, via a nose mask, on genioglossus (EMGgg), sternomastoid (EMGsm), and diaphragm electromyogram (EMGdia) activity in sleeping humans. Ten patients with sleep apnea and six normal subjects were studied. The pressure oscillations were applied through the mask for a single breath. The subjects were studied in non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. In the normal subjects, during NREM sleep, peak EMGgg, EMGsm, and EMGdia activity increased significantly in response to the oscillations in 63, 51, and 46%, respectively, of all trials. During REM sleep, significant increases occurred in 73, 88, and 13%, respectively, of all trials. Similar responses were observed in the patients with obstructive sleep apnea. Peak EMGgg, EMGsm, and EMGdia activity increased significantly in 74, 50, and 67%, respectively, of all NREM sleep trials and in 55, 81, and 76%, respectively, of all REM sleep trials. An important finding was that in 46% of the trials in the patients with sleep apnea the oscillation-induced increase in EMGgg activity was associated with a partial or complete reversal of the upper airway obstruction with an increase in tidal volume. This was observed in NREM and REM sleep. We conclude that there are upper airway receptors that respond to low-pressure-high-frequency oscillations applied to the upper airway that have input to the genioglossus and other muscles of respiration. These responses may be utilized in future treatment for sleep apnea.

Upper airway resistance and geniohyoid muscle activity in normal men during wakefulness and sleep

1990 ◽  
Vol 69 (4) ◽  
pp. 1252-1261 ◽  
Author(s):  
D. A. Wiegand ◽  
B. Latz ◽  
C. W. Zwillich ◽  
L. Wiegand
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Muscle Activity ◽  
Airway Resistance ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Supraglottic Airway ◽  
Rapid Eye Movement ◽  
Upper Airway Resistance ◽  
Normal Men

Sleep-related reduction in geniohyoid muscular support may lead to increased airway resistance in normal subjects. To test this hypothesis, we studied seven normal men throughout a single night of sleep. We recorded inspiratory supraglottic airway resistance, geniohyoid muscle electromyographic (EMGgh) activity, sleep staging, and ventilatory parameters in these subjects during supine nasal breathing. Mean inspiratory upper airway resistance was significantly (P less than 0.01) increased in these subjects during all stages of sleep compared with wakefulness, reaching highest levels during non-rapid-eye-movement (NREM) sleep [awake 2.5 +/- 0.6 (SE) cmH2O.l-1.s, stage 2 NREM sleep 24.1 +/- 11.1, stage 3/4 NREM sleep 30.2 +/- 12.3, rapid-eye-movement (REM) sleep 13.0 +/- 6.7]. Breath-by-breath linear correlation analyses of upper airway resistance and time-averaged EMGgh amplitude demonstrated a significant (P less than 0.05) negative correlation (r = -0.44 to -0.55) between these parameters in five of seven subjects when data from all states (wakefulness and sleep) were combined. However, we found no clear relationship between normalized upper airway resistance and EMGgh activity during individual states (wakefulness, stage 2 NREM sleep, stage 3/4 NREM sleep, and REM sleep) when data from all subjects were combined. The timing of EMGgh onset relative to the onset of inspiratory airflow did not change significantly during wakefulness, NREM sleep, and REM sleep. Inspiratory augmentation of geniohyoid activity generally preceded the start of inspiratory airflow. The time from onset of inspiratory airflow to peak inspiratory EMGgh activity was significantly increased during sleep compared with wakefulness (awake 0.81 +/- 0.04 s, NREM sleep 1.01 +/- 0.04, REM sleep 1.04 +/- 0.05; P less than 0.05). These data indicate that sleep-related changes in geniohyoid muscle activity may influence upper airway resistance in some subjects. However, the relationship between geniohyoid muscle activity and upper airway resistance was complex and varied among subjects, suggesting that other factors must also be considered to explain sleep influences on upper airway patency.

Sleep Disorders

2015 ◽  
Author(s):  
Sudhansu Chokroverty
Keyword(s):  
Sleep Apnea ◽  
Sleep Disorders ◽  
Eye Movement ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Circadian Rhythm Sleep Disorders ◽  
Apnea Syndrome ◽  
Sleep Mechanism

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.

Sleep Disorders

2015 ◽  
Author(s):  
Sudhansu Chokroverty
Keyword(s):  
Sleep Apnea ◽  
Sleep Disorders ◽  
Eye Movement ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Circadian Rhythm Sleep Disorders ◽  
Apnea Syndrome ◽  
Sleep Mechanism

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.

Arousal Characteristics in Patients with Parkinson’s Disease and Isolated Rapid Eye Movement Sleep Behavior Disorder

SLEEP ◽  
2021 ◽  
Author(s):  
Andreas Brink-Kjær ◽  
Matteo Cesari ◽  
Friederike Sixel-Döring ◽  
Brit Mollenhauer ◽  
Claudia Trenkwalder ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Eye Movement ◽  
Rem Sleep ◽  
Regression Models ◽  
Muscle Tone ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Sleep Behavior

Abstract Study objectives Patients diagnosed with isolated rapid eye movement (REM) sleep behavior disorder (iRBD) and Parkinson’s disease (PD) have altered sleep stability reflecting neurodegeneration in brainstem structures. We hypothesize that neurodegeneration alters the expression of cortical arousals in sleep. Methods We analyzed polysomnography data recorded from 88 healthy controls (HC), 22 iRBD patients, 82 de novo PD patients without RBD and 32 with RBD (PD+RBD). These patients were also investigated at a 2-year follow-up. Arousals were analyzed using a previously validated automatic system, which used a central EEG lead, electrooculography, and chin electromyography. Multiple linear regression models were fitted to compare group differences at baseline and change to follow-up for arousal index (ArI), shifts in electroencephalographic signals associated with arousals, and arousal chin muscle tone. The regression models were adjusted for known covariates affecting the nature of arousal. Results In comparison to HC, patients with iRBD and PD+RBD showed increased ArI during REM sleep and their arousals showed a significantly lower shift in α-band power at arousals and a higher muscle tone during arousals. In comparison to HC, the PD patients were characterized by a decreased ArI in NREM sleep at baseline. ArI during NREM sleep decreased further at the 2-year follow-up, although not significantly Conclusions Patients with PD and iRBD present with abnormal arousal characteristics as scored by an automated method. These abnormalities are likely to be caused by neurodegeneration of the reticular activation system due to alpha-synuclein aggregation.

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