Arousal and ventilatory responses during sleep in children with obstructive sleep apnea

Marcus, Carole L.; Lutz, Janita; Carroll, John L.; Bamford, Owen S.

doi:10.1152/jappl.1998.84.6.1926

Cited by 130 publications

(83 citation statements)

References 25 publications

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“…We have previously demonstrated that children with OSAS had blunted arousal responses to hypercapnia (29), and impaired arousal responses to inspiratory loading during sleep compared with control subjects (16) but had a similar acoustic arousal threshold (30). This study, using a more sophisticated measure of respiratory and auditory processing stimuli, has confirmed our previous findings.…”

Section: Aep During Sleepsupporting

confidence: 86%

Respiratory and Auditory Cortical Processing in Children with Obstructive Sleep Apnea Syndrome

Huang¹,

Marcus²,

Davenport³

et al. 2013

Am J Respir Crit Care Med

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Rationale: Children with obstructive sleep apnea syndrome (OSAS) have impaired cortical processing of respiratory afferent stimuli, manifested by blunted sleep respiratory-related evoked potentials (RREP). However, whether this impairment is limited to respiratory stimuli, or reversible after successful treatment, is unknown. We hypothesized that, during sleep, children with OSAS have (1) abnormal RREP, (2) normal cortical processing of nonrespiratory stimuli, and (3) persistence of abnormal RREP after treatment. Objectives: To measure sleep RREP and auditory evoked potentials in normal control subjects and children with OSAS before and after treatment. Methods: Twenty-four children with OSAS and 24 control subjects were tested during N3 sleep. Thirteen children with OSAS repeated testing 4-6 months after adenotonsillectomy. Measurements and Main Results: RREP were blunted in OSAS compared with control subjects (N350 at Cz 227 6 15.5 vs. 247.4 6 28.5 mV; P ¼ 0.019), and did not improve after OSAS treatment (N350 at Cz pretreatment 225.1 6 7.4 vs. 229.8 6 8.1 posttreatment). Auditory evoked potentials were similar in OSAS and control subjects at baseline (N350 at Cz 258 6 33.1 vs. 266 6 31.1 mV), and did not change after treatment (N350 at Cz 267.5 6 36.8 vs. 6 20.3).Conclusions: Children with OSAS have persistent primary or irreversible respiratory afferent cortical processing deficits during sleep that could put them at risk of OSAS recurrence. OSAS does not seem to affect the cortical processing of nonrespiratory (auditory) afferent stimuli during sleep.Keywords: evoked potentials; children; auditory; respiratory; obstructive sleep apnea syndromeThe pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS) is not clear. In most children, OSAS is related to adenotonsillar hypertrophy or obesity. However, these structural factors cannot fully explain the degree of upper airway collapsibility (1, 2). Studies have shown that upper airway neuromotor tone and reflexes during sleep play an important role in maintaining airway patency during sleep in the pediatric population (3, 4). Recently, it has been shown that central nervous system processing of upper airway respiratory stimuli is abnormal during sleep in children with OSAS (5). However, it is not known whether this abnormal afferent processing is limited to respiratory stimuli, or whether it is an indicator of broader abnormalities in stimulus processing, secondary to the hypoxemia, hypercapnia, and sleep fragmentation of OSAS. Furthermore, it is not known whether this deficit resolves after treatment of OSAS. Determining reversibility would help elucidate whether the blunted responses were a primary and perhaps predisposing abnormality, or were secondary to the OSAS.Respiratory-related evoked potentials (RREP) have been used to study the central nervous system processing of upper airway stimuli (6, 7). Auditory evoked potentials (AEP) are a useful tool to investigate cortical responses to nonrespiratory stimuli and produce the same set of longer...

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Section: Aep During Sleepsupporting

confidence: 86%

Respiratory and Auditory Cortical Processing in Children with Obstructive Sleep Apnea Syndrome

Huang¹,

Marcus²,

Davenport³

et al. 2013

Am J Respir Crit Care Med

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“…However, most patients with OSA have arousal thresholds that are within the normal range after therapy (1,6). In those who have high arousal thresholds despite CPAP treatment (z25% of the patoents with OSA we studied), OSA is typically very severe (6,7). Increased arousal thresholds in these patients may be inherent or slowly/incompletely reversible.…”

Section: From the Authorsmentioning

confidence: 95%

Reply: Arousal Threshold in Obstructive Sleep Apnea

Eckert

White

Jordan

et al. 2014

Am J Respir Crit Care Med

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children with OSA have higher arousal thresholds to a number of respiratory stimuli (such as hypercapnia [2] and inspiratory resistance loading [3]), but not to nonrespiratory stimuli (4), compared with age-matched control subjects.The arousal threshold changes over the course of normal development, with children having a higher arousal threshold compared with adults (5). However, the study by Eckert and coworkers showing blunted respiratory arousal thresholds in adults with OSA suggests that deficits in arousal are a common pathogenic mechanism for OSA across the age spectrum. n

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“…In the current study, both CO 2 and subatmospheric pressure application resulted in increased flow and a change from a flow-limited to a nonflow-limited pattern. This was probably due to stimulation of the CNS, resulting in augmentation of upper airway neuromotor tone (7,34,35). Previously, we showed that children with OSAS had normal ventilatory responses to hypoxia and hypercapnia during both wakefulness (36) and sleep (35).…”

Section: Neuromotor Control Of the Upper Airwaymentioning

confidence: 95%

“…The neuromotor theory is supported by the literature. Previous studies have shown normalization of arousal responses to hypercapnia following T&A in children (35). In addition, adults with OSAS have an improvement in the hypercapnic ventilatory drive following tracheostomy (41), and have improvement in upper airway sensation following CPAP administration (42).…”

Section: Neuromotor Causesmentioning

confidence: 99%

Upper Airway Dynamic Responses in Children with the Obstructive Sleep Apnea Syndrome

et al. 2005

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Normal children have a smaller upper airway than adults, but, nevertheless, snore less and have less apnea. We have previously shown that normal children have an upper airway that is resistant to collapse during sleep. We hypothesized that this resistance to collapse is due to preservation of upper airway neuromotor responses during sleep. Furthermore, we hypothesized that upper airway responses would be diminished in children with the obstructive sleep apnea syndrome (OSAS). We therefore compared the upper airway pressure-flow relationship during sleep between children with OSAS and controls. Measurements were made by correlating maximal inspiratory airflow with the level of nasal pressure applied via a mask. Neuromotor upper airway activation was assessed by evaluating the upper airway response to 1) hypercapnia and 2) intermittent, acute negative pressure. We found that children with OSAS had no significant response to either hypercapnia or negative pressure during sleep, compared with the normal children. After treatment of OSAS by tonsillectomy and adenoidectomy, there was a trend for normalization of upper airway responses. We conclude that upper airway dynamic responses are decreased in children with OSAS but recover after treatment. We speculate that the pharyngeal airway neuromotor responses present in normal children are a compensatory response for a relatively narrow upper airway. Further, we speculate that this compensatory response is lacking in children with OSAS, most likely due to either habituation to chronic respiratory abnormalities during sleep or to mechanical damage to the upper airway. In children, OSAS is related to adenotonsillar hypertrophy. Most children with OSAS have large tonsils and adenoids, and improve after T&A (1). Nevertheless, studies suggest that childhood OSAS is not due to anatomic abnormalities alone. Most obvious is the fact that patients with OSAS do not obstruct during wakefulness, when upper airway muscle tone is high. Although the upper airway may be narrower in children with OSAS than in those without, there is overlap between the groups (2). A small percentage of children with adenotonsillar hypertrophy but no other known risk factors for OSAS are not cured by T&A (1). Furthermore, a small percentage of children who were cured of their OSAS by T&A have been reported to develop a recurrence during adolescence (3,4). Thus, it appears that childhood OSAS is a dynamic process resulting from a combination of structural and neuromotor abnormalities, rather than from structural abnormalities alone. The upper airway above the level of the cartilaginous airway is a collapsible muscular tube that usually remains patent but has the potential to collapse to facilitate such functions as speech and swallowing. It comprises more than 30 pairs of muscles (5). Thus, neuromotor control of this area is important to maintain airway patency. Upper airway collapsibility during sleep is modulated by the central ventilatory drive (6). The upper airway dilatory muscles are respiratory musc...

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Arousal and ventilatory responses during sleep in children with obstructive sleep apnea

Cited by 130 publications

References 25 publications

Respiratory and Auditory Cortical Processing in Children with Obstructive Sleep Apnea Syndrome

Respiratory and Auditory Cortical Processing in Children with Obstructive Sleep Apnea Syndrome

Reply: Arousal Threshold in Obstructive Sleep Apnea

Upper Airway Dynamic Responses in Children with the Obstructive Sleep Apnea Syndrome

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