Ventilatory responses during wakefulness in children with obstructive sleep apnea.

Marcus, Carole L.; Gozal, David; Arens, Raanan; Basinski, D. J.; Omlin, K. J.; Keens, Thomas G.; Ward, Sally L. Davidson

doi:10.1164/ajrccm.149.3.8118641

Cited by 56 publications

(35 citation statements)

References 22 publications

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“…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). Thus, their overall ventilatory drive appears to be normal.…”

Section: Neuromotor Control Of the Upper Airwaymentioning

confidence: 95%

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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Section: Neuromotor Control Of the Upper Airwaymentioning

confidence: 95%

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

et al. 2005

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“…A number of studies have been performed in patients with OSAHS and their family members regarding hypercapnic and hypoxia ventilatory responses. The numbers are small and the results conflicting [14,49,50,51,52,53,54,55]. Whether respiratory control problems are implicated in the pathogenesis of OSAHS is open to debate.…”

Section: Intermediate Phenotypes Of Osahsmentioning

confidence: 99%

Genetic Aspects of the Obstructive Sleep Apnoea/Hypopnoea Syndrome – Is There a Common Link with Obesity?

Riha¹

2009

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Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is the third most common respiratory condition after asthma and chronic obstructive airway disease affecting approximately 2–4% of the middle-aged population. OSAHS has a hereditary component but owing to difficulties with phenotyping, its genetic basis has been difficult to elucidate. Despite this, limited progress has been made in considering the genetic basis of the ‘intermediate phenotypes’ of OSAHS such as craniofacial structure and upper airway control. Obesity is a risk factor for the development of OSAHS. The genetics of obesity are complex, but advances have been made recently using genome-wide association studies. Some authors postulate that OSAHS and common obesity share many pathophysiological pathways. However, the genes underpinning the development of sleep-disordered breathing and obesity are likely to be different, despite phenotypes that appear to overlap and influence each other’s expression. This paper focuses on human studies over-viewing the most recent work in the area and includes a brief discussion on methods of genetic studies.

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“…1,2 Children with SDB are more frequent users of health care services, 3 experience more frequent comorbid chronic illnesses, 4,5 and may develop significant clinical cardiovascular morbidity. 1,[6][7][8][9] They also display significant behavioral and cognitive comorbidities, 10 as well as reduced quality of life and mood alterations. 11 Animal models of SDB display long-term, partially irreversible neurocognitive consequences after intermittent hypoxia during sleep, particularly when such exposures occur early during development.…”

mentioning

confidence: 99%

Infant-Feeding Methods and Childhood Sleep-Disordered Breathing

et al. 2007

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Ventilatory responses during wakefulness in children with obstructive sleep apnea.

Cited by 56 publications

References 22 publications

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

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

Genetic Aspects of the Obstructive Sleep Apnoea/Hypopnoea Syndrome – Is There a Common Link with Obesity?

Infant-Feeding Methods and Childhood Sleep-Disordered Breathing

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