Developmental changes in response to subatmospheric pressure loading of the upper airway

Marcus, Carole L.; Lutz, Janita; Hamer, Audrey; Smith, Philip L.; Schwartz, Alan R.

doi:10.1152/jappl.1999.87.2.626

Cited by 75 publications

(62 citation statements)

References 35 publications

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“…First, our subjects were older (11.9 Ϯ 1.9 yr; range, 9.1-16.4 yr) than the peak incidence of OSAS in children (aged 2-8 yr), and there is the confounding variable of pubertal status. We do not believe that this adversely affects our conclusions insofar as a previous developmental study indicates that there is little difference in airway collapsibility in this age range (34). Furthermore, only four of our subjects were older than 13 yr, and the EMGgg responsiveness of these subjects was not different from the remainder of the control population.…”

Section: Limitationsmentioning

confidence: 56%

Influence of Airway Pressure on Genioglossus Activity during Sleep in Normal Children

Katz

Marcus

White

2006

Am J Respir Crit Care Med

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Section: Limitationsmentioning

confidence: 56%

Influence of Airway Pressure on Genioglossus Activity during Sleep in Normal Children

Katz

Marcus

White

2006

Am J Respir Crit Care Med

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“…Alternatively, it is possible that the obese control subjects did not develop OSAS despite enlargement of upper airway soft tissues, owing to the presence of compensatory upper airway neuromotor reflexes during sleep. It has been shown that healthy children have increased upper airway reflexes to stimuli such as subatmospheric pressure and carbon dioxide during sleep (9) and that these reflexes decline during adolescence (35). However, the rate of decline during adolescence is variable, and we have shown that obese adolescents without OSAS have increased upper airway reflexes during sleep compared with BMI-matched adolescents with OSAS (19).…”

mentioning

confidence: 58%

“…In adults, there are known anatomic risk factors for OSAS, including enlargement of the tongue, soft palate, parapharyngeal fat pads, and lateral pharyngeal walls (5) in conjunction with craniofacial restriction (retrognathia) (6). In addition to anatomic factors, physiologic mechanisms increase OSAS risk in both children and adults (7)(8)(9)(10)(11)(12). Although these risk factors for OSAS have been well described in children and adults, few studies have addressed the important transitional developmental phase of adolescence.…”

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confidence: 99%

Understanding the Anatomic Basis for Obstructive Sleep Apnea Syndrome in Adolescents

Schwab

Kim

Bagchi

et al. 2015

Am J Respir Crit Care Med

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Rationale: Structural risk factors for obstructive sleep apnea syndrome (OSAS) in adolescents have not been well characterized. Because many adolescents with OSAS are obese, we hypothesized that the anatomic OSAS risk factors would be more similar to those in adults than those in children.Objectives: To investigate the anatomic risk factors in adolescents with OSAS compared with obese and lean control subjects using magnetic resonance imaging (MRI).Methods: Three groups of adolescents (age range: 12-16 yr) underwent MRI: obese individuals with OSAS (n = 49), obese control subjects (n = 38), and lean control subjects (n = 50). Measurements and Main Results:We studied 137 subjects and found that (1) obese adolescents with OSAS had increased adenotonsillar tissue compared with obese and lean control subjects; (2) obese OSAS adolescents had a smaller nasopharyngeal airway than control subjects; (3) the size of other upper airway soft tissue structures (volume of the tongue, parapharyngeal fat pads, lateral walls, and soft palate) was similar between subjects with OSAS and obese control subjects; (4) although there were no major craniofacial abnormalities in most of the adolescents with OSAS, the ratio of soft tissue to craniofacial space surrounding the airway was increased; and (5) there were sex differences in the pattern of lymphoid proliferation.Conclusions: Increased size of the pharyngeal lymphoid tissue, rather than enlargement of the upper airway soft tissue structures, is the primary anatomic risk factor for OSAS in obese adolescents. These results are important for clinical decision making and suggest that adenotonsillectomy should be considered as the initial treatment for OSAS in obese adolescents, a group that has poor continuous positive airway pressure adherence and difficulty in achieving weight loss.Keywords: adenoid; adolescents; MRI; obstructive sleep apnea syndrome; tonsils The obstructive sleep apnea syndrome (OSAS) is common in children and adults, but it has not been well studied in adolescents. In one study, researchers reported the prevalence of OSAS in adolescents to be 2% (1), but the prevalence is probably higher in the United States because of the adolescent obesity epidemic (2). OSAS in children is thought to be secondary to a combination of enlargement of the lymphoid tissue (tonsils and adenoid) (3) and, sometimes, obesity, as well as to reductions in neuromuscular tone (4). In adults, there are known anatomic risk factors for OSAS, including enlargement of the tongue, soft palate, parapharyngeal fat pads, and lateral pharyngeal walls (5) in conjunction with craniofacial restriction (retrognathia) (6). In addition to anatomic factors, physiologic mechanisms increase OSAS risk in both children and adults (7-12). Although these risk factors for OSAS have been well described in children and adults, few Supported by grants from the National Institutes of Health (R01 HL058585, R01 HL089447, and P01 HL094307).Author Contributions: Conception and design: R.J.S., R.M.B., S.H., and C.L...

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“…PFR were obtained during a second, overnight study, using modifications of previously published techniques (6,9,18). Upper airway function was measured under the following conditions, in random order:…”

Section: Measurement Of Pfr and Upper Airway Responsesmentioning

confidence: 99%

“…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 muscles and, therefore, are activated in response to increases in the central ventilatory drive (7).…”

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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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Developmental changes in response to subatmospheric pressure loading of the upper airway

Cited by 75 publications

References 35 publications

Influence of Airway Pressure on Genioglossus Activity during Sleep in Normal Children

Influence of Airway Pressure on Genioglossus Activity during Sleep in Normal Children

Understanding the Anatomic Basis for Obstructive Sleep Apnea Syndrome in Adolescents

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

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