What is the role of neural regulation in the pathophysiology of childhood obstructive sleep apnea (OSA)?

Updated: Feb 13, 2019
  • Author: Mary E Cataletto, MD; Chief Editor: Denise Serebrisky, MD  more...
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Answer

Abnormal respiratory control does not appear to play a significant role in upper airway obstruction during sleep in children with obstructive sleep apnea. In one study, the ventilatory response to hyperoxic hypercapnic challenge in children and adolescents with obstructive sleep apnea was similar to that measured in age-matched and sex-matched controls. [3] Similarly, no differences were found in the ventilatory response to isocapnic hypoxia. Blunting in central chemosensitivity was reported in some children with obstructive sleep apnea undergoing surgery; however, despite such reports, central chemosensitivity during sleep in children with obstructive sleep apnea was similar to that in matched controls. However, arousal to hypercapnia was blunted, suggesting that subtle alterations in the central chemosensitive arousal network may have occurred in these children.

These subtle changes have been further substantiated by examining the ventilatory response to repeated hypercapnia, whereby reciprocal changes in respiratory frequency and tidal volume occur. In addition, children with obstructive sleep apnea demonstrate impaired arousal responses to inspiratory loads during rapid eye movement (REM) and non-REM sleep, compared to controls. Neural responses to hypoxia and hypercapnia have not been well studied in children with obstructive sleep apnea and underlying syndromes.

In addition to the aforementioned considerations, diminished laryngeal reflexes to mechanoreceptor and chemoreceptor stimulation, with reduced afferent inputs into central neural regions underlying inspiratory inputs, can be present. For example, chemoreceptor stimuli, such as increased PaCO2 or decreased PaO2, stimulate the airway, dilating muscles in a preferential mode (ie, upper airway musculature is more stimulated than the diaphragm).

This preferential recruitment tends to correct an imbalance of forces acting on the airway and, therefore, maintains airway patency. Similarly, stimuli that result from suction pressures in the nose, pharynx, or larynx rapidly stimulate the activity of upper airway dilators. This effect is also preferential to the upper airway, causing some degree of diaphragmatic inhibition and, thus, compensating for increases in upstream resistance. The function of these upper airway receptors in children with adenotonsillar hypertrophy with and without obstructive sleep apnea is not known.


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