Sleep deprivation may also lead to poor neurologic function. OSA results from pathophysiology of the upper airway. Airway patency depends on airway caliber as well as appropriately functioning oropharyngeal reflexes. As the airway obstructs, local reflexes respond by increasing upper airway muscular activity and tone in order to relieve the obstruction. In children, these protective responses are not fully developed.
Neuronal recruitment leading to increased upper airway muscle tone is sluggish.
Also, respiratory control in children is dominated by inhibitory responses. The predominance of inhibitory responses during airway obstruction results in apnea rather than stimulation of respiration. Obstruction of the airway is more of a problem with sleep because oropharyngeal muscle tone is at its lowest during sleep. The majority of children with OSA do not appear to arouse in response to either upper airway obstruction, hypercapnia, or hypoxia and are able to maintain normal sleep architecture at the expense of oxygenation and hypercarbia. Thus a child with an adequate airway and no complaints of hypersomnolence during the day can still have significant OSA while asleep.