Normal children have a smaller upper airway than adults, but, nevertheless, sn ore 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 tha t 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 sle ep between children with OSAS and controls. Measurements were made by correlatin g maximal inspiratory airflow with the level of nasal pressure applied via a mas k. Neuromotor upper airway activationwas assessed by evaluating the upper airway response to 1) hypercapnia and 2) intermittent, acute negative pressure. We fou nd that children with OSAS had no significant response to either hypercapnia or negative pressure during sleep, compared with the normal children. After treatme nt of OSAS by tonsillectomy and adenoidectomy, there was a trend for normalizati on of upper airway responses. We conclude that upper airway dynamic responses ar e decreased in children with OSAS but recover after treatment. We speculate that the pharyngeal airway neuromotor responses present in normal children are a com pensatory response for a relatively narrow upper airway. Further, we speculate t hat this compensatory response is lacking in children with OSAS, most likely due to either habituation to chronic respiratory abnormalities during sleep or to m echanical damage to the upper airway. Normal children have a smaller upper airway than adults, but, nevertheless, sn ore 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 tha t this resistance to collapse is due to preservation of upper airway 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 sle ep between children with OSAS and controls. Measurements were made by correlatin g maximal inspiratory airflow with the level of nasal pressure applied via a mas k. Neuromotor upper airway activation was assessed by evaluating the upper airway response to 1) hypercapnia and 2) intermittent, acute negative pressure. We fou nd that children with OSAS had no significant response to either hypercapnia or negative pressure during sleep, comp are treated with tonsillectomy and adenoidectomy, there was a trend for normalizati on of upper airway responses. We conclude that upper airway dynamic responses ar e decreased in children with OSAS but recover after treatment. We speculate that the pharyngeal airway neuromotor responses present in normal children are a com pensatory response for rather than in children with OSAS, most likely due to either habituation to chronic respiratory abnormalities during sleep or to m echanical damage to the upper airway.