The pathophysiology of obstructive sleep apnoea (OSA) is complex and i
ncompletely understood, A narrowed upper airway is very common among O
SA patients, and is usually in adults due to nonspecific factors such
as fat deposition in the neck, or abnormal bony morphology of the uppe
r airway. Functional impairment of the upper airway dilating muscles i
s particularly important in the development of OSA, and patients have
a reduction both in tonic and phasic contraction of these muscles duri
ng sleep when compared to normals, A variety of defective respiratory
control mechanisms are found in OSA, including impaired chemical drive
, defective inspiratory load responses, and abnormal upper airway prot
ective reflexes, These defects may play an important role in the abnor
mal upper airway muscle responses found among patients with OSA. Local
upper airway reflexes mediated by surface receptors sensitive to intr
apharyngeal pressure changes appear to be important in this respect. A
rousal plays an important role in the termination of each apnoea, but
may also contribute to the development of further apnoea, because of a
reduction in respiratory drive related to the hypocapnia which result
s from postapnoeic hyperventilation, A cyclical pattern of repetitive
obstructive apnoeas may result.A better understanding of the integrate
d pathophysiology of OSA should help in the development of new therape
utic techniques.