We hypothesized that subatmospheric intraluminal pressure is not requi
red for pharyngeal occlusion during sleep. Six normal subjects and six
subjects with sleep apnea or hypopnea (SAH) were studied during non-r
apid-eye-movement sleep. Pharyngeal patency was determined by using fi
ber-optic nasopharyngoscopy during spontaneous central sleep apnea (n
= 4) and induced hypocapnic central apnea via nasal mechanical ventila
tion (n = 10). Complete pharyngeal occlusion occurred in 146 of 160 sp
ontaneously occurring central apneas in patients with central sleep ap
nea syndrome. During induced hypocapnic central apnea, gradual progres
sive pharyngeal narrowing occurred. More pronounced narrowing was note
d at the velopharynx relative to the oropharynx and in subjects with S
AH relative to normals. Complete pharyngeal occlusion frequently occur
red in subjects with SAH (31 of 44 apneas) but rarely occurred in norm
als (3 of 25 apneas). Resumption of inspiratory effort was associated
with persistent narrowing or complete occlusion unless electroencephal
ogram signs of arousal were noted. Thus pharyngeal cross-sectional are
a is reduced during central apnea in the absence of inspiratory effort
. Velopharyngeal narrowing consistently occurs during induced hypocapn
ic central apnea even in normal subjects. Complete pharyngeal occlusio
n occurs during spontaneous or induced central apnea in patients with
SAH. We conclude that subatmospheric intraluminal pressure is not requ
ired for pharyngeal occlusion to occur. Pharyngeal narrowing or occlus
ion during central apnea may be due to passive collapse or active cons
triction.