Subjects with isolated complaints of chronic daytime sleepiness are us
ually classified as ''idiopathic hypersomniacs'' and treated symptomat
ically. A group of these subjects was investigated during nocturnal sl
eep and daytime naps. In a subgroup of them, sleep was fragmented by v
ery short alpha EEG arousals throughout the sleeping period. These sho
rt arousals are usually ignored in sleep analyses, but their impact is
significant (in the 15 subjects identified with the syndrome, the mea
n sleep latency in multiple sleep latency tests was 5.1 +/- 1 min). Th
ese arousals are directly related to an abnormal increase in respirato
ry efforts during sleep (the mean peak inspiratory esophageal pressure
measured in our subjects in the respiratory cycle just preceding a tr
ansient arousal was - 33 +/- 7 cm H2O). Typically, an arousal occurs w
ithin one to three breaths of flow limitation associated with abrupt b
ut limited reduction in tidal volume (ie, abnormal increase in upper a
irway resistance during sleep). The arousal restores normal breathing.
Snoring was noted in association with these transient arousals in 10
of the 15 subjects; however, snoring was neither sufficient nor necess
ary for the identification of the clinical syndrome. Both sexes were e
qually represented in the affected group. All studied subjects had upp
er airway anatomy that was mildly abnormal. Nasal continuous positive
airway pressure, used as an experimental tool, eliminated the daytime
sleepiness (multiple sleep latency mean score = 13.5 min), the transie
nt arousals (mean alpha EEG arousal index decreased from 31.3 +/- 12.4
to 8 +/- 2 per hour of sleep), and the abnormal upper airway resistan
ce. Chronic daytime sleepiness is a major cause of social, economic, a
nd medical impairment. Recognition of this syndrome and its cause is i
mportant, as specific treatments can be developed to eliminate the pro
blem.