Upper Airway Resistance Syndrome (UARS)
The term Upper Airway Resistance Syndrome (UARS) was first coined by Guilleminault in 1993 and used to describe chronic daytime sleepiness in the absence of actual apneas or hypopneas, but often associated with snoring in turn associated with brief, frequent arousals with an only slightly abnormal breathing pattern.  Patients may present with the clinical features of hypersomnolence but lack the typical findings of apnea, hypopnea and nocturnal oxygen desaturation during polysomnography (PSG).
Patients with UARS lack the typical findings of apnea on PSG and, therefore, are often not diagnosed. The arousals and sleep fragmentation are related to an increased effort to breathe which can be diagnosed by measurement of pressure changes in the esophagus [Pes].

References:
Stoohs R The Upper Airway Resistance Syndrome (UARS)
In Sleep-Wake Disorders, edited by K. Meier-Ewert and M. Okawa, Plenum Press, New York, 1998, pp 165-174

Guilleminault C, Stoohs R, Clerk A, Cetel M, Maistros P
A cause of excessive daytime sleepiness. The upper airway resistance syndrome [see comments]
In: Chest (1993 Sep) 104(3):781-7   ISSN: 0012-3692
Subjects with isolated complaints of chronic daytime sleepiness are usually classified as "idiopathic hypersomniacs" and treated symptomatically. A group of these subjects was investigated during nocturnal sleep and daytime naps. In a subgroup of them, sleep was fragmented by very short alpha EEG arousals throughout the sleeping period. These short arousals are usually ignored in sleep analyses, but their impact is significant (in the 15 subjects identified with the syndrome, the mean sleep latency in multiple sleep latency tests was 5.1 +/- 1 min). These arousals are directly related to an abnormal increase in respiratory efforts during sleep (the mean peak inspiratory esophageal pressure measured in our subjects in the respiratory cycle just preceding a transient arousal was -33 +/- 7 cm H2O). Typically, an arousal occurs within one to three breaths of flow limitation associated with abrupt but limited reduction in tidal volume (ie, abnormal increase in upper airway 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 necessary for the identification of the clinical syndrome. Both sexes were equally represented in the affected group. All studied subjects had upper 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 transient arousals (mean alpha EEG arousal index decreased from 31.3 +/- 12.4 to 8 +/- 2 per hour of sleep), and the abnormal upper airway resistance. Chronic daytime sleepiness is a major cause of social, economic, and medical impairment. Recognition of this syndrome and its cause is important, as specific treatments can be developed to eliminate the problem.
Comment in: Chest 1993 Sep;104(3):665-6
Comment in: Chest 1994 Aug;106(2):646
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Stanford University School of Medicine
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