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The term, "Upper Airway Resistance Syndrome," (UARS) was first coined by Dr. Guilleminault at Stanford in 1993, to signify 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. There is no actual cessation of breathing, nor any decrease in oxygen saturation, but with measurement of air flow through the nose and mouth there are signs of decreased flow on breathing in. The arousals and resulting sleep fragmentation are related to increased effort to breathe, detectable with measurement of pressure changes in the esophagus. Just before the arousal, the esophageal pressure starts to decrease, indicating increased effort to maintain the flow of air, which is only slightly reduced.
Guilleminault's original group of 15 UARS patients had fairly high arousal indices of 31/hour, abnormally low percentages of stages 3 and 4 sleep (see Glossary) and fairly normal REM sleep(see Glossary). On Multiple Sleep Latency Testing or MSLT (see Glossary) there was a significantly reduced sleep latency of only 5.3 minutes, corroborating the patients' reports of increased sleepiness. Treatment with CPAP at low pressures (7) reduced the arousal index to an average of 7.9, all patients ending up in a "normal range" of less than 10, and MSLT results showed improvement to sleep latencies averaging 13.5, with increases in stage 3 and 4 sleep. In other words, despite their lack of real apneas or hypopneas, these patients who merely seemed to require extra effort to maintain their respiratory flow had respiratory-related arousals, symptoms, and CPAP response very similar to sleep apneics. Systolic and diastolic blood pressures were increased in association with the arousals, and patients with UARS who had borderline hypertension improved their blood pressures with CPAP.
Research done by these authors suggested improved was of diagnosing UARS with various measures, since the direct measurement of esophageal pressure with a pressure sensor which must go down the patient's nose into the throat may disturb sleep. The authors note that the curve of inspiratory air flow as the patient breathes is normally rounded, looking something like a sine wave, whereas the flow tracing in apneics and UARS patients show a flattening at the peak of inspiration, indicating airway narrowing limiting flow increase as the patient breathes against increasing resistance. However, this indicator has yet to be validated and is difficult to define by visual inspection. The authors developed a resistance tube added to a CPAP mask to allow forced oscillation of breathing and the parallel respiratory impedance (or resistance) which parallels the degree of effort during UARS. In their own patients, with daytime somnolence but without increased apnea-hypopnea indices, the number of EEG arousals added up to 43.2/hour, but most (32.7) of these were not associated with apneas or hypopneas. The forced oscillation technique allowed the authors to identify 19.2 of these arousals as related to partial airway obstruction, thereby making the diagnosis of UARS without needing to measure esophageal pressure. They note other alternatives for identifying respiratory-related arousals, such as rises in blood pressure.
This article represents more a review than a report of original research, but I included it anyway because of the importance of sleep apneics being aware of the syndrome of UARS and how it might be diagnosed in people with otherwise typical sleep apnea syndromes but low AHI indices. Also, it may be that even in people with typical sleep apnea, some arousals may go unrecognized as respiratory-related because of being in the nature of UARS. This would lead to maladjustment of CPAP titration if the technician relied on suppression of apneas and hypopneas alone, and might result in the patient remaining symptomatic despite CPAP which seemingly eliminates apneas and hypopneas, yet has not other obvious cause of sleep fragmentation like periodic leg movements of sleep. It is important to realize that it is sleep fragmentation which is probably the main culprit in causing many of the symptoms of sleep apnea, not hypoxia, which may be quite minimal with hypopneas and quite absent with UARS or PLMS.
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