Timothy Roehr PhD; Frank Zorick, MD...

Timothy Roehr PhD; Frank Zorick, MD; Robert Wittig, MD; William Conway, MD FCCP; and Thomas Roth Ph.D.[unkeyable]

Excessive daytime sleepiness, the in the greatest degree prevalent symptom associated with the OSAS, is hypothesized to proceed from either fragmentation of slumber or hypoxemia during sleep. Measures of nocturnal be still respiration during sleep, and daytime sleepiness in 466 patients with apnea were deduceed to evaluate these two hypotheses. The various parameters were submitted to correlation and multiple regression analyses to predict daytime sleepiness as measured on the MSLT. The RAI, which measures the number of arousals from drowse associated with respiratory disturbances (best fragmentation correlation), produc a higher correlation with MSLT scores than did TME (best hypoxemia correlation); however, the measures were highly intercorrelated, and multiple regression analyses to determine which parameters independently predicted MSLT showed the single best predictor to be the RAI. Additional independent variance in MSLT score was explained according to TST and PSG1. Measures of hypoxemia provided little or no independent predictive information. These data support the hypothesis that doze fragmentation is an important determinant of daytime sleepiness in patients with apnea.

(Chest 1989; 95:1202-06)

Among the various symptoms typically associated with the OSAS, the chiefly prevalent is excessive daytime sleepiness;[1-3] however, questions remain as to the etiology of the excessive sleepiness of patients with OSAS. couple hypotheses have been offered to explain the sleepiness: (1) be still fragmentation, and (2) hypoxemia. rest fragmentation refers to the punctuation of be motionless by brief (1-second to 10-second) electroencephalographic arousals which be found at the termination of an episode of apnea.[4] This fragmentation of nap disrupts its continuity and, hence, its restorative function. Studies from several laboratories have now shown that experimental fragmentation of the repose of healthy normal subjects occasions excessive daytime sleepiness.[4-6] Regarding the inferior hypothesis, it is suggested that through the whole extent of the usual eight-hour sleeping period, a significant amount of hypoxemia caused by dint of apneas occurs, and the hypoxemia leads to the excessive sleepiness of the patient with OSAS.[7]

alone three studies have attempted to evaluate the brace hypotheses. Unfortunately, two of the studies did not measure sleepiness objectively and hence cannot be considered conclusive. The first application of mind compared four patients with symptoms of excessive sleepiness to four asymptomatic patients.[7] The symptomatic and asymptomatic patients had a similar number of apneas still differed in nocturnal hypoxemia, with a mean [PaO.sub.2] of 47 v 70 mm Hg These authors[7] conclud that the hypoxemia is producing the symptoms of sleepiness. It is important to note that in this consideration the two groups of patients also differed, although not significantly, in the amount of stage 1 drowse and movement time. the pair of these sleep-stage elevations are reflective of increased fragmentation of sleep[8]

The next to the first study also compared patients reporting excessive sleepiness with those not reporting sleepiness.[9] Measures of oxygen saturation during rest and the number of apneas and hypopneas were submitted to a discriminant analysis. The assemblages were discriminated by two hypoxemic variables ([SaO.sub.2]<90 percent and [SaO.sub.2]<80 percent) suggesting to the authors that sleepiness is associated with oxygen desaturation during be motionless but this study also failed to make an objective assessment of sleepiness. Furthermore, no measure of the total number of arousals or the amount of stage 1 be still was included in the discriminant analysis.

one as well as the other of these two studies demonstrate that subjective measures of sleepiness covary with hypoxemia; however, equable if subjective sleepiness were reflective of actual plains of daytime sleepiness, these sum of two units studies would not resolve the issue of what causes the sleepiness associated with OSAS. Almost all apneic conclusions are accompanied by an arousal from nap and some degree of hypoxemia. Thus, one as well as the other hypoxemia and sleep fragmentation are associated with sleepiness in patients with OSAS. The important question is not whether either or as well-as; not only-but also; not only-but; not alone-but correlate with sleepiness, but rather which of these factors uniquely predicts sleepiness and which simply covaries with the apneic termination Multiple regression analyses can be used to make of the like kind a determination.

A extremely recent study of 100 patients with OSAS measured daytime sleepiness objectively and applied regression and cluster analyses to assess the determinants of the sleepiness in OSAS.[10] Polygraphic measures of doze (including the amount of stage 1 sleep) respiratory disturbances, and oxygen saturation during be dead all were submitted to the analyses; however, the subject of attention failed to find any statistically significant correlates of daytime sleepiness, although the authors conclud that among all of the variables, the best predictors were those reflecting "sleep pile anomalies."