Nm. Punjabi et al., Modeling hypersomnolence in sleep-disordered breathing - A novel approach using survival analysis, AM J R CRIT, 159(6), 1999, pp. 1703-1709
The etiology of excessive daytime sleepiness in patients with sleep-disorde
red breathing (SDB) is not well defined. In this study, we examined the rel
ationships between several clinical and polysomnographic parameters and the
degree of hypersomnolence in 741 patients with SDB (apnea-hypopnea index [
AHI] greater than or equal to 10 events/h). The study sample was obese (bod
y mass index [BMI]: 35.3 +/- 8.5 kg/m(2)) and had evidence of moderate SDB
(AHI: 47.6 +/- 29.3 events/h). Hypersomnolence was quantified with the mult
iple sleep latency test (MSLT) and survival analysis was used to assess the
risk factors for hypersomnolence. In a multivariate proportional hazards m
odel, AHI and nocturnal hypoxemia were independent predictors of hypersomno
lence (MSLT < 10 min). The adjusted relative risks (RR) of hypersomnolence
were 1.00, 1.30, and 1.65 for patients with an AHI of 10 to 29.9, 30 to 59.
9, and greater than or equal to 60 events/h, respectively. A positive assoc
iation between hypersomnolence and oxyhemoglobin desaturation (Delta Sa(O2)
) was observed with RR of 1.00, 1.18, 1.43, and 1.94 for a Delta Sa(O2) of
less than or equal to 5%, 5.1 to 10%, 10.1 to 15%, and >15%, respectively.
Sleep fragmentation, as assessed by the distribution of sleep stages, was a
lso an independent predictor of hypersomnolence. Using stage 1 sleep as a r
eference, an increase in stage 2 and slow wave sleep (SWS) were protective
from hypersomnolence. For a 10% increase in stage 2 or SWS the adjusted RR
for hypersomnolence were 0.93 and 0.79, respectively. REM sleep showed no s
ignificant association with the degree of hypersomnolence. These results su
ggest that AHI, nocturnal hypoxemia, and sleep fragmentation are independen
t determinants of hypersomnolence in SDB.