ライフサイエンスコーパス: sleepiness

1 epiness) to 24 points (high level of daytime sleepiness).

2 0-24, with values <10 suggesting no daytime sleepiness).

3 ] >or= 5/hour, and >or= 2 symptoms including sleepiness).

4 study for patients with unexplained daytime sleepiness.

5 y significant sleep disturbances and daytime sleepiness.

6 is a common disease, responsible for daytime sleepiness.

7 excessive sleep, and its links to excessive sleepiness.

8 p deprivation-induced increase in subjective sleepiness.

9 ociated with reduced alertness and increased sleepiness.

10 iness scale, 1312 (28.5%) reported excessive sleepiness.

11 y significant decrease in subjective daytime sleepiness.

12 on reward sensitivity either directly or via sleepiness.

13 thalamic injury, with inactivity and daytime sleepiness.

14 imilar in terms of their impact on objective sleepiness.

15 mon in older adults, was not associated with sleepiness.

16 44) complaints of frequent excessive daytime sleepiness.

17 ven beverages per week) reduced the risk for sleepiness.

18 hase advances, respectively, without causing sleepiness.

19 commonly present in those with complaints of sleepiness.

20 ective reports of depressed mood and current sleepiness.

21 rtant consequences such as excessive daytime sleepiness.

22 ve useful in prediction of excessive daytime sleepiness.

23 ce sleep fragmentation and excessive daytime sleepiness.

24 effects may not be directly attributable to sleepiness.

25 ariation of obesity with snoring and daytime sleepiness.

26 e important outcome, the severity of daytime sleepiness.

27 healthy subjects, which are associated with sleepiness.

28 This effect was related to the level of sleepiness.

29 se (CAD), many of whom do not report daytime sleepiness.

30 Food consumption is thought to induce sleepiness.

31 he relationship between mild OSA and daytime sleepiness.

32 y, poor sleep quality, and excessive daytime sleepiness.

33 omycin on objective vigilance and subjective sleepiness.

34 ansient but substantial increases in daytime sleepiness.

35 so associated with reduced AHI and excessive sleepiness.

36 delayed sleep habits, and excessive daytime sleepiness.

37 ures include snoring, witnessed apnoeas, and sleepiness.

38 /hypocretin (OH) neurons causes pathological sleepiness [1-4], whereas OH hyperactivity is associated

39 nterval): 2.97 (2.65-3.34)), regular daytime sleepiness (2.66 (2.34-3.01)), and regular insomnia (2.3

40 nd 1.33; P < 0.001 for all domains), daytime sleepiness (-2.92; P < 0.001), mood state (-4.24; P = 0.

41 h risk for OSAS, 46.3% had excessive daytime sleepiness, 41.5% were positive for both the Bq and ESS,

42 Excessive daytime sleepiness affected 32% of the patients, sometimes with

43 annoyance, disturbs sleep and causes daytime sleepiness, affects patient outcomes and staff performan

44 ions, moving violations, aggressive driving, sleepiness, alcohol abuse, metabolic disorders, and mult

45 Acute melatonin suppression and subjective sleepiness also had a dose-dependent response to light e

46 Excessive sleepiness among the elderly is multifactorial.

47 in performance were independent of reported sleepiness and awareness of stimulus changes, arguing ag

48 sleep, is characterized by excessive daytime sleepiness and cataplexy, a loss of muscle tone triggere

49 Narcolepsy is characterized by chronic sleepiness and cataplexy, episodes of profound muscle we

50 Narcolepsy is characterized by excessive sleepiness and cataplexy, sudden episodes of muscle weak

51 Narcolepsy is characterized by chronic sleepiness and cataplexy-sudden muscle paralysis trigger

52 olepsy, a condition characterized by chronic sleepiness and cataplexy.

53 disorder characterized by excessive daytime sleepiness and cataplexy.

54 which is characterized by excessive daytime sleepiness and cataplexy.

55 a significant increase in daytime subjective sleepiness and changes in the EEG architecture of a subs

56 toms, and well-being, and objective tests of sleepiness and cognition.

57 as been implicated in pathways that generate sleepiness and cognitive impairments, but existing mathe

58 Sleepiness and distress, when modeled together, showed l

59 nificantly more likely to experience daytime sleepiness and dozing during daytime activities.

60 vative strategies to minimize the effects of sleepiness and fatigue on patient care and resident safe

61 n, which is often characterized by excessive sleepiness and fatigue.

62 oor maintenance of wakefulness indicative of sleepiness and fragmented sleep and lacked any electroph

63 ocytes throughout the brain causes excessive sleepiness and fragmented wakefulness during the nocturn

64 d with modafinil continued to have excessive sleepiness and impaired performance at night.

65 d breathing (SDB) is associated with daytime sleepiness and impaired quality of life.

66 choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.

67 etween increased levels of excessive daytime sleepiness and increased measures for adiposity traits (

68 es recurrent arousals from sleep, leading to sleepiness and increased risk of motor vehicle and occup

69 older people with OSA syndrome, CPAP reduces sleepiness and is marginally more cost effective over 12

70 not only because of the negative impacts of sleepiness and its root causes on health and social func

71 Because of the strong interactions between sleepiness and motivation, the role of sleepiness was al

72 nts receiving escitalopram had more frequent sleepiness and obstipation than did those in the other t

73 Increases in objective sleepiness and performance lapses, as well as poorer lan

74 , respectively, narcolepsy excessive daytime sleepiness and poor sleep quality.

75 nd substantially improving excessive daytime sleepiness and quality of life.

76 Narcolepsy with cataplexy, characterized by sleepiness and rapid onset into REM sleep, affects 1 in

77 iness Scale (ESS) was used to assess daytime sleepiness and standardized questionnaires assessed snor

78 to explore the relationship between daytime sleepiness and the risk of ischemic stroke and vascular

79 Daytime sleepiness and time to fall asleep decreased during weig

80 of characteristic history (snoring, daytime sleepiness) and physical examination (increased neck cir

81 ted with increases in fatigue (tiredness and sleepiness) and with deterioration in cognitive performa

82 e in obesity, 40% of the variance in daytime sleepiness, and 23% of the variability in self-reports o

83 ted sleep characteristics, excessive daytime sleepiness, and chronotype using the Pittsburgh Sleep Qu

84 s; polysomnography; and symptoms of fatigue, sleepiness, and depression.

85 lf-reported parental sleep duration, daytime sleepiness, and dozing among employed adults.

86 triction, irregular sleep schedules, daytime sleepiness, and elevated risk for sleep disturbances.

87 cating patients about the risks of excessive sleepiness, and encouraging clinicians to become familia

88 The degree of performance impairment, sleepiness, and homeostatic sleep-pressure response to s

89 ivid dreams, insomnia, nausea, constipation, sleepiness, and indigestion.

90 ant interactions between eczema and fatigue, sleepiness, and insomnia as predictors of poorer overall

91 ent-reported measures of depression, daytime sleepiness, and quality of life.

92 e, the visual analog scale score for daytime sleepiness, and sleep log-derived and actigraphy-derived

93 ep are not associated with excessive daytime sleepiness, and therefore appear unlikely to contribute

94 reased nocturnal activity, excessive daytime sleepiness, and weight loss.

95 clinical features (i.e., significant daytime sleepiness, anxiety and depression symptoms, potential f

96 igue (aOR, 1.59; 95% CI, 1.16-2.19), daytime sleepiness (aOR, 1.81; 95% CI, 1.28-2.55), or insomnia (

97 ng from chest at night, and medications with sleepiness as a side effect.

98 ith the respiratory cycle predicted next-day sleepiness as measured by the multiple sleep latency tes

99 s minimal oxygen saturation, did not predict sleepiness as well.

100 .6]; 13 trials, 543 participants), excessive sleepiness assessed by ESS score (WMD, -2.0 [95% CI, -2.

101 ine/after AAC; (3) hourly ammonia/subjective sleepiness assessment for 8 hours after AAC; (4) sleep E

102 Self-reported daytime sleepiness associated with increased risk for all-cause

103 oving wakefulness in patients with excessive sleepiness associated with narcolepsy, obstructive sleep

104 Secondary outcomes were subjective sleepiness at 12 months, plus objective sleepiness, qual

105 ystem disorders, including excessive daytime sleepiness, attention deficit hyperactivity disorder, Al

106 e associated with improvements in attention, sleepiness, behavior, and quality of life, and that chan

107 In contrast, sleepiness best predicted vigilance.

108 This study supports the notion that daytime sleepiness, but not nighttime sleeping duration, is one

109 Subjective sleepiness, but not psychomotor vigilance, improved duri

110 designing a drug that could treat excessive sleepiness by promoting alertness.

111 Sleep Latency Test in all subjects, problem sleepiness by self-rating in 873, and subjective sleep p

112 ctive strategy for identifying biomarkers of sleepiness by using genetic and pharmacological tools th

113 disorder characterized by excessive daytime sleepiness, cataplexy, and other pathological manifestat

114 disorder characterized by excessive daytime sleepiness, cataplexy, hypnagonic hallucinations, sleep

115 criteria for diencephalic encephalitis with sleepiness, cataplexy, hypocretin deficiency, and centra

116 Objective sleepiness, cognitive performance, and preference for tr

117 The complaint of excessive daytime sleepiness, commonly encountered in neurological practic

118 anxiety and depressive symptoms, and daytime sleepiness compared with conservative treatment.

119 nal-assist servoventilation improves daytime sleepiness compared with the control.

120 neurological underpinnings of alertness and sleepiness deepens, improved treatment methods are bound

121 Subjects had few symptoms, that is, sleepiness, depression, anxiety, and cognitive deficits.

122 nea syndrome can experience residual daytime sleepiness despite regular use of nasal continuous posit

123 Narcolepsy is a common cause of chronic sleepiness distinguished by intrusions into wakefulness

124 rial stiffness), neurobehavioral (subjective sleepiness, driving simulator performance), and quality

125 In contrast, sleepiness, driving simulator performance, and disease-s

126 rk sleep disorder chronically have excessive sleepiness during night work and insomnia when attemptin

127 ng chronotypes reported a faster increase in sleepiness during the day than evening chronotypes, whic

128 xploring the links between excessive daytime sleepiness (EDS) and vulnerability to infectious disease

129 tment of disorders such as excessive daytime sleepiness (EDS) as well as other sleep or cognitive dis

130 fety and efficacy of LT on excessive daytime sleepiness (EDS) associated with PD.

131 We assessed whether excessive daytime sleepiness (EDS) at baseline was associated with subsequ

132 Excessive daytime sleepiness (EDS) is common and disabling in Parkinson's

133 ng and between obesity and excessive daytime sleepiness (EDS), although for the most part the genetic

134 g risk, inquiring about additional causes of sleepiness, educating patients about the risks of excess

135 rcentage of patients with normalized daytime sleepiness (Epworth score < 10) was significantly higher

136 urgh Sleep Quality Index [PSQI]) and daytime sleepiness (Epworth Sleepiness Scale [ESS]).

137 sleepiness, patients with excessive daytime sleepiness (Epworth Sleepiness Scale score >/=10) had a

138 Patients with self-reported daytime sleepiness (Epworth Sleepiness Scale score >10) and an a

139 pnea-hypopnea index >/=15/h) without daytime sleepiness (Epworth Sleepiness Scale score <10) were ran

140 (Pittsburgh Sleep Quality Index) and daytime sleepiness (Epworth Sleepiness Scale), and circadian mar

141 r 1 wk at home and sleep apnea in subjective sleepiness (Epworth Sleepiness Scale), objective sleepin

142 tual snorers, 18% reported excessive daytime sleepiness (ESS > or = 11), and 29% were obese (body mas

143 olepsy is characterized by excessive daytime sleepiness, fragmentation of nighttime sleep, and catapl

144 n/hypocretin signaling, resulting in chronic sleepiness, fragmented non-rapid eye movement sleep, and

145 Excessive daytime sleepiness has emerged as one of the most common, but of

146 rome occurs, which includes fever, anorexia, sleepiness, hyperalgesia and elevated corticosteroid sec

147 sleepier on the MSLT and reported increased sleepiness, hypnagogic hallucinations and cataplexy-like

148 es sleep architecture, and decreases daytime sleepiness in abstinent cocaine users.

149 dered the first-line treatment for excessive sleepiness in adult patients with narcolepsy.

150 ncrease in ammonia concentrations/subjective sleepiness in both patients and healthy volunteers; (ii)

151 morning-dosed modafinil on sleep and daytime sleepiness in chronic cocaine users.

152 bles associated with longitudinal changes in sleepiness in early PD.

153 differential diagnosis of excessive daytime sleepiness in older adults.

154 elf-reported symptoms of snoring and daytime sleepiness in older men have a genetic basis that is lar

155 multiple risk factors for excessive daytime sleepiness in older subjects (mean age, 78 years; range

156 However, treatment of mild OSA may improve sleepiness in patients who are sleepy at baseline and im

157 produces an improvement in excessive daytime sleepiness in patients with Cheyne-Stokes breathing and

158 tment for the management of residual daytime sleepiness in patients with obstructive sleep apnea/hypo

159 on (SF) appear to underlie excessive daytime sleepiness in patients with sleep apnea (OSA).

160 evaluated the use of modafinil for treating sleepiness in patients with this disorder.

161 Circadian dysfunction may underlie excessive sleepiness in PD.

162 le increases in subjective and physiological sleepiness in response to chronic sleep loss.

163 afinil for the treatment of residual daytime sleepiness in such patients.

164 There was a significant reduction in sleepiness in the positive airway pressure therapy group

165 ion, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586).

166 clarithromycin, have been reported to reduce sleepiness in these patients.

167 developing an effective method for detecting sleepiness in vulnerable populations.

168 ibe the effectiveness of countermeasures for sleepiness, including recent work-hour restrictions.

169 Sleepiness increased motivation to choose the high-effor

170 dical disorder that causes excessive daytime sleepiness, increasing the risk for drowsy driving two t

171 gether, our findings show that the excessive sleepiness incurred by recurrent arousals during sleep m

172 iated with atopy, fatigue, excessive daytime sleepiness, insomnia, and only 0 to 3 nights of sufficie

173 by neurologists, including excessive daytime sleepiness, insomnia, narcolepsy, rapid eye movement sle

174 Daytime sleepiness is an independent risk factor for stroke and

175 h and social function, but because excessive sleepiness is generally remediable with appropriate trea

176 ), but its value in patients without daytime sleepiness is uncertain.

177 To cope with sleepiness, many teens regularly consume highly caffeina

178 not affect rhythms of subjective hunger and sleepiness, master clock markers (plasma melatonin and c

179 Sleepiness may account for up to 20% of crashes on monot

180 SA in individuals who demonstrate subjective sleepiness may be beneficial.

181 Preliminary evidence suggests that daytime sleepiness may predate clinical diagnosis of Parkinson d

182 Increased sleepiness may reduce the likelihood of arousal with eac

183 ference, -0.42 [0.09], P < .001) and daytime sleepiness (mean [SE] difference, -0.24 [0.09], P = .006

184 Subjective sleepiness, melatonin and cortisol were assessed hourly.

185 ondary endpoints included changes in daytime sleepiness, mood state, anxiety, and depression.

186 circadian effects were observed for reported sleepiness, mood, and reported effort; the effects on wo

187 diurnal preference, sleep quality/timing and sleepiness/mood questionnaires.

188 ion, cardiovascular disease, stroke, daytime sleepiness, motor vehicle accidents, and diminished qual

189 males and WDR27 in males), excessive daytime sleepiness (near AR-OPHN1) and a composite sleep trait (

190 tle change in point estimates of effect, but sleepiness no longer had a statistically significant ass

191 t the physiologic process that underlies the sleepiness of narcolepsy is unknown.

192 osterior hypothalamus completely rescued the sleepiness of these mice, but their fragmented sleep was

193 ion, consistent with decreased self-reported sleepiness on SYN115.

194 rovements in attention deficits (P < 0.001); sleepiness on the Epworth Sleepiness Scale (P < 0.001);

195 om NREM1 are a marker of severity, either of sleepiness or REM instability.

196 howed no association with subjective problem sleepiness or sleep propensity.

197 (P = .009, I2 = 74%), and excessive daytime sleepiness (OR, 2.27; 95% CI, 1.54-3.35) (P < .001, I2 =

198 2.65; P=0.023), those with excessive daytime sleepiness (OR, 2.51; P=0.037), and those with >/=2 medi

199 (P = .003, I2 = 76%), and excessive daytime sleepiness (OR, 2.72; 95% CI, 1.32-5.61) (P = .007, I2 =

200 that eczema associated with fatigue, daytime sleepiness, or insomnia was associated with even higher

201 y and fatigue, depression, excessive daytime sleepiness, or rapid eye movement sleep behaviour disord

202 al women with complaints of snoring, daytime sleepiness, or unsatisfactory sleep.

203 Daytime sleepiness (Osler test) was measured before and after th

204 measured duration and fragmentation, daytime sleepiness, overall quality, self-reported duration) wer

205 .008); and symptoms of snoring, fatigue, and sleepiness (P < 0.001).

206 iated with arousals predicted less objective sleepiness (p = 0.008); rates of leg movements without a

207 nts were associated with decreased objective sleepiness (p = 0.03) but explained less than 1% of the

208 ng history, pRBD was associated with greater sleepiness (p=0.001), depression (p=0.001) and cognitive

209 CPAP improved objective sleepiness (p=0.024), mobility (p=0.029), total choleste

210 d with PD patients without excessive daytime sleepiness, patients with excessive daytime sleepiness (

211 Sleepiness plays an important role in major crashes of c

212 circadian rhythms in core body temperature, sleepiness, power in the theta band of the wake EEG, sle

213 led clinical trials with the endpoints being sleepiness, quality of life, and 24-h ambulatory blood p

214 s not only patient-reported outcomes such as sleepiness, quality of life, and mood but also intermedi

215 tive sleepiness at 12 months, plus objective sleepiness, quality of life, mood, functionality, noctur

216 +/- 5, respectively), functional outcomes of sleepiness questionnaire, short-form 36 health survey me

217 battery consisting of cognitive subtests, a sleepiness rating scale, and a mood scale, to predict ne

218 piness (Epworth Sleepiness Scale), objective sleepiness (reduced sleep latency as determined by the M

219 onger to fall asleep and had reduced evening sleepiness, reduced melatonin secretion, later timing of

220 , as the syndrome may increase their risk of sleepiness-related accidents.

221 ological fragmentation of wakefulness (i.e., sleepiness), respectively.

222 Obstructive sleep apnoea causes sleepiness, road traffic accidents, and probably systemi

223 13], P = .01) and incident OSA with habitual sleepiness (RR, 1.18 [95% CI, 1.07-1.31], P = .02).

224 associated with new-onset OSA with habitual sleepiness (RR, 2.72 [95% CI, 1.26-5.89], P = .045).

225 erns to rate fatigue on the 7-point Stanford Sleepiness Scale (7 is most tired).

226 rimary outcome was 6-month change in Epworth Sleepiness Scale (ESS) score, which ranges from 0 (no da

227 art) were negatively associated with Epworth sleepiness scale (ESS) scores and sex (male).

228 ty, area under the curve (AUC), AHI, Epworth Sleepiness Scale (ESS) scores, blood pressure, mortality

229 The Epworth Sleepiness Scale (ESS) was used to assess daytime sleepi

230 he Berlin questionnaire (Bq) and the Epworth sleepiness scale (ESS) were applied to determine the ris

231 Secondary outcomes included the Epworth Sleepiness Scale (ESS), the Sleep Apnea Symptoms Questio

232 EDS was measured with the Epworth Sleepiness Scale (ESS).

233 h Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS, which assesses daytime hypersomno

234 icits (P < 0.001); sleepiness on the Epworth Sleepiness Scale (P < 0.001); behavior (P < 0.001); and

235 ndex [PSQI]) and daytime sleepiness (Epworth Sleepiness Scale [ESS]).

236 the Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale and Morningness-Eveningness Questionnai

237 ses in subjective somnolence (via Karolinska Sleepiness Scale and Visual Analogue Scale measures) and

238 correlation between the decrease in Epworth Sleepiness Scale at 3 months and adherence (r = 0.411; P

239 d subjective sleep propensity by the Epworth Sleepiness Scale in 201.

240 The main outcome was the Epworth Sleepiness Scale measurement.

241 We obtained the Epworth Sleepiness Scale on 2088 community residents.

242 s with excessive daytime sleepiness (Epworth Sleepiness Scale score >/=10) had a significantly lower

243 th self-reported daytime sleepiness (Epworth Sleepiness Scale score >10) and an apnea-hypopnea index

244 >/=15/h) without daytime sleepiness (Epworth Sleepiness Scale score <10) were randomized to auto-titr

245 rovements in EDS, as assessed by the Epworth Sleepiness Scale score (mean [SD], 15.81 [3.10] at basel

246 sequent self-reported error with the Epworth Sleepiness Scale score (odds ratio [OR], 1.10 per unit i

247 utcome measure was the change in the Epworth Sleepiness Scale score comparing the bright LT with the

248 index of 20 h(-1) or greater and an Epworth Sleepiness Scale score of 10 or less (scores range from

249 th coexistent EDS, as assessed by an Epworth Sleepiness Scale score of 12 or greater, and without cog

250 of 57.1 (10.1) years and a mean (SD) Epworth Sleepiness Scale score of 9.8 (4.4), and 77.5% were post

251 o 1.20 per one-point increase in the Epworth Sleepiness Scale score).

252 reater mean changes from baseline in Epworth Sleepiness Scale scores at Weeks 1 and 4 (p < 0.001) and

253 s in the intervention group, with Karolinska sleepiness scale scores of 6.65 (95% CI, 6.35-6.97) vs 7

254 of the Northern Manhattan Study, the Epworth Sleepiness Scale was collected during the 2004 annual fo

255 ed by using a questionnaire with the Epworth Sleepiness Scale) were assessed before and immediately a

256 ality Index) and daytime sleepiness (Epworth Sleepiness Scale), and circadian markers of the melatoni

257 leep apnea in subjective sleepiness (Epworth Sleepiness Scale), objective sleepiness (reduced sleep l

258 Of the 4608 participants who completed the sleepiness scale, 1312 (28.5%) reported excessive sleepi

259 ypopnea index, 41 [35-53]; mean [SD] Epworth sleepiness scale, 9.3 [4.2]) were randomized to effectiv

260 luded the Epworth Sleepiness Scale, Stanford Sleepiness Scale, Functional Outcomes of Sleep Questionn

261 Secondary outcomes included the Epworth Sleepiness Scale, Stanford Sleepiness Scale, Functional

262 igit Span Test Forward and Backward, Epworth Sleepiness Scale, SteerClear, Digit Symbol, Controlled O

263 Secondary outcome measures were the Epworth Sleepiness Scale, the Functional Outcomes of Sleep Quest

264 to noon) by day of call cycle and Karolinska sleepiness scale.

265 ession screening instrument, and the Epworth Sleepiness Scale.

266 Epworth Sleepiness Score (ESS) and Functional Outcomes of Sleep

267 Coprimary endpoints were Epworth sleepiness score (ESS) at 3 months and cost-effectivenes

268 , the respiratory disturbance index (RDI), a sleepiness score, the arousal index, and sleep-associate

269 h a specialist model did not result in worse sleepiness scores, suggesting that the 2 treatment modes

270 ously significant risk factors for excessive sleepiness: severe sleep-disordered breathing (apnea-hyp

271 ement that described the relationships among sleepiness, sleep apnea, and driving risk.

272 We investigated the associations of sleepiness, sleep disorders, and work environment (inclu

273 y, poor sleep quality, and excessive daytime sleepiness, studied according to an a priori protocol.

274 For example, sleepiness surpasses alcohol and drugs as the greatest i

275 tudy, subjective ratings of treatment value, sleepiness, symptoms, and well-being, and objective test

276 However, the residual sleepiness that was observed in the treated patients und

277 with 200 mg of modafinil reduced the extreme sleepiness that we observed in patients with shift-work

278 and after the trial with change in measured sleepiness the primary endpoint.

279 In patients with OSA without daytime sleepiness, the prescription of CPAP compared with usual

280 Active treatment reduced excessive daytime sleepiness; the mean Osler change was +7.9 minutes (SEM

281 Although OSA is a risk factor for excessive sleepiness, there is developing evidence that it is also

282 arefully monitor changes in mood and daytime sleepiness throughout the intervention.

283 (ESS) score, which ranges from 0 (no daytime sleepiness) to 24 points (high level of daytime sleepine

284 hy might be unable, due to excessive daytime sleepiness, to accumulate the need/ability to produce re

285 .2, chronotype was 63.6 +/- 10.8 and daytime sleepiness was 7.4 +/- 4.8.

286 Daytime sleepiness was also associated with NC (P = 0.02) and PP

287 tween sleepiness and motivation, the role of sleepiness was also determined.

288 Objective sleepiness was assessed by the Multiple Sleep Latency Te

289 ost part the genetic variance in snoring and sleepiness was nonoverlapping with the genetic variance

290 The prevalence of insomnia and daytime sleepiness was not significantly higher compared with th

291 Daytime sleepiness was trichotomized using previously reported c

292 nt efficacy and satisfaction, and subjective sleepiness were also better with CPAP than with MRS (eff

293 Increases in subjective sleepiness were associated with shorter sleep durations

294 t) and OSA concomitant with habitual daytime sleepiness were estimated using repeated-measures Poisso

295 Polysomnography, cognitive performance, and sleepiness were monitored.

296 Subjective measures of sleepiness were significantly improved on clarithromycin

297 ression, along with changes in alertness and sleepiness, were assessed.

298 ted with the increased alertness and reduced sleepiness when methylphenidate was administered after s

299 Modafinil significantly improved daytime sleepiness, with significantly greater mean changes from

300 /= 2 hallmarks of OSA: loud snoring, daytime sleepiness, witnessed apnea, and hypertension.