ライフサイエンスコーパス: sleep disorder

1 and without cognitive impairment or primary sleep disorder.

2 nxiety, learning disability, depression, and sleep disorder.

3 related sleep disorder, and circadian rhythm sleep disorder.

4 : Narcolepsy is a chronic rapid eye movement sleep disorder.

5 sfunction in these circuits can give rise to sleep disorders.

6 ible new therapeutic targets in the field of sleep disorders.

7 tentially contribute to the genesis of these sleep disorders.

8 d with comorbid medical conditions including sleep disorders.

9 eep and wake signals, potentially preventing sleep disorders.

10 nificant differences in Parkinson disease or sleep disorders.

11 ight be effective in treating certain modern sleep disorders.

12 vents were primarily nausea and vomiting and sleep disorders.

13 ns in PD, the PPN could be involved in these sleep disorders.

14 nt of multiple conditions such as stress and sleep disorders.

15 this cohort had underlying mental health and sleep disorders.

16 al vulnerability to altered communication in sleep disorders.

17 es that may be unrelated to their effects on sleep disorders.

18 s to identify genetic underpinnings of human sleep disorders.

19 lex relationship between epilepsy, sleep and sleep disorders.

20 ns and their treatments can affect sleep and sleep disorders.

21 related co-morbidities including anxiety and sleep disorders.

22 onist under development for the treatment of sleep disorders.

23 nsure optimal treatment of both epilepsy and sleep disorders.

24 ulators for the treatment of heart, lung and sleep disorders.

25 herapy for the treatment of circadian rhythm sleep disorders.

26 ers three areas: (a) Genetic determinants of sleep disorders.

27 ep health and potentially screening for some sleep disorders.

28 ential therapeutic utility in treating human sleep disorders.

29 billion people worldwide suffer from various sleep disorders.

30 -existing factors that could be exacerbating sleep disorders.

31 f conditions such as heart, lung, blood, and sleep disorders.

32 genes influencing risk for some neurological sleep disorders.

33 ts and anxiety phenotype, without detectable sleeping disorders.

34 ms of hypomania, agitation, impulsivity, and sleeping disorders.

35 lay in the development and severity of these sleeping disorders.

36 95% confidence interval [CI], 22.4 to 32.3), sleep disorders (11.6 excess cases per 1000; 95% CI, 8.3

37 (95% CI, 33.2 to 45.4), 23.5 excess cases of sleep disorders (95% CI, 19.4 to 27.6), 18.7 excess case

38 rupt natural circadian rhythms; as a result, sleep disorders affect a substantial population in moder

39 proposed theories for the pathophysiology of sleep disorders after TBI.

40 Insomnia is the most common sleep disorder among adults, especially affecting indivi

41 the high prevalence of gastrointestinal and sleep disorders among ASD children.

42 Untreated sleep disorders among police officers may adversely affe

43 Furthermore, QOL for many symptoms such as sleep disorder and malaise/feebleness was also significa

44 licated in an exceedingly common and complex sleep disorder and the development of an RLS animal mode

45 Lewy body dementia, rapid eye movement (REM) sleep disorder and/or multiple system atrophy, following

46 Hypersomnia, rapid eye movement sleep disorder and/or narcolepsy were identified in 11 s

47 ep but is also a manifestation of medical or sleep disorders and a side effect of medications.

48 e development of novel therapeutics to treat sleep disorders and anxiety.

49 erences in the progression of, for instance, sleep disorders and congestive heart failure in diabetic

50 overuse, stressful life events, depression, sleep disorders and cutaneous allodynia.

51 se (PD) is highly comorbid for a spectrum of sleep disorders and deep brain stimulation (DBS) of the

52 eurological comorbidities: motor impairment, sleep disorders and epilepsy.

53 ported in the setting of movement disorders, sleep disorders and even internal medicine disorders, su

54 ng as a new potential therapeutic target for sleep disorders and for neuropsychiatric diseases accomp

55 MOD) is used clinically for the treatment of sleep disorders and has been investigated as a potential

56 epresents a potential therapeutic target for sleep disorders and migraine-associated photophobia.

57 timizing therapeutic choice in patients with sleep disorders and neuropsychiatric conditions.

58 naptic GABA(A) receptors in the treatment of sleep disorders and other neurological conditions.

59 not examined the relationship between other sleep disorders and SCI.

60 ntions to prevent and treat circadian rhythm-sleep disorders and social jet-lag.

61 Sleep disorders and substance abuse are highly comorbid

62 lticentre studies are needed to characterise sleep disorders and their mechanisms in autoimmune encep

63 as modafinil, are used for the treatment of sleeping disorders and investigated as potential therape

64 general medical condition, breathing-related sleep disorder, and circadian rhythm sleep disorder.

65 d phase, headache, pyrexia, nasopharyngitis, sleep disorder, and tremor were the most frequent advers

66 ing indications, such as insomnia, circadian sleep disorders, and depression, new potential therapeut

67 morbidities such as anxiety, depression, and sleep disorders, and explore how to apply these findings

68 ass index, smoking, physical activity, other sleep disorders, and snoring status.

69 chemotherapy, weight gain in HIV infection, sleep disorders, and Tourette syndrome.

70 investigated the associations of sleepiness, sleep disorders, and work environment (including truck c

71 are," "critical care," "earplugs," "sleep," "sleep disorders," and "delirium." STUDY SELECTION: Inter

72 estigate whether l-dopa treatment alleviates sleep disorders; and (3) to determine whether a choliner

73 r manifestations (such as rapid eye movement sleep disorder, anosmia, constipation and depression) ap

74 ortant drug target group in the treatment of sleep disorders, anxiety, epileptic seizures, and many o

75 Individuals with this sleep disorder are also at increased risk for establishe

76 Many genetic variants associated with sleep disorders are also implicated in neurological diso

77 Sleep disorders are among the most debilitating comorbid

78 Sleep disorders are common in humans, and sleep loss inc

79 Evidence suggests that sleep disorders are common in individuals with CKD, but

80 Sleep disorders are commonly encountered in people livin

81 However, sleep disorders are frequent, often severe, and usually

82 However, sleep health and sleep disorders are not equitably distributed across rac

83 encephalitis exemplify two diseases in which sleep disorders are prominent.

84 Sleeping disorders are one of the underrecognized sequal

85 Accurate identification and diagnosis of sleep disorders as well as epilepsy is clinically import

86 rhythm may be beneficial in the treatment of sleep disorders as well as metabolic diseases.

87 Obstructive sleep apnea (OSA) is a common sleep disorder associated with obesity.

88 implicated, including apnoea of prematurity, sleep disordered breathing and congestive heart failure.

89 Obstructive sleep disordered breathing can cause death and significa

90 breathing and HVR, which may protect against sleep disordered breathing in obesity.

91 ment V(E) and HVR, which may protect against sleep disordered breathing in obesity.

92 In addition, sleep disordered breathing, inflammation, left ventricul

93 CIH-induced neuropathology in patients with sleep disordered breathing.

94 le lung disease, pulmonary hypertension, and sleep disordered breathing.

95 The prevalence of moderate-to-severe sleep-disordered breathing (>/=15 events per h) was 23.4

96 t prevalence estimates of moderate to severe sleep-disordered breathing (apnea-hypopnea index, measur

97 Sleep-disordered breathing (characterized by recurrent a

98 Sleep-disordered breathing (respiratory event index >=10

99 ing evidence suggests an association between sleep-disordered breathing (SDB) and cognitive decline i

100 Sleep-disordered breathing (SDB) during pregnancy has be

101 Sleep-disordered breathing (SDB) in children is associat

102 Sleep-disordered breathing (SDB) is a common disorder in

103 Whether sleep-disordered breathing (SDB) is a risk factor for le

104 Rationale: Sleep-disordered breathing (SDB) is associated with incr

105 Sleep-disordered breathing (SDB) is associated with path

106 Prior studies have found that sleep-disordered breathing (SDB) is common among those w

107 Sleep-disordered breathing (SDB) is common in patients w

108 ng of intrinsic information in children with sleep-disordered breathing (SDB) is different from healt

109 Sleep-disordered breathing (SDB) is frequently associate

110 Yet, sleep-disordered breathing (SDB) is highly prevalent in

111 Genetic determinants of sleep-disordered breathing (SDB), a common set of disord

112 iciency), sleep duration, sleep consistency, sleep-disordered breathing (SDB), and sleep architecture

113 Primary sleep disorders such as sleep-disordered breathing (SDB), sleep-related movement

114 Obstructive sleep-disordered breathing (SDB), which includes primary

115 en linked to disrupted sleep associated with sleep-disordered breathing (SDB).

116 ial triggers for arrhythmia in patients with sleep-disordered breathing (SDB).

117 Sleep-disordered breathing accounted for 9 to 10% of eth

118 ongest in older participants in whom overall sleep-disordered breathing also increased atrial fibrill

119 events, we aimed to assess the prevalence of sleep-disordered breathing and associated clinical featu

120 Although research supports a sleep-disordered breathing and atrial fibrillation assoc

121 ights the complex interrelationships between sleep-disordered breathing and cardiovascular disease, p

122 e directionality of the relationship between sleep-disordered breathing and heart failure is controve

123 born preterm exhibit increased incidence of sleep-disordered breathing and hypertension, suggesting

124 els were used to assess associations between sleep-disordered breathing and outcomes, adjusted for so

125 more in-depth discussion of indications for sleep-disordered breathing and recurrent throat infectio

126 Clinical signs of insomnia and sleep-disordered breathing are common in mid-to-late pre

127 ent in HFpEF patients, but renal disease and sleep-disordered breathing burdens are similar.

128 Central sleep-disordered breathing can occur with associated car

129 Among older women, those with sleep-disordered breathing compared with those without s

130 Sleep-disordered breathing contributes to cardiac chambe

131 articipants who had objective assessments of sleep-disordered breathing during pregnancy were asked t

132 Prospective data suggest that sleep-disordered breathing enhances risk for incident an

133 dered breathing, can itself trigger specific sleep-disordered breathing events including air leaks, p

134 airway resistance can increase the risk for sleep-disordered breathing events.

135 rdered breathing compared with those without sleep-disordered breathing had an increased risk of deve

136 Sleep-disordered breathing has also been linked to these

137 thway whereby incident CVD causes or worsens sleep-disordered breathing has not been studied.

138 Sleep-disordered breathing in neuromuscular diseases is

139 e in addressing pitfalls in the diagnosis of sleep-disordered breathing in neuromuscular diseases, id

140 ptin will bypass leptin resistance and treat sleep-disordered breathing in obesity.

141 We estimated the prevalence of sleep-disordered breathing in the United States for the

142 m the brain, and hypoxemia characteristic of sleep-disordered breathing increases Abeta production.

143 ptin resistance and significantly attenuated sleep-disordered breathing independently of body weight.

144 Sleep-disordered breathing is a common disorder with a r

145 Sleep-disordered breathing is also more common in patien

146 Sleep-disordered breathing is associated with an increas

147 Sleep-disordered breathing is associated with major morb

148 Sleep-disordered breathing is associated with worse func

149 These results suggest that sleep-disordered breathing is highly prevalent, with imp

150 logical mechanisms underlying the effects of sleep-disordered breathing on the brain.

151 lectively studied in populations at risk for sleep-disordered breathing or cardiovascular diseases.

152 ent studies show either absence of change in sleep-disordered breathing or improved sleep cardiovascu

153 , incident CVD was associated with worsening sleep-disordered breathing over 5 years.

154 gnition; however, it remains unclear whether sleep-disordered breathing precedes cognitive impairment

155 tion association, prospective data examining sleep-disordered breathing predicting incident atrial fi

156 oing obesity epidemic, previous estimates of sleep-disordered breathing prevalence require updating.

157 The high prevalence of sleep-disordered breathing recorded in our population-ba

158 (2010-2015), were offered participation in a sleep-disordered breathing study including a home sleep

159 Cross-sectional studies have linked sleep-disordered breathing to poor cognition; however, i

160 re reasonable endpoints for future trials of sleep-disordered breathing treatment in stroke.

161 If effective, sleep-disordered breathing treatment may somewhat lessen

162 thing in neuromuscular diseases, identifying sleep-disordered breathing triggered by noninvasive vent

163 Sleep-disordered breathing was ascertained by apnea-hypo

164 Sleep-disordered breathing was associated with worse fun

165 Sleep-disordered breathing was defined as an apnea-hypop

166 The prevalence of sleep-disordered breathing was modeled as a function of

167 Sleep-disordered breathing was not associated with globa

168 rdered breathing, the 105 women (35.2%) with sleep-disordered breathing were more likely to develop m

169 the diagnosis of OHS in obese patients with sleep-disordered breathing when suspicion for OHS is not

170 ted with cardiorespiratory diseases, such as sleep-disordered breathing with apnoea, congestive heart

171 to determine the independent association of sleep-disordered breathing with risk of mild cognitive i

172 been previously reported that some patient's sleep-disordered breathing worsened following surgery.

173 for sleep duration, sleep fragmentation, and sleep-disordered breathing) in the development of cognit

174 Obesity is a strong causal factor for sleep-disordered breathing, and because of the ongoing o

175 trategies for management of hypoventilation, sleep-disordered breathing, and cough insufficiency are

176 icity and alcohol's contribution to obesity, sleep-disordered breathing, and hypertension.

177 re, specific exercise, opioids, treatment of sleep-disordered breathing, and interventions to address

178 sure of physiological stress associated with sleep-disordered breathing, and this measure predicts in

179 The primary outcome was prevalence of sleep-disordered breathing, assessed by the apnoea-hypop

180 on, a standard-of-care management option for sleep-disordered breathing, can itself trigger specific

181 s, dyslipidemia, obstructive sleep apnea and sleep-disordered breathing, certain cancers, and major c

182 ry artery disease, congestive heart failure, sleep-disordered breathing, gastro-oesophageal reflux di

183 owever, its indication for all patients with sleep-disordered breathing, regardless of daytime sympto

184 Compared with the 193 women without sleep-disordered breathing, the 105 women (35.2%) with s

185 entral apnea, Cheyne-Stokes respiration, and sleep-disordered breathing-age interaction terms were si

186 me individuals may partially protect against sleep-disordered breathing.

187 When abnormal, these interactions lead to sleep-disordered breathing.

188 effects of oral antihistamines on asthma and sleep-disordered breathing.

189 omnography studies to assess the presence of sleep-disordered breathing.

190 malities in children with SCD are related to sleep-disordered breathing.

191 otype and cognitive decline in patients with sleep-disordered breathing.

192 y event index was 14 (IQR = 6-25); 62.8% had sleep-disordered breathing.

193 of specific tryptamines for the treatment of sleeping disorders, bupropion for substance abuse disord

194 As epilepsy and sleep disorders can be treated and may contribute signif

195 a may worsen epilepsy and treatment of these sleep disorders can lead to improved seizure control.

196 leep initiation and regulation, all types of sleep disorders can occur, with varying distinct associa

197 arm); physical disorders (cancers, diabetes, sleep disorder, cardiovascular diseases, chronic lower r

198 Narcolepsy is a chronic sleep disorder caused by a loss of hypocretin (hcrt) neu

199 rcolepsy with cataplexy is a rare and severe sleep disorder caused by the destruction of orexinergic

200 Obstructive sleep apnea (OSA) is a sleep disorder characterized by disruptions of normal sl

201 Variation in chronotype has been linked to sleep disorders, cognitive and physical performance, and

202 e, idiopathic insomnia, and circadian rhythm sleep disorder-delayed sleep phase type.

203 resence of psychiatric complications such as sleep disorder, depression, anxiety and somatoform disor

204 xt revision; International Classification of Sleep Disorders: Diagnostic and Coding Manual II, Intern

205 ly lower rates of dizziness (8.8% vs 37.1%), sleep disorders/disturbances (12.1% vs 25.2%), and alter

206 hm disorders have been associated with other sleep disorders (e.g., insomnia, obstructive sleep apnea

207 led receptors that may be useful targets for sleep disorders, eating disorders, or addictive behavior

208 Sleep disorders, especially insomnia, occur in up to 83%

209 positive for obstructive sleep apnea or any sleep disorder had an increased prevalence of reported p

210 Further, some treatments for sleep disorders have direct effects on neuropsychiatric

211 Sleep duration, mostly short sleep, and sleep disorders have emerged as being related to adverse

212 Inadequate sleep and sleep disorders have important adverse consequences on m

213 pathophysiologic processes such as epilepsy, sleep disorders, hypertension, and cancer.

214 disturbance, cognitive decline and dementia, sleep disorders, hyposmia and autonomic failure.

215 teria by the International Classification of Sleep Disorders (ICSD).

216 nd video polysomnography to identify a novel sleep disorder in three patients referred to the Sleep U

217 s study were as follows: (1) to characterize sleep disorders in a monkey model of PD; (2) to investig

218 we explored the mechanistic basis for these sleep disorders in a mouse model of Angelman syndrome (U

219 Sleep disorders in adolescents are both very common and

220 ese findings reveal potential treatments for sleep disorders in AS patients.

221 pport the validity of the RIM model to study sleep disorders in fibromyalgia, and provide new insight

222 e sleep apnea(OSA) is one of the most common sleep disorders in kidney transplant recipients, however

223 ing, and the presence of physician-diagnosed sleep disorders in metropolitan, urban, and rural US Geo

224 of 2911 men in the observational Outcomes of Sleep Disorders in Older Men (MrOS) Sleep Study cohort u

225 llow-up (2009-2012) waves of the Outcomes of Sleep Disorders in Older Men Study (an ancillary study t

226 he efficacy of l-dopa treatment in improving sleep disorders in parkinsonian monkeys, and that adding

227 Sleep disorders in people with autoimmune encephalitis h

228 ve illnesses, but this is the first study of sleep disorders in PPND.

229 n promise for the treatment of insomnias and sleep disorders in several recent clinical trials in vol

230 an deficits that we report may contribute to sleep disorders in severe myoclonic epilepsy of infancy

231 s with some of the more commonly encountered sleep disorders in this age group, and to review their d

232 ut the prevalence of insomnia, a distressing sleep disorder, in these populations has yet to be deter

233 tablishes the prevalence of gaming, mood and sleep disorders, in a large African sample.

234 that occur in PD such as depression, apathy, sleep disorders (including rapid-eye movement sleep beha

235 nts in maintenance hemodialisys (HD) present sleep disorders, increased inflammation, unbalanced redo

236 The development of new therapeutics for sleep disorders is increasingly dependent upon understan

237 iency epidemic, as is the high prevalence of sleep disorders like insomnia.

238 Narcolepsy is a chronic sleep disorder, likely with an autoimmune component.

239 patients undergoing sleep evaluation for any sleep disorders (low pretest probability for narcolepsy)

240 Narcolepsy is a sleep disorder marked by chronic, debilitating excessive

241 avioral and circuit development, and suggest sleep disorders may be of neurodevelopmental origin.

242 avior with implications for the treatment of sleep disorders, metabolic disease, and cancer.

243 ants, 40.4% screened positive for at least 1 sleep disorder, most of whom had not been diagnosed prev

244 d with comorbid medical conditions including sleep disorders, motor hyperactivity, and seizures.

245 determine whether patients with a non-apnea sleep disorder (NA-SD) and comorbidity have an increased

246 The sleep disorder narcolepsy is characterized by excessive

247 ss of HCRT (ligands or receptors) causes the sleep disorder narcolepsy with cataplexy in humans and i

248 he discovery of a single gene underlying the sleep disorder narcolepsy, and identification of loci th

249 xin neurons in humans is associated with the sleep disorder narcolepsy, which is characterized by exc

250 of the amygdala (CeA) triggered cataplexy of sleep disorder narcolepsy.

251 An increased incidence in the sleep-disorder narcolepsy has been associated with the 2

252 ebilitating symptom of the neurodegenerative sleep disorder, narcolepsy.

253 t guidelines pertaining to the management of sleep disorders of children on the autism spectrum.

254 plications of drowsy driving, and the common sleep disorders of obstructive sleep apnea and insomnia.

255 Sleep disorders often remain undiagnosed.

256 ble evidence on the effects of therapies for sleep disorders on neuropsychiatric conditions and also

257 (c) The impact of sleep disorders on obesity and diabetes.

258 e for clinical treatment of AD patients with sleep disorders, pathophysiological stimulation of neuro

259 erent samples: controls, patients with other sleep disorders, patients with other hypersomnias, and p

260 neck pain, myalgia, arthralgia, paresthesia, sleep disorder, poor appetite and concentration difficul

261 neck pain, myalgia, arthralgia, paresthesia, sleep disorder, poor appetite, and concentration difficu

262 toms including anxiety, cognitive defect and sleep disorder precede the onset of motor impairment, an

263 ndependent Scandinavian cohorts and on other sleep disorders (restless legs syndrome, insomnia) and s

264 colepsy type 1 is a devastating neurological sleep disorder resulting from the destruction of orexin-

265 Narcolepsy is a human sleep disorder resulting from the loss of neurons contai

266 International Classification of Sleep Disorders, second edition (ICSD2) derived insomnia

267 orders, or in the context of another primary sleep disorder such as restless legs syndrome, or second

268 n rhythm period and phase, which can lead to sleep disorders such as Familial Advanced Sleep Phase Sy

269 In addition, sleep disorders such as insomnia, obstructive sleep apne

270 The understanding of the neurophysiology of sleep disorders such as insomnia, parasomnias, and narco

271 especially with respect to the treatment of sleep disorders such as narcolepsy.

272 of the switching mechanism may contribute to sleep disorders such as narcolepsy.

273 More recent studies have shown that primary sleep disorders such as obstructive sleep apnoea may wor

274 Additionally, symptoms of some sleep disorders such as parasomnias and narcolepsy can b

275 f REM sleep mechanisms underlie debilitating sleep disorders such as REM sleep behaviour disorder and

276 Sleep disorders such as short sleep duration and increas

277 Primary sleep disorders such as sleep-disordered breathing (SDB)

278 wever, a positive MSLT may be found in other sleep disorders, such as behaviourally induced inadequat

279 imately 14 loci increasing susceptibility to sleep disorders, such as narcolepsy and restless leg syn

280 Given that insomnia is a common sleep disorder that disrupts the ability to initiate and

281 Heart failure has previously been linked to sleep disorders that are often associated with frequent

282 1,2,3,6-tetrahydropyridine treatment induced sleep disorders that comprised sleep episodes during day

283 odel and to evaluate if the model mimics the sleep disorders that occur in fibromyalgia patients.

284 nsider the pathophysiological basis of major sleep disorders that often are seen by neurologists, inc

285 ature's solutions to heart, lung, blood, and sleep disorders through future research in this area.

286 iew the evidence relating sleep duration and sleep disorders to cardiometabolic risk and call for hea

287 ehavior, fueled by evidence directly linking sleep disorders to genetic mutations affecting circadian

288 pulation-based controls or all patients with sleep disorders undergoing a nocturnal sleep study (area

289 een healthy adults (age 35-65 years) without sleep disorders underwent 5-14 days of actigraphy, follo

290 whereas in anti-NMDA receptor encephalitis, sleep disorders vary according to the disease stage alon

291 hose respondents who screened positive for a sleep disorder vs those who did not had a higher rate of

292 t visit of 5 years (range 2-12); in four the sleep disorder was the initial and most prominent featur

293 g a group of North American police officers, sleep disorders were common and were significantly assoc

294 ent with NA-SD, two matched controls without sleep disorders were randomly selected for comparison.

295 In anti-IgLON5 disease, sleep disorders were the core symptoms that led to the d

296 ng physical disorders, such as cirrhosis and sleep disorders, were also noted as well as the use of m

297 on with broad medical implications including sleep disorders, which can exacerbate metabolic disturba

298 t of circuit-selective drugs might alleviate sleep disorders with fewer side effects.

299 Combinations of other sleep disorders with RLS further increased the risk of E

300 Insomnia is a common sleep disorder, yet its pathophysiological basis remains