ライフサイエンスコーパス: apnoea

1 ated startle reflexes, muscle hypertonia and apnoea.

2 ve airway pressure-treated obstructive sleep apnoea.

3 /=45%) treated for predominant central sleep apnoea.

4 ia and hypercapnia associated with prolonged apnoea.

5 elevated blood pressure in obstructive sleep apnoea.

6 severe hypoxaemia associated with prolonged apnoea.

7 oxygen deprivation associated with prolonged apnoea.

8 developed specifically for obstructive sleep apnoea.

9 ertension, angina, MI, and obstructive sleep apnoea.

10 ormal sleep behaviours and obstructive sleep apnoea.

11 rome, type 2 diabetes, and obstructive sleep apnoea.

12 ay motor disorders such as obstructive sleep apnoea.

13 death syndrome (SIDS) and obstructive sleep apnoea.

14 x evoked exaggerated increases in SNA during apnoea.

15 spiratory chemosensitivity and central sleep apnoea.

16 impaired in patients with obstructive sleep apnoea.

17 ertension in patients with obstructive sleep apnoea.

18 ry activity, with intense activation causing apnoea.

19 inical problem of cyclical obstructive sleep apnoea.

20 sm linking hypertension to obstructive sleep apnoea.

21 O2 -7 +/- 1 mmHg vs. baseline) occurred post-apnoea.

22 r disease in patients with obstructive sleep apnoea.

23 seline blood pressure, and severity of sleep apnoea.

24 coupled with an increased incidence of sleep apnoea.

25 ast three breaths prior to each hypopnoea or apnoea.

26 dic alternation between hyperventilation and apnoea.

27 ent for patients with mild obstructive sleep apnoea.

28 sure in patients with mild obstructive sleep apnoea.

29 life in patients with mild obstructive sleep apnoea.

30 hold, in participants with obstructive sleep apnoea.

31 e the global prevalence of obstructive sleep apnoea.

32 rostimulation in patients with central sleep apnoea.

33 ising therapeutic approach for central sleep apnoea.

34 be baroreflex mediated, and disappear during apnoea.

35 e markedly reduced the occurrence of central apnoeas.

36 e ataxic breathing pattern emerged with many apnoeas.

37 rescuing plasticity following hypoxic neural apnoeas.

38 oses of morphine increased the occurrence of apnoeas.

39 tion also results in unstable breathing with apnoeas.

40 28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.55 (95% CI 0.40-0.87).

41 ubjects performing repetitive end-expiratory apnoeas (20 s) every minute for 30 min during intermitte

42 1 mmHg-1), or the CFV responses to voluntary apnoea (+51 +/- 19 vs. +50 +/- 18 %).

43 mittent hypoxia (CIH) is a hallmark of sleep apnoea, a condition associated with diverse clinical dis

44 n the global prevalence of obstructive sleep apnoea, a disorder associated with major neurocognitive

45 Obstructive sleep apnoea, a syndrome that leads to recurrent intermittent

46 ions in respiratory neural activity ('neural apnoea') accompanied by cessations in ventilation that r

47 Prevalence estimates for obstructive sleep apnoea across studies using different diagnostic criteri

48 The assessment of how obstructive sleep apnoea affects cognition depends on the specificity and

49 oring criteria to identify obstructive sleep apnoea, allowing determination of an equivalent apnoea-h

50 and hypercapnia, it is unknown if repetitive apnoeas also elicit LTF.

51 d by approximately 29% at the termination of apnoea, although there was no change in the non-oxidativ

52 sorders, including cerebral ischaemia, sleep apnoea, Alzheimer's disease, multiple sclerosis, amyotro

53 bited hypertension, irregular breathing with apnoeas, an augmented CB chemosensory reflex as indicate

54 Thirteen participants with sleep apnoea and 13 controls completed two trials.

55 women) have mild to severe obstructive sleep apnoea and 425 million (399-450) adults aged 30-69 years

56 CBD) chemoreceptors would reduce SNA, reduce apnoea and arrhythmia incidence and improve ventricular

57 tly in clinical trials for obstructive sleep apnoea and atrial fibrillation(16).

58 bited hypertension, irregular breathing with apnoea and augmented the CB chemosensory reflex, with al

59 Typically, postictal apnoea and bradycardia progress to asystole and death.

60 a consequence of increased obstructive sleep apnoea and cardiovascular disease.

61 as many undesirable side effects (sedation, apnoea and dependence) by binding to and activating the

62 hypoxia (CIH) occurs in patients with sleep apnoea and has adverse effects on multiple physiological

63 g. essential hypertension, obstructive sleep apnoea and heart failure.

64 V-positive cases were associated with cough, apnoea and hospitalization among infants.

65 in both adults and children during untreated apnoea and hypopnoea, along with changes in cerebral blo

66 iring plasticity following concurrent neural apnoea and hypoxia is indicated since recurrent hypoxic

67 of RTN neurons probably underlies the sleep apnoea and lack of chemoreflex that characterize congeni

68 inspiration after swallow, prolonged swallow apnoea and multiple swallows per bolus.

69 ut the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive

70 The prevalence of central apnoea and periodic breathing is increased in the elderl

71 fic physiological sleep disorders--eg, sleep apnoea and periodic limb movement disorder--are essentia

72 on the association between obstructive sleep apnoea and stroke reviewing both the epidemiological dat

73 of the association between obstructive sleep apnoea and the brain.

74 region of the pons reduced the incidence of apnoea and the respiratory irregularity of Rett female m

75 Obstructive sleep apnoea and type 2 diabetes are common medical disorders

76 otrapezoid nucleus (RTN) displayed increased apnoeas and blunted CO(2)-stimulated breathing; re-expre

77 T respiratory phenotype of recurrent central apnoeas and prolonged post-inspiratory activity.

78 n premature infants who suffer from frequent apnoeas and respiratory depression.

79 Central apnoeas and respiratory irregularity are a common featur

80 n (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hyperte

81 should be screened for the presence of sleep apnoea, and if present, administration of intermittent h

82 n, chronic kidney disease, obstructive sleep apnoea, and metabolic disease including diabetes and obe

83 aroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result fr

84 y be impaired in some individuals with sleep apnoea, and that exogenously activating pathways giving

85 usual breathing frequencies disappear during apnoea, and thus cannot provide evidence for the existen

86 Features include snoring, witnessed apnoeas, and sleepiness.

87 elated disorders including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and n

88 Male participants with obstructive sleep apnoea (apnoea-hypopnoea index > 5 events/h), matched fo

89 s to <=80 years) with mild obstructive sleep apnoea (apnoea-hypopnoea index [AHI] >=5 to <=15 events

90 CIH and sleep apnoea are characterized by increased reactive oxygen sp

91 Many forms of sleep apnoea are characterized by recurrent reductions in resp

92 uggest that responses of healthy subjects to apnoea are driven importantly, and possibly prepotently,

93 Although repetitive apnoeas are a frequent natural occurrence producing brie

94 reatening breathing irregularity and central apnoeas are highly prevalent in children suffering from

95 REM sleep could explain why certain central apnoeas are less frequent during this sleep stage.

96 esis that repeated, brief ventilator-induced apnoeas are sufficient to induce serotonin-dependent phr

97 vements and behaviours and obstructive sleep apnoea, as confirmed by polysomnography.

98 e study cohort was an episode of significant apnoea at presentation, found to have been recorded in 7

99 ss, startles and stumbles' of hyperekplexia, apnoea attacks (50 of 89) and delayed development (47 of

100 c outcomes for affected cases such as severe apnoea attacks, learning difficulties and developmental

101 O2 ) will be reduced near the termination of apnoea, attributed in part to the hypercapnia.

102 outcome was prevalence of obstructive sleep apnoea based on AASM 2012 diagnostic criteria in individ

103 eporting the prevalence of obstructive sleep apnoea based on objective testing methods.

104 of the phrenic motor nucleus prior to neural apnoea blocked long-lasting iPMF (2 +/- 8% baseline; P >

105 nary chemoreflex responses, characterized by apnoea, bradycardia and hypotension.

106 in the cerebral metabolic reduction near the apnoea breakpoint.

107 rtly explain the reduction in CMRO2 near the apnoea breakpoint.

108 sleep apnoea than those who had less severe apnoea, but was independent of the baseline blood pressu

109 CFV increased during apnoeas (by 42 +/- 3 %) and decreased below baseline (by

110 Obstructive sleep apnoea can be diagnosed on the basis of characteristic h

111 agmatic activity emerged out of a background apnoea caused by mechanical hyperventilation an average

112 Obstructive sleep apnoea causes sleepiness, road traffic accidents, and pr

113 iciency in diverse conditions, such as sleep apnoea, cervical spinal injury or amyotrophic lateral sc

114 1, Cohen's d = 1.18) near the termination of apnoea compared to baseline, although non-oxidative meta

115 ontrolled and random frequency breathing and apnoea, conceived to perturb their autonomic function an

116 ses, such as sleep-disordered breathing with apnoea, congestive heart failure and essential hypertens

117 rain hypoperfusion such as obstructive sleep apnoea, congestive heart failure, cardiac arrhythmias, a

118 The subjects' responses to apnoea could not be attributed to changes of central che

119 hypoxia characteristic of obstructive sleep apnoea could promote hypertension by increasing sNVT.

120 bnormalities in those with obstructive sleep apnoea could reduce cardiovascular disease risk and impr

121 e discussed, management of obstructive sleep apnoea could soon transition from a so-called one size f

122 The post-apnoea decrease in CFV did not occur when hyperventilati

123 tion of patients with mild obstructive sleep apnoea diagnosed using the American Academy of Sleep Med

124 f oxyhaemoglobin desaturation caused by 20 s apnoea did not affect CFV.

125 Dips suggestive of obstructive sleep apnoea did not predict CNS events, and adenotonsillectom

126 Fourteen elite apnoea-divers performed a maximal apnoea (range 3 min 36

127 In addition to altering baseline V(I) and apnoea duration, DNE is associated with subtle but signi

128 decreased the number of sighs and post-sigh apnoeas during wakefulness in both the light and the dar

129 Thus, brief ventilator apnoeas elicit phrenic and XII LTF.

130 uced inspiratory motor output, such as sleep apnoea, endogenous mechanisms of compensatory plasticity

131 d pressure in 118 men with obstructive sleep apnoea (Epworth score > 9, and a > 4% oxygen desaturatio

132 Patients with obstructive sleep apnoea experience chronic intermittent hypoxia-hypercapn

133 iated with an abnormal pattern (i.e. swallow apnoeas followed by inspiration) and to clarify whether

134 Our results might account for increases in apnoea frequency and duration previously observed during

135 rs have moderate to severe obstructive sleep apnoea globally.

136 ted pathologies, including obstructive sleep apnoea, heart failure and diabetes.

137 d below baseline (by 20 +/- 2 %) during post-apnoea hyperventilation.

138 e and (ii) is most efficacious (reduction in apnoea-hypopnea index; AHI) in patients with a posterior

139 the P(CO2) required to produce hypopnoea or apnoea (hypopnoea/apnoeic threshold) in sleeping humans.

140 ttenuation of irregular breathing, decreased apnoea-hypopnoea incidence (11.1 +/- 2.9 vs.

141 participants with obstructive sleep apnoea (apnoea-hypopnoea index > 5 events/h), matched for age, b

142 iable adjustment, the upper quartile for the apnoea-hypopnoea index (>20.6 events per h) was associat

143 (11 men, 11 women) with OSA (mean +/-s.e.m., apnoea-hypopnoea index (AHI) 48.9 +/- 5.9 events h(-1))

144 Oscillatory breathing was quantified as the apnoea-hypopnoea index (AHI) and respiratory rate variab

145 oea, allowing determination of an equivalent apnoea-hypopnoea index (AHI) for publications that used

146 Eligible patients with an apnoea-hypopnoea index (AHI) of at least 20 events per h

147 plain of poor sleep quality despite a normal apnoea-hypopnoea index (AHI).

148 The apnoea-hypopnoea index (AHI)was assessed on separate nig

149 0 years) with mild obstructive sleep apnoea (apnoea-hypopnoea index [AHI] >=5 to <=15 events per h us

150 ated obesity hypoventilation syndrome and an apnoea-hypopnoea index of 30 or more events per h.

151 Zolpidem did not change the apnoea-hypopnoea index versus placebo (40.6 +/- 12.3 vs.

152 The median apnoea-hypopnoea index was 6.9 events per h (IQR 2.7-14.

153 coefficient of variation of tidal volume and apnoea-hypopnoea index were increased in CHF-sham animal

154 ured by plethysmography and quantified by an apnoea-hypopnoea index, respiratory rate variability ind

155 lly decrease OSA severity as measured by the apnoea-hypopnoea index.

156 sleep-disordered breathing, assessed by the apnoea-hypopnoea index.

157 was detected between circulating HMW-HA and apnoea-hypopnoea-index (r = - 0.195, p = 0.043), HYAL-1

158 a-index (r = - 0.195, p = 0.043), HYAL-1 and apnoea-hypopnoea-index (r = 0.30, p < 0.01) as well as o

159 Apnoea/hypopnoea incidence (AHI), breathing variability,

160 d SNP were significantly correlated with the apnoea/hypopnoea index (AHI) (P = 0.035, 0.042 and 0.026

161 Obstructive sleep apnoea/hypopnoea syndrome, depression and anxiety were i

162 5% (13/53); five of these patients had sleep apnoea/hypopnoea syndrome, six had depression and five a

163 ively] a marked increase in the incidence of apnoeas/hypopnoeas (20.2 +/- 4.0 vs. 9.7 +/- 2.6 events

164 mprovements in severity of obstructive sleep apnoea (i.e. reduction in event frequency by 83%, in con

165 observed in patients with obstructive sleep apnoea (i.e. reflex compensation for an anatomically sma

166 on of Piezo2(+) vagal sensory neurons causes apnoea in adult mice.

167 of perinatal mortality in infants and sleep apnoea in adults, but the mechanisms of respiratory cont

168 ce of OSA and the emergence of central sleep apnoea in conditions such as high altitude.

169 Prolonged apnoea in humans is reflected in progressive hypoxaemia

170 The swallow apnoea in patients with brain, spinal cord and periphera

171 Early identification of obstructive sleep apnoea in patients with metabolic dysfunction, including

172 the abdominal muscles during opioid-induced apnoea in the newborn rat.

173 spiratory chemosensitivity and central sleep apnoea in this disorder.

174 cause of central (and possibly obstructive) apnoeas in this population.

175 by administration of opioids (opioid-induced apnoea) in neonatal rats, abdominal muscles continue to

176 spiratory output and lower the threshold for apnoea, inactivity-induced inspiratory motor facilitatio

177 cantly reduced the severity of central sleep apnoea, including improvements in sleep metrics, and was

178 Three and six ventilator apnoeas induced phrenic and XII LTF with a magnitude sim

179 Both apnoea-induced and AIH-induced LTF were associated with

180 We conclude that apnoea-induced fluctuations in CFV were caused primarily

181 Hyperoxia also had no effect on the apnoea-induced increase in CFV (40 +/- 4 %).

182 played a smaller but significant role in the apnoea-induced increase in CFV; however, negative intrat

183 ockade, which abolished the increase in MAP, apnoea-induced increases in CFV were partially attenuate

184 de, a serotonin receptor antagonist, blocked apnoea-induced LTF but not changes in the CO(2)-recruitm

185 Similar to AIH-induced LTF, apnoea-induced LTF is serotonin dependent, and the relev

186 Apnoea-induced LTF may have implications for the mainten

187 Apnoea-induced LTF may preserve upper airway patency dur

188 It seems likely that post-swallowing apnoea inspiration is a non-specific concomitant of diso

189 Obstructive sleep apnoea is a common disease that is now more widely recog

190 Obstructive sleep apnoea is a disease of increasing importance because of

191 is convincing evidence to believe that sleep apnoea is a modifiable risk factor for stroke; however,

192 Central sleep apnoea is a serious breathing disorder associated with p

193 Obstructive sleep apnoea is an increasingly common disorder of repeated up

194 Obstructive sleep apnoea is associated with raised blood pressure.

195 A co-morbidity of sleep apnoea is hypertension associated with elevated sympathe

196 ypocapnia-induced apnoeic threshold, whereby apnoea is initiated by small transient reductions in art

197 rol and thus could explain why central sleep apnoea is less frequent in REM sleep.

198 for the treatment of mild obstructive sleep apnoea is limited and definitions of disease severity va

199 analgesia, but maternal desaturation or even apnoea is more likely.

200 , increase sleep efficiency without changing apnoea length, oxygen desaturation, next-day perceived s

201 ry sleep disorders such as obstructive sleep apnoea may worsen epilepsy and treatment of these sleep

202 eceptor afferents terminate produced central apnoea, mimicking the effect of lung inflation.

203 In patients with most severe sleep apnoea, nCPAP reduces blood pressure, providing signific

204 pnoea (failure to trigger the ventilator) or apnoea (no breathing effort) occurred.

205 lation syndrome and severe obstructive sleep apnoea, non-invasive ventilation and continuous positive

206 Mixed or obstructive apnoeas occurred with 9% of these seizures.

207 iratory depression are implicated, including apnoea of prematurity, sleep disordered breathing and co

208 respiratory disturbances featuring prolonged apnoeas of variable durations.

209 3 months typically present with a history of apnoea or other breathing abnormalities, show axonal dam

210 OR (LAUP) OR (LAVP) OR (laser AND (apnea OR apnoea OR sleep))).

211 Central apnoeas or hypopnoeas occurred with 50% of 100 seizures.

212 ut central adverse effects such as sedation, apnoea, or addiction.

213 Obstructive sleep apnoea (OSA) and type 2 diabetes frequently co-exist and

214 f elderly individuals with obstructive sleep apnoea (OSA) for comparison (n = 3, age 68 +/- 1 years,

215 Obstructive sleep apnoea (OSA) is a heterogeneous and complex disease; how

216 Obstructive sleep apnoea (OSA) is characterised by intermittent hypoxia an

217 oral appliance therapy for obstructive sleep apnoea (OSA) is that therapeutic responses remain unpred

218 A and vLTF are enhanced in obstructive sleep apnoea (OSA) participants compared to matched healthy co

219 f the main contributors to obstructive sleep apnoea (OSA) pathogenesis.

220 *Some patients with obstructive sleep apnoea (OSA) respond well to oral appliance therapy, whe

221 AP) for moderate to severe obstructive sleep apnoea (OSA) syndrome have been established in middle-ag

222 saturation profiles during obstructive sleep apnoea (OSA), have been shown to exhibit a heightened ca

223 saturation profiles during obstructive sleep apnoea (OSA), have been shown to exhibit a heightened ca

224 (SF), a primary feature of obstructive sleep apnoea (OSA), impairs hippocampal long-term potentiation

225 Obstructive sleep apnoea (OSA), which is characterized by periodic inspira

226 gain (LG) in patients with obstructive sleep apnoea (OSA), yet its effects on the other traits respon

227 in people with and without obstructive sleep apnoea (OSA).

228 to sleep in patients with obstructive sleep apnoea (OSA).

229 atively high prevalence of obstructive sleep apnoea (OSA).

230 nts with SS and those with obstructive sleep apnoea (OSA).

231 atively high prevalence of obstructive sleep apnoea (OSA).

232 acetazolamide may improve obstructive sleep apnoea (OSA).However, how acetazolamide affects the key

233 tion, atrial fibrillation, obstructive sleep apnoea, osteoporosis and venous thromboembolism.

234 yed recovery of eupnoea from hypoxic-induced apnoea (P < 0.001).

235 crement in muscle activity is greater in the apnoea patient than in healthy controls.

236 sleep onset, and the decrement is greater in apnoea patients than in healthy controls.

237 obstruction determine the phenotype of sleep apnoea patients who benefit maximally from oral applianc

238 d risk for hypertension in obstructive sleep apnoea patients.

239 rogression of, obstructive and central sleep apnoea, possibly through the development of peripheral n

240 Further, we found that, during central apnoeas, post-inspiratory drive (adductor motor) to the

241 Countries without obstructive sleep apnoea prevalence data were matched to a similar country

242 mental component summary (MCS) and the sleep apnoea quality-of-life index symptoms domain (sym).

243 teen elite apnoea-divers performed a maximal apnoea (range 3 min 36 s to 7 min 26 s) under dry labora

244 idative metabolism in man during a prolonged apnoea (ranging from 3 min 36 s to 7 min 26 s) that gene

245 In the post-apnoea recovery period, CFV returned to baseline in 45 +

246 Our aim was to see whether nCPAP for sleep apnoea reduces blood pressure compared with the most rob

247 he treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.

248 Apnoea responses of healthy subjects may result from cha

249 ring apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, barorecepto

250 at short-term exposure to repetitive hypoxic apnoeas (RHA) produces prolonged impairment in barorefle

251 more likely to have had recurrent infantile apnoeas (RR1.9; P < 0.005) than those with GLRA1 mutatio

252 The increased awareness of obstructive sleep apnoea's (OSA) links to Alzheimer's disease and major ps

253 Apnoea sets in motion a continuous and ever changing reo

254 Respiratory crisis related to recurrent apnoeas, sometimes triggered by chest infections, were c

255 ography showed features of obstructive sleep apnoea, stridor, and abnormal sleep architecture (undiff

256 in the pathophysiology of obstructive sleep apnoea syndrome (OSA).

257 in the pathophysiology of obstructive sleep apnoea syndrome (OSA).

258 tion of genetic factors to obstructive sleep apnoea syndrome (OSAS) has led to a better understanding

259 holic fatty liver disease, obstructive sleep apnoea syndrome, erectile dysfunction, periodontitis, in

260 ant in the pathogenesis of obstructive sleep apnoea syndrome.

261 At apnoea termination when the airway opens, we observed (1

262 the absence of brainstem function, including apnoea testing, would suffice.

263 as larger in patients with more severe sleep apnoea than those who had less severe apnoea, but was in

264 of PACAP in RTN neurons displayed increased apnoeas that were further exacerbated by changes in ambi

265 Similarly to the apnoea, there was no change in the non-oxidative metabol

266 Clinically the apnoea threshold appears important only because of its a

267 tors were high gain and high mean CO(2); the apnoea threshold did not independently influence system

268 Increasing the apnoea threshold F(ETCO(2)) from 0.02 to 0.03 had no eff

269 Second, high apnoea threshold itself does not create instability.

270 0.0001), irrespective of chemoreflex gain or apnoea threshold.

271 de range of values of steady state CO(2) and apnoea thresholds.

272 two decades indicates that obstructive sleep apnoea, through the effects of intermittent hypoxaemia a

273 huttle mission with controlled breathing and apnoea, to identify autonomic changes that might contrib

274 is indicated since recurrent hypoxic neural apnoeas triggered increased phrenic inspiratory output i

275 tilated rats were exposed to a 30 min neural apnoea; upon resumption of respiratory neural activity,

276 nce, insomnia, restless legs syndrome, sleep apnoea, urinary dysfunction, orthostatic symptoms, depre

277 233 had mild obstructive sleep apnoea using AASM 2012 criteria and were included in the

278 , gastroesophageal reflux, obstructive sleep apnoea, vocal cord dysfunction, obesity, dysfunctional b

279 decrease in P(ET,CO2) required to induce an apnoea was greater after treatment with leuprolide (2.56

280 and on landing day, but their control during apnoea was sharply altered: astronauts increased their b

281 Intrathecal TNFalpha without neural apnoea was sufficient to elicit long-lasting phrenic mot

282 ratures, whereas the duration of spontaneous apnoeas was longer in DNE pups than in controls at 33 de

283 racterized by pontocerebellar hypoplasia and apnoea, we discovered a missense mutation and an exonic

284 hogenesis and treatment of obstructive sleep apnoea, we have developed a novel application of magneti

285 liable prevalence data for obstructive sleep apnoea were available for 16 countries, from 17 studies.

286 Additionally, augmented breaths followed by apnoea were recorded and were not usually associated wit

287 late both burst areas and frequencies during apnoea were sharply diminished.

288 Hypopnoeas and apnoeas were induced in all subjects during both normoxi

289 creased, breathing patterns were normalized, apnoeas were reduced, body weight was increased to near

290 The number and duration of apnoeas were similar between control and treatment perio

291 mechanical ventilation resulted in a central apnoea which demarcated the threshold of the ventilatory

292 reathing, and normally the great majority of apnoeas which accompany a swallow are followed by expira

293 patients with stroke have concomitant sleep apnoea, which can affect recovery potential.

294 rate depression and increased risk of fatal apnoea, which correlate with increasing irregularities i

295 o this region could account for the observed apnoea, which could in turn lead to hypoxic damage and b

296 uch mechanisms (as in the patient with sleep apnoea) will be prone to collapse during sleep.

297 E-HF) showed that treatment of central sleep apnoea with adaptive servoventilation in patients with h

298 were exposed to three or six 25 s ventilator apnoeas with 5 min intervals, and compared to time contr

299 nsights and discoveries in obstructive sleep apnoea, with a focus on diagnostics and therapeutics.

300 eport global prevalence of obstructive sleep apnoea; with almost 1 billion people affected, and with