ライフサイエンスコーパス: intracranial pressure

1 as the primary intervention to reduce raised intracranial pressure.

2 that microgravity reduces central venous and intracranial pressure.

3 , correlated with CT-edema and preceded peak intracranial pressure.

4 ity (95% CI, 41%-79%) for detecting elevated intracranial pressure.

5 patients with acute brain injury and raised intracranial pressure.

6 tion spaceflight rarely increased postflight intracranial pressure.

7 if all stage 2 treatments failed to control intracranial pressure.

8 ncreased inflammatory response and to reduce intracranial pressure.

9 osmotherapy) were added as needed to control intracranial pressure.

10 added only if hypothermia failed to control intracranial pressure.

11 en with either large hemorrhage or increased intracranial pressure.

12 provement in survival, regardless of initial intracranial pressure.

13 t and an over 50% reduction effect on raised intracranial pressure.

14 minute-by-minute mean arterial pressure and intracranial pressure.

15 o why glaucoma develops in patients with low intracranial pressure.

16 ultrasonography can help diagnose increased intracranial pressure.

17 rm outcomes and may be more significant than intracranial pressure.

18 ssure and two reported that mannitol lowered intracranial pressure.

19 asive, quick method for diagnosing increased intracranial pressure.

20 thy volunteers but not on patients with high intracranial pressure.

21 CT parameters and directly measured elevated intracranial pressure.

22 OCT were correlated with invasively measured intracranial pressure.

23 . 24+/-2 mmHg, p=0.006) but had no effect on intracranial pressure (14+/-1 vs. 15+/-1 mmHg, p=0.72).

24 ch included: 1) brain tissue oxygenation, 2) intracranial pressure, 3) jugular venous continuous oxim

25 Complications in CNS disease included raised intracranial pressure (42%), hydrocephalus (30%), neurol

26 , statistically significant correlation with intracranial pressure, a predetermined level of diagnost

27 ertension exposure: area under the curve for intracranial pressure above 20 mm Hg (area under the cur

28 s had fewer hours than medical patients with intracranial pressure above 25 mm Hg after randomization

29 tomy (DC) is often required to manage rising intracranial pressure after traumatic brain injury (TBI)

30 CNS requires aggressive management of raised intracranial pressure along with standard antifungal the

31 ic participants had the largest increases in intracranial pressure (AMS present, Delta7mmHg, 95% CI =

32 ry, closed traumatic brain injury; increased intracranial pressure; an initial head injury less than

33 of patients had at least one episode of high intracranial pressure and 36% had a highest mean intracr

34 yr) with acute CNS infections having raised intracranial pressure and a modified Glasgow Coma Scale

35 gnificant relationship between the change in intracranial pressure and AMS symptom severity (R(2) = 0

36 f perfusion could contribute to increases in intracranial pressure and an associated impairment of vi

37 Waveforms of intracranial pressure and arterial blood pressure, basel

38 ons in each arm were specified and impact on intracranial pressure and brain tissue oxygenation measu

39 raumatic brain injury informed by multimodal intracranial pressure and brain tissue oxygenation monit

40 Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure ac

41 Intracranial pressure and cerebral perfusion pressure we

42 high frequency correlated significantly with intracranial pressure and cerebral perfusion pressure, b

43 arming at a rate compatible with maintaining intracranial pressure and cerebral perfusion pressure.

44 I) causes brain edema that induces increased intracranial pressure and decreased cerebral perfusion.

45 uration astronauts develop signs of elevated intracranial pressure and have neuro-ophthalmological fi

46 pertonic saline and mannitol appear to lower intracranial pressure and improve clinical outcomes in p

47 Elevated intracranial pressure and inadequate cerebral perfusion

48 Elevated intracranial pressure and inadequate cerebral perfusion

49 negative intrathoracic pressure would lower intracranial pressure and increase cerebral perfusion, t

50 We characterized the occurrence of elevated intracranial pressure and low cerebral perfusion pressur

51 y two routinely monitored signals as inputs (intracranial pressure and mean arterial blood pressure)

52 erating curve; adding dynamic information of intracranial pressure and mean arterial pressure during

53 Adding information of the first 24 hrs of intracranial pressure and mean arterial pressure monitor

54 ng the dynamic characteristics of continuous intracranial pressure and mean arterial pressure monitor

55 adding dynamic characteristics of continuous intracranial pressure and mean arterial pressure monitor

56 ar drain (EVD) is used clinically to relieve intracranial pressure and occasionally to deliver medica

57 a life-threatening disorder causing elevated intracranial pressure and papilledema.

58 screening test for the detection of elevated intracranial pressure and prediction of intracranial pre

59 forts should be made to aggressively control intracranial pressure and select a proper donor to minim

60 Continuous monitoring of intracranial pressure and temperature illustrates functi

61 erformed to evaluate the percent decrease in intracranial pressure and the 95% confidence intervals,

62 ive likelihood ratio, may indicate increased intracranial pressure and the need for additional confir

63 dies do not support the speculation that low intracranial pressure and the resulting pressure-depende

64 Nine reported that hypertonic saline lowered intracranial pressure and two reported that mannitol low

65 e relationships between autonomic functions, intracranial pressure, and cerebral autoregulation.

66 nuous monitoring of arterial blood pressure, intracranial pressure, and cerebral perfusion pressure,

67 = 0.078; control vs 4-hr delay, p = 0.150), intracranial pressure, and microdialysis values.

68 o primary management objectives are reducing intracranial pressure, and optimising cerebral perfusion

69 intracranial pressure, and partial brain tissue oxygenat

70 ally throbs, intensifies with an increase in intracranial pressure, and presents itself in associatio

71 Episodes of increased intracranial pressure are secondary injuries associated

72 oreflex sensitivity, heart rate variability, intracranial pressure, arterial blood pressure, cerebral

73 lts of this study suggest that complexity of intracranial pressure assessed by multiscale entropy was

74 mm; p = 0.03) and were associated with high intracranial pressure at first measurement and over 24 h

75 curve, 0.74 [95% CI, 0.61-0.87]), monitoring intracranial pressure + brain tissue PO2 (area under the

76 g characteristic curve, 0.84 [0.74-0.93]) or intracranial pressure + brain tissue PO2+ cerebral micro

77 Under general anesthesia, probes to measure intracranial pressure, brain oxygen tension (PbtO2), and

78 Intracranial pressure, brain tissue PO2, and cerebral mi

79 Brain multimodal monitoring-including intracranial pressure, brain tissue PO2, and cerebral mi

80 of the eye has been correlated with elevated intracranial pressure, but optimal cutoffs have been inc

81 as recorded during the stepwise elevation of intracranial pressure by inflation of an epidural balloo

82 Markov model yielded states characterized by intracranial pressure, cerebral perfusion pressure, comp

83 erwent monitoring with brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean

84 Unsupervised clustering of hourly values of intracranial pressure/cerebral perfusion pressure, the c

85 y in real time as well as to monitor in vivo intracranial pressure continuously in proof-of-concept m

86 Intracranial pressure control was similar in both groups

87 Intracranial pressure correlated with maximal retinal ne

88 Our algorithm can predict the onset of intracranial pressure crises with 30-minute advance warn

89 r scale, rebleeding, global cerebral oedema, intracranial pressure crisis, pneumonia and sepsis, hype

90 Similar mortality rates and refractory intracranial pressure deaths suggest that children with

91 tic hypothermia plus standard care to reduce intracranial pressure did not result in outcomes better

92 ith poor neurologic prognosis, but measuring intracranial pressure directly requires an invasive proc

93 and coronal) in patients with suspected high intracranial pressure due to trauma, bleeding, tumor, or

94 Chronic exposure to elevated intracranial pressure during spaceflight is hypothesized

95 tress syndrome, status asthmaticus, elevated intracranial pressure, elevated intra-abdominal pressure

96 Intracranial pressure elevation and brain water accumula

97 We developed a model to predict increased intracranial pressure episodes 30 mins in advance, by us

98 Increased intracranial pressure episodes could be predicted 30 min

99 ess of the model to predict future increased intracranial pressure events 30 minutes in advance, in a

100 m Hg lasting at least 5 minutes and the mean intracranial pressure for every 12-hour interval were an

101 lysis estimated that the percent decrease in intracranial pressure from baseline to either 60 minutes

102 Patients with highest mean intracranial pressure greater than 20 mm Hg had signific

103 from less than 65 to less than 90 mm Hg and intracranial pressure greater than 20 mm Hg in spans wer

104 Episodes of intracranial pressure greater than 20 mm Hg lasting at l

105 Highest mean intracranial pressure greater than 20 mm Hg was signific

106 an/peak intracranial pressure, proportion of intracranial pressure greater than 20 mm Hg, use of edem

107 han 18 to greater than 30 mm Hg and combined intracranial pressure greater than 20 plus cerebral perf

108 s than 65 to less than 90 mm Hg and combined intracranial pressure greater than 20 plus cerebral perf

109 asured optic nerve sheath diameter to detect intracranial pressure greater than 22 mm Hg was 0.81 (0.

110 hest measured optic disc elevation to detect intracranial pressure greater than 22 mm Hg was 0.84 (0.

111 ranial pressure, with test-positivity set at intracranial pressure greater than 22 mm Hg.

112 2% (48-98%) and specificity 79% (70-86%) for intracranial pressure greater than 22 mm Hg.

113 was associated with increased mortality for intracranial pressure greater than or equal to 20 mm Hg

114 A 90-day mortality in intracranial pressure group (38.2%) was significantly hi

115 perfusion pressure group in comparison with intracranial pressure group had significantly higher med

116 ) had evidence of intracranial hypertension (intracranial pressure > 25 mm Hg) and overall 21-day mor

117 severe intraventricular hemorrhage, although intracranial pressure >30 mm Hg predicts higher short-te

118 aumatic brain injury and refractory elevated intracranial pressure (>25 mm Hg) to undergo decompressi

119 An intracranial pressure>18 mm Hg was an exclusion criterio

120 ears promising for the detection of elevated intracranial pressure, however, verification from larger

121 Persistently elevated intracranial pressure (ICP) above upright values is a su

122 Mean arterial blood pressure, heart rate, intracranial pressure (ICP) and cerebral perfusion press

123 d treatment variables associated with raised intracranial pressure (ICP) and immune reconstitution in

124 improvement in blood pH and in parameters of intracranial pressure (ICP) and oxygenation.

125 Both intracranial pressure (ICP) and the cerebrovascular pres

126 rence between intraocular pressure (IOP) and intracranial pressure (ICP) at the level of lamina cribr

127 Intracranial pressure (ICP) control is a mainstay of tra

128 at uses near-infrared spectroscopy (NIRS) or intracranial pressure (ICP) decreases index variability

129 ctions did not mirror the large increases in intracranial pressure (ICP) during locomotion, indicatin

130 es the effects of aircraft cabin pressure on intracranial pressure (ICP) elevation of a pneumocephalu

131 Patients with elevated intracranial pressure (ICP) exhibit neuro-ocular symptom

132 ure of the current methods for monitoring of intracranial pressure (ICP) has prevented their use in m

133 m and/or shed capsule is postulated to raise intracranial pressure (ICP) in cryptococcal meningitis (

134 c function in TBI, we examined how increased intracranial pressure (ICP) influences the meningeal lym

135 P) is a well-known risk factor for glaucoma, intracranial pressure (ICP) is attracting heightened int

136 Raised intracranial pressure (ICP) is common in cryptococcosis.

137 An elevation in intracranial pressure (ICP) lowers conventional outflow

138 Intracranial pressure (ICP) monitoring forms an integral

139 tudy is the largest on the use and effect of intracranial pressure (ICP) monitoring in pediatric trau

140 Intracranial pressure (ICP) monitoring is a mainstay of

141 nerve elevation in the setting of increased intracranial pressure (ICP) of unclear cause.

142 culous meningitis (TBM) often lead to raised intracranial pressure (ICP) resulting in high morbidity

143 Intracranial pressure (ICP), CBF, and mean arterial pres

144 in CSF outflow did not cause an increase in intracranial pressure (ICP), consistent with an alterati

145 venous transmission of pressure and elevated intracranial pressure (ICP), could explain these finding

146 itoring of arterial blood pressure (ABP) and intracranial pressure (ICP), were retrospectively analyz

147 and tumor-induced edema result in increased intracranial pressure (ICP), which, in turn, is responsi

148 ss the lamina cribrosa (LC) related to a low intracranial pressure (ICP).

149 ntation that resembles syndromes of elevated intracranial pressure (ICP).

150 have various causes, including disorders of intracranial pressure (ICP).

151 minal pressure may have a negative effect on intracranial pressure (ICP).

152 tis (CM) are commonly attributed to elevated intracranial pressure (ICP).

153 ertension is generally assessed by measuring intracranial pressure (ICP).

154 relationships between autonomic impairment, intracranial pressure, impaired cerebral autoregulation,

155 th acute CNS infection, management of raised intracranial pressure improves mortality and neuromorbid

156 Stage 3 treatments were required to control intracranial pressure in 54% of the patients in the cont

157 etween peak sulfonylurea receptor-1 and peak intracranial pressure in 91.7% of patients with intracra

158 re-targeted therapy for management of raised intracranial pressure in children with acute CNS infecti

159 Detecting elevated intracranial pressure in children with subacute conditio

160 nce current treatment paradigms for elevated intracranial pressure in children.

161 re no observed increases in serum lactate or intracranial pressure in either group.

162 ric hypoxia causes elevated brain volume and intracranial pressure in individuals with symptoms consi

163 is the most predictive of patients with high intracranial pressure in our population.

164 It has been suggested that a low intracranial pressure in patients with normal intraocula

165 Direct assessment of intracranial pressure in space is required to verify the

166 oring allows to accurately predict increased intracranial pressure in the neuro-ICU.

167 l pressure-targeted approach to treat raised intracranial pressure in these children.

168 for early detection of episodes of increased intracranial pressure in traumatic brain injury patients

169 rds for non-resorbable devices by monitoring intracranial pressures in rats for 25 days.

170 Intracranial pressure increased to a mean maximum of 19

171 bital area and the eye, and intensifies when intracranial pressure increases.

172 n damage is influenced by the speed at which intracranial pressure increases.

173 High intracranial pressure is a common complication in the fi

174 Mean intracranial pressure is associated with the severity of

175 Recent studies have reported that intracranial pressure is lower in patients with NTG when

176 Intracranial pressure is not frequently elevated during

177 This being said, intracranial pressure is not reduced to the levels obser

178 Elevated intracranial pressure is one of the proposed mechanisms

179 The natural history indicates that increased intracranial pressure is transient in survivors.

180 This low intracranial pressure, leading to an abnormally high tra

181 Elevated intracranial pressure leads to structural changes in the

182 oward effects (including promoting increased intracranial pressure), little is known about the regula

183 ure is applied in the brain to represent the intracranial pressure loading caused by the tissue swell

184 ume of the brain tissue as a function of the intracranial pressure loading under a specific geometry

185 ssure-targeted therapy (n = 55) (maintaining intracranial pressure < 20 mm Hg using osmotherapy while

186 disease, a finding that suggests that raised intracranial pressure may contribute to a fatal outcome.

187 hat increased brain volume leading to raised intracranial pressure may play a role.

188 No significant difference in intracranial pressure, mean cerebral artery transcranial

189 rating characteristic 0.87-0.94) and highest intracranial pressure measurement (area under the receiv

190 serve as an effective surrogate for invasive intracranial pressure measurement.

191 ol patients, underwent direct intraoperative intracranial pressure measurement.

192 ting characteristic curve of 0.86 using only intracranial pressure measurements and time since last c

193 Outcomes included CT edema, intracranial pressure measurements, therapies targeting

194 opriate indication underwent placement of an intracranial pressure monitor and only 134 of 335 (45.6%

195 The use of intracranial pressure monitor in acetaminophen acute liv

196 nophen status and adjusting for confounders, intracranial pressure monitor placement did not impact 2

197 Hemorrhagic complications from intracranial pressure monitor placement were uncommon an

198 However, intracranial pressure monitor was associated with increa

199 Intracranial pressure monitored (n = 140) versus nonmoni

200 Overall 21-day mortality was similar (intracranial pressure monitored 33% vs controls 38%, p =

201 able, hemorrhagic complications were rare in intracranial pressure monitored patients (4 of 56 [7%];

202 Forty-one percent of intracranial pressure monitored patients received liver

203 During the first 7 days, intracranial pressure monitored patients received more i

204 Intracranial pressure monitored patients were younger th

205 In intracranial pressure monitored patients with acute live

206 Of 87 intracranial pressure monitored patients with detailed i

207 outcomes whereas white race (p=0.01), use of intracranial pressure monitoring (p=0.001), and increasi

208 ion in continuous mean arterial pressure and intracranial pressure monitoring allows to accurately pr

209 Compared with intracranial pressure monitoring alone (area under the r

210 erebral microdialysis--is more accurate than intracranial pressure monitoring alone in detecting cere

211 s brain tissue oxygenation monitoring versus intracranial pressure monitoring alone.

212 vel compliance ranged from 9.6% to 65.2% for intracranial pressure monitoring and 6.7% to 76.2% for c

213 with Brain Trauma Foundation guidelines for intracranial pressure monitoring and craniotomy.

214 cal characteristics with a propensity score, intracranial pressure monitoring guideline compliance wa

215 The role of intracranial pressure monitoring has been challenged; ho

216 he complex nature of examining the effect of intracranial pressure monitoring in observational studie

217 onclusively confirm or refute the utility of intracranial pressure monitoring in patients with acute

218 Intracranial pressure monitoring is a widely but inconsi

219 Invasive intracranial pressure monitoring is often unavailable an

220 Intracranial pressure monitoring is standard of care aft

221 Intracranial pressure monitoring plays a critical role i

222 otocol based on brain tissue oxygenation and intracranial pressure monitoring reduced the proportion

223 Intracranial pressure monitoring was not associated with

224 ive and nonaggressive based on the frequency intracranial pressure monitoring) on outcome was assesse

225 atic brain injury (Glasgow Coma Scale </= 8; intracranial pressure monitoring).

226 In the patient subgroup with intracranial pressure monitoring, prolonged time spent i

227 mobile medical team, mechanical ventilation, intracranial pressure monitoring, vasopressors, acute ne

228 els in those patients with an indication for intracranial pressure monitoring.

229 the first week of therapy, 29% did not have intracranial pressure monitoring.

230 raniectomy and external ventricular draining/intracranial pressure monitoring.

231 Intracranial-pressure monitoring is considered the stand

232 ents had a higher proportion of samples with intracranial pressure more than 20 mm Hg (13% vs 30%), b

233 acranial pressure and 36% had a highest mean intracranial pressure more than 20 mm Hg.

234 ue oxygenation crisis events were defined as intracranial pressure of greater than or equal to 20 mm

235 In patients with an intracranial pressure of more than 20 mm Hg after trauma

236 We randomly assigned adults with an intracranial pressure of more than 20 mm Hg despite stag

237 IIH is a condition of raised intracranial pressure of unknown cause, usually observed

238 ntation that resembles syndromes of elevated intracranial pressure on Earth.

239 entobarbital infusion, or markedly increased intracranial pressure on interruption of continuous seda

240 remains controversy about how best to manage intracranial pressure on the ICU; we review the recent l

241 tissue oxygenation data were recorded in the intracranial pressure -only group in blinded fashion.

242 after severe traumatic brain injury (0.45 in intracranial pressure-only group and 0.16 in intracrania

243 of patients with good recovery compared with intracranial pressure-only management; however, the stud

244 r mortality and more favorable outcomes than intracranial pressure-only treatment.

245 PHOMS in MS is due to intermittently raised intracranial pressure or an otherwise impaired "glymphat

246 s complications as related to an increase in intracranial pressure or as a direct result from cranial

247 caused by the seizure disorder or increased intracranial pressure or by the underlying disorder (tha

248 eflex sensitivity showed no correlation with intracranial pressure or cerebral perfusion pressure; th

249 s between autonomic impairment and increased intracranial pressure or impaired cerebral autoregulatio

250 m to be independent of age, trauma severity, intracranial pressure, or autoregulatory status, and thu

251 romise as surrogate, noninvasive measures of intracranial pressure, outperforming other conventional

252 Intracranial pressure over 20 mm Hg is associated with p

253 had a sensitivity of 100% in predicting high intracranial pressure over the following 24 hours.

254 ore likely to receive treatment for elevated intracranial pressure (P < .001).

255 g cerebral perfusion pressure (p = 0.03) and intracranial pressure (p = 0.06) seen after seizure onse

256 The number of patients with high intracranial pressure peaked 3 days after subarachnoid h

257 or age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral

258 intracranial pressure-only group and 0.16 in intracranial pressure plus brain tissue oxygenation grou

259 re randomized to treatment protocol based on intracranial pressure plus brain tissue oxygenation moni

260 al to assess impact on neurologic outcome of intracranial pressure plus brain tissue oxygenation-dire

261 values (+/- SDs) of arterial blood pressure, intracranial pressure, pressure reactivity index, and ot

262 dently of age, admission Glasgow Coma Scale, intracranial pressure, pressure reactivity index, or cer

263 rmation extraction from radiographic images, intracranial pressure processing, low back pain and real

264 n/peak sulfonylurea receptor-1 and mean/peak intracranial pressure, proportion of intracranial pressu

265 Proportion of intracranial pressure readings from greater than 18 to g

266 Of 21,954 intracranial pressure readings, median interquartile ran

267 ta-analysis of the effect of 23.4% saline on intracranial pressure reduction.

268 Elevated intracranial pressure requiring acute intervention is a

269 Elevated intracranial pressure requiring acute intervention was a

270 H due to vascular malformation, and elevated intracranial pressure requiring urgent intervention woul

271 The intracranial pressure response to hypoxia varied between

272 AMS symptomology is explained by a variable intracranial pressure response to hypoxia.

273 Intracranial pressure significantly increases with abdom

274 sure-targeted approach with the conventional intracranial pressure-targeted approach to treat raised

275 py-dopamine, and if needed noradrenaline) or intracranial pressure-targeted therapy (n = 55) (maintai

276 ventilation and osmotherapy, was superior to intracranial pressure-targeted therapy for management of

277 toward an early warning system for increased intracranial pressure that can be generally applied.

278 bri is a disorder characterized by increased intracranial pressure that predominantly affects obese y

279 ension is a disorder characterised by raised intracranial pressure that predominantly affects young,

280 edema develops quickly after trauma, raising intracranial pressure that results in a decrease of bloo

281 ions in the gradient between intraocular and intracranial pressures that direct the movement of fluid

282 Adverse consequences of intracranial pressure-time burden and cerebral perfusion

283 he area under the curve from high-resolution intracranial pressure-time plots was calculated to repre

284 ypothermia as a first line measure to reduce intracranial pressure to less than 20 mm Hg is harmful i

285 ated intracranial pressure and prediction of intracranial pressure treatment intensity.

286 bral blood flow, regional brain volumes, and intracranial pressure, using high-resolution magnetic re

287 injury based on brain tissue oxygenation and intracranial pressure values was consistent with reduced

288 Clinical manifestations due to increased intracranial pressure, visual impairment and endocrine d

289 The highest mean intracranial pressure was analyzed in relation to demogr

290 In the present study, intracranial pressure was estimated non-invasively (nICP

291 An intraparenchymal intracranial pressure was inserted.

292 f heart rate responses to acute increases in intracranial pressure was not affected by Cx43 deficienc

293 disability at 6 months were pooled, however, intracranial pressure was not an independent predictor o

294 Intracranial pressure was recorded every 4 hrs in all pa

295 At the end of the experiment, the intracranial pressure was significantly higher in c-ECPR

296 h a protocol for monitoring intraparenchymal intracranial pressure was used (pressure-monitoring grou

297 te the correlation between the complexity of intracranial pressure waveform and outcome after traumat

298 likelihood ratio that may rule out increased intracranial pressure, whereas an elevated measurement,

299 ference standard was the concurrent invasive intracranial pressure, with test-positivity set at intra

300 ese women, producing a syndrome of increased intracranial pressure without identifiable cause.