ライフサイエンスコーパス: intracranial

1 tential therapeutic benefits associated with intracranial 2-HG inhibition.

2 deposits in neural tissues of patients with intracranial abnormalities following intravenous gadolin

3 CT of the head revealed intracranial abnormalities in 35 of 193 patients (18.1%)

4 GBCA administration occurs in the absence of intracranial abnormalities that might affect the permeab

5 n study, lorlatinib showed both systemic and intracranial activity in patients with advanced ALK-posi

6 hown robust anti-tumour efficacy, along with intracranial activity, in patients with ALK-rearranged n

7 each must be tested with both intranasal and intracranial administration to ensure the absence of let

8 bsent in both the brain and spinal cord when intracranial and intrathecal injections of the same AAV

9 Using intracranial and magnetoencephalography (MEG) recordings

10 leeding events (n=218 gastrointestinal, n=45 intracranial, and n=142 other) during 13 509 patient-yea

11 oking history vs 163 of 564 patients without intracranial aneurysm (28.9%; P < .001).

12 ntracranial aneurysm: 42 of 78 patients with intracranial aneurysm (53.8%) had a smoking history vs 1

13 The presence of intracranial aneurysm did not vary with location of extr

14 The prevalence of intracranial aneurysm in patients with fibromuscular dys

15 though the clinical benefit of screening for intracranial aneurysm in patients with FMD has yet to be

16 The prevalence of intracranial aneurysm in women diagnosed with FMD is sig

17 To examine the prevalence of intracranial aneurysm in women diagnosed with FMD.

18 The only known risk factor was an intracranial aneurysm that was found on her grandmother'

19 ith FMD with intracranial imaging who had an intracranial aneurysm.

20 hese 86 patients, 25 (53.8%) had more than 1 intracranial aneurysm.

21 (12.9%; 95% CI, 10.3%-15.9%) had at least 1 intracranial aneurysm.

22 of smoking was significantly associated with intracranial aneurysm: 42 of 78 patients with intracrani

23 in 32 of 74 patients (43.2%), and 24 of 128 intracranial aneurysms (18.8%) were in the posterior com

24 Unruptured intracranial aneurysms (UIAs) are increasingly diagnosed

25 Small unruptured intracranial aneurysms (UIAs) are increasingly diagnosed

26 Intracranial aneurysms 5 mm or larger occurred in 32 of

27 ness and safety of endovascular treatment of intracranial aneurysms with the use hydrogel coils.

28 Acute ischemic stroke caused by proximal intracranial arterial occlusion of the anterior circulat

29 troke caused by atherosclerosis of the major intracranial arteries.

30 ed internal carotid, vertebral, or suspected intracranial artery aneurysms were reviewed.

31 using search terms intracranial stenosis and intracranial atherosclerosis.

32 Intracranial atherosclerotic disease (ICAD) is an import

33 Intracranial atherosclerotic disease is a highly prevale

34 ajor modifiable risk factors associated with intracranial atherosclerotic disease.

35 andard of care for symptomatic patients with intracranial atherosclerotic disease.

36 Intracranial atherosclerotic stenosis (ICAS) is a common

37 level of AD and MD comorbidity, while larger intracranial (beta = 1.07; 95% CI, 0.50 to 1.64) and sma

38 0.72 to 1.09]) but were less likely to have intracranial bleeding (0.39 vs. 0.77 events per 100 pers

39 arin therapy, the risk factors for traumatic intracranial bleeding are unique from those for ischemic

40 There was no significant increase in intracranial bleeding or other critical organ bleeding.

41 introduce an experimental paradigm in which intracranial brain activity, a video of the real-life vi

42 phaly; reported brain abnormalities included intracranial calcifications, corpus callosum abnormaliti

43 py (WBRT) is the standard of care to improve intracranial control following resection of brain metast

44 tients undergoing monitoring of seizures via intracranial depth electrodes viewed a series of neutral

45 s and three females) who were implanted with intracranial depth electrodes.

46 ns were limited to their activation from the intracranial dura but not facial skin or cornea.

47 was compared with the seizure onset zone at intracranial EEG and with surface IED-related potentials

48 Using intracranial EEG recordings from rare patients with medi

49 ing a multimodal analysis of functional MRI, intracranial EEG recordings, and large-scale neural popu

50 Using tools combining MEG and intracranial EEG with brain connectivity analyses, we pr

51 Using intracranial EEG, we recorded ventral striatum activity

52 f high-gamma activity recorded using MEG and intracranial EEG.

53 e show that pre- vs. postmortem, TES-induced intracranial electric fields differ significantly in bot

54 Intracranial electrical brain stimulation in awake neuro

55 Yet, insufficient data on intracranial electrical connectivity has precluded a dir

56 oencephalographic recordings obtained during intracranial electrical stimulation in a cohort of three

57 By analyzing intracranial electrode data from humans, we demonstrate

58 recorded directly from the human brain using intracranial electrodes implanted in patients undergoing

59 Here we used intracranial electrodes to record single-neuron activiti

60 Recent intracranial electroencephalographic (iEEG) work has sho

61 We recorded intracranial electroencephalographic activity from parti

62 Finally, we analyze intracranial electroencephalography (IEEG) recordings of

63 We examine this question using intracranial electroencephalography captured from nine h

64 vices and in automatic parsing of continuous intracranial electroencephalography data.

65 opment of seizure detection algorithms using intracranial electroencephalography from canines and hum

66 on refractory epilepsy undergoing continuous intracranial electroencephalography monitoring engaged i

67 However, no intracranial electrophysiological evidence for replay ex

68 Using intracranial electrophysiological recordings during an a

69 Intracranial ependymomas are segregated on the basis of

70 ng of vitrectomy in relation to the inciting intracranial event was recorded.

71 Our results provide initial intracranial evidence for the neurophysiological reality

72 ons whereas MRI is more useful in evaluating intracranial extension.

73 Imaging was used to quantify distribution of intracranial extracellular free water (FW).

74 ved that 2 mA currents generated substantial intracranial fields, which were much stronger in the sti

75 Major intracranial findings were seen in only 15 of 549 (2.7%)

76 The median time from groin puncture to first intracranial flow restoration with CS was 47 minutes (in

77 ctly assessed mesial temporal activity using intracranial foramen ovale electrodes in two patients wi

78 tion with radiotherapy in treating mice with intracranial GBM xenograft markedly slows tumor growth a

79 small interfering (si) and micro (mi)RNAs to intracranial glioblastoma (GBM) tumor sites.

80 ation into the clinical setting supported on intracranial grid or strip electrodes.

81 6OTD suppressed the intracranial growth of GSC-derived tumors in a mouse xen

82 ilure [120 mg/day], haemoptysis [80 mg/day], intracranial haemorrhage [20 mg/day], ventricular fibril

83 teria included: CNS involvement, a stroke or intracranial haemorrhage less than 12 months before enro

84 icularly when the syndrome is complicated by intracranial haemorrhage or brain infarction.

85 d as: initial failure of aneurysm treatment, intracranial haemorrhage or residual aneurysm on 1-year

86 Symptomatic intracranial hemorrhage (1% vs 4%) and parenchymal hemor

87 ted in 356 patients (7.1%), and included 181 intracranial hemorrhage (42.5%), 100 brain deaths (23.5%

88 h survival between patients with and without intracranial hemorrhage (68.3% vs 76.0%; p = 0.350).

89 were safer with respect to the reduction of intracranial hemorrhage (HR, 0.38; 95% CI, 0.26-0.56).

90 agnostic performance of APT MRI in detecting intracranial hemorrhage (ICH) at hyperacute, acute and s

91 Spontaneous intracranial hemorrhage (ICH) is also a frequent occurre

92 Intracranial hemorrhage (ICH) was the most common site o

93 SSRIs) may increase the risk for spontaneous intracranial hemorrhage (ICH), an effect that is in theo

94 temic embolic events (SSEE), major bleeding, intracranial hemorrhage (ICH), and all-cause death.

95 tigated the frequency and characteristics of intracranial hemorrhage (ICH), the factors associated wi

96 rebral artery occlusion leading to increased intracranial hemorrhage and mortality.

97 e as monitored warfarin, with lower rates of intracranial hemorrhage and reduced mortality.

98 h, myocardial infarction, major bleeding, or intracranial hemorrhage as an outcome.

99 The rate of symptomatic intracranial hemorrhage did not differ significantly bet

100 ion, the adjusted odds ratio for symptomatic intracranial hemorrhage for those on NOACs was 0.92 (95%

101 Bleeding occurred in 70.2%, including intracranial hemorrhage in 16%, and was independently as

102 A mathematical model that can predict acute intracranial hemorrhage in infants at increased risk of

103 Accurate and timely identification of intracranial hemorrhage in infants without a history of

104 Unadjusted rates of symptomatic intracranial hemorrhage in the NOAC, warfarin, and none

105 e basis of a multivariable model to identify intracranial hemorrhage in well-appearing infants using

106 emorrhagic effect of NAC in a mouse model of intracranial hemorrhage induced by in situ collagenase t

107 It is unclear whether intracranial hemorrhage is a consequence of the extracor

108 real membrane oxygenation, the occurrence of intracranial hemorrhage is associated with a high mortal

109 efined as brain death, seizures, stroke, and intracranial hemorrhage occurring during extracorporeal

110 department visit with a primary diagnosis of intracranial hemorrhage or gastrointestinal, urogenital,

111 We report a higher prevalence of intracranial hemorrhage than has previously been describ

112 significantly more likely to have died from intracranial hemorrhage than were all other deceased org

113 vealed factors independently associated with intracranial hemorrhage to be duration of ventilation (d

114 The prevalence of intracranial hemorrhage was 16.4% in extracorporeal memb

115 Intracranial hemorrhage was lower with higher-dose NOACs

116 Intracranial hemorrhage was the most frequent type, and

117 tients at greatest risk of suffering a major intracranial hemorrhage with anticoagulation.

118 leeding (blood loss requiring transfusion or intracranial hemorrhage) and thrombosis during ECMO supp

119 injury; mortality was 79.6% in patients with intracranial hemorrhage, 68.2% in patients with stroke,

120 ity fracture, pelvic fracture, central line, intracranial hemorrhage, and blood transfusion).

121 Ischemic stroke, intracranial hemorrhage, and death.

122 f 0-2) and mortality at 90 days, symptomatic intracranial hemorrhage, emboli to new territory, and va

123 Ischemic stroke, intracranial hemorrhage, extracranial bleeding, and myoc

124 ly confirmed single spontaneous or traumatic intracranial hemorrhage, of whom 39 (83%) had hearing lo

125 logically confirmed spontaneous or traumatic intracranial hemorrhage, of whom none had hearing loss,

126 parable outcomes regarding the occurrence of intracranial hemorrhage, regardless of the antenatal man

127 48.0% specific (95% CI, 47.3-48.9) for acute intracranial hemorrhage.

128 hemoglobin, can identify infants with acute intracranial hemorrhage.

129 l support, are independently associated with intracranial hemorrhage.

130 lities, isolated skull fractures, or chronic intracranial hemorrhage.

131 ls to alert physicians to the possibility of intracranial hemorrhage.

132 gic outcomes; and 3) factors associated with intracranial hemorrhage.

133 rain imaging, we sought 1) the prevalence of intracranial hemorrhage; 2) survival and neurologic outc

134 tinal bleeding and 98 (32.6%) presented with intracranial hemorrhage; among the patients who could be

135 a consideration, but its risks of major and intracranial hemorrhages rival overall harms from interm

136 eritis nodosa, lacunar ischemic strokes, and intracranial hemorrhages), immunodeficiency and bone mar

137 remarkable synergistic anticancer effect on intracranial human and murine glioblastoma via induction

138 Primary intracranial hydatid cyst is a rare location of human ec

139 The ability to detect intracranial hypertension (ICP >/= 20 mm Hg) was highest

140 the population-based incidence of idiopathic intracranial hypertension (IIH) and to determine if it m

141 ociated with papilledema owing to idiopathic intracranial hypertension (IIH) at presentation.

142 ed MR venography in patients with idiopathic intracranial hypertension (IIH).

143 of patients with hydrocephalus and suspected intracranial hypertension (n = 5), and the negative cont

144 tanding of the pathophysiology of idiopathic intracranial hypertension and glaucoma.

145 Hyperammonemia has been associated with intracranial hypertension and mortality in patients with

146 8) months in the hydrocephalus and suspected intracranial hypertension cohort (60% female), and 59.7

147 A similar proportion died due to refractory intracranial hypertension in each group (abusive head tr

148 Hypothermia reduces intracranial hypertension in patients with traumatic bra

149 o month 12 in participants of the Idiopathic Intracranial Hypertension Treatment Trial (IIHTT).

150 ated with the development of cerebral edema, intracranial hypertension, and secondary neuronal injury

151 for identifying critically ill patients with intracranial hypertension.

152 arious forms of hydrocephalus and ideopathic intracranial hypertension.

153 racranial pressure in 91.7% of patients with intracranial hypertension.

154 had low sensitivity (11%-42%) for detecting intracranial hypertension.

155 arious forms of hydrocephalus and idiopathic intracranial hypertension.SIGNIFICANCE STATEMENT Effecti

156 Intracranial hypotension (IH) is an uncommon, benign, an

157 Intracranial hypotension can mimic other conditions such

158 In previous human intracranial (iEEG) work we found that excitatory broadb

159 s in the registry, 669 (60.2%) had undergone intracranial imaging at the time of enrollment (mean [SD

160 mendation that all patients with FMD undergo intracranial imaging if not already performed.

161 ross-sectional study included 669 women with intracranial imaging registered in the US Registry for F

162 Percentage of women with FMD with intracranial imaging who had an intracranial aneurysm.

163 We used bilateral intracranial infusions of propranolol into either the in

164 alters drug-taking behavior, we administered intracranial injections of plasmid DNA encoding IL-10 (p

165 atus to 759 of 767 patients with significant intracranial injuries (sensitivity, 99.0% [95% CI: 98.0%

166 ain is essential for diagnostic screening of intracranial injuries in need of neurosurgical intervent

167 Clinicians, afraid of missing intracranial injuries, liberally obtain computed tomogra

168 rvention and 306 (3.94%) who had significant intracranial injuries.

169 with mild traumatic brain injury (mTBI) and intracranial injury (ICI) on computed tomographic imagin

170 Based on these results, the Children's Intracranial Injury Decision Aid score is a potentially

171 Based on this modeling, the Children's Intracranial Injury Decision Aid score was created.

172 n this modeling, we developed the Children's Intracranial Injury Decision Aid score, which ranged fro

173 cal intervention, and clinically significant intracranial injury, respectively).

174 Intracranial inoculation of 1-d-old immunocompetent CD-1

175 the CWD agent following experimental oral or intracranial inoculation.

176 subcutaneously but replicate well following intracranial inoculation.

177 tients with proximal occlusion after stroke (intracranial internal carotid artery and/or middle cereb

178 We enrolled patients with occlusion of the intracranial internal carotid artery or proximal middle

179 n patients with acute ischemic stroke due to intracranial large vessel occlusion, to determine the cl

180 Among cohort A, 14 patients who had intracranial large-vessel occlusion/stenosis with sparse

181 ent (IAT) in the setting of extracranial and intracranial lesions is considered challenging, and whet

182 with structural changes on intraorbital and intracranial magnetic resonance imaging and in-flight an

183 d microglia in treatment of murine syngeneic intracranial malignant gliomas.

184 d detection of the transosseous extension of intracranial meningiomas compared with CE-MRI.

185 Transosseous extension of intracranial meningiomas is known to be an important ris

186 s and an unexpected shared pathogenesis with intracranial meningiomas.

187 o patients also underwent SRS for additional intracranial metastases.

188 In intracranial mouse xenograft models of glioblastoma, inh

189 Using intracranial multiphoton imaging, we found that infusion

190 (1%) had fourth nerve palsy owing to a known intracranial neoplasm.

191 itary adenoma (PA) is one of the most common intracranial neoplasms.

192 Mice subjected to bioimaging after neonatal intracranial or intravascular administration of biosenso

193 conscious, unrestrained mice after neonatal intracranial or intravascular administration of lentivir

194 benefit of CGRP-mAb in reducing headaches of intracranial origin such as migraine with aura and why t

195 lp differentiate lesions of extracranial and intracranial origins.

196 Specific MRI findings include intracranial pachymeningeal enhancement, sagging of the

197 Intracranial plaque presence, size (maximum normalized w

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

199 Both intracranial pressure (ICP) and the cerebrovascular pres

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

201 Intracranial pressure (ICP) monitoring is a mainstay of

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

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

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

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

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

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

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

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

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

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

212 Intracranial pressure control was similar in both groups

213 Intracranial pressure correlated with maximal retinal ne

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

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

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

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

218 Detecting elevated intracranial pressure in children with subacute conditio

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

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

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

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

223 Elevated intracranial pressure leads to structural changes in the

224 ol patients, underwent direct intraoperative intracranial pressure measurement.

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

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

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

228 Intracranial pressure monitoring is a widely but inconsi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 OCT were correlated with invasively measured intracranial pressure.

248 as the primary intervention to reduce raised intracranial pressure.

249 that microgravity reduces central venous and intracranial pressure.

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

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

252 CT parameters and directly measured elevated intracranial pressure.

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

254 EGFR-TKI versus EGFR-TKI followed by SRS at intracranial progression is urgently needed.

255 Overall survival (OS) and intracranial progression-free survival were measured fro

256 -TKI, or EGFR-TKI followed by SRS or WBRT at intracranial progression.

257 esence of ECD modified the effect of IAT for intracranial proximal anterior circulation occlusion.

258 atients with acute ischemic stroke caused by intracranial proximal occlusion.

259 tigate this boundary setting mechanism using intracranial recordings (ECoG), in 12 patients undergoin

260 Here, we used human intracranial recordings and visual word-by-word presenta

261 Here, using intracranial recordings from the human hippocampus we fo

262 d calibrate current-flow models with in vivo intracranial recordings in humans, providing a solid fou

263 Here a large dataset of intracranial recordings obtained during encoding of word

264 A new study using human intracranial recordings offers a fresh perspective on ho

265 Intracranial response by investigator assessment was als

266 e primary endpoint was investigator-assessed intracranial response in cohort A in the all-treated-pat

267 Secondary endpoints included intracranial response in cohorts B, C, and D.

268 6-69) of 76 patients in cohort A achieved an intracranial response.

269 I 12-88]) of six patients in cohort 5 had an intracranial response.

270 uld serve as a direct positive reinforcer on intracranial self-photostimulation assays.

271 of VTA glutamatergic neurons produced robust intracranial self-stimulation (ICSS) behavior, which was

272 Intracranial self-stimulation in rats showed that elonga

273 In addition, we performed intracranial self-stimulation in rats to understand how

274 ed from 1955 to June 2016 using search terms intracranial stenosis and intracranial atherosclerosis.

275 ve management of vascular risk factors) with intracranial stenting plus aggressive medical management

276 Prior intracranial stimulation or cortical cooling studies hav

277 ons or if CAIS occurred as a complication of intracranial surgery or brain tumor.

278 rom pseudo-occlusion (defined as an isolated intracranial thrombus that impedes ascending blood flow)

279 ortem examination, FACS-based enumeration of intracranial tumor-infiltrating lymphocytes directly cor

280 fourth nerve palsy the presenting sign of an intracranial tumor.

281 ls with impaired proliferation but increased intracranial tumorigenicity.

282 the brain or leaky vasculature of late-stage intracranial tumors.

283 g the host antitumor immune response against intracranial tumors.

284 P/L-selectins and accumulate selectively in intracranial tumors.

285 vivo transient depletion of PRMT5 decreased intracranial tumour size and growth rate in mice implant

286 IC) cohort study who underwent 3-dimensional intracranial vessel wall magnetic resonance imaging from

287 ges of Parkinson disease and that the entire intracranial visual system can be involved.

288 Purpose To assess intracranial visual system changes of newly diagnosed Pa

289 ippocampus (d=-0.11), putamen (d=-0.14), and intracranial volume (d=-0.10) were smaller in individual

290 2 vs -0.06), putamen (d=-0.18 vs -0.08), and intracranial volume (d=-0.14 vs 0.01).

291 CM exposure was associated with lower child intracranial volume (F1,70 = 6.84, p = .011), which was

292 ngs identify the biological underpinnings of intracranial volume and their link to physiological and

293 ol differences in subcortical structures and intracranial volume through pooling of all individual da

294 riers (P = 0.047), after adjusting for total intracranial volume, age, sex, follow-up years in the re

295 ot be explained by differences in verbal IQ, intracranial volume, anxiety/depression, or attention or

296 22q11.2 gene dosage varied positively with intracranial volume, gray and white matter volume, and c

297 re defined manually and normalized for total intracranial volume.

298 ion in the respective tissues when comparing intracranial with intrathecal injections.

299 g and prolonged the survival of mice bearing intracranial xenografts of MI cells harboring these muta

300 of animal subjects bearing reporter-modified intracranial xenografts, we quantitatively assessed MGMT