ライフサイエンスコーパス: intracerebral hemorrhage

1 rtality of 31% in ischemic stroke and 42% in intracerebral hemorrhage.

2 it hematoma/iron-mediated brain injury after intracerebral hemorrhage.

3 esponses are associated with the outcomes of intracerebral hemorrhage.

4 A TSPO ligand attenuates brain injury after intracerebral hemorrhage.

5 to several clinical complications, including intracerebral hemorrhage.

6 7), but no association with stable angina or intracerebral hemorrhage.

7 nslational target for secondary injury after intracerebral hemorrhage.

8 come); the secondary outcome was symptomatic intracerebral hemorrhage.

9 -0.16%) seizures, and 4% (95% CI, 0.01-0.1%) intracerebral hemorrhage.

10 they could not be assessed in patients with intracerebral hemorrhage.

11 edema expansion rate predicts outcome after intracerebral hemorrhage.

12 tients, including 53 with sepsis and 59 with intracerebral hemorrhage.

13 n increased risk of both ischemic stroke and intracerebral hemorrhage.

14 roke-related mortality, incident stroke, and intracerebral hemorrhage.

15 differences in rates of death or symptomatic intracerebral hemorrhage.

16 n mortality or the occurrence of symptomatic intracerebral hemorrhage.

17 may increase the development or severity of intracerebral hemorrhage.

18 are associated with long-term outcome after intracerebral hemorrhage.

19 the effect of fingolimod in a mouse model of intracerebral hemorrhage.

20 in atrophy was evaluated two weeks following intracerebral hemorrhage.

21 ress syndrome is common after intubation for intracerebral hemorrhage.

22 .21 (95% confidence interval, 1.10-1.33) for intracerebral hemorrhage.

23 on mast cell activation in a mouse model of intracerebral hemorrhage.

24 and at 14 days, 28 days, and 3 months after intracerebral hemorrhage.

25 ceived standard critical care management for intracerebral hemorrhage.

26 c stroke, and 13.7% (95% CI, 3.6%-23.9%) for intracerebral hemorrhage.

27 s were investigated at 24 and 72 hours after intracerebral hemorrhage.

28 gulants, and both developed life-threatening intracerebral hemorrhage.

29 by prevention of mast cell activation after intracerebral hemorrhage.

30 irmed in an autologous blood injection model intracerebral hemorrhage.

31 muL) in the brain was established to induce intracerebral hemorrhage.

32 risk of any stroke, cerebral infarction, or intracerebral hemorrhage.

33 ties, on inflammation and brain injury after intracerebral hemorrhage.

34 a expansion and poor clinical outcomes after intracerebral hemorrhage.

35 ts with warfarin-associated coagulopathy and intracerebral hemorrhage.

36 s and safer therapy for TBI with no risk for intracerebral hemorrhage.

37 ementia, often without clinically manifested intracerebral hemorrhage.

38 threatening cerebral edema that occurs after intracerebral hemorrhage.

39 nt advances in the management of spontaneous intracerebral hemorrhage.

40 , 4,072 with ischemic stroke, and 2,974 with intracerebral hemorrhage.

41 essel stroke but not cardioembolic stroke or intracerebral hemorrhage.

42 loci influenced both small vessel stroke and intracerebral hemorrhage.

43 and distal brain region alteration following intracerebral hemorrhage.

44 The most common etiology was intracerebral hemorrhage.

45 upregulated centrally and peripherally after intracerebral hemorrhage.

46 to start or restart anticoagulation after an intracerebral hemorrhage.

47 neurological outcomes in an animal model of intracerebral hemorrhage.

48 increased bleeding complications, including intracerebral hemorrhages.

49 nd blood-brain barrier (BBB) disruption with intracerebral hemorrhages.

50 (SRF), suffer from loss of BBB integrity and intracerebral hemorrhaging.

51 subarachnoid hemorrhage 0.17 (0.06-0.45) and intracerebral hemorrhage 0.57 (0.34-0.94).

52 Within 1 year of intracerebral hemorrhage, 224 (56%) of 402 patients died

53 iagnoses were subarachnoid hemorrhage (38%), intracerebral hemorrhage (31%), and acute ischemic strok

54 ge (32%), and 1,404 ventilated patients with intracerebral hemorrhage (49%) of whom 1,084 (38%) were

55 129 patients with stroke (with infarction or intracerebral hemorrhage, 57 women and 72 men; mean age,

56 The patient died of an intracerebral hemorrhage 6 months after the assessment.

57 In contrast, rates of intracerebral hemorrhage (6% vs 8%; p = 0.35) did not di

58 type of intracranial hemorrhage, followed by intracerebral hemorrhage (8%), and subdural hemorrhage (

59 red with those without CAA more commonly had intracerebral hemorrhage (9.3% vs 3.5%, respectively; P

60 Articles relevant to prognosis in intracerebral hemorrhage, acute ischemic stroke, traumat

61 and an increased probability of symptomatic intracerebral hemorrhage (adjusted OR per 30 minutes inc

62 tcomes included thrombolysis rate, secondary intracerebral hemorrhage after thrombolysis, and 7-day m

63 tients, including 53 with sepsis and 59 with intracerebral hemorrhage, along with 53 control particip

64 direct thrombin inhibitor with a low risk of intracerebral hemorrhage, ameliorates AD pathogenesis in

65 ses and 404,630 noncases, and 1,545 cases of intracerebral hemorrhage and 1,481 noncases.

66 A total of 46,735 intracerebral hemorrhage and 331,521 ischemic stroke cas

67 m 0, no symptoms, to 6, death) scores before intracerebral hemorrhage and at 14 days, 28 days, and 3

68 erebral cortex and is a major cause of lobar intracerebral hemorrhage and cognitive impairment in the

69 r CMBs were similar to those for symptomatic intracerebral hemorrhage and differed for lobar and deep

70 per patient (p=.01; but not >20 mm Hg), both intracerebral hemorrhage and intraventricular hemorrhage

71 re readings per patient>30 mm Hg and initial intracerebral hemorrhage and intraventricular hemorrhage

72 Intracerebral hemorrhage and ischemic stroke admissions

73 determine whether palliative care use after intracerebral hemorrhage and ischemic stroke differs bet

74 Assessment of all-cause mortality of intracerebral hemorrhage and ischemic stroke patients ad

75 Hematoma expansion occurs in children with intracerebral hemorrhage and may require urgent treatmen

76 sted odds ratio, 0.65; 95% CI, 0.50-0.84 for intracerebral hemorrhage and odds ratio, 0.62; 95% CI, 0

77 Beyond 30 days, there was one fatal intracerebral hemorrhage and one transient ischemic atta

78 ening capillary nets, increasing the risk of intracerebral hemorrhage and stroke.

79 Finally, hospitalization rates for intracerebral hemorrhage and subarachnoid hemorrhage rem

80 ated with an increased rate of mortality and intracerebral hemorrhage and with a decreased rate of fa

81 hout neurologic symptoms, 6 with prior lobar intracerebral hemorrhage) and 17 mutation noncarriers (M

82 ents, including 10 with sepsis and five with intracerebral hemorrhage, and 11 healthy controls.

83 with subarachnoid hemorrhage, 1% to 21% with intracerebral hemorrhage, and 30% of patients following

84 Twelve patients had intracerebral hemorrhage, and 4 had subarachnoid hemorrh

85 197% increase (95% CI = 59-457%) in risk of intracerebral hemorrhage, and an increase in white matte

86 mbolysis, 7- and 90-day mortality, secondary intracerebral hemorrhage, and discharge home.

87 Subarachnoid hemorrhage, intracerebral hemorrhage, and ischemic stroke hospitaliz

88 , Tenth Revision, codes for ischemic stroke, intracerebral hemorrhage, and stroke not otherwise speci

89 and secondary outcomes were ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage as

90 d ratio <1.5) for transient ischemic attack, intracerebral hemorrhage, and unstable angina, and inver

91 which 225 were cerebral infarctions, 42 were intracerebral hemorrhages, and 99 were unspecified strok

92 ding two posttreatment delayed ruptures, two intracerebral hemorrhages, and one thromboembolism.

93 the wall), clinical presentation, number of intracerebral hemorrhages, and other imaging markers not

94 At 24 and 72 hours post intracerebral hemorrhage, animals showed blood-brain bar

95 icance of hematoma expansion after childhood intracerebral hemorrhage are unknown.

96 , and activated microglia/macrophages in the intracerebral hemorrhage area and measuring plasma tumor

97 tilization of palliative care in spontaneous intracerebral hemorrhage at a population level using a l

98 Symptomatic intracerebral hemorrhage based on the European Cooperati

99 t study of adults diagnosed with spontaneous intracerebral hemorrhage between June 1, 2010 and May 31

100 Three days after intracerebral hemorrhage, brain edema, hematoma volume a

101 Delirium is common after intracerebral hemorrhage, but severe neurologic deficits

102 sponse was determined at set intervals after intracerebral hemorrhage by counting peripheral neutroph

103 o, 1.23; 95% CI, 1.18-1.30; p < 0.001), high intracerebral hemorrhage case volume (p < 0.001), antico

104 A challenge with collagenase to induce intracerebral hemorrhage caused marked brain damage and

105 Exclusion criteria included other intracerebral hemorrhage causes, anticoagulation, coagul

106 of acute respiratory distress syndrome after intracerebral hemorrhage, characterize risk factors for

107 in Alzheimer disease (chr2p21 and chr10q24), intracerebral hemorrhage (chr1q22), neuroinflammatory di

108 Other endpoints included: asymptomatic intracerebral hemorrhage; clinical improvement in NIHSS;

109 Activation of mast cells following intracerebral hemorrhage contributed to increase of bloo

110 motes neuroprotection or neurotoxicity after intracerebral hemorrhage depending on the time of admini

111 atrial fibrillation who are also at risk of intracerebral hemorrhage due to cerebral amyloid angiopa

112 on in patients with both ischemic stroke and intracerebral hemorrhage, especially compared with other

113 inimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation Phase III trial.

114 Fifty percent of participants with intracerebral hemorrhage experienced augmented renal cle

115 s with aneurysmal subarachnoid hemorrhage or intracerebral hemorrhage experienced enhanced renal clea

116 gist rated the diagnostic brain CT for acute intracerebral hemorrhage features and SVD biomarkers.

117 All 5 patients with an intracerebral hemorrhage had lobar microbleeds at baseli

118 sing trend of palliative care utilization in intracerebral hemorrhage has occurred over the last deca

119 piratory distress syndrome after spontaneous intracerebral hemorrhage have not been reported.

120 ellar microbleeds) were at increased risk of intracerebral hemorrhage (hazard ratio, 5.27; 95% confid

121 onfirmed NHS including primary and secondary intracerebral hemorrhage, hemorrhagic transformation of

122 nly modifiable predictor of outcome in adult intracerebral hemorrhage; however, the frequency and cli

123 ude of association appeared to be higher for intracerebral hemorrhage (HR, 1.9; 95% CI, 1.5-2.4) and

124 s further divided into those with past lobar intracerebral hemorrhage (ICH) (n = 21) and those with c

125 Ischemic stroke (IS) and intracerebral hemorrhage (ICH) account for an equal numb

126 Intracerebral hemorrhage (ICH) accounts for a disproport

127 age (IVH) is a negative prognostic factor in intracerebral hemorrhage (ICH) and is associated with pe

128 Autophagy occurs in the brain after intracerebral hemorrhage (ICH) and thrombin contributes

129 cal treatment for supratentorial spontaneous intracerebral hemorrhage (ICH) and whether it is modifie

130 Patients who have experienced intracerebral hemorrhage (ICH) appear to develop cogniti

131 sive blood pressure (BP) reduction for acute intracerebral hemorrhage (ICH) are inconsistent.

132 Transient symptoms from an intracerebral hemorrhage (ICH) are not well recognized a

133 e cortex is a key brain region vulnerable to intracerebral hemorrhage (ICH) associated with stroke an

134 (OAT) resumption is a therapeutic dilemma in intracerebral hemorrhage (ICH) care, particularly for lo

135 seizure is frequently the presenting sign of intracerebral hemorrhage (ICH) caused by stroke, head tr

136 ortant determinant of outcome in spontaneous intracerebral hemorrhage (ICH) due to small vessel disea

137 giography (CTA) spot sign is associated with intracerebral hemorrhage (ICH) expansion and may mark th

138 e accuracy of using the spot sign to predict intracerebral hemorrhage (ICH) expansion with standardiz

139 oding a collagen-binding Cnm protein induced intracerebral hemorrhage (ICH) experimentally and was al

140 of these markers for the differentiation of intracerebral hemorrhage (ICH) from ischemic stroke (IS)

141 linical outcomes in patients with cerebellar intracerebral hemorrhage (ICH) has not been established.

142 The role of CD47 in intracerebral hemorrhage (ICH) has not been investigated

143 n APOE alleles epsilon2/epsilon4 and risk of intracerebral hemorrhage (ICH) have been inconsistent an

144 onary events (MCE), ischemic stroke (IS) and intracerebral hemorrhage (ICH) in a cohort of Chinese ad

145 effect and improve functional recovery after intracerebral hemorrhage (ICH) in rats.

146 Intracerebral hemorrhage (ICH) is a devastating disease

147 Intracerebral hemorrhage (ICH) is a devastating form of

148 Intracerebral hemorrhage (ICH) is a devastating form of

149 Intracerebral hemorrhage (ICH) is a devastating stroke s

150 Spontaneous deep intracerebral hemorrhage (ICH) is a devastating subtype

151 Intracerebral hemorrhage (ICH) is a devastating type of

152 Persistent intracerebral hemorrhage (ICH) is a major cause of death

153 Intracerebral hemorrhage (ICH) is an especially feared c

154 Intracerebral hemorrhage (ICH) is one of the most devast

155 Intracerebral hemorrhage (ICH) is the most devastating a

156 Intracerebral hemorrhage (ICH) is the most severe form o

157 Concern about intracerebral hemorrhage (ICH) is the primary reason for

158 Intracerebral hemorrhage (ICH) is the stroke subtype wit

159 ma, and improves neurological function in an intracerebral hemorrhage (ICH) mouse model.

160 of specific antidotes is a major concern in intracerebral hemorrhage (ICH) related to direct anticoa

161 IVH and intracerebral hemorrhage (ICH) volume were measured manu

162 t ischemic attack (TIA), ischemic stroke, or intracerebral hemorrhage (ICH), aged 18 to 50 years, adm

163 s deposited in perihematomal tissue after an intracerebral hemorrhage (ICH), and may contribute to ox

164 in injuries (TBIs), multiple sclerosis (MS), intracerebral hemorrhage (ICH), and neuromyelitis optica

165 important modulators of tissue damage after intracerebral hemorrhage (ICH), but how this function is

166 protein (LDL) cholesterol levels and risk of intracerebral hemorrhage (ICH), but it remains unclear w

167 stricting hematoma expansion following acute intracerebral hemorrhage (ICH), but selecting those pati

168 cognitive decline commonly occurs following intracerebral hemorrhage (ICH), but the mechanisms under

169 Following intracerebral hemorrhage (ICH), the activation of mast c

170 In primary intracerebral hemorrhage (ICH), the most fatal type of s

171 MDMs in the murine brain after experimental intracerebral hemorrhage (ICH), we found robust phenotyp

172 nd tissue diffusion changes in patients with intracerebral hemorrhage (ICH).

173 predictor of poor outcome following an acute intracerebral hemorrhage (ICH).

174 ypertension is a significant risk factor for intracerebral hemorrhage (ICH).

175 rove long-term functional outcomes following intracerebral hemorrhage (ICH).

176 nd may play a role in the pathophysiology of intracerebral hemorrhage (ICH).

177 ) has been associated with increased risk of intracerebral hemorrhage (ICH).

178 erebral microbleeds, porencephaly, and fatal intracerebral hemorrhage (ICH).

179 lack of data on how to treat OAC-associated intracerebral hemorrhage (ICH).

180 ts of TSC were also tested in a rat model of intracerebral hemorrhage (ICH).

181 use has a similar effect among patients with intracerebral hemorrhage (ICH).

182 stem cells (BMSCs) transplantation following intracerebral hemorrhage (ICH).

183 ume is the strongest predictor of outcome in intracerebral hemorrhage (ICH).

184 has a detrimental role in brain injury after intracerebral hemorrhage (ICH).

185 ms in neonates and children with spontaneous intracerebral hemorrhage (ICH).

186 vertently administering tPA in patients with intracerebral hemorrhage (ICH).

187 highly penetrant cerebrovascular disease and intracerebral hemorrhage (ICH).

188 hemic lesions in patients with acute primary intracerebral hemorrhage (ICH).

189 y key mediators, such as thrombin, following intracerebral hemorrhage (ICH).

190 uiding treatment in patients presenting with intracerebral hemorrhage (ICH).

191 etamine use has emerged as a risk factor for intracerebral hemorrhage (ICH).

192 itical care might all be beneficial in acute intracerebral hemorrhage (ICH).

193 ccasionally to deliver medications following intracerebral hemorrhage (ICH).

194 pathophysiological mechanisms after onset of intracerebral hemorrhage (ICH).

195 n in vitro model of hematoma clearance after intracerebral hemorrhage [ICH]), and (3) reduced proinfl

196 sion protects blood-brain barrier(BBB) after intracerebral hemorrhage(ICH) remains unexplored.

197 Intracerebral hemorrhages (ICHs) are common in patients

198 tations contribute to sporadic, nonfamilial, intracerebral hemorrhages (ICHs).

199 s hospitalized with acute ischemic stroke or intracerebral hemorrhage in a large, urban academic medi

200 Intracerebral hemorrhage in patients with warfarin-assoc

201 TSC administered in combination with tPA on intracerebral hemorrhage incidence.

202 iated with 1-year death and dependence after intracerebral hemorrhage, independent of known predictor

203 ebral hemorrhage, neutrophils infiltrate the intracerebral hemorrhage-injured brain.

204 In patients with intracerebral hemorrhage, intensive lowering of blood pr

205 Intracerebral hemorrhage, intraventricular hemorrhage, a

206 Intracerebral hemorrhage is a devastating disorder with

207 Intracerebral hemorrhage is accompanied by a pronounced

208 e would improve the outcome in patients with intracerebral hemorrhage is not known.

209 Risk of intracerebral hemorrhage is the primary factor limiting

210 The ERICH study (Ethnic/Racial Variations of Intracerebral Hemorrhage) is a prospective, multicenter,

211 stroke (HS), ie, subarachnoid hemorrhage and intracerebral hemorrhage, is more common than ischemic s

212 rebral arteries and is an important cause of intracerebral hemorrhage, ischemic stroke, and cognitive

213 Preventing readmission after intracerebral hemorrhage may depend primarily on optimiz

214 Collagenase-induced intracerebral hemorrhage model in 8-week-old male CD-1 m

215 TIA (n = 262), ischemic stroke (n = 606), or intracerebral hemorrhage (n = 91) was assessed as of Nov

216 ORM-3 is given either before or 3 days after intracerebral hemorrhage, namely, as a prophylactic agen

217 ognized as an important component leading to intracerebral hemorrhage, neuroinflammation, and cogniti

218 Shortly after intracerebral hemorrhage, neutrophils infiltrate the int

219 "beneficial" phenotype for the treatment of intracerebral hemorrhage.Neutrophils are important modul

220 Symptomatic intracerebral hemorrhage occurred in 3.6% of participant

221 = .04) and CAA presentation with symptomatic intracerebral hemorrhage (odds ratio, 2.23; 95% CI, 1.07

222 e evidence to guide treatment strategies for intracerebral hemorrhage on vitamin K antagonists (VKA-I

223 Small focal intracerebral hemorrhages only visible on exquisitely se

224 Worthwhile interventions for intracerebral hemorrhage or subarachnoid hemorrhage gene

225 weeks) who had additional increased odds of intracerebral hemorrhage (OR = 1.84; 95% CI, 1.11-3.03)

226 .16]; p = 5.3 x 10(-5) ; N = 3,670), but not intracerebral hemorrhage (OR [95% CI] = 0.97 [0.84-1.12]

227 in a composite end point of ischemic stroke, intracerebral hemorrhage, or death from any cause.

228 the WARCEF primary outcome (ischemic stroke, intracerebral hemorrhage, or death), with death alone, i

229 me to the first to occur of ischemic stroke, intracerebral hemorrhage, or death.

230 ical," "stroke," "subarachnoid hemorrhage," "intracerebral hemorrhage," or "brain injury." DATA EXTRA

231 isability warrant careful prognostication of intracerebral hemorrhage outcomes and should be consider

232 hospital and day-90 SG utilities (SGU) among intracerebral hemorrhage patients and report a 3-way ass

233 puted tomography (CT) perfusion can identify intracerebral hemorrhage patients at high risk of hemato

234 prediction rule for short-term mortality in intracerebral hemorrhage patients but discriminated mort

235 azard ratio, 1.57; 95% CI, 1.39-1.77) and in intracerebral hemorrhage patients compared with these gr

236 Intracerebral hemorrhage patients discharged between Sep

237 ppear to influence palliative care use among intracerebral hemorrhage patients in the United States.

238 val curve gradient among ischemic stroke and intracerebral hemorrhage patients stabilized.

239 From 158 intracerebral hemorrhage patients that underwent MRI, on

240 ride >/= 115 mmol/L) on clinical outcomes in intracerebral hemorrhage patients treated with continuou

241 palliative care for both white and minority intracerebral hemorrhage patients was lower in minority

242 smal subarachnoid hemorrhage patients and 30 intracerebral hemorrhage patients were enrolled, contrib

243 Intracerebral hemorrhage patients with and without palli

244 Of the 311,217 intracerebral hemorrhage patients, 32,159 (10.3%) receiv

245 s moderate elevations may impact outcomes in intracerebral hemorrhage patients.

246 verse events (AEs), including death, stroke, intracerebral hemorrhage, pericardial complications, hem

247 To propose and validate a modified pediatric intracerebral hemorrhage (PICH) (mPICH) score and to com

248 hypoactive, were detected mean 6 days after intracerebral hemorrhage presentation, and were associat

249 (CMBs), which are asymptomatic precursors of intracerebral hemorrhage, reflects specific underlying m

250 ncy, (4) status post cardiac arrest, and (5) intracerebral hemorrhage requiring mechanical ventilatio

251 schemic stroke, and 3.9 [95% CI, 1.9-7.2 for intracerebral hemorrhage, respectively).

252 troke (RR: 0.91; 95% CI: 0.87, 0.96) but not intracerebral hemorrhage (RR: 0.96; 95% CI: 0.84, 1.10)

253 Discrimination was affected by study mean Intracerebral Hemorrhage score (beta = -0.05), and calib

254 ed after adjusting for all components of the intracerebral hemorrhage score (odds ratio, 2.21; 95% CI

255 oducible across cohorts for patients with an Intracerebral Hemorrhage score 0-1 (I = 15%).

256 s (mean age 68.0 [SD 18.4], 62% male, median intracerebral hemorrhage score 1.5 [interquartile range

257 sociation persisted after adjustment for all intracerebral hemorrhage score components (odds ratio, 2

258 Overall, the Intracerebral Hemorrhage score discriminated well (poole

259 verestimating mortality for patients with an Intracerebral Hemorrhage score greater than 3 (observed:

260 The Intracerebral Hemorrhage score is a valid clinical predi

261 also overestimated mortality in the highest Intracerebral Hemorrhage score patients, with significan

262 easurement, mean study year, and mean cohort Intracerebral Hemorrhage score.

263 ional Institutes of Health Stroke Scale, and intracerebral hemorrhage scores (P<0.001).

264 cluded patients with age less than 18 years, intracerebral hemorrhage secondary to trauma, tumor, isc

265 the newborn, infective pneumonia, asphyxia, intracerebral hemorrhage, seizure, cardiomyopathy, periv

266 pans (>= 2) of readings after adjustment for intracerebral hemorrhage severity.

267 Treatments for symptomatic intracerebral hemorrhage (sICH) are based on expert opin

268 n of CMB burden with the risk of symptomatic intracerebral hemorrhage (sICH) in patients with acute i

269 . 16.0%, P < 0.001), and similar symptomatic intracerebral hemorrhage (SICH) rates (1.7% vs. 1.8%, P

270 The primary safety outcome was symptomatic intracerebral hemorrhage (sICH) with preplanned stopping

271 t admission, MCA recanalization, symptomatic intracerebral hemorrhage (SICH), and 3-month clinical ou

272 chemic attack/systemic embolism, symptomatic intracerebral hemorrhage (sICH), and major extracranial

273 The influence of warfarin on symptomatic intracerebral hemorrhage (SICH), arterial recanalization

274 reatment is thrombolysis-related symptomatic intracerebral hemorrhage (sICH), which occurs in nearly

275 2) and mortality at 3 months and symptomatic intracerebral hemorrhage (SICH).

276 MO deployment incurred no increased risk for intracerebral hemorrhage (STEMO deployment: 7/200; conve

277 61), and (3) the Ethnic/Racial Variations of Intracerebral Hemorrhage study (n = 209).

278 the final vascular events (brain infarction, intracerebral hemorrhage, subarachnoid hemorrhage, coron

279 h HN improved outcomes in an animal model of intracerebral hemorrhage, suggesting that this process c

280 xerts protective effects in a mouse model of intracerebral hemorrhage; the mechanisms underlying thes

281 In patients with intracerebral hemorrhage, there was a higher mean measur

282 despite the early hazards (chiefly of fatal intracerebral hemorrhage), thrombolysis within 6 h did n

283 rkinson's diseases), carcinogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischem

284 linical role of hyperoxemia in patients with intracerebral hemorrhage treated in the ICU remains cont

285 Adult patients with intracerebral hemorrhage under antiplatelet treatment an

286 telet transfusion (2 U) within 60 minutes of intracerebral hemorrhage under antiplatelet treatment di

287 ic efficacy of early platelet transfusion in intracerebral hemorrhage under antiplatelet treatment.

288 Patients with intracerebral hemorrhage underwent in-hospital and day-9

289 Scale scores = 4-6) 1 year after first-ever intracerebral hemorrhage using logistic regression, adju

290 ociation of smoking with ischemic stroke and intracerebral hemorrhage using summary statistics data f

291 t not with thrombolytic treatment (p=.05) or intracerebral hemorrhage volume (p=.14).

292 Intracerebral hemorrhage volume measured from the comput

293 djusted for age, gender, Glasgow Coma Scale, intracerebral hemorrhage volume, intraventricular hemorr

294 ic territory, and a 3- to 5-fold increase in intracerebral hemorrhage volumes.

295 ars) and the standardized mortality rate for intracerebral hemorrhage was 8.4 (95% CI, 7.4-9.3; obser

296 No statistical difference in symptomatic intracerebral hemorrhage was found (5.6% vs 2.1% for the

297 ks' gestation to 18 years) with nontraumatic intracerebral hemorrhage were enrolled in a study from 2

298 kin Scale score, 0-1), and occurrence of any intracerebral hemorrhage within 24 to 36 hours after tre

299 the proportion of patients with symptomatic intracerebral hemorrhage within 30 hours after initiatio

300 gned 2839 patients who had had a spontaneous intracerebral hemorrhage within the previous 6 hours and