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

1 to start or restart anticoagulation after an intracerebral hemorrhage.

2 n mortality or the occurrence of symptomatic intracerebral hemorrhage.

3 may increase the development or severity of intracerebral hemorrhage.

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

5 in atrophy was evaluated two weeks following intracerebral hemorrhage.

6 ress syndrome is common after intubation for intracerebral hemorrhage.

7 .21 (95% confidence interval, 1.10-1.33) for intracerebral hemorrhage.

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

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

10 ceived standard critical care management for intracerebral hemorrhage.

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

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

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

14 by prevention of mast cell activation after intracerebral hemorrhage.

15 irmed in an autologous blood injection model intracerebral hemorrhage.

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

17 neurological outcomes in an animal model of intracerebral hemorrhage.

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

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

20 a expansion and poor clinical outcomes after intracerebral hemorrhage.

21 ts with warfarin-associated coagulopathy and intracerebral hemorrhage.

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

23 ementia, often without clinically manifested intracerebral hemorrhage.

24 threatening cerebral edema that occurs after intracerebral hemorrhage.

25 nt advances in the management of spontaneous intracerebral hemorrhage.

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

27 improve survival or functional outcome after intracerebral hemorrhage.

28 ction in experimental models of ischemia and intracerebral hemorrhage.

29 diagnosis and treatment of acute spontaneous intracerebral hemorrhage.

30 esponses are associated with the outcomes of intracerebral hemorrhage.

31 hemorrhage, and the prevention of recurrent intracerebral hemorrhage.

32 occurs in nearly one fifth of patients with intracerebral hemorrhage.

33 parenchymal arteriovenous malformations and intracerebral hemorrhage.

34 , predisposes both newborn and adult mice to intracerebral hemorrhage.

35 A TSPO ligand attenuates brain injury after intracerebral hemorrhage.

36 yolk sac, or shortly after birth with severe intracerebral hemorrhage.

37 II (rFVIIa) can reduce hematoma growth after intracerebral hemorrhage.

38 ccurate than CT for the detection of chronic intracerebral hemorrhage.

39 to several clinical complications, including intracerebral hemorrhage.

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

41 nslational target for secondary injury after intracerebral hemorrhage.

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

43 edema expansion rate predicts outcome after intracerebral hemorrhage.

44 upregulated centrally and peripherally after intracerebral hemorrhage.

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

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

47 differences in rates of death or symptomatic intracerebral hemorrhage.

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

49 ischemic strokes and a larger proportion of intracerebral hemorrhages.

50 increased bleeding complications, including intracerebral hemorrhages.

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

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

53 hemorrhage (60%), cerebral infarction (23%), intracerebral hemorrhage (11%), and traumatic brain inju

54 Of the 98 patients with acute intracerebral hemorrhage, 22 patients (22%) showed PND d

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

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

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

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

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

60 h (95% CI, 1.08 to 1.46) but similar risk of intracerebral hemorrhage (adjusted odds ratio, 0.81; 95%

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

62 ites to have do-not-resuscitate orders after intracerebral hemorrhage although the association was at

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

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

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

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

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

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

69 Intracerebral hemorrhage and ischemic stroke admissions

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

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

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

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

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

75 activation of MMP-2 and MMP-9 in donors with intracerebral hemorrhage and subsequent development of a

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

77 age, 24% had traumatic brain injury, 23% had intracerebral hemorrhage, and 13% had ischemic stroke.

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

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

80 e acute setting after ischemic brain injury, intracerebral hemorrhage, and cardiac arrest has a negat

81 of brain capillary endothelial cells (BCEC), intracerebral hemorrhage, and death.

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

83 Subarachnoid hemorrhage, intracerebral hemorrhage, and ischemic stroke hospitaliz

84 gender, and diagnostic categories of trauma, intracerebral hemorrhage, and neurologic disease were as

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

86 e, the treatment of medical complications of intracerebral hemorrhage, and the prevention of recurren

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

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

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

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

91 rials of glucocorticoids in ischemic stroke, intracerebral hemorrhage, aneurysmal subarachnoid hemorr

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

93 care and end-of-life issues in patients with intracerebral hemorrhage are examined.

94 ical approaches for treatment of spontaneous intracerebral hemorrhage are presented.

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 The mean estimated increase in volume of the intracerebral hemorrhage at 24 hours was 26% in the plac

98 was the percent change in the volume of the intracerebral hemorrhage at 24 hours.

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

100 Symptomatic intracerebral hemorrhage based on the European Cooperati

101 Similarly, in an experimental model of intracerebral hemorrhage, both AbetaPP(-/-) and APLP2(-/

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

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

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

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

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 We randomly assigned 399 patients with intracerebral hemorrhage diagnosed by CT within three ho

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

113 ne the prevalence of PND among patients with intracerebral hemorrhage during Emergency Medical Servic

114 erioration has been studied in patients with intracerebral hemorrhage during hospitalization, but rat

115 A total of 270 cases of intracerebral hemorrhage from 2000-2003 were analyzed.

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

117 lative to CT for the detection of hyperacute intracerebral hemorrhage has not been demonstrated.

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 s in bleeding events, defined as symptomatic intracerebral hemorrhage, hemopericardium, or other syst

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

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

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

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

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

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

128 Neurodegeneration occurs after intracerebral hemorrhage (ICH) and tissue-type transglut

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

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

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

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

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

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

135 Since intracerebral hemorrhage (ICH) causes dramatic neurologi

136 Intracerebral hemorrhage (ICH) causes morbidity and mort

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

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

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

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

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

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

145 We characterized acute intracerebral hemorrhage (ICH) in the rat by sequential

146 Intracerebral hemorrhage (ICH) is a devastating acute ne

147 Intracerebral hemorrhage (ICH) is a devastating disease

148 Intracerebral hemorrhage (ICH) is a devastating form of

149 Intracerebral hemorrhage (ICH) is a devastating stroke s

150 Intracerebral hemorrhage (ICH) is a devastating type of

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

152 We hypothesized that donor intracerebral hemorrhage (ICH) is associated with activa

153 Intracerebral hemorrhage (ICH) is associated with neurol

154 ntrollable and reproducible animal models of intracerebral hemorrhage (ICH) is essential for the syst

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

156 Intracerebral hemorrhage (ICH) is the most devastating a

157 Spontaneous intracerebral hemorrhage (ICH) is the most devastating t

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

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

160 Intracerebral hemorrhage (ICH) is the stroke subtype wit

161 We test this duplex ELISA on our porcine intracerebral hemorrhage (ICH) model and show that it is

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

163 nomenon, we evaluated the effects of a focal intracerebral hemorrhage (ICH) on cortical excitability

164 Severe intracerebral hemorrhage (ICH) produces gastric patholog

165 ting in multiple sources adjacent to a focal intracerebral hemorrhage (ICH) propagate into brain regi

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

167 to validate a double blood infusion model of intracerebral hemorrhage (ICH) that does not use anticoa

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

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

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

171 pathy (CAA) is a common cause of symptomatic intracerebral hemorrhage (ICH), as well as small asympto

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

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

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

175 After intracerebral hemorrhage (ICH), the brain parenchyma is

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

177 rrent study examines nestin expression after intracerebral hemorrhage (ICH), the role of different bl

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

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

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

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

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

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

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

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

189 There are few data on platelet function in intracerebral hemorrhage (ICH).

190 ogical functional recovery in a rat model of intracerebral hemorrhage (ICH).

191 ed that DNA injury occurs in the brain after intracerebral hemorrhage (ICH).

192 within the first 6 h of collagenase-induced intracerebral hemorrhage (ICH).

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

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

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

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

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

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

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

200 is necessary to eliminate the hematoma after intracerebral hemorrhage (ICH); however, release of proi

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

202 Intracerebral hemorrhages (ICHs) are common in patients

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

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

205 We introduced intracerebral hemorrhage in each of eight anesthetized N

206 Of the total 46 patients admitted with intracerebral hemorrhage in our service, 29 patients wer

207 ay a role in the pathogenesis of spontaneous intracerebral hemorrhage in patients with CAA.

208 Intracerebral hemorrhage in patients with warfarin-assoc

209 a substantially greater ischemic stroke and intracerebral hemorrhage incidence compared with non-His

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

211 did not result in any significant change in intracerebral hemorrhage incidence.

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

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

214 Intracerebral hemorrhage, intraventricular hemorrhage, a

215 Intracerebral hemorrhage is a devastating disorder with

216 Intracerebral hemorrhage is accompanied by a pronounced

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

218 Intracerebral hemorrhage is the least treatable form of

219 Intracerebral hemorrhage is the least treatable form of

220 Risk of intracerebral hemorrhage is the primary factor limiting

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

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

223 if they a) suffered subarachnoid hemorrhage, intracerebral hemorrhage, ischemic infarction, or trauma

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

225 Intraventricular extension of intracerebral hemorrhage (IVH) is an independent predict

226 rFVIIa within four hours after the onset of intracerebral hemorrhage limits the growth of the hemato

227 Preventing readmission after intracerebral hemorrhage may depend primarily on optimiz

228 sure, observed in up to 56% of patients with intracerebral hemorrhage, may predispose to hematoma exp

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

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

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

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

233 Shortly after intracerebral hemorrhage, neutrophils infiltrate the int

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

235 Symptomatic intracerebral hemorrhage occurred in 3.6% of participant

236 Symptomatic intracerebral hemorrhage occurred in three patients in t

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

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

239 y (CT) within three hours after the onset of intracerebral hemorrhage, one third have an increase in

240 Worthwhile interventions for intracerebral hemorrhage or subarachnoid hemorrhage gene

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

242 .16]; p = 5.3 x 10(-5) ; N = 3,670), but not intracerebral hemorrhage (OR [95% CI] = 0.97 [0.84-1.12]

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

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

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

246 e studies of patients with new-onset stroke, intracerebral hemorrhage, or subarachnoid hemorrhage sup

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

248 ically null for all alphav integrins develop intracerebral hemorrhage owing to defective interactions

249 Intracerebral hemorrhage patients discharged between Sep

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

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

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

253 Intracerebral hemorrhage patients with and without palli

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

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

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

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

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

259 t endogenous tPA assists in the clearance of intracerebral hemorrhage, presumably by affecting microg

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

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

262 s post cardiac arrest; or e) diagnosis of an intracerebral hemorrhage requiring mechanical ventilatio

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

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

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

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

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

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

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

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

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

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

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 hemorrhage, traumatic brain injury, primary intracerebral hemorrhage, subdural hematoma, brain tumor

280 uidelines are presented for the diagnosis of intracerebral hemorrhage, the management of increased ar

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

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

283 We randomly assigned 841 patients with intracerebral hemorrhage to receive placebo (268 patient

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

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

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

287 Intracerebral hemorrhage volume measured from the comput

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

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

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

291 Intracerebral hemorrhage was more common in Mexican Amer

292 The growth in volume of intracerebral hemorrhage was reduced by 2.6 ml (95% conf

293 Growth in the volume of intracerebral hemorrhage was reduced by 3.3 ml, 4.5 ml,

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

295 zed patients with a diagnosis of spontaneous intracerebral hemorrhage were identified by codes of the

296 e developed larger hematomas in experimental intracerebral hemorrhage, whereas AbetaPP gene knockout

297 igh rate of tolerability among patients with intracerebral hemorrhage who were treated with intraveno

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