ライフサイエンスコーパス: intracranial hemorrhage

1 reatment, or antiplatelet therapy) after the intracranial hemorrhage.

2 did not show increased risk of developmental intracranial hemorrhage.

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

4 ent with occult brain metastasis had grade 4 intracranial hemorrhage.

5 All these agents reduced intracranial hemorrhage.

6 ted a significant predictive performance for intracranial hemorrhage.

7 sk of moderate or severe bleeding, including intracranial hemorrhage.

8 urrent stroke, including ischemic stroke and intracranial hemorrhage.

9 MAIN OUTCOME MEASURE: Symptomatic intracranial hemorrhage.

10 ith a history of stroke owing to the risk of intracranial hemorrhage.

11 reased the risk of major bleeding, including intracranial hemorrhage.

12 group (88% vs. 16%, p< 0.001) and 31% had an intracranial hemorrhage.

13 hemorrhage were compared with those without intracranial hemorrhage.

14 If severe, the thrombocytopenia can lead to intracranial hemorrhage.

15 improved with increasing risk for stroke and intracranial hemorrhage.

16 48.0% specific (95% CI, 47.3-48.9) for acute intracranial hemorrhage.

17 sequence for the detection of acute and old intracranial hemorrhage.

18 rnal platelet antigens and can lead to fetal intracranial hemorrhage.

19 ous abortion, and a high rate of spontaneous intracranial hemorrhage.

20 activity possibly contributory to brain AVM intracranial hemorrhage.

21 gher mortality and increased rates of severe intracranial hemorrhage.

22 -induced thrombocytopenia without increasing intracranial hemorrhage.

23 cts cerebral microbleeds - a risk factor for intracranial hemorrhage.

24 rs) due to major arterial occlusion, without intracranial hemorrhage.

25 of major bleeding complications, especially intracranial hemorrhage.

26 computed tomography revealed no evidence of intracranial hemorrhage.

27 rized by venous sinusoids that predispose to intracranial hemorrhage.

28 Two presented with acute intracranial hemorrhage.

29 sis for acute pulmonary embolism suffered an intracranial hemorrhage.

30 nst myocardial infarction and predisposes to intracranial hemorrhage.

31 hemoglobin, can identify infants with acute intracranial hemorrhage.

32 l support, are independently associated with intracranial hemorrhage.

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

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

35 n oral anticoagulant treatment with incident intracranial hemorrhage.

36 presenting the risk of thrombolytic-related intracranial hemorrhage.

37 und to be relatively safe, with no excess in intracranial hemorrhage.

38 ticoagulation does not increase the risk for intracranial hemorrhage.

39 %; P = .87), and total (44% vs 37%; P = .13) intracranial hemorrhages.

40 creased rate of recurrent cardiac events and intracranial hemorrhages.

41 ortality (9% vs. 12%, P=0.50) or symptomatic intracranial hemorrhage (0% vs. 3%, P=0.12).

42 .11; P=0.44), with significant reductions in intracranial hemorrhage (0.5% vs. 0.7%, P=0.02) and fata

43 rough 30 days (1.6% versus 2.2%, P=0.27) and intracranial hemorrhage (0.6% versus 0.8%, P=0.37) were

44 ajor bleeding (2.2% vs. 0.6%, p < 0.001) and intracranial hemorrhage (0.6% vs. 0.1%, p = 0.015) witho

45 bypass grafting (2.1% vs. 0.6%, P<0.001) and intracranial hemorrhage (0.6% vs. 0.2%, P=0.009), withou

46 ajor bleeding event; 31 of these events were intracranial hemorrhages (0.8%/year).

47 follows: ischemic stroke, 0.80 (0.67-0.96); intracranial hemorrhage, 0.34 (0.26-0.46); major gastroi

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

49 monary embolism (12.1% versus 7.8%; P=0.02), intracranial hemorrhage (1.6% versus 0.2%; P=0.03), and

50 t complications were infrequent: symptomatic intracranial hemorrhage, 1.8%; life-threatening or serio

51 to a congenital disorder developed an acute intracranial hemorrhage 10 days after surgery.

52 and brain trauma (29% [CI, 19% to 38%]), and intracranial hemorrhage (11% [CI, 7.7% to 14%]) were the

53 ll as a significant increase in asymptomatic intracranial hemorrhages (19.0% vs 10.7%; P=.01).

54 in-hospital deaths, 2873 (4.9%) patients had intracranial hemorrhage, 19,491 (33.4%) patients achieve

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

56 ) patients, with 66 (0.6%) nonhemorrhagic, 6 intracranial hemorrhages, 3 cerebral infarctions with he

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

58 codes for ischemic stroke (433-434, 436) and intracranial hemorrhage (430-432) identified 1812 stroke

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

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

61 of death, nonfatal reinfarction, or nonfatal intracranial hemorrhage (a measure of net clinical benef

62 l 22% (17%-26%), normal 52% (48%-56%); adult intracranial hemorrhage: absent 1% (0%-4%), present 38%

63 [95% CI: 1.31 to 1.97]) and greater risk of intracranial hemorrhage (adjusted HR: 2.04 [95% CI: 1.25

64 ot associated with risk-adjusted symptomatic intracranial hemorrhage (adjusted odds ratio, 1.0; 95% c

65 There was 1 death from intracranial hemorrhage after coronary artery dissection

66 age, and nonwhite race, all risk factors for intracranial hemorrhage after fibrinolytic therapy, were

67 atopulmonary syndrome who developed multiple intracranial hemorrhages after transplantation.

68 ociated with lower in-hospital mortality and intracranial hemorrhage, along with an increase in the p

69 ospital risk-adjusted mortality, symptomatic intracranial hemorrhage, ambulatory status at discharge,

70 time and in-hospital mortality, symptomatic intracranial hemorrhage, ambulatory status at discharge,

71 .1%, 29.6%, and 25.2%, respectively), severe intracranial hemorrhage among survivors (23.3%, 19.1%, a

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

73 -year-old extended criteria donor died of an intracranial hemorrhage and had undergone cardiopulmonar

74 platelet antigen-1a (HPA-1a), can result in intracranial hemorrhage and intrauterine death.

75 The management of intracranial hemorrhage and intraventricular hemorrhage

76 Acute intracranial hemorrhage and intraventricular hemorrhage

77 Patients with intracranial hemorrhage and intraventricular hemorrhage

78 ansion and limit the medical consequences of intracranial hemorrhage and intraventricular hemorrhage.

79 information pertaining to the acute care of intracranial hemorrhage and intraventricular hemorrhage.

80 hibitors were associated with lower rates of intracranial hemorrhage and mortality compared with warf

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

82 rimary safety variables included symptomatic intracranial hemorrhage and mortality.

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

84 Primary outcomes evaluated were symptomatic intracranial hemorrhage and serious systemic hemorrhage;

85 common conditions associated with LRDA were intracranial hemorrhage and subarachnoid hemorrhage.

86 ies; 28% to 43% and 1% to 30%, respectively) intracranial hemorrhage and vessel perforation or dissec

87 iated through a reduction in rates of severe intracranial hemorrhage and/or cystic periventricular le

88 ANS-associated reductions in rates of severe intracranial hemorrhage and/or cystic periventricular le

89 ockdown of a zebrafish ADA2 homologue caused intracranial hemorrhages and neutropenia - phenotypes th

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

91 , 2.20 (95% CI: 1.26, 3.84) for nontraumatic intracranial hemorrhage, and 2.17 (95% CI: 1.60, 2.96) f

92 s during acute traumatic brain injury, acute intracranial hemorrhage, and acutely growing brain tumor

93 sk for ischemic stroke or systemic embolism, intracranial hemorrhage, and all-cause mortality without

94 subluxations and/or dislocations, fractures, intracranial hemorrhage, and arterial injury.

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

96 ciated with reduced risk of ischemic stroke, intracranial hemorrhage, and death and increased risk of

97 Ischemic stroke, intracranial hemorrhage, and death.

98 iated with reduced mortality and symptomatic intracranial hemorrhage, and higher rates of independent

99 a group, NOACs significantly reduce stroke, intracranial hemorrhage, and mortality, with lower to si

100 e risk of bleeding complications, especially intracranial hemorrhage, and no laboratory test is appli

101 atide was not associated with an increase in intracranial hemorrhage, and no significant effect on no

102 Risks of all-cause mortality, intracranial hemorrhage, and parenchymal hematoma at 90

103 There were no reports of intracranial hemorrhage, and the most common site of ble

104 eviewed for the presence of skull fractures, intracranial hemorrhage, and traumatic DVST.

105 vator, but bleeding complications, including intracranial hemorrhage, are a recognized complication.

106 requires precise information on the risk for intracranial hemorrhage as a function of patient age and

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

108 anticoagulant treatment reintroduction after intracranial hemorrhage as feasible.

109 To assess the risk for intracranial hemorrhage associated with the administrati

110 he authors report on a series of spontaneous intracranial hemorrhages associated with vein of Galen a

111 nces observed in the cumulative incidence of intracranial hemorrhage at 1 year in the enoxaparin and

112 Intracranial hemorrhage at diagnosis was rare (0.6%).

113 The risk for intracranial hemorrhage at INRs less than 2.0 did not di

114 Sixteen patients (12.2%) had evidence of intracranial hemorrhage at or near the time of diagnosis

115 Intracranial hemorrhage at presentation was defined as t

116 systemic emboli prevented by warfarin minus intracranial hemorrhages attributable to warfarin, multi

117 ban increased the risk of major bleeding and intracranial hemorrhage but not the risk of fatal bleedi

118 e intracranial hemorrhage or develop delayed intracranial hemorrhage but respond to treatment using s

119 tely increase or decrease the probability of intracranial hemorrhage, but no finding or combination o

120 ted a significant predictive performance for intracranial hemorrhage (c-index: 0.75; p = 0.03).

121 gastrointestinal, or genitourinary bleeding; intracranial hemorrhage; cardiac tamponade; nonbypass su

122 2.0 were not associated with lower risk for intracranial hemorrhage compared with INRs between 2.0 a

123 nfection, bronchopulmonary dysplasia, severe intracranial hemorrhage, cystic periventricular leukomal

124 difference between the groups in the risk of intracranial hemorrhage, cystic periventricular leukomal

125 The rates of intracerebral and intracranial hemorrhage did not differ significantly bet

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

127 However, massive intracranial hemorrhage distinguishes these patients fro

128 When intracranial hemorrhage does occur, it is often due to o

129 A third child developed acute intracranial hemorrhage due to delayed dural sinus throm

130 170 case-patients who developed intracranial hemorrhage during warfarin therapy and 1020

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

132 Intracranial hemorrhage events associated with NOACs in

133 anagement of minimally injured patients with intracranial hemorrhage exclusively by trauma surgeons.

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

135 ensitive to the rates of ischemic stroke and intracranial hemorrhage for LAA closure and medical anti

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

137 In patients with VKA-related intracranial hemorrhage, four-factor PCC might be superi

138 c brain injury, subarachnoid hemorrhage, and intracranial hemorrhage have demonstrated that prolonged

139 atio, 1.15; 95% CI, 1.00 to 1.32), including intracranial hemorrhage (hazard ratio, 1.42; 95% CI, 1.1

140 These findings included intracranial hemorrhages, hemorrhages involving the opti

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

142 onade (HR: 2.38 [95% CI: 0.56 to 10.1]), and intracranial hemorrhage (HRs for 1-year mortality were n

143 The risk of further intracranial hemorrhage (ICH) and the benefit of stroke

144 dy racial/ethnic differences in the risk for intracranial hemorrhage (ICH) and the effect of warfarin

145 ence of cerebral hyperperfusion syndrome and intracranial hemorrhage (ICH) and the risk factors for t

146 The risks of major bleeding and intracranial hemorrhage (ICH) are higher in Asian patien

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

148 Estimating risk of intracranial hemorrhage (ICH) for patients with unruptur

149 eports of statin usage and increased risk of intracranial hemorrhage (ICH) have been inconsistent.

150 nticoagulation does not increase the risk of intracranial hemorrhage (ICH) in patients with solid tum

151 Intracranial hemorrhage (ICH) is a rare but devastating

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

153 NAIT) is a life-threatening disease in which intracranial hemorrhage (ICH) is the major risk.

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

155 mized studies have shown a decreased risk of intracranial hemorrhage (ICH) with use of novel oral ant

156 The primary safety end point was the rate of intracranial hemorrhage (ICH) within 5 days of treatment

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

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

159 We assessed ACT-associated intracranial hemorrhage (ICH), including frequency, clin

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

161 outcomes were risk of recurrent embolism and intracranial hemorrhage (ICH).

162 results in a sequence of events that lead to intracranial hemorrhage (ICH).

163 Epidemiological data on the risk of intracranial hemorrhage (ICrH) after ischemic stroke are

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

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

166 was cerebral ischemia in 73.3% of patients, intracranial hemorrhage in 22.8%, and a stroke-mimicking

167 is associated with clinical presentation of intracranial hemorrhage in brain arteriovenous malformat

168 of Hedgehog signaling increased the risk of intracranial hemorrhage in ciliary mutants, activation o

169 As a potential treatment to prevent fetal intracranial hemorrhage in HPA-1a alloimmunized pregnanc

170 brain pericytes are associated with neonatal intracranial hemorrhage in human fetuses, as well as str

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

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

173 ilar or reduced rates of ischemic stroke and intracranial hemorrhage in patients with AF compared wit

174 Early reperfusion was associated with fatal intracranial hemorrhage in patients with the Malignant p

175 Hypernatremia is associated with intracranial hemorrhage in term infants.

176 Four were symptomatic, including fatal intracranial hemorrhage in the index case.

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

178 There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs

179 ficantly increase the risk of transfusion or intracranial hemorrhage in this non-randomized cohort.

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

181 There was a trend toward more symptomatic intracranial hemorrhages in the ancrod group vs placebo

182 There were more intracranial hemorrhages in the tenecteplase group.

183 ompared with warfarin for any outcome except intracranial hemorrhage, in which case dabigatran risk w

184 factors were identified in association with intracranial hemorrhage, including age at initial diagno

185 The risk for intracranial hemorrhage increased at 85 years of age or

186 The risk for intracranial hemorrhage increases at age 85 years.

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

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

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

190 We conclude that intracranial hemorrhage is frequently observed in patien

191 The rate of intracranial hemorrhage is higher among infants delivere

192 Symptomatic intracranial hemorrhage is infrequent, but approximately

193 PA with regard to mortality, but the rate of intracranial hemorrhage is significantly higher.

194 e while the absolute increase in the risk of intracranial hemorrhage is small.

195 Intracranial hemorrhage is the most feared complication

196 h the true risk of thrombolysis-precipitated intracranial hemorrhage is unknown.

197 were included when subarachnoid hemorrhage, intracranial hemorrhage, ischemic stroke, sub/epidural h

198 red with warfarin, was associated with fewer intracranial hemorrhages, less adverse consequences foll

199 Treatment complications included symptomatic intracranial hemorrhage, life-threatening or serious sys

200 Our findings suggest that intracranial hemorrhage may not be an infrequent occurre

201 ggest that the IL-6 genotype associated with intracranial hemorrhage modulates IL-6 expression in bra

202 For intracranial hemorrhage, mortality was not improved with

203 sk for ischemic stroke or systemic embolism, intracranial hemorrhage, myocardial infarction, or morta

204 Intracranial hemorrhage occurred in 1 of 860 infants del

205 as reported in 8%, 11% and 6%, respectively; intracranial hemorrhage occurred in 1%, 3% and 2% of pat

206 Intracranial hemorrhage occurred in 1.0%, 0.6%, and 1.7%

207 Intracranial hemorrhage occurred in 1.0%.

208 Symptomatic intracranial hemorrhage occurred in 2 patients (5%).

209 More intracranial hemorrhages occurred in the fibrinolysis gr

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

211 Intracranial hemorrhage occurs in 0.5-1.0% of affected c

212 ds ratio, 1.63 [CI, 1.51 to 1.77]), previous intracranial hemorrhage (odds ratio, 0.33 [CI, 0.21 to 0

213 ts were preserved when weighting factors for intracranial hemorrhage of 1.0 and 2.0 were used.

214 th and low birth weight, birth asphyxia, and intracranial hemorrhage of the newborn significantly dec

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

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

217 with TBI (findings of skull fracture and/or intracranial hemorrhage on an initial computed tomograph

218 ase on all patients with TBI (skull fracture/intracranial hemorrhage on head computed tomography) pre

219 ome measures were findings of progression of intracranial hemorrhage on repeated computed tomographic

220 9 patients [16.6%]; P = .89), progression of intracranial hemorrhage on repeated scans (post-BIG grou

221 but no significant difference in symptomatic intracranial hemorrhage or all-cause mortality at 90 day

222 urysmal malformations can present with acute intracranial hemorrhage or develop delayed intracranial

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

224 gnificant differences in the rates of severe intracranial hemorrhage or periventricular leukomalacia.

225 d with higher unadjusted odds of symptomatic intracranial hemorrhage or serious systemic hemorrhage,

226 (p =.006), having an acute diagnosis such as intracranial hemorrhage or trauma (p =.007), not having

227 ity (OR, 1.40; 95% CI: 0.37, 5.25; P = .62), intracranial hemorrhage (OR, 0.55; 95% CI: 0.03, 8.91; P

228 I, 0.95-0.98; P < .001), reduced symptomatic intracranial hemorrhage (OR, 0.96; 95% CI, 0.95-0.98; P

229 ing muscle, liver, or retinal abnormalities, intracranial hemorrhage, or death, in the very low LDL g

230 pendently associated with older patient age, intracranial hemorrhage (other than epidural), skull fra

231 m (p = 0.0004 and p = 0.0006, respectively), intracranial hemorrhage (p = 0.0007 and p = 0.0005, resp

232 imilar association was noted for the risk of intracranial hemorrhage (P=0.015) and progressive aortic

233 gic transformation (P=0.001) and symptomatic intracranial hemorrhage (P=0.036).

234 Subdural hematoma is a common type of intracranial hemorrhage, particularly among the elderly,

235 Secondary safety outcomes included severe intracranial hemorrhage, periventricular leukomalacia, a

236 nction, bacterial infection, length of stay, intracranial hemorrhage, periventricular leukomalacia, c

237 treatment reduced the combined end point of intracranial hemorrhage, periventricular leukomalacia, o

238 port genes in respective mutants rescued the intracranial hemorrhage phenotype.

239 crease the risk of aneurysm formation, acute intracranial hemorrhage, play a vital role in neurosurgi

240 s both risk for thromboembolism and risk for intracranial hemorrhage provides a more quantitatively i

241 rsus 1.5%; P=0.04) with a trend toward lower intracranial hemorrhage rates compared with low-volume c

242 Intracranial hemorrhage rates were 1.1% and 0.2%, respec

243 Stroke unit admission, symptomatic intracranial hemorrhage rates, and in-hospital mortality

244 d with lower in-hospital mortality and lower intracranial hemorrhage rates.

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

246 Three patients had intracranial hemorrhages related to the intracranial pre

247 ents with atrial fibrillation who survive an intracranial hemorrhage remains unknown.

248 f life-saving treatments among patients with intracranial hemorrhage, representing a self-fulfilling

249 neonatal complications, such as nontraumatic intracranial hemorrhage, respiratory distress syndrome,

250 ents (an absolute hemoglobin drop >/=4 g/dL, intracranial hemorrhage, retroperitoneal bleed, or trans

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

252 , 0.72-1.02) with a significant reduction of intracranial hemorrhage (RR, 0.46; 95% CI, 0.39-0.56).

253 ly no detectable differences in the risks of intracranial hemorrhage (RR, 1.15; 95% CI, 0.67-1.97; RD

254 p a score for assessing risk for symptomatic intracranial hemorrhage (sICH) in ischemic stroke patien

255 Symptomatic intracranial hemorrhage (sICH) was evaluated with Nation

256 Symptomatic intracranial hemorrhage (sICH), in-hospital mortality, d

257 lin were favored in subarachnoid hemorrhage, intracranial hemorrhage, spine, demyelinating disease, a

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

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

260 Compared with the 115 patients without intracranial hemorrhage, the 16 patients presenting with

261 rtality (per 100 person-years) for recurrent intracranial hemorrhage, the rate of ischemic stroke/sys

262 Adverse events (AEs), such as intracranial hemorrhage, thromboembolic event, and progr

263 ) recordings were averaged up to the time of intracranial hemorrhage, thromboembolic event, or progre

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

265 ents receiving antiplatelet therapy who have intracranial hemorrhage (traumatic or spontaneous).

266 an increased frequency of early symptomatic intracranial hemorrhage, treatment with IA r-proUK withi

267 5, reflecting the greater clinical impact of intracranial hemorrhage versus thromboembolism.

268 Fatal bleeding or intracranial hemorrhage was 0.9% with both treatments in

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

270 rtality was 21%, and the rate of symptomatic intracranial hemorrhage was 4%; neither rate differed ac

271 Intracranial hemorrhage was associated with higher doses

272 The risk for intracranial hemorrhage was fourfold higher (adjusted ha

273 Intracranial hemorrhage was induced by the injection of

274 val, 0.69 to 0.90; P<0.0003) and symptomatic intracranial hemorrhage was less frequent (4.7% versus 5

275 Intracranial hemorrhage was lower with higher-dose NOACs

276 Intracranial hemorrhage was noted in 2 neonates (nadir p

277 Intracranial hemorrhage was noted in two patients (2.4%)

278 The risk of symptomatic intracranial hemorrhage was similar with either treatmen

279 Intracranial hemorrhage was the most frequent type, and

280 Intracranial hemorrhage was uncommon, but the rate was m

281 Major or severe bleeding (but not intracranial hemorrhage) was higher with orbofiban; it o

282 At 90 days, the rates of symptomatic intracranial hemorrhage were 1.9% in both the thrombecto

283 py, and outcomes in patients presenting with intracranial hemorrhage were compared with those without

284 hemorrhage, the 16 patients presenting with intracranial hemorrhage were more frequently women, less

285 No cases of intracranial hemorrhage were observed.

286 The rates of major bleeding and intracranial hemorrhage were similar in the two groups.

287 w of radiographic imaging was performed, and intracranial hemorrhages were categorized as trace, meas

288 ial fractures, more severe injuries, such as intracranial hemorrhages, were associated with a higher

289 farin therapy may face an increased risk for intracranial hemorrhage when treated with tPA.

290 s, displayed increased risk of developmental intracranial hemorrhage, whereas the morphology of the v

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

292 ble from warfarin except for a lower risk of intracranial hemorrhage with dabigatran.

293 Intracranial hemorrhage with neurological deterioration

294 ncluded MCA recanalization, the frequency of intracranial hemorrhage with neurological deterioration,

295 logistic regression to determine the odds of intracranial hemorrhage with regard to age and internati

296 [95% CI, 0.83-0.94], P < .001), symptomatic intracranial hemorrhage within 36 hours was less likely

297 Fatal or nonfatal symptomatic intracranial hemorrhage within 7 days occurred in 6% of

298 gnificant difference in rates of symptomatic intracranial hemorrhage within 90 days (70 events [5.7%]

299 c revascularization at 24 hours, symptomatic intracranial hemorrhage within 90 days, and all-cause mo

300 as obtained and demonstrated a left parietal intracranial hemorrhage without midline shift or hydroce