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

1 evere stroke increasing the absolute risk of intracerebral haemorrhage).

2 ong independent risk factor for future lobar intracerebral haemorrhage.

3 idence of dementia and risk factors after an intracerebral haemorrhage.

4 es on long-term functional performance after intracerebral haemorrhage.

5 ally invasive surgery (MIS) in patients with intracerebral haemorrhage.

6 cal management as a therapeutic strategy for intracerebral haemorrhage.

7 o differentiate between ischaemic stroke and intracerebral haemorrhage.

8 or people taking antiplatelet therapy before intracerebral haemorrhage.

9 s, does not improve functional outcome after intracerebral haemorrhage.

10 rgical interventions are investigational for intracerebral haemorrhage.

11 complications and no increase in symptomatic intracerebral haemorrhage.

12 redict a poor outcome in patients with acute intracerebral haemorrhage.

13 lth Stroke Scale >3) versus those with acute intracerebral haemorrhage.

14 ical deficits without infarction, seizure or intracerebral haemorrhage.

15 in and is associated with dementia and lobar intracerebral haemorrhage.

16 age-matched stroke service referrals without intracerebral haemorrhage.

17 specialty practice can improve outcome after intracerebral haemorrhage.

18 ial conservative treatment for patients with intracerebral haemorrhage.

19 ay be a risk factor for thrombolysis-related intracerebral haemorrhage.

20 weighted scans) and lacunar infarcts, but no intracerebral haemorrhage.

21 emorrhage, cortical superficial siderosis or intracerebral haemorrhage.

22 re no significant differences in symptomatic intracerebral haemorrhage.

23 a substantially increased risk of recurrent intracerebral haemorrhage.

24 evant in patients at low risk of symptomatic intracerebral haemorrhage.

25 come for people with spontaneous severe deep intracerebral haemorrhage.

26 blocker propranolol might reduce the risk of intracerebral haemorrhage.

27 One patient had an asymptomatic intracerebral haemorrhage.

28 schaemic stroke and 338 (30.6%) of 1104 with intracerebral haemorrhage.

29 e associated with greater risks of recurrent intracerebral haemorrhage.

30 effects of blood pressure lowering in acute intracerebral haemorrhage.

31 who achieved a good response 365 days after intracerebral haemorrhage.

32 improve functional outcome in patients with intracerebral haemorrhage.

33 lood is implicated in secondary injury after intracerebral haemorrhage.

34 50% of patients presented with intracerebral haemorrhage.

35 in patients with probable CAA without lobar intracerebral haemorrhage.

36 traventricular haemorrhage size and thalamic intracerebral haemorrhage.

37 , and loss of functional independence) after intracerebral haemorrhage.

38 controls, though none had major CAA-related intracerebral haemorrhages.

39 idence declined by more than 50% for primary intracerebral haemorrhage (0.47, 0.27-0.83, p=0.01) but

40 11]), and asthma (1.15 [1.04-1.27]), whereas intracerebral haemorrhage (1.00 [0.95-1.06]), other cere

41 chaemic stroke (1.68, 95% CI 1.60-1.77), and intracerebral haemorrhage (1.24, 95% CI 1.07-1.44).

42 of 266 vs 46 [19.3%] of 238) or symptomatic intracerebral haemorrhage (14 [5.3%] of 266 vs eight [3.

43 hyperintensities (WMH): 10 597 individuals; intracerebral haemorrhage: 1545 cases, 1481 controls].

44 lic blood pressure was much lower than after intracerebral haemorrhage (158.5 mm Hg [SD 30.1] vs 189.

45 CI 3-4) for ischaemic stroke, 47% (46-48)for intracerebral haemorrhage, 19% (17-22; 52% for rural are

46 95% CI 1.06 to 1.38) with increased risk of intracerebral haemorrhage (2.07, 95% CI 1.37 to 3.13) an

47 eeded the absolute increase in risk of fatal intracerebral haemorrhage (2.2% [1.5% to 3.0%]) and the

48 score 2 vs 1, p<0.001), and more often with intracerebral haemorrhage (20% vs 13%, p=0.002).

49 s 17% ([17-18] ischaemic stroke 16% [15-16], intracerebral haemorrhage 28% [26-29], subarachnoid haem

50 We included 114 patients with intracerebral haemorrhage (39 with clinically probable c

51 ke at 5 years (ischaemic stroke 41% [41-42], intracerebral haemorrhage 44% [42-46], subarachnoid haem

52 visual acuity (77.8%), headache (16.7%), and intracerebral haemorrhage (5.55%), and 5.55% were asympt

53 cipants were enrolled, of whom 525 (98%) had intracerebral haemorrhage: 507 (97%) were diagnosed on C

54 strokes were also ischaemic stroke; after an intracerebral haemorrhage, 56% of recurrent strokes were

55 troke were ischaemic stroke, 7440 (16%) were intracerebral haemorrhage, 702 (2%) were subarachnoid ha

56 associated with higher rates of symptomatic intracerebral haemorrhage (8.4% vs 3.0%, adjusted OR 3.5

57 bsolute excess 3.1% [2.4-3.8]); and of fatal intracerebral haemorrhage (91 [2.7%] of 3391 vs 13 [0.4%

58 changes in the population-based incidence of intracerebral haemorrhage according to age and likely ae

59 port, we analysed eligible participants with intracerebral haemorrhage according to their treatment a

60 Spontaneous supratentorial intracerebral haemorrhage accounts for 20% of all stroke

61 Intracerebral haemorrhage accounts for about 10-15% of a

62 mortality (1.6, 0.8-3.4; p=0.27) or rates of intracerebral haemorrhage after treatment with thromboly

63 Brain imaging features of intracerebral haemorrhage and cerebral small vessel dise

64 ognised as an important cause of spontaneous intracerebral haemorrhage and cognitive impairment in th

65 lated small vessel pathology associated with intracerebral haemorrhage and cognitive impairment.

66 l disease and a largely untreatable cause of intracerebral haemorrhage and contributor to age-related

67 ed cerebral small vessel disorder leading to intracerebral haemorrhage and dementia.

68 19-99 years with spontaneous (non-traumatic) intracerebral haemorrhage and elevated systolic blood pr

69 ploratory analyses to assess mortality after intracerebral haemorrhage and examine the absolute risks

70 f patients within 24 h of the onset of acute intracerebral haemorrhage and is associated with death a

71 isease (cSVD) causes lacunar stroke (LS) and intracerebral haemorrhage and is the most common patholo

72 gression models for association with primary intracerebral haemorrhage and ischaemic stroke subtypes.

73 Primary intracerebral haemorrhage and lacunar ischaemic stroke a

74 ar instability, leading to increased primary intracerebral haemorrhage and lacunar stroke risk.

75 loperoxidase levels increase risk of primary intracerebral haemorrhage and lacunar stroke, directly i

76 Key safety outcomes were symptomatic intracerebral haemorrhage and mortality within 90 days.

77 cerebrovascular permeability, development of intracerebral haemorrhage and neurovascular injury in ex

78 sability, and 8% died - one in the course of intracerebral haemorrhage and one due to other sustained

79 improve clinical management of patients with intracerebral haemorrhage and promise to reduce mortalit

80 Intracerebral haemorrhage and small vessel ischaemic str

81 icipant eligibility and rate features of the intracerebral haemorrhage and surrounding brain.

82 After combining intracerebral haemorrhage and SVS datasets, our sample s

83 Our cross-phenotype genetic study of intracerebral haemorrhage and SVS demonstrates novel gen

84 lying this novel genome-wide approach across intracerebral haemorrhage and SVS.

85 lator deferoxamine mesylate in patients with intracerebral haemorrhage and to establish whether the d

86 t decreases in DBS complications, with fewer intracerebral haemorrhages and infections with general a

87 y participants or patients with non-CAA deep intracerebral haemorrhage) and patients with Alzheimer's

88 ticipants for primary (recurrent symptomatic intracerebral haemorrhage) and secondary (ischaemic stro

89 dwide (91.5% for ischaemic stroke, 87.1% for intracerebral haemorrhage), and were consistent across r

90 haemic stroke, 4.36 million (3.69-5.05) were intracerebral haemorrhage, and 1.58 million (1.32-1.91)

91 l haemorrhage, 56% of recurrent strokes were intracerebral haemorrhage, and 41% of recurrent strokes

92 ose with ischaemic stroke, 69% of those with intracerebral haemorrhage, and 52% of those with subarac

93 frequent but previously underestimated after intracerebral haemorrhage, and are three times more comm

94 hnoid haemorrhage predominantly results from intracerebral haemorrhage, and early and delayed cerebra

95 ng surgery for the evacuation of spontaneous intracerebral haemorrhage, and had a high risk of postop

96 of 14.2% (95% CI 10.0-19.3) at 1 year after intracerebral haemorrhage, and incidence reached 28.3% (

97 l burden of vascular-related brain damage in intracerebral haemorrhage, and may be a useful surrogate

98 have recently been described in spontaneous intracerebral haemorrhage, and may be important to under

99 ascular disease (including ischaemic stroke, intracerebral haemorrhage, and myocardial infarction) by

100 ge, year, stroke subtypes (ischaemic stroke, intracerebral haemorrhage, and subarachnoid haemorrhage)

101 separately for cerebral infarction, primary intracerebral haemorrhage, and subarachnoid haemorrhage.

102 dified Rankin scale [mRS]), the incidence of intracerebral haemorrhages, and technical observations.

103 cases [10 388 with ischaemic stroke and 3059 intracerebral haemorrhage] and 13 472 controls).

104 Delayed seizures after intracerebral haemorrhage are associated with different

105 of CAA in patients with thrombolysis-related intracerebral haemorrhage are required.

106 n but the benefits and risks in survivors of intracerebral haemorrhage are uncertain.

107 as on cognition in the context of ageing and intracerebral haemorrhage, as well as in Alzheimer's and

108 2 locus previous seen in traditional GWAS of intracerebral haemorrhage, as well as the rediscovery of

109 are alone, reduced death or dependence after intracerebral haemorrhage associated with antiplatelet t

110 n older age-groups, in part due to a rise in intracerebral haemorrhage associated with antithrombotic

111 7, 0.20-0.69; p=0.002), but the incidence of intracerebral haemorrhage associated with antithrombotic

112 The incidence of intracerebral haemorrhage associated with premorbid hype

113 novel genome-wide associations for non-lobar intracerebral haemorrhage at 2q33 and 13q34.

114 29-0.95; p=0.03), but the number of cases of intracerebral haemorrhage at all ages were similar in OX

115 mplications (cerebrospinal fluid leakage and intracerebral haemorrhage) at days 3-7 after AAV2 gene t

116 were aged 18 years or older with spontaneous intracerebral haemorrhage, atrial fibrillation, an indic

117 published arteriovenous malformation-related intracerebral haemorrhage (AVICH) score showed better ou

118 alteplase seems to be safe in patients with intracerebral haemorrhage, but increased asymptomatic bl

119 or arteriolosclerosis), we performed GWAS of intracerebral haemorrhage by location in 1813 subjects (

120 embolic events outnumbered warfarin-related intracerebral haemorrhages by about 15-fold (280 vs 19),

121 Neither incidence of symptomatic intracerebral haemorrhage (by SITS-MOST definition, 1/52

122 If the incidence of intracerebral haemorrhage can be decreased, then in the

123 We used a discovery cohort of 1409 primary intracerebral haemorrhage cases and 1624 controls from t

124 ght reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antipla

125 ght reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antipla

126 d high-dose tinzaparin developed symptomatic intracerebral haemorrhage compared with one in the aspir

127 haemic stroke constituted 65.3% (62.4-67.7), intracerebral haemorrhage constituted 28.8% (28.3-28.8),

128 nd 138 controls (96 healthy elderly, 42 deep intracerebral haemorrhage controls) and 72 patients with

129 ulation aged under 75 years the incidence of intracerebral haemorrhage decreased substantially (rate

130 nts in the alteplase group died, symptomatic intracerebral haemorrhage (defined by SITS-MOST criteria

131 er with first or recurrent spontaneous lobar intracerebral haemorrhage diagnosed by non-contrast brai

132 number of outflows and outflow diameter) of intracerebral haemorrhage due to intracranial dural arte

133 ant associations were observed for non-lobar intracerebral haemorrhage enhanced by SVS with rs2758605

134 From the 560 patients with spontaneous intracerebral haemorrhage enrolled in the PITCH cohort b

135 n, 3/52 [6%] vs 4/51 [8%], p=0.59) nor total intracerebral haemorrhage events (8/52 [15%] vs 14/51 [2

136 e CT-only criteria (1620 patients with lobar intracerebral haemorrhage from eight cohorts, median age

137 We studied consecutive patients with intracerebral haemorrhage from four specialist stroke ce

138 al cohort study in patients with spontaneous intracerebral haemorrhage from the Prognosis of Intracer

139 Intracerebral haemorrhage GWAS results by location were

140 Patients with intracerebral haemorrhage had higher prevalences of sick

141 they had a structural cerebral cause for the intracerebral haemorrhage, had a low score (3-5) on the

142 though the number of hospital admissions for intracerebral haemorrhage has increased worldwide in the

143 preclinical and clinical studies focused on intracerebral haemorrhage has risen.

144 h systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1.44 [95% CI 1.3

145 Microbleeds are strongly associated with intracerebral haemorrhage, hypertension, lacunar stroke

146 mic stroke (OR 1.22, 99% CI, 1.00-1.49), and intracerebral haemorrhage (ICH) (OR 2.05, 99% CI 1.40-2.

147 Antithrombotic agents increase risks of intracerebral haemorrhage (ICH) and associated adverse o

148 mine the strength of the association between intracerebral haemorrhage (ICH) and cerebral amyloid ang

149 ERACT2 enrolled 2839 adults with spontaneous intracerebral haemorrhage (ICH) and high systolic blood

150 the relationship between laterality of acute intracerebral haemorrhage (ICH) and poor clinical outcom

151 Patients with primary intracerebral haemorrhage (ICH) are at increased long-te

152 onists oral anticoagulants (NOAC)-associated intracerebral haemorrhage (ICH) are largely unknown.

153 Inflammatory responses to intracerebral haemorrhage (ICH) are potential therapeuti

154 surgical treatment of spontaneous cerebellar intracerebral haemorrhage (ICH) differ.

155 ilon2 and epsilon4 have an increased risk of intracerebral haemorrhage (ICH) in lobar regions, presum

156 Whether statins increase the risk of intracerebral haemorrhage (ICH) in patients with a previ

157 study, we examined injury progression after intracerebral haemorrhage (ICH) induced by collagenase i

158 Intracerebral haemorrhage (ICH) is a devastating conditi

159 Intracerebral haemorrhage (ICH) is a dramatic condition

160 Intracerebral haemorrhage (ICH) is a life-threatening em

161 Intracerebral haemorrhage (ICH) is an acute neurological

162 of blood pressure (BP) at the acute phase of intracerebral haemorrhage (ICH) is beneficial.

163 Poor prognosis after intracerebral haemorrhage (ICH) is related to haemorrhag

164 Intracerebral haemorrhage (ICH) is the most devastating

165 Intracerebral haemorrhage (ICH) is the most severe subty

166 BACKGROUND AND Intraventricular extension of intracerebral haemorrhage (ICH) predicts poor outcome, b

167 Intraventricular extension of intracerebral haemorrhage (ICH) predicts poor outcome, b

168 Intracerebral haemorrhage (ICH) remains the most devasta

169 ith arteriovenous malformation (AVM)-related intracerebral haemorrhage (ICH) than other AVM or ICH sc

170 dictor of poor outcome only in patients with intracerebral haemorrhage (ICH) volumes </=30 cm(3) (OR

171 myloid angiopathy (CAA) is a common cause of intracerebral haemorrhage (ICH) with a high recurrence r

172 (CAA)) is an important cause of spontaneous intracerebral haemorrhage (ICH), a devastating and still

173 Intracerebral haemorrhage (ICH), a subtype of stroke, ca

174 kidney and cerebrovascular disease including intracerebral haemorrhage (ICH), and common collagen IV

175 3/uL, fibrinogen <150 mg/dL, the presence of intracerebral haemorrhage (ICH), and the presence of cer

176 ion rate may be a predictor of outcome after intracerebral haemorrhage (ICH).

177 health-related quality of life (HRQoL) after intracerebral haemorrhage (ICH).

178 id angiopathy (CAA) is associated with lobar intracerebral haemorrhage (ICH).

179 ut the long-term prognosis after spontaneous intracerebral haemorrhage (ICH).

180 ve outcome after spontaneous (non-traumatic) intracerebral haemorrhage (ICH).

181 cible HO-1 to early brain injury produced by intracerebral haemorrhage (ICH).

182 (95% CI 57-64) in people with non-traumatic intracerebral haemorrhage (ICH).

183 no specific therapies improved outcome after intracerebral haemorrhage (ICH).

184 echanisms underlying brain injury induced by intracerebral haemorrhage (ICH).

185 health-related quality of life (HRQoL) after intracerebral haemorrhage (ICH).

186 m the Tranexamic Acid for Hyperacute Primary Intracerebral Haemorrhage (ie, TICH-2) international mul

187 subjects, including seizures in 5 (0.6%) and intracerebral haemorrhage in 4 (0.5%).

188 Patients with spontaneous supratentorial intracerebral haemorrhage in neurosurgical units show no

189 s, but not in the overall number of cases of intracerebral haemorrhage in older age-groups, in part d

190 ipants who received 35 mg BIIB078, traumatic intracerebral haemorrhage in one participant who receive

191 transfusion after acute spontaneous primary intracerebral haemorrhage in people taking antiplatelet

192 hazards of antiplatelet therapy on recurrent intracerebral haemorrhage in primary subgroup analyses o

193 aemorrhage and examine the absolute risks of intracerebral haemorrhage in the context of functional o

194 Cumulative 5-year incidence of recurrent intracerebral haemorrhage in the low-risk CT-only cerebr

195 effect of antiplatelet therapy on recurrent intracerebral haemorrhage in the presence of cerebral mi

196 e interventions (seizure after discharge and intracerebral haemorrhage in the recreational activity g

197 ital with acute stroke (ischaemic or primary intracerebral haemorrhage) in England and Wales between

198 1384 strokes (1193 ischaemic strokes and 191 intracerebral haemorrhages) in patients admitted during

199 ta on 86 strokes (81 ischaemic strokes and 5 intracerebral haemorrhages) in patients with evidence of

200 than two times higher in patients with lobar intracerebral haemorrhage (incidence at 1 year 23.4%, 14

201 14.6-33.3) than for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9.2%, 5.1

202 ke severity, but the absolute excess risk of intracerebral haemorrhage increased with increasing stro

203 tzerland, adults (18-75 years) with a severe intracerebral haemorrhage involving the basal ganglia or

204 Intracerebral haemorrhage is a complication of thromboly

205 Intracerebral haemorrhage is an important public health

206 Intracerebral haemorrhage is an unmet medical need affec

207 Acute stroke due to supratentorial intracerebral haemorrhage is associated with high morbid

208 a DOAC or no anticoagulation, stratified by intracerebral haemorrhage location and sex.

209 Because intracerebral haemorrhage location is an adequate surrog

210 prespecified subgroup analysis, according to intracerebral haemorrhage location.

211 s use, improved data collection, low rate of intracerebral haemorrhage, low technical complications,

212 ow age 75 years, absolute number of cases of intracerebral haemorrhage might increase in future.

213 For moderate to large intracerebral haemorrhage, MISTIE did not improve the pr

214 bsolute effects of alteplase on the risks of intracerebral haemorrhage, mortality, and functional imp

215 he incidence of ischaemic stroke (n=14 930), intracerebral haemorrhage (n=3496), and acute myocardial

216 stroke), and outnumbered disabling or fatal intracerebral haemorrhage (n=45 vs n=18), with an absolu

217 Late seizures after intracerebral haemorrhage occur after the initial acute

218 9-60) in 2013; symptomatic post-thrombolysis intracerebral haemorrhages occurred in 28 of 675 patient

219 or conscious patients with superficial lobar intracerebral haemorrhage of 10-100 mL and no intraventr

220 -80 years with a non-traumatic (spontaneous) intracerebral haemorrhage of 20 mL or higher to standard

221 h spontaneous, non-traumatic, supratentorial intracerebral haemorrhage of 30 mL or more.

222 h favourable outcomes in patients with acute intracerebral haemorrhage of predominantly mild-to-moder

223 tratified by trial, to model the log odds of intracerebral haemorrhage on allocation to alteplase, tr

224 mopressin improves outcomes in patients with intracerebral haemorrhage on antiplatelet drug therapy.

225 P-lowering initiated within several hours of intracerebral haemorrhage onset was safe and improved fu

226 patients with CAA versus patients with deep intracerebral haemorrhage or healthy controls.

227 early treatment did not increase the risk of intracerebral haemorrhage or other bleeding.

228 ple size included 241 024 participants (6255 intracerebral haemorrhage or SVS cases and 233 058 contr

229 % CI = -0.13 to -0.02), but a higher risk of intracerebral haemorrhage (OR: 1.64, 95% CI = 1.26-2.13)

230 e of recurrent ischaemic stroke, symptomatic intracerebral haemorrhage, or unclassified stroke within

231 ia in dementia-free survivors of spontaneous intracerebral haemorrhage; our results suggest that unde

232 280 [50%] male), 69 patients had a recurrent intracerebral haemorrhage over 1381 person-years' follow

233 T-APOE criteria, 74 patients had a recurrent intracerebral haemorrhage over 1495 person-years' follow

234 57 [53%] male), 171 patients had a recurrent intracerebral haemorrhage over 3208 person-years' follow

235 substantial fall in hypertension-associated intracerebral haemorrhage over the past 25 years, but no

236 sus 6/75 (8%) in the remaining patients with intracerebral haemorrhage (P = 0.024); no diffusion-weig

237 ients with infection at onset, patients with intracerebral haemorrhage (p=0.014), dysphagia (p=0.003)

238 racerebral haemorrhage from the Prognosis of Intracerebral Haemorrhage (PITCH) cohort who were admitt

239 l haemorrhage survivors for association with intracerebral haemorrhage recurrence.

240 creased steeply in the days and weeks before intracerebral haemorrhage (regression p<0.0001) but not

241 ssociation with risk, which was stronger for intracerebral haemorrhage (relative risk [RR] per 280 g

242 eria were pure intraventricular haemorrhage; intracerebral haemorrhage resulting from intracranial va

243 Stroke, including acute ischaemic stroke and intracerebral haemorrhage, results in neuronal cell deat

244 k (odds ratio, 1.07, P = 0.04) and recurrent intracerebral haemorrhage risk (hazards ratio, 1.45, P =

245 ase levels were associated with both primary intracerebral haemorrhage risk (odds ratio, 1.07, P = 0.

246 the contrary, there was no association with intracerebral haemorrhage risk among statin non-users (P

247 mong statin users was associated with higher intracerebral haemorrhage risk in a model adjusting for

248 sity lipoprotein response is associated with intracerebral haemorrhage risk using Mendelian randomiza

249 uous) and baseline severity according to the intracerebral haemorrhage score were assessed by adding

250 djusted for stratification variables and the Intracerebral Haemorrhage Score.

251 In patients with intracerebral haemorrhage seen within 90 min, the highes

252 CAAH and thrombolysis-related intracerebral haemorrhage share some clinical features,

253 ture clinical trials including patients with intracerebral haemorrhage should assess cognitive endpoi

254 prespecified baseline covariates (stability intracerebral haemorrhage size, age, Glasgow Coma Scale,

255 iod were recorded by type (ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and

256 Patients with comorbid dementia, intracerebral haemorrhage, subarachnoid haemorrhage, oes

257 odels in a prospective cohort of 174 primary intracerebral haemorrhage survivors for association with

258 ective longitudinal follow-up of consecutive intracerebral haemorrhage survivors presenting to a sing

259 enrolled adults within 6 h of supratentorial intracerebral haemorrhage symptom onset if they had used

260 ommon in cerebral amyloid angiopathy-related intracerebral haemorrhage than in other intracerebral ha

261 Hypertension was more associated with intracerebral haemorrhage than with ischaemic stroke, wh

262 ever, the risk of dementia after spontaneous intracerebral haemorrhage that accounts for about 15% of

263 th increasing stroke severity: for SITS-MOST intracerebral haemorrhage the absolute excess risk range

264 For first recurrent intracerebral haemorrhage, the DOAC group did not meet t

265 ts with atrial fibrillation and a history of intracerebral haemorrhage, the latest data from randomis

266 ubarachnoid haemorrhages and, of all primary intracerebral haemorrhages, they are responsible for 4%

267 P = 0.007), older donor age (P = 0.010), and intracerebral haemorrhage/thrombosis in donor (P = 0.023

268 e lowering strategies in patients with acute intracerebral haemorrhage to determine the strength of a

269 nd median time from the onset of symptoms of intracerebral haemorrhage to randomisation of 3.6 h (2.7

270 CH-2 (Tranexamic Acid for Hyperacute Primary Intracerebral Haemorrhage) trial, we assessed baseline s

271 ified assessment of three classifications of intracerebral haemorrhage: type 2 parenchymal haemorrhag

272 ated intracerebral haemorrhage than in other intracerebral haemorrhage types.

273 magnetic resonance imaging (<3 months after intracerebral haemorrhage) using diffusion-weighted imag

274 probable cerebral amyloid angiopathy-related intracerebral haemorrhage versus 6/75 (8%) in the remain

275 tensive care unit with stable, non-traumatic intracerebral haemorrhage volume less than 30 mL, intrav

276 Cumulative 3-year incidence of recurrent intracerebral haemorrhage was 34 (15%) of 320 patients i

277 Primary intracerebral haemorrhage was excluded by computed tomog

278 The incidence of primary intracerebral haemorrhage was increased at low temperatu

279 e-phase blood pressure reading after primary intracerebral haemorrhage was more likely than after isc

280 owever defined, the proportional increase in intracerebral haemorrhage was similar irrespective of tr

281 the mean first systolic blood pressure after intracerebral haemorrhage was substantially higher than

282 ajor ischaemic stroke and those with primary intracerebral haemorrhage, we compared acute-phase and p

283 owever, alteplase also increases the risk of intracerebral haemorrhage; we aimed to determine the pro

284 only and those with frontal infarcts and/or intracerebral haemorrhage were both significantly more l

285 ury, aneurysmal subarachnoid haemorrhage, or intracerebral haemorrhage were eligible for the study.

286 A total of 872 survivors of intracerebral haemorrhage were enrolled and followed for

287 Association estimates for intracerebral haemorrhage were negatively correlated wit

288 rs with primary, spontaneous, supratentorial intracerebral haemorrhage were randomly assigned (1:1) t

289 ysmal subarachnoid haemorrhage, and 151 with intracerebral haemorrhage) were enrolled.

290 d compared with usual premorbid levels after intracerebral haemorrhage, whereas acute-phase systolic

291 sible to randomise patients with spontaneous intracerebral haemorrhage who are taking antiplatelet dr

292 INTERACT1-3 included adults with acute intracerebral haemorrhage who presented within 6 h of th

293 ly prevent ischaemic strokes in survivors of intracerebral haemorrhage with atrial fibrillation but a

294 s in the UK and were eligible if they had an intracerebral haemorrhage with stroke symptom onset with

295 ) to investigate changes in the incidence of intracerebral haemorrhage with time, above and below age

296 While the association between CAA and lobar intracerebral haemorrhage (with its high recurrence risk

297 Intraventricular haemorrhage is a subtype of intracerebral haemorrhage, with 50% mortality and seriou

298 st an association with a high risk of future intracerebral haemorrhage, with potential implications f

299 s of Health Stroke Scale [NIHSS]); and fatal intracerebral haemorrhage within 7 days.

300 ge for patients with spontaneous superficial intracerebral haemorrhage without intraventricular haemo