ライフサイエンスコーパス: ICH

1 ICH occurred at a rate of 0.80% per year with warfarin r

2 ICH occurred in 174 patients; most ICH events were spont

3 ICH was adjudicated by a central committee.

4 an the number needed to harm for producing 1 ICH with warfarin use for patients with a CHA2DS2-VASc s

5 CETP variants in a discovery cohort of 1,149 ICH cases and 1,238 controls from 3 studies, followed by

6 ars, prehospital modified Rankin Scale </=3, ICH volume < 60ml, Glasgow Coma Scale of <9, and severe

7 clusion criteria, for a total of 4,385 acute ICH patients in this meta-analysis.

8 Hypodensities within an acute ICH detected on an NCCT scan may predict hematoma expans

9 d safety of intensive BP reduction for acute ICH by analyzing data from several recent randomized con

10 be a promising therapeutic target for acute ICH treatment trials.

11 included 123 consecutive patients with acute ICH (onset <6 hours).

12 intensive BP lowering in patients with acute ICH is safe and effective in improving clinical outcomes

13 =3;efficacy outcome), in patients with acute ICH randomised to either intensive BP-lowering or standa

14 For patients with acute ICH similar to those included in RCTs and without contra

15 e studies including 4360 patients with acute ICH were pooled in meta-analysis.

16 herapeutic potential for patients with acute ICH.

17 After ICH, the immediate infiltration of leukocytes and activa

18 After ICH, the modified Rankin scale score at discharge was >/

19 entrations had better outcomes 90 days after ICH, confirming the role of TGF-beta1 in functional reco

20 ury and blood-brain barrier disruption after ICH can be assessed with multimodal MRI, and that periha

21 icits, brain edema, and BBB disruption after ICH, in association with RhoA activation and down-regula

22 e impairment at high rates, both early after ICH and over the long term.

23 Incident dementia early after ICH is strongly associated with hematoma size and locati

24 deficits and perihematomal brain edema after ICH induction by injection of either autologous blood or

25 othelial junction proteins' expression after ICH.

26 improvement of neurological functions after ICH.

27 nd improving of neurological functions after ICH.

28 by tail vein injection within 24 hours after ICH induction.

29 E expansion rate in the first 72 hours after ICH predicts outcome, and how it compares against other

30 at endogenous P2X7R increased at 3 hrs after ICH with peak at 24 hrs, then returned to normal at 72 h

31 ar structure around hematoma at 24 hrs after ICH, along with perivascular astrocytes and endothelial

32 hrs, then returned to normal at 72 hrs after ICH.

33 tenuates brain injury and inflammation after ICH.

34 ppression could preserve BBB integrity after ICH through inhibiting RhoA activation.

35 alternative activation of macrophages after ICH.

36 cluded EPID, diagnosed within 6 months after ICH, and DPID, diagnosed beyond 6 months after ICH.

37 H, and DPID, diagnosed beyond 6 months after ICH.

38 le to decrease mortality and morbidity after ICH in experimental models.

39 s microglia-mediated neuroinflammation after ICH and promotes functional recovery, suggesting that TG

40 g soluble AXL had poor 1-year outcomes after ICH onset, suggesting that therapeutically augmenting ef

41 ht to determine whether OAT resumption after ICH is associated with long-term outcome, accounting for

42 e risks and benefits of OAT resumption after ICH.

43 ts with computed tomographic images allowing ICH volume calculation and MRI allowing imaging markers

44 Hypodensities within an ICH detected by noncontrast computed tomography (NCCT) h

45 ed the association between treatment arm and ICH expansion at 24 hours.

46 iscriminatory ability for major bleeding and ICH in an Asian/Chinese AF population.

47 as an interaction between race/ethnicity and ICH risk (P<0.0001).

48 < 0.05, apart from mOBRI, HEMORR2HAGES) and ICH (all p < 0.05), and additionally, resulted in a net

49 cial disparities related to hypertension and ICH have been reported, these previous studies were limi

50 a volume and between serum calcium level and ICH expansion were investigated in multivariable linear

51 e associations between these SVD markers and ICH volume, as well as hematoma expansion, were investig

52 source of assessment, clinical severity and ICH characteristics.

53 The annual ICH and ischemic stroke rates in warfarin users were 5.9

54 etween NOAC-ICH versus vitamin K antagonists-ICH (VKA-ICH).

55 -6) at discharge and at 3 months, as well as ICH volumes and haematoma expansion rates in the two gro

56 n K antagonist oral anticoagulant-associated ICH has a high mortality and an unfavorable outcome, and

57 Antithrombotic-associated ICH (364 patients, 11%) was not associated with a signif

58 ients with/without antithrombotic-associated ICH in the Intensive Blood Pressure Reduction in Acute C

59 (25 of 61) of patients with NOAC-associated ICH were female, and the mean (SD) patient age was 76.1

60 e patients with nontraumatic NOAC-associated ICH, of whom 45 (74%) qualified for the hematoma expansi

61 mprove the poor prognosis of NOAC-associated ICH.

62 review and meta-analysis to compare baseline ICH volume, haematoma expansion and clinical outcomes be

63 ndependently associated with higher baseline ICH volume (beta = -0.13, SE = .03, P < .001).

64 d an AUC of 0.86 for differentiating between ICH and IS within 4.5hrs of symptom onset with a sensiti

65 Hispanics and inadequate power to analyze by ICH location.

66 dy (n = 542), (2) a U.S.-based single-center ICH study (n = 261), and (3) the Ethnic/Racial Variation

67 patients admitted with primary lobar or deep ICH to a single tertiary care medical center between Jan

68 patients admitted with primary lobar or deep ICH to a single tertiary care medical center, the presen

69 0 [55.1%] female) and 164 patients with deep ICH (mean [SD] age 67 [14] years and 71 [43.3%] female).

70 ds was associated with larger lobar and deep ICHs.

71 Our results showed that APT MRI could detect ICH at hyperacute, acute and subacute stages.

72 noninvasive imaging biomarker for detecting ICH at hyperacute, acute and subacute stages.

73 en cohorts from six studies, 204 experienced ICH during 5197 person-years of follow-up (Kaplan-Meier

74 123 without missing data (19.5%) experienced ICH expansion.

75 Among 738 patients who had experienced ICH (mean [SD] age, 74.3 [12.1] years; 384 men [52.0%]),

76 study enrolled patients who had experienced ICH from January 1, 2006, to December 31, 2013.

77 frequent among patients who have experienced ICH and is not prominently associated with acute charact

78 decline among patients who have experienced ICH.

79 p (odds ratio per quintile increase in final ICH volume, 1.49; 95% CI, 1.14-1.94; P = .004).

80 case-control approach, each case of a first ICH identified during follow-up was matched with as many

81 ness and suitability were assessed following ICH (Q2 [R1]) guidelines.

82 he specific responses of microglia following ICH with the aim of identifying pathways that may aid in

83 between OAT resumption and outcome following ICH, regardless of hematoma location.

84 ality and poor functional outcomes following ICH.

85 Moreover, TGF-beta1 treatment following ICH decreased microglial Il6 gene expression in vivo and

86 For ICH cases, untreated hypertension was higher in blacks (

87 jor bleeding events and 0.83 (0.75-0.91) for ICH (all p < 0.001).

88 iated with long-term outcome, accounting for ICH location (ie, lobar vs nonlobar).

89 logistic regression models were computed for ICH as an overall group and separately for the location

90 d untreated hypertension as risk factors for ICH.

91 se was associated with an increased risk for ICH (RR, 1.17; 95% CI, 1.02-1.35) relative to TCAs, high

92 onin reuptake actually increase the risk for ICH and the effect of concomitant use of antithrombotics

93 To assess the risk for ICH associated with the use of SSRIs compared with tricy

94 ke are associated with an increased risk for ICH, particularly in the first 30 days of use and when u

95 ted with higher HDL-C also increase risk for ICH.

96 predictive performance of the spot sign for ICH expansion was lower than in prior reports from singl

97 ctoferrin to present a potential therapy for ICH.

98 t limits bleeding and rescues the brain from ICH.

99 phenotype and contributing to recovery from ICH.

100 ole of TGF-beta1 in functional recovery from ICH.

101 We determined whether, within 1 year from ICH, OAT resumption was associated with: (1) mortality,

102 Untreated hypertension confers a greater ICH risk in blacks and Hispanics relative to whites acro

103 though linked to factors determining greater ICH growth including poor SBP control, dIVH is independe

104 score, larger (>/=15 mL) ICH volume, greater ICH growth and higher achieved SBP over 24 h.

105 ts with ineffective hemostasis with PCCs had ICH (n = 16; 61.5%).

106 increase risks of intracerebral haemorrhage (ICH) and associated adverse outcomes.

107 (NOAC)-associated intracerebral haemorrhage (ICH) are largely unknown.

108 progression after intracerebral haemorrhage (ICH) induced by collagenase in mice using a preclinical

109 he acute phase of intracerebral haemorrhage (ICH) is beneficial.

110 ular extension of intracerebral haemorrhage (ICH) predicts poor outcome, but the significance of dela

111 ular extension of intracerebral haemorrhage (ICH) predicts poor outcome, but the significance of dela

112 ion (AVM)-related intracerebral haemorrhage (ICH) than other AVM or ICH scores.

113 ife (HRQoL) after intracerebral haemorrhage (ICH).

114 of outcome after intracerebral haemorrhage (ICH).

115 e International Conference on Harmonisation (ICH) guidelines which evaluate linearity, detection limi

116 se with past lobar intracerebral hemorrhage (ICH) (n = 21) and those with cerebral microbleeds only a

117 ognostic factor in intracerebral hemorrhage (ICH) and is associated with permanent shunt dependency i

118 o have experienced intracerebral hemorrhage (ICH) appear to develop cognitive impairment at high rate

119 eduction for acute intracerebral hemorrhage (ICH) are inconsistent.

120 t symptoms from an intracerebral hemorrhage (ICH) are not well recognized and have previously not bee

121 apeutic dilemma in intracerebral hemorrhage (ICH) care, particularly for lobar hemorrhages related to

122 ome in spontaneous intracerebral hemorrhage (ICH) due to small vessel disease (SVD), but the associat

123 is associated with intracerebral hemorrhage (ICH) expansion and may mark those patients most likely t

124 ot sign to predict intracerebral hemorrhage (ICH) expansion with standardized multiphase computed tom

125 nm protein induced intracerebral hemorrhage (ICH) experimentally and was also associated with cerebra

126 Intracerebral hemorrhage (ICH) is a devastating disease without effective treatmen

127 Intracerebral hemorrhage (ICH) is a devastating form of stroke that results from t

128 Intracerebral hemorrhage (ICH) is one of the most devastating and disabling forms

129 Intracerebral hemorrhage (ICH) is the most devastating adverse event in patients r

130 Concern about intracerebral hemorrhage (ICH) is the primary reason for withholding tPA therapy f

131 issue damage after intracerebral hemorrhage (ICH), but how this function is regulated is not clear.

132 Following intracerebral hemorrhage (ICH), the activation of mast cell contributes to brain i

133 after experimental intracerebral hemorrhage (ICH), we found robust phenotypic changes in the infiltra

134 s in patients with intracerebral hemorrhage (ICH).

135 following an acute intracerebral hemorrhage (ICH).

136 nt risk factor for intracerebral hemorrhage (ICH).

137 outcomes following intracerebral hemorrhage (ICH).

138 pathophysiology of intracerebral hemorrhage (ICH).

139 increased risk of intracerebral hemorrhage (ICH).

140 major bleeding and intracranial hemorrhage (ICH) are higher in Asian patients with atrial fibrillati

141 PT MRI in detecting intracranial hemorrhage (ICH) at hyperacute, acute and subacute stages by compari

142 Spontaneous intracranial hemorrhage (ICH) is also a frequent occurrence in these patients, bu

143 Intracranial hemorrhage (ICH) was the most common site of bleeding requiring reve

144 isk for spontaneous intracranial hemorrhage (ICH), an effect that is in theory linked to the strength

145 E), major bleeding, intracranial hemorrhage (ICH), and all-cause death.

146 characteristics of intracranial hemorrhage (ICH), the factors associated with the risk of ICH, and o

147 barrier(BBB) after intracerebral hemorrhage(ICH) remains unexplored.

148 (CAV-1) causes infectious canine hepatitis (ICH), a frequently fatal disease which primarily affects

149 fty-eight white, 880 black, and 766 Hispanic ICH patients were enrolled.

150 However, exclusively GFAP differed in ICH compared with IS (p < 0.0001).

151 concentrations were significantly greater in ICH patients than in controls (p < 0.0001).

152 rget that requires further investigations in ICH.

153 ve been implicated in playing vital roles in ICH outcomes.

154 results were verified in collagenase induced ICH model.

155 In collagenase-induced ICH mice, the protection of etifoxine was associated wit

156 s from mice subjected to collagenase-induced ICH.

157 High (>/=14) NIHSS score, larger ICH and proxy responders were associated with low scores

158 of Health Stroke Scale (NIHSS) score, larger ICH, presence of intraventricular extension and use of p

159 independent variable associated with larger ICH volume in the lobar ICH group (odds ratio per quinti

160 Apixaban resulted in significantly less ICH (0.33% per year), regardless of type and location, t

161 28%) resumed OAT, whereas 86/379 (23%) lobar ICH survivors did.

162 OAT resumption after lobar ICH was also associated with decreased mortality (HR = 0

163 We separately analyzed nonlobar and lobar ICH cases using propensity score matching and Cox regres

164 endent variable associated with larger lobar ICH volume, and the absence of cerebral microbleeds was

165 sociated with larger ICH volume in the lobar ICH group (odds ratio per quintile increase in final ICH

166 This study analyzed 254 patients with lobar ICH (mean [SD] age, 75 [11] years and 140 [55.1%] female

167 group having noninflammatory CAA with lobar ICH, 1 of 21 (5%) met the criteria for possible CAA-ri,

168 nt hematoma expansion in patients with lobar ICH.

169 ly shorter for patients who suffered a major ICH on enoxaparin compared with patients not receiving a

170 n was 3 times more likely to develop a major ICH than those not treated with anticoagulation (14.7% v

171 essure, stroke), and observed that all major ICHs on enoxaparin occurred in the setting of a PANWARDS

172 There was no difference in mean ICH-volume between the two groups (standard mean differe

173 Health Stroke Scale score, larger (>/=15 mL) ICH volume, greater ICH growth and higher achieved SBP o

174 ICH occurred in 174 patients; most ICH events were spontaneous (71.7%) versus traumatic (28

175 rol group having noninflammatory CAA with no ICH, 11 of 16 (69%) met the criteria for possible CAA-ri

176 Twelve studies including 393 NOAC-ICH and 3482 VKA-ICH were pooled in meta-analysis.

177 expansion and clinical outcomes between NOAC-ICH versus vitamin K antagonists-ICH (VKA-ICH).

178 tional outcome appear to be similar for NOAC-ICH versus VKA-ICH.

179 haematoma expansion were comparable in NOAC-ICH versus VKA-ICH (OR: 0.76; 95% CI 0.49 to 1.19, p=0.2

180 nd any difference between patients with NOAC-ICH versus VKA-ICH in all-cause mortality at discharge (

181 teristics and outcomes in patients with NOAC-ICH versus VKA-ICH using an appropriate keyword/MeSH ter

182 iate analyses, OAT resumption after nonlobar ICH was associated with decreased mortality (hazard rati

183 Among nonlobar ICH survivors, 178/633 (28%) resumed OAT, whereas 86/379

184 stroke incidence in both lobar and nonlobar ICH (both p < 0.01).

185 [SD] age, 47.9 [18.5] years), 3036 cases of ICH were identified during follow-up and matched to 8970

186 tly associated with acute characteristics of ICH.

187 In foxes with no evidence of ICH on post-mortem examination, 29 of 154 (18.8%) red fo

188 Expansion of ICH was defined as hematoma growth of greater than 33%,

189 cerebral microbleeds only and no history of ICH (n = 16).

190 core >==2, 12 917 patients with a history of ICH were identified and were assigned to 1 of 3 groups,

191 In sum, the profound impact of ICH on the immune system involves the coordinated action

192 ntial of GFAP as a tool for early rule-in of ICH, while UCH-L1 was not clinically useful.

193 eighted (APTw) and SWI signal intensities of ICH at hyperacute, acute and subacute stages.

194 001 for heterogeneity) and lobar location of ICH (HR, 2.04; 95% CI, 1.06-3.91; P = .02 for heterogene

195 nificant risk factor across all locations of ICH in whites (odds ratio [OR], 1.57; 95% confidence int

196 e to whites across all anatomic locations of ICH.

197 racial/ethnic groups across all locations of ICH: whites (OR, 8.79; 95% CI, 5.66-13.66; P<0.0001), bl

198 eurobehavioral outcomes in a murine model of ICH, suggesting therapeutic potential for patients with

199 Finally, in mouse models of ICH, spleen shrinkage could be related to innervations f

200 injury and inflammation in 2 mouse models of ICH.

201 The primary outcome of ICH within 5 years of CCM diagnosis was associated with

202 ia during the acute and resolution phases of ICH in vivo and found increases in TGF-beta1 pathway act

203 mong patients with previous ICH, the rate of ICH and ischemic stroke in untreated patients was 4.2 an

204 To determine the rate of ICH in patients treated with enoxaparin, we performed a

205 t associated with a significant reduction of ICH expansion (relative risk, 0.83; 95% CI, 0.27-2.51; P

206 gh-grade gliomas given the increased risk of ICH and poor prognosis after a major hemorrhage on antic

207 elevant biomarker for evaluating the risk of ICH before tPA administration.

208 cise estimates and predictors of the risk of ICH during untreated follow-up in an individual patient

209 The 5-year estimated risk of ICH during untreated follow-up was 3.8% (95% CI 2.1-5.5)

210 um level was associated with reduced risk of ICH expansion (odds ratio, 0.55 [95% CI, 0.35-0.86]; P =

211 nt factors associated with increased risk of ICH were enrollment in Asia or Latin America, older age,

212 CH), the factors associated with the risk of ICH, and outcomes post-ICH overall and by randomized tre

213 iated with increased HDL-C raise the risk of ICH.

214 Incidence rate ratios (RRs) of ICH.

215 spective, multicenter, case-control study of ICH among whites, blacks, and Hispanics.

216 cerebral haemorrhage (ICH) than other AVM or ICH scores.

217 ry exchange and spleen shrinkage by d 3 post-ICH, with recovery by d 14.

218 rris water maze latencies on Days 29-32 post-ICH.

219 increased Rotarod latencies on Days 1-5 post-ICH, and long-term improvement in neurocognitive perform

220 tivation/degranulation, IVIG attenuated post-ICH mast cell activation.

221 ere included in the analyses of delayed post-ICH dementia (DPID).

222 were included in the analyses of early post-ICH dementia (EPID).

223 ependency for aresorptive hydrocephalus post-ICH.

224 ated with the risk of ICH, and outcomes post-ICH overall and by randomized treatment.

225 in a substantial proportion of patients post-ICH.

226 data suggest that laropiprant treatment post-ICH attenuates brain damage by targeting primary as well

227 2.6 (2.1, 3.0); 78.5% of patients had a pre-ICH INR <3.0.

228 participants 18 years or older, without pre-ICH dementia, who presented to a tertiary care academic

229 bleeding events and 29.5-67.3% in predicting ICH (all p < 0.05).

230 who have atrial fibrillation with a previous ICH having a CHA2DS2-VASc score >==6.

231 who have atrial fibrillation with a previous ICH treated with warfarin or antiplatelet drugs in compa

232 Among patients with previous ICH, the rate of ICH and ischemic stroke in untreated pa

233 dy of 2103 consecutive patients with primary ICH ascertained during the period between 1994 and 2015

234 tiary care academic institution with primary ICH were included in the analyses of early post-ICH deme

235 sults: A total of 2123 patients with primary ICH were screened, and 2103 patients met the inclusion c

236 s included consecutive patients with primary ICH who underwent a CTA within 8 hours from onset at 59

237 ighlights the clinical relevance of reducing ICH by using apixaban rather than warfarin and avoiding

238 The association among BP reduction, ICH expansion, and outcome was investigated with multiva

239 There is only sparse evidence regarding ICH related to the use of non-vitamin K antagonist oral

240 We included 1,012 OAT-related ICH survivors (633 nonlobar and 379 lobar).

241 SCORE-IT (Spot Sign Score in Restricting ICH Growth) is a preplanned prospective observational st

242 d with a trend for lower risk of significant ICH expansion compared with standard treatment (OR: 0.82

243 poor outcome in acute small to moderate-size ICH.

244 ed trials of patients with acute spontaneous ICH and elevated systolic blood pressure (SBP)-randomly

245 re measured in 418 patients with spontaneous ICH without anticoagulant therapy, and hematoma expansio

246 , all single parameters forming the SM, sSM, ICH and AVICH score and the scores itself were significa

247 ldtype (WT) and DP1(-/-) mice were subjected ICH and neurologic deficits and hemorrhagic lesion outco

248 Our results confirm that ICH volume, haematoma expansion, mortality and functiona

249 utcomes were evaluated at 72 hours after the ICH.

250 treated with laropiprant at 1 hour after the ICH.

251 We hypothesized that IVIG will attenuate the ICH-induced mast cell activation via FcgammaRIIB/SHIP1 p

252 To prove this hypothesis we employed the ICH collagenase mouse model.

253 could provide additional information for the ICH compared with SWI.

254 n AUROC of 0.765 compared with 0.705 for the ICH score and 0.682 for the sSM grade.

255 grade, the supplemented SM (sSM) grade, the ICH score and the AVICH score.

256 computed tomography and were included in the ICH expansion analysis.

257 Main Outcomes and Measures: The ICH volumes at baseline and within 48 hours after sympto

258 ajor risk factor for fatal post-thrombolysis ICH, but rapidly assessing BBB damage before tPA adminis

259 his evaluation system is set up according to ICH/GCP, World Medical Association Declaration of Helsin

260 cent international normalized ratio (INR) to ICH was 13 days (6, 21 days).

261 Median INR prior to ICH was 2.6 (2.1, 3.0); 78.5% of patients had a pre-ICH

262 tential of laropiprant, WT mice subjected to ICH were treated with laropiprant at 1 hour after the IC

263 outcome was also comparable between the two ICH groups.

264 We applied a validated ICH prediction risk score PANWARDS (platelets, albumin,

265 studies including 393 NOAC-ICH and 3482 VKA-ICH were pooled in meta-analysis.

266 AC-ICH versus vitamin K antagonists-ICH (VKA-ICH).

267 nsion were comparable in NOAC-ICH versus VKA-ICH (OR: 0.76; 95% CI 0.49 to 1.19, p=0.236).

268 ce between patients with NOAC-ICH versus VKA-ICH in all-cause mortality at discharge (OR: 0.66; 95% C

269 utcomes in patients with NOAC-ICH versus VKA-ICH using an appropriate keyword/MeSH term search strate

270 appear to be similar for NOAC-ICH versus VKA-ICH.

271 Patients aged at least 18 years with VKA-ICH who presented within 12 h after symptom onset with a

272 mplex concentrate (PCC) in patients with VKA-ICH.

273 We demonstrated that while ICH induced mast cell activation/degranulation, IVIG att

274 with transient ischemic attack, and 27 with ICH.

275 ate whether the spot sign is associated with ICH expansion across a wide range of centers and whether

276 tics Consortium was strongly associated with ICH risk (OR = 1.86, SE = 0.13, p = 1.39 x 10(-6) ).

277 M location are independently associated with ICH within 5 years of CCM diagnosis.

278 ere used to identify factors associated with ICH.

279 n CETP demonstrated nominal association with ICH, with the strongest association at the rs173539 locu

280 ciates apolipoprotein E (apoE) genotype with ICH incidence and outcome.

281 lood pressure (BP) lowering in patients with ICH (<6 hours) and elevated systolic BP (150-220 mm Hg).

282 analyzed a large cohort of 784 patients with ICH (the development cohort; 55.6% female), examined NCC

283 No evidence suggested that patients with ICH and a spot sign specifically benefit from intensive

284 ansion and improves outcome in patients with ICH and a spot sign.

285 n Iba1(+) cells from brains of patients with ICH and in CD11b(+)CD45(int) cells from mice subjected t

286 F alone-on shunt dependency in patients with ICH and severe IVH.

287 e in the extent of bleeding in patients with ICH as measured by baseline hematoma volume and risk of

288 el, lymphopenia was present in patients with ICH at admission and persisted up to 14 d.

289 were performed on 33 included patients with ICH by using a 3-T MRI unit.

290 We identified patients with ICH from the overall trial population enrolled in the Ap

291 Among 3207 consecutive patients with ICH initially screened, 17 fulfilled study criteria (med

292 A total of 596 patients with ICH were included.

293 o August 31, 2014, to identify patients with ICH who had transient deficits that resolved completely

294 In addition, patients with ICH with infection had significant deficiencies of T and

295 In patients with ICH, prior antithrombotic therapy is associated with gre

296 with the extent of bleeding in patients with ICH.

297 s associated with clinical presentation with ICH or new focal neurological deficit (FND) without brai

298 eople with non-brainstem CCM presenting with ICH or FND, and 30.8% (26.3-35.2) for 495 people with br

299 95 people with brainstem CCM presenting with ICH or FND.

300 people with brainstem CCM presenting without ICH or FND, 18.4% (13.3-23.5) for 327 people with non-br

301 le with non-brainstem CCM presenting without ICH or FND, 8.0% (0.1-15.9) for 80 people with brainstem