ライフサイエンスコーパス: microbleed

1 matter hyperintensities (WMH), lacunes, and microbleeds.

2 ging scanner to 222 patients with AD without microbleeds.

3 ated in a separate group of patients without microbleeds.

4 on, haemosiderin leakage, microinfarcts, and microbleeds.

5 to assess the presence of microinfarcts and microbleeds.

6 2 lesion volume, brain atrophy, and cerebral microbleeds.

7 or 'punctate' petechial-appearing traumatic microbleeds.

8 SWI is a highly sensitive way of identifying microbleeds.

9 yze the spatial relationship between CAA and microbleeds.

10 bral haemorrhage in the presence of cerebral microbleeds.

11 people, including 192 with multiple (>or=2) microbleeds.

12 a surrogate markers of axonal injury such as microbleeds.

13 ith amyloid-beta on tau after accounting for microbleeds.

14 ring blood vessel homeostasis and preventing microbleeds.

15 ed with the occurrence of new postprocedural microbleeds.

16 ed with the occurrence of new postprocedural microbleeds.

17 4 of 5 incident lacunes and 3 of 10 incident microbleeds.

18 tients with punctate versus linear appearing microbleeds.

19 re used for subsequent analysis of traumatic microbleeds.

20 matter hyperintensities volume and cerebral microbleeds.

21 vascular sealing and provoking inflammatory microbleeding.

22 of cerebral microbleeds (SHR for >5 cerebral microbleeds 2.33, 1.38-3.94), and older age (SHR per 10-

23 that of ischemic stroke in those with 2 to 4 microbleeds (25 vs 12 per 1,000 patient-years) and >= 11

24 ranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95% CI 48-84] per 100

25 er 1000 patient-years; and for >=20 cerebral microbleeds, 73 ischaemic strokes [46-108] per 1000 pati

26 (25 vs 12 per 1,000 patient-years) and >= 11 microbleeds (94 vs 48 per 1,000 patient-years).

27 analysis based on the presence or absence of microbleeds (a marker of diffuse axonal injury) revealed

28 progress to infarction and detects cerebral microbleeds - a risk factor for intracranial hemorrhage.

29 eGFR was lower in those with strictly lobar microbleeds (adjusted mean difference (aMD) -2.10 mL/min

30 ted risk ratio, 2.54; 95% CI, 1.76-3.68) and microbleeds (adjusted risk ratio, 1.43; 95% CI, 1.18-1.7

31 k of stroke in comparison with those without microbleeds, adjusting for demographic, genetic, and car

32 from infarct volume, SN-AI(95) at baseline, microbleeds, age, and sex (beta = 4.99; P < .001).

33 ischaemic stroke (for five or more cerebral microbleeds, aHR 4.55 [95% CI 3.08-6.72] for intracrania

34 r ischaemic stroke; for ten or more cerebral microbleeds, aHR 5.52 [3.36-9.05] vs 1.43 [1.07-1.91]; a

35 ] vs 1.43 [1.07-1.91]; and for >=20 cerebral microbleeds, aHR 8.61 [4.69-15.81] vs 1.86 [1.23-1.82]).

36 crobleeds, confirming that WMH, lacunes, and microbleeds, although heterogeneous on MRI, can have a c

37 % CI -3.70 to -1.15)), but not strictly deep microbleeds (aMD -0.67 (95% CI -1.85 to 0.51)).

38 .73 cm(2) (95% CI -3.39 to -0.81)) and mixed microbleeds (aMD -2.42 (95% CI -3.70 to -1.15)), but not

39 However, irrespective of cerebral microbleed anatomical distribution or burden, the rate o

40 Vasculoprotection was assessed as microbleed and intracranial hemorrhage (ICH) rates.

41 In total, 1,168 cortical microbleeds and 472 cortical microinfarcts were observed

42 ssifiers discriminated between patients with microbleeds and age-matched controls with a high degree

43 e observed a significant interaction between microbleeds and amyloid-beta pathology on greater baseli

44 More specifically, the co-occurrence of microbleeds and amyloid-beta pathology was associated wi

45 t in emphasis towards neuroimaging, cerebral microbleeds and diagnostic aspects and away from patholo

46 WMH), enlarged perivascular spaces, cerebral microbleeds and lacunes.

47 Cerebral microbleeds and larger hemorrhages developed upon postna

48 The relationship between CAA severity and microbleeds and microinfarcts as well as the sequence of

49 basis of magnetic resonance imaging-defined microbleeds and microinfarcts in cerebral amyloid angiop

50 walls of cortical vessels and the accrual of microbleeds and microinfarcts over time.

51 ere cerebral amyloid angiopathy are cortical microbleeds and microinfarcts.

52 arcts, between diagnosis of AD and number of microbleeds and number of microinfarcts, and between cog

53 Cerebral microbleeds and other markers of cerebral small vessel d

54 Measures associated with new microbleeds and postprocedural outcome including neurolo

55 s a modest correlation between the number of microbleeds and the number of cognitive domains impaired

56 , better sensitivity of SWI for detection of microbleeds and the use of a 3 T MRI platform.

57 (FDG-PET), and presence and distribution of microbleeds and white matter hyperintensities (WMHs) wer

58 ations of cerebral small vessel disease (eg, microbleeds and white matter hyperintensities in strateg

59 of small vessel disease, including cerebral microbleeds and white matter hyperintensities.

60 Proportion of microbleeds and WMH was higher in lvPPA-high than lvPPA-

61 and volume; perivascular spaces; lacunes and microbleeds), and vascular risk measures were assessed i

62 acune (3 with cavity <3mm), 3 evolved into a microbleed, and 27 were not detectable on follow-up.

63 imaging, with white matter hyperintensities, microbleeds, and brain atrophy reflecting key structural

64 atter hyperintensities, perivascular spaces, microbleeds, and brain atrophy.

65 (ml/mo), and number of incident lacunes and microbleeds, and calculated for each marker the proporti

66 hyperlipidaemia, prior stroke, lacunes, deep microbleeds, and carry the apolipoprotein E varepsilon3

67 covert brain infarcts, white matter lesions, microbleeds, and cortical microinfarcts, are also common

68 r hyperintensities (WMH), infarcts, cerebral microbleeds, and enlarged perivascular spaces (PVS), as

69 line MRI allowing quantification of cerebral microbleeds, and followed-up participants for ischaemic

70 icrovascular (subcortical infarcts, cerebral microbleeds, and higher white matter lesion volume), and

71 s (WMH), enlarged perivascular spaces (PVS), microbleeds, and infarcts emerge in relation to demograp

72 Incident subcortical infarcts, cerebral microbleeds, and progression of white matter hyperintens

73 lated perivascular spaces, lacunar infarcts, microbleeds, and spontaneous intracerebral hemorrhage.

74 lar amyloid accumulation, neuroinflammation, microbleeds, and white matter (WM) degeneration, is a co

75 LNCCIs), small noncortical infarcts (SNCIs), microbleeds, and white matter lesions were quantified by

76 Cerebral microbleeds are a neuroimaging biomarker of stroke risk.

77 Microbleeds are also frequently found in healthy elderly

78 roke or transient ischaemic attack, cerebral microbleeds are associated with a greater relative hazar

79 Cerebral microbleeds are associated with cognitive deficits, but

80 This study provides novel evidence that microbleeds are associated with cognitive dysfunction, i

81 Cerebral microbleeds are associated with the risks of ischemic st

82 Cerebral microbleeds are highly prevalent in people with clinical

83 Cerebral microbleeds are hypothesized downstream markers of brain

84 Microbleeds are more prevalent in patients with Alzheime

85 Traumatic microbleeds are small foci of hypointensity seen on T2*-

86 Microbleeds are strongly associated with intracerebral h

87 bral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurr

88 ds cannot be excluded, recognizing traumatic microbleeds as a form of traumatic vascular injury may a

89 detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life.

90 vasculature has facilitated the detection of microbleeds associated with long-term effects of radiati

91 Furthermore, TBI moderated microbleed associations with vascular risk factors and c

92 inal analysis restricted to subjects without microbleed at baseline, COPD was an independent predicto

93 sessed the presence, number, and location of microbleeds at baseline (August 2005 to December 2011) o

94 s with an intracerebral hemorrhage had lobar microbleeds at baseline; 4 of them used antithrombotics.

95 Microbleeds at other locations were associated with an i

96 hm identifies the anatomical localization of microbleeds based on brain atlases, and greatly reduces

97 s typical of hypertensive arteriopathy: deep microbleeds (beta=0.63, F(1,35)=35.24, p<0.001), deep WM

98 Brain microbleeds (BMBs) are seen as small, homogeneous, round

99 Serial sectioning revealed that for (n = 28) microbleeds, both Abeta (4%) and smooth muscle cells (4%

100 The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this

101 r than intracranial hemorrhage regardless of microbleed burden.

102 a higher risk of recurrent stroke and higher microbleeds burden, compared with those with normal kidn

103 Logistic regression confirmed that microbleeds (but not white matter changes) were an indep

104 angiopathy, CAA) is associated with cerebral microbleeds, but the precise relationship between CAA bu

105 r particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient i

106 crovascular lesions (e.g., microinfarcts and microbleeds) can now be visualized in vivo.

107 axonal injury in association with traumatic microbleeds cannot be excluded, recognizing traumatic mi

108 e cerebral parameters (white matter lesions, microbleeds), cardiovascular parameters (carotid plaque,

109 hite matter hyperintensities (WMH), cerebral microbleeds (CMB) and lacunes.

110 mal, subarachnoid, or subdural, and cerebral microbleed [CMB]).Twenty-six patients with COVID-19 ARDS

111 Restricted lobar cerebral microbleeds (CMBs) and cortical superficial siderosis (C

112 Define the concept of cerebral microbleeds (CMBs) and describe the most useful MRI sequ

113 (>40 EPVS)), white-matter changes, cerebral microbleeds (CMBs) and lacunes were rated using validate

114 Lobar cerebral microbleeds (CMBs) and localized non-hemorrhage iron dep

115 Cerebral microbleeds (CMBs) are an important risk factor for stro

116 Cerebral microbleeds (CMBs) are collections of blood breakdown pr

117 Cerebral microbleeds (CMBs) are defined as hypointense foci visib

118 Cerebral microbleeds (CMBs) are increasingly recognised neuroimag

119 agnetic resonance imaging to detect cerebral microbleeds (CMBs) as a marker of occult hemorrhage.

120 prevalence of brain infarctions and cerebral microbleeds (CMBs) between breast cancer survivors expos

121 We aimed to analyse the impact of cerebral microbleeds (CMBs) burden on HT subtypes and outcome aft

122 Cerebral microbleeds (CMBs) have been established as an independe

123 Cerebral microbleeds (CMBs) have been observed in healthy elderly

124 To characterize cerebral microbleeds (CMBs) in lacunar stroke patients in the Sec

125 ntally and was also associated with cerebral microbleeds (CMBs) in our population-based cohort study.

126 , to assess whether the presence of cerebral microbleeds (CMBs) on prethrombolysis MRI scans is assoc

127 Cerebral microbleeds (CMBs) were evaluated from magnetic resonanc

128 silon4 allele shows male excess for cerebral microbleeds (CMBs), a marker of SVD, which is opposite t

129 The spatial distribution of cerebral microbleeds (CMBs), which are asymptomatic precursors of

130 spaces (ePVS), lacunar strokes, and cerebral microbleeds (CMBs).

131 emorrhagic markers, including lobar cerebral microbleeds (CMBs).

132 tem imaging and histology revealed traumatic microbleed co-localization with iron-laden macrophages,

133 Imaging of the blood-brain barrier, cerebral microbleeds, coexistent ischemia, associated vascular le

134 ive cortical vessels was lower surrounding a microbleed compared to a simulated control lesion, and h

135 risk (95% CI 2.57-10.32) of having multiple microbleeds compared to a dose of 18 Gy.

136 n = 165) had a higher prevalence of cerebral microbleeds compared with subjects with normal lung func

137 sonance imaging we observed an additional 48 microbleeds (compared to high resolution), which proved

138 l cavities, and almost one-third of incident microbleeds, confirming that WMH, lacunes, and microblee

139 patients with microbleeds (n = 25) and a non-microbleed control group (n = 30) matched for age, gende

140 gic lesions (ARIA-H) in the form of cerebral microbleeds, convexity subarachnoid haemorrhage, cortica

141 Cerebral microbleeds, cortical superficial siderosis, and white m

142 Brain MRIs were rated for lobar cerebral microbleeds, cortical superficial siderosis, centrum sem

143 in injury, including strictly lobar cerebral microbleeds, cortical superficial siderosis, centrum sem

144 s characterized by individual focal lesions (microbleeds, cortical superficial siderosis, microinfarc

145 In the general population, a high microbleed count was associated with an increased risk f

146 Lobar microbleed count, another marker of CAA severity, also r

147 The risk increased with greater microbleed count.

148 A subset had cerebral microbleeds detected on T2* gradient recall echo scans.

149 Compared with having no microbleeds, eGFR was lower in those with strictly lobar

150 white matter damage in 25 TBI patients with microbleed evidence of TAI compared to neurologically he

151 with traumatic brain injury, 21 of whom had microbleed evidence of traumatic axonal injury, and 25 a

152 anced iron imaging, facilitating amyloid and microbleed examination; for example, higher microbleed p

153 white matter connectivity matrices from the microbleed group were able to identify patients with a h

154 ge, clinical measures of injury severity and microbleeds (>50% for fractional anisotropy versus <5% f

155 Patients with lobar microbleeds had an increased risk for stroke and stroke-

156 injury, whilst 40% of patients with visible microbleeds had no diffusion evidence of axonal injury.

157 In addition, microbleeds have been found to predict mortality in AD.

158 Microbleeds have generally been considered to be clinica

159 rd ratio 2.50, P = 0.038), exclusively lobar microbleeds (hazard ratio 2.22, P = 0.008) and presence

160 sociated with white matter lesions, cerebral microbleeds, hypertension, diabetes and ischemic heart d

161 rs (WMH/EPVS: age/hypertension, lacunes/deep microbleeds: hypertension/obesity).

162 d in 387 patients (22%), SNCIs in 368 (21%), microbleeds in 372 (22%), and white matter lesions in 17

163 describe the pathology underlying traumatic microbleeds in an index patient.

164 OPD had a significantly higher prevalence of microbleeds in deep or infratentorial locations (OR, 3.3

165 n independent predictor of incident cerebral microbleeds in deep or infratentorial locations (OR, 7.1

166 ncreased risk of the development of cerebral microbleeds in deep or infratentorial locations.

167 diation on cumulative number and location of microbleeds in each brain region, and multiple linear re

168 Compared with having no microbleeds, microbleeds in lobar locations were associated with an i

169 those without microbleeds, participants with microbleeds in locations suggestive of cerebral amyloid

170 4; 95% CI, -0.64 to -0.03; P = .03), whereas microbleeds in other brain regions were associated with

171 Greater prevalence of microbleeds in our study compared to prior reports is li

172 -dimensional T2*-weighted neuroimaging: more microbleeds in patients who are aging or with dementia o

173 to: (i) identify and characterize traumatic microbleeds in patients with acute traumatic brain injur

174 uited to the CROMIS-2 (Clinical Relevance of Microbleeds in Stroke) ICH study were included (mean age

175 Clinical Relevance of Microbleeds in Stroke-2 comprised two independent multic

176 of OAC from CROMIS-2 (Clinical Relevence Of Microbleeds In Stroke-2), a prospective observational in

177 emorrhages) are more likely to have multiple microbleeds in the brain.

178 Patients with executive dysfunction had more microbleeds in the frontal region (mean count 1.54 versu

179 rucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stro

180 used pooled individual patient data from the Microbleeds International Collaborative Network, includi

181 precise relationship between CAA burden and microbleeds is undefined.

182 ulation in which the clinical implication of microbleeds is unknown.

183 markers (white matter hyperintensity - WMH, microbleeds, lacunes, enlarged perivascular spaces, brai

184 Regarding the specific microbleed location, subjects with COPD had a significan

185 Our results strengthen the notion that microbleeds mark progression of cerebrovascular patholog

186 etinal microvascular abnormalities and brain microbleeds may occur together in older adults.

187 matter hyperintensities (WMH), lacunes, and microbleeds (MBs) on brain MRI.

188 The total susceptibility of a cerebral microbleed measured by using QSM is a physical property

189 Besides numerous lobar microbleeds (median 16 at baseline, 53 at last follow-up

190 with CAA-ri had more numerous lobar cerebral microbleeds (median 207[IQR 33-811] vs 19[IQR 7-58], p <

191 Compared with having no microbleeds, microbleeds in lobar locations were associa

192 tly have more white matter hyperintensities, microbleeds, microinfarctions and cerebral atrophy on ma

193 January 2, 2002, and December 16, 2009, and microbleeds (n = 111) and matched those (1:2) for age, s

194 We therefore studied patients with microbleeds (n = 25) and a non-microbleed control group

195 ain infarctions (n = 9/23, 39%) and cerebral microbleeds (n = 8/23, 35%).

196 te matter disease (n=5), haemorrhages (n=4), microbleeds (n=1), hippocampal microvasculature (n=1).

197 [0.13-4.61]; p(interaction)=0.41), cerebral microbleed number 0-1 versus 2-4 versus 5 or more (HR 0.

198 Cerebral microbleeds, observed as small, spherical hypointense re

199 These findings indicate that microbleeds occur preferentially in local regions of con

200 Mechanistically, these microbleeds occurred in the absence of peripheral immune

201 and the presence of strictly lobar cerebral microbleeds (odds ratio 3.85, 95% confidence interval 1.

202 The striking effect of microbleeds on executive dysfunction is likely to result

203 ven cerebral amyloid angiopathy and multiple microbleeds on in vivo clinical magnetic resonance imagi

204 In conclusion, these findings suggest that microbleeds on in vivo magnetic resonance imaging are sp

205 ion in primary subgroup analyses of cerebral microbleeds on MRI and in exploratory subgroup analyses

206 Microbleeds on MRI are associated with an increased risk

207 evidence of punctate and/or linear traumatic microbleeds on MRI.

208 d CT findings were associated with traumatic microbleeds on MRI.

209 tiple linear regression was used to evaluate microbleeds on neurocognitive outcomes, adjusting for ag

210 -echo sequence at 3.0 T and who had cerebral microbleeds on T2*-weighted images.

211 171 microbleeds were detected compared to 66 microbleeds on the corresponding in vivo magnetic resona

212 rhage (ICH) (n = 21) and those with cerebral microbleeds only and no history of ICH (n = 16).

213 level was not associated with the number of microbleeds or microinfarcts.

214 establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebra

215 cores with either the absence or presence of microbleeds or their location.

216 Low education was associated with more microbleeds (OR = 1.90, 95% CI = 1.33 to 2.72) and lower

217 ties (OR, 1.29; 95% CI, 1.19-1.39), cerebral microbleeds (OR, 1.18; 95% CI, 1.03-1.34), and cerebral

218 acunes (OR: 1.25; 95% CI: 1.04 to 1.48), and microbleeds (OR: 1.16; 95% CI: 1.03 to 1.31).

219 atter hyperintensities, small deep infarcts, microbleeds, or enlarged perivascular spaces) to severe

220 ate-to-severe white matter hyperintensities, microbleeds, or lacunes on baseline MRI.

221 d declined with increasing distance from the microbleed (p < 0.0001).

222 tern correlated strongly with lobar cerebral microbleeds (P < 0.001, age and sex adjusted Cohen's d =

223 tricular hemorrhage (p = 0.019), presence of microbleeds (p = 0.024), and large, early reductions in

224 or stroke (p = 0.012), presence of 1 or more microbleeds (p = 0.04), black race (p = 0.641), and pres

225 nce of microinfarcts (P = 0.025), though not microbleeds (P = 0.973).

226 In comparison with those without microbleeds, participants with microbleeds in locations

227 microbleed patients compared with 30% of non-microbleed patients (P = 0.03).

228 ive dysfunction, which was present in 60% of microbleed patients compared with 30% of non-microbleed

229 classifiers were applied to patients without microbleeds, patients having likely TAI showed evidence

230 cal and subcortical infarcts, microinfarcts, microbleeds, perivascular spacing, and white matter atte

231 cerebrovascular diseases, including cerebral microbleeds, porencephaly, and fatal intracerebral hemor

232 i) determine whether appearance of traumatic microbleeds predict clinical outcome; and (iii) describe

233 The MISTRAL (do MIcrobleeds predict STRoke in ALzheimer's disease) Study

234 age in primary subgroup analyses of cerebral microbleed presence (2 or more) versus absence (0 or 1)

235 Microbleed presence was associated with an increased ris

236 Microbleed presence was associated with lower CSF Abeta4

237 acranial haemorrhage, regardless of cerebral microbleed presence, antomical distribution, or burden.

238 Cerebral microbleed presence, location, and number.

239 Microbleed prevalence was 15.3% (median [interquartile r

240 Microbleed prevalence was 18.7% (median count 1 [1-111])

241 microbleed examination; for example, higher microbleed prevalence was found in AD than previously re

242 g significantly greater distances toward the microbleed relative to their female counterparts.

243 mber and anatomical distribution of cerebral microbleeds reliably using consensus criteria and valida

244 fidence interval (CI): 0.61, 1.10), cerebral microbleeds (RR = 0.69, 95% CI: 0.37, 1.32), total brain

245 enic edema and multiple cortical/subcortical microbleeds, sharing several aspects with the recently d

246 .61, 1.70-4.01), a higher number of cerebral microbleeds (SHR for >5 cerebral microbleeds 2.33, 1.38-

247 , lacunes, chronic infarctions, and [on MRI] microbleeds, siderosis, and enlarged perivascular spaces

248 The source of traumatic microbleed signal on MRI appeared to be iron-laden macro

249 d MRI images, PiB retention was increased at microbleed sites compared to simulated control lesions (

250 Cerebral microbleed size was measured by two neuroradiologists on

251 .07-1.60]; p(interaction)=0.75), or cerebral microbleed strictly lobar versus other location (HR 0.52

252 ions strongly correlated with lobar cerebral microbleeds suggesting that cerebral amyloid angiopathy

253 iated with white matter changes and cerebral microbleeds, suggesting that they result from an occlusi

254 ar appearance and location of some traumatic microbleeds suggests a vascular origin.

255 Of 13 sampled microbleeds that were matched on histology, five proved

256 Following injury (microbleed), the fraction of mobile microglia increased

257 Microbleeds thus mark the presence of diffuse vascular a

258 ratio [aHR] comparing patients with cerebral microbleeds to those without was 1.35 (95% CI 1.20-1.50)

259 ures of infarct-like brain lesions, cerebral microbleeds, total brain volume, and white matter lesion

260 total brain volume (P = 0.02), and number of microbleeds (trend P = 0.06).

261 following death for evaluation of traumatic microbleeds using MRI targeted pathology methods.

262 nsity volume, subcortical infarcts, cerebral microbleeds, Virchow-Robin spaces, and total brain paren

263 imately 20 to 40 msec, the measured cerebral microbleed volume increased by mean factors of 1.49 +/-

264 tibility over a region containing a cerebral microbleed was also estimated on QSM images as its total

265 At least one microbleed was present in 85% of survivors, occurring mo

266 The presence of traumatic microbleeds was an independent predictor of disability (

267 rence of cortical microinfarcts and cerebral microbleeds was assessed on fluid-attenuated inversion r

268 n patients with AD, the presence of nonlobar microbleeds was associated with an increased risk for ca

269 The presence of microbleeds was associated with an increased risk for de

270 The presence of more than 4 microbleeds was associated with cognitive decline.

271 ultivariable models, the absence of cerebral microbleeds was associated with larger ICH volume for bo

272 obar ICH volume, and the absence of cerebral microbleeds was associated with larger lobar and deep IC

273 Evidence of brain microbleeds was found in 485 (11.5%) people, including 1

274 The absence of cerebral microbleeds was independently associated with more frequ

275 iron precipitation in aggregates typical of microbleeds was shown by the Perl's staining.

276 49 patients, chronic hemorrhage, most often microbleeds, was visualized on MRI but not on CT.

277 Study, the presence, number, and location of microbleeds were assessed at baseline on brain MRI of 47

278 Lobar (with or without cerebellar) microbleeds were associated with a decline in executive

279 , 33.9; 95% CI, 2.5-461.7), whereas nonlobar microbleeds were associated with an increased risk for c

280 In addition, lobar microbleeds were associated with an increased risk for i

281 tional hazards to investigate if people with microbleeds were at increased risk of stroke in comparis

282 xels) ex vivo magnetic resonance images, 171 microbleeds were detected compared to 66 microbleeds on

283 Cerebral microbleeds were detected using high-resolution magnetic

284 nsity volume, lacunar infarcts, and cerebral microbleeds were estimated on magnetic resonance imaging

285 Microbleeds were most common in the basal ganglia but we

286 rast, the presence of focal brain injury and microbleeds were not associated with an increased risk o

287 After TAVR, new microbleeds were observed in 19 (23% [95% CI, 14%-33%])

288 16 at baseline, 53 at last follow-up), deep microbleeds were present in 19.6% of patients at baselin

289 Microbleeds were present in 41% of control subjects and

290 Traumatic microbleeds were prevalent in the population studied and

291 White matter changes and cerebral microbleeds were rated with validated scales.

292 The presence and number of microinfarcts or microbleeds were unrelated to cognitive performance.

293 angiopathy (lobar with or without cerebellar microbleeds) were at increased risk of intracerebral hem

294 I has high sensitivity in detecting cerebral microbleeds, which appear as small dot-like hypointense

295 WI) is a highly sensitive way of identifying microbleeds, which are a marker of TAI.

296 small (<20 mm) infarcts or lacunes, cerebral microbleeds, white matter hyperintensities, enlarged per

297 oke (HR, 3.8; 95% CI, 1.5-10.1) and nonlobar microbleeds with an increased risk for cardiovascular ev

298 The association of microbleeds with cognitive decline and dementia was stud

299 hite matter hyperintensities (WMH), lacunes, microbleeds with CSF beta-amyloid 42 (Abeta42), total ta

300 ts appear to develop in the early 30s, while microbleeds, WMH, amyloid, and tau emerge in the mid to