ライフサイエンスコーパス: microbleed

1 2 lesion volume, brain atrophy, and cerebral microbleeds.

2 SWI is a highly sensitive way of identifying microbleeds.

3 yze the spatial relationship between CAA and microbleeds.

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

5 matter hyperintensities volume and cerebral microbleeds.

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

7 ging scanner to 222 patients with AD without microbleeds.

8 ated in a separate group of patients without microbleeds.

9 to assess the presence of microinfarcts and microbleeds.

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

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

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

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

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

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

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

17 Cerebral microbleeds and larger hemorrhages developed upon postna

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

19 ere cerebral amyloid angiopathy are cortical microbleeds and microinfarcts.

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

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

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

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

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

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

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

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

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

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

30 Microbleeds are also frequently found in healthy elderly

31 Cerebral microbleeds are associated with cognitive deficits, but

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

33 Cerebral microbleeds are highly prevalent in people with clinical

34 Cerebral microbleeds are hypothesized downstream markers of brain

35 Microbleeds are more prevalent in patients with Alzheime

36 Microbleeds are strongly associated with intracerebral h

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

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

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

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

41 Microbleeds at other locations were associated with an i

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

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

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

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

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

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

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

49 (>40 EPVS)), white-matter changes, cerebral microbleeds (CMBs) and lacunes were rated using validate

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

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

52 Cerebral microbleeds (CMBs) are increasingly recognised neuroimag

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

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

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

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

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

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

59 Cerebral microbleeds (CMBs) were evaluated from magnetic resonanc

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

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

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

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

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

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

66 Cerebral microbleeds, cortical superficial siderosis, and white m

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

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

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

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

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

72 The risk increased with greater microbleed count.

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

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

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

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

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

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

79 Microbleeds have generally been considered to be clinica

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

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

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

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

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

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

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

87 4; 95% CI, -0.64 to -0.03; P = .03), whereas microbleeds in other brain regions were associated with

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

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

90 precise relationship between CAA burden and microbleeds is undefined.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Microbleeds on MRI are associated with an increased risk

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

108 171 microbleeds were detected compared to 66 microbleeds on the corresponding in vivo magnetic resona

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

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

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

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

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

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

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

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

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

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

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

120 Microbleed presence was associated with an increased ris

121 Microbleed presence was associated with lower CSF Abeta4

122 Cerebral microbleed presence, location, and number.

123 Microbleed prevalence was 15.3% (median [interquartile r

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

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

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

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

128 .61, 1.70-4.01), a higher number of cerebral microbleeds (SHR for >5 cerebral microbleeds 2.33, 1.38-

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

130 Cerebral microbleed size was measured by two neuroradiologists on

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

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

133 Microbleeds thus mark the presence of diffuse vascular a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 49 patients, chronic hemorrhage, most often microbleeds, was visualized on MRI but not on CT.

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

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

151 , 33.9; 95% CI, 2.5-461.7), whereas nonlobar microbleeds were associated with an increased risk for c

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

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

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

155 Cerebral microbleeds were detected using high-resolution magnetic

156 Microbleeds were most common in the basal ganglia but we

157 Microbleeds were present in 41% of control subjects and

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

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

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

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

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

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

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

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