ライフサイエンスコーパス: hyperintensity

1 eterogeneity) from enhancing tumor and FLAIR hyperintensity.

2 ests subtle injury even in the absence of T2 hyperintensity.

3 et not all iron-staining lesions had R2* rim hyperintensity.

4 hich is significantly correlated with MBH T2 hyperintensity.

5 odified by baseline severity of white matter hyperintensities.

6 atter T2/fluid-attenuated inversion recovery hyperintensities.

7 iovale perivascular spaces, and white matter hyperintensities.

8 iovale perivascular spaces, and white matter hyperintensities.

9 wed global brain atrophy and white matter T2 hyperintensities.

10 iated with increasing volume of white matter hyperintensities.

11 d with a topographic pattern of white matter hyperintensities.

12 ller infarctions and volumes of white matter hyperintensities.

13 elationship between amyloid and white matter hyperintensities.

14 vealed longitudinal spindle-shaped T2-signal hyperintensity (100%) and cord enlargement (79%) accompa

15 migraine with progression of infratentorial hyperintensities: 21 participants (15%) in the migraine

16 RT also reversed progression of white matter hyperintensities, a biomarker of cerebrovascular disease

17 l group had progression of deep white matter hyperintensities (adjusted odds ratio [OR], 2.1; 95%CI,

18 e and clinical significance of persistent T2 hyperintensity after acute ST-segment-elevation myocardi

19 Hippocampal T2 hyperintensity after FSE represents acute injury often e

20 ns, cases carrying c.1909+22G>A demonstrated hyperintensities along the superior cerebellar peduncles

21 White matter hyperintensities also contribute to brain atrophy patter

22 More severe periventricular white matter hyperintensities also correlated with a lower proportion

23 ion probability map showed that white matter hyperintensities also had a wide anatomical distribution

24 02) and with the progression of white matter hyperintensity among participants with systolic blood pr

25 ve found an association between white matter hyperintensities and Alzheimer's disease pathologies.

26 l cord MRI abnormalities such as T2-weighted hyperintensities and atrophy are commonly associated wit

27 degenerations who show unusual white matter hyperintensities and atrophy on magnetic resonance imagi

28 White matter hyperintensities and brain atrophy, seen on magnetic res

29 pe design using distribution of white matter hyperintensities and brain infarcts in a population-base

30 White matter hyperintensities and brain infarcts were measured using

31 ity of periventricular and deep white matter hyperintensities and calculated the number and percentag

32 ect on SPARE-BA was mediated by white matter hyperintensities and cardiovascular risk score each expl

33 diates the relationship between white matter hyperintensities and chronic post-stroke aphasia severit

34 Over time, progression of hyperintensities and cognitive deficits predicts a poor

35 thological substrate, linked to white matter hyperintensities and frontal white matter changes, which

36 ass (grey matter, white matter, white matter hyperintensities and lacunes) for each individual.

37 rebral microvessels that causes white matter hyperintensities and several other common abnormalities

38 the cerebrovascular pathology (white-matter hyperintensities and small- and large-vessel infarcts).

39 T2-weighted hyperintensity and contrast enhancement both yielded 100

40 al disconnectivity strongly correlated to T2 hyperintensity and marginally to atrophy.

41 se imaging features include (a) confluent T2 hyperintensity and mild restricted diffusion in bilatera

42 T2 hyperintensity and volume alterations of C5, C6, and C7

43 2-weighted imaging for atrophy, white matter hyperintensities, and infarcts.

44 hite matter hyperintensities, infratentorial hyperintensities, and posterior circulation territory in

45 volumes of total brain tissue, white matter hyperintensities, and regional tissues/structures, adjus

46 maller brain volumes, increased white matter hyperintensities, and worse cognitive performances.

47 resented with marked ipsilateral atrophy, T2 hyperintensity, and mean diffusivity increases across al

48 We hypothesized that: (i) white matter hyperintensities are associated with damage to fibres of

49 White matter hyperintensities are associated with increased risk of d

50 Leukoaraiosis or white matter hyperintensities are frequently observed on magnetic res

51 ilent brain infarcts (SBIs) and white matter hyperintensities are subclinical cerebrovascular lesions

52 fications, when associated with white matter hyperintensities, are of major importance in the decisio

53 Hyperintensity around the injection tracts on T2-weighte

54 ed in conventional LGE, which results in the hyperintensity artifact.

55 E technique produced severe, uninterpretable hyperintensity artifacts in the anterior and lateral por

56 band LGE MR imaging technique eliminates the hyperintensity artifacts seen in patients with cardiac d

57 re performed to test the hypothesis that the hyperintensity artifacts that are typically observed on

58 To examine white matter hyperintensities as a neurobiological mechanism of these

59 White matter hyperintensities as seen on brain T2-weighted magnetic r

60 control subjects by MRI and analyzed the T2 hyperintensity as a measure of HI.

61 e matter fluid-attenuated inversion recovery hyperintensities, as well as a contrast-enhancing sellar

62 ar disease, such as lacunes and white matter hyperintensities, as well as dementia.

63 ate the topographic patterns of white matter hyperintensities associated with Alzheimer's disease bio

64 Measured areas of hyperintensity at acute DW imaging were used as the stan

65 ta = -0.25) and increased brain white matter hyperintensities (beta = 0.17).

66 In a subgroup, white matter hyperintensities, bicaudate index, global cortical (GCA)

67 igates the relationship between white matter hyperintensities burden and patterns of brain atrophy as

68 vascular disease risk score and white matter hyperintensities burden on SPARE-BA, revealing a statist

69 Individuals with high white matter hyperintensities burden showed significantly (P < 0.0001

70 lues compared to those with low white matter hyperintensities burden, indicating that the former had

71 White matter hyperintensity burden and ECV predict rapid cognitive de

72 ith LLD+MCI also showed greater white matter hyperintensity burden compared with LLD+NC (P=0.015).

73 den, older individuals with low white matter hyperintensity burden, and young adults were assessed in

74 , older individuals with severe white matter hyperintensity burden, older individuals with low white

75 had a higher incidence of deep white matter hyperintensities but did not have significantly higher p

76 cerebrospinal fluid biomarkers, white matter hyperintensities, cognitive and clinical measures, and l

77 assess the relationship between white matter hyperintensities, connectome fibre-length measures and a

78 lts support the hypothesis that white matter hyperintensities contribute to patterns of brain atrophy

79 White matter hyperintensities contribute to the presentation of AD an

80 severe periventricular and deep white matter hyperintensities correlated with a lower proportion of l

81 elop cardiovascular disease and white matter hyperintensities could decrease the incidence or delay t

82 s, bariatric surgery had no effect on MBH T2 hyperintensity despite inducing significant weight loss

83 microbleeds, and progression of white matter hyperintensities detected on MRI; cognitive decline defi

84 -0.334, P = 0.020), while deep white matter hyperintensities did not correlate with mid-range fibres

85 plication and deletion revealed white matter hyperintensities, dilated perivascular spaces, and lacun

86 We assessed loss of dorsolateral nigral hyperintensity (DNH) on high-field susceptibility-weight

87 e demonstrate that the rates of white matter hyperintensity expansion and grey matter atrophy are str

88 le CAA-ri (requiring asymmetric white matter hyperintensities extending to the subcortical white matt

89 pocampal volume), white matter (white matter hyperintensities, fractional anisotropy [theoretical ran

90 Hyperintensity from gadopentetate dimeglumine enabled vi

91 sities included periventricular white matter hyperintensities (frontal and parietal lobes).

92 define the relationship between white matter hyperintensity growth and brain atrophy, we applied a se

93 ficantly associated with faster white matter hyperintensity growth in the frontal and parietal region

94 Additionally, the rate of white matter hyperintensity growth was heterogeneous, occurring more

95 Although white matter hyperintensities have traditionally been viewed as a mar

96 r hyperintensities (with severe white matter hyperintensities; hazard ratio, 1.54; 95% confidence int

97 ohorts and also associated with white matter hyperintensities in a general population sample.

98 d imaging lesions and posterior white matter hyperintensities in adjusted analyses.

99 h corresponds to the top 25% of white matter hyperintensities in an independent non-demented sample).

100 tricular enlargement in one, periventricular hyperintensities in another and frontal atrophy of the l

101 n white matter connectivity and white matter hyperintensities in BD than UD depression, habenula volu

102 of age-related accumulation of white matter hyperintensities in both periventricular and deep white

103 el disease (eg, microbleeds and white matter hyperintensities in strategically important regions of t

104 ing (MRI) of the brain showed characteristic hyperintensities in the basal ganglia and thalamus that

105 L patients showed more frequent white matter hyperintensities in the bilateral posterior temporal reg

106 eing in the highest quartile of white matter hyperintensities in those with depressive symptoms only

107 han or equal to three vertebral segments) T2-hyperintensity in 44 of 50 (88%) ring enhancing myelitis

108 ree precession images showed areas of signal hyperintensity in only 17 of 30 patients.

109 Purpose To explore the extent of signal hyperintensity in the brain on unenhanced T1-weighted ma

110 koencephalopathy; diffusion-weighted imaging hyperintensity in the corticomedullary junction and skin

111 Obese subjects exhibited T2 hyperintensity in the left but not the right MBH, which

112 ructural study showed that the strong signal hyperintensity in the white matter of FCD IIb was relate

113 patterns of amyloid-associated white matter hyperintensities included periventricular white matter h

114 icant basal ganglia lesions and white matter hyperintensities, including periventricular regions and

115 through cerebral vasculature and persistent hyperintensities indicated occlusion.

116 n of MRI-measured cerebral deep white matter hyperintensities, infratentorial hyperintensities, and p

117 g results were normal, without basal ganglia hyperintensity, lacunae, calcification, or heavy metal d

118 nts showed brain abnormalities (white matter hyperintensities, lacunar lesions suggestive of ischemic

119 marker of vascular risk (total white matter hyperintensity lesion volume).

120 c resonance imaging evidence of white matter hyperintensity lesions.

121 they had a brain infarct and/or white matter hyperintensities load >/=1.11% of total intracranial vol

122 1 and P=0.050) and with greater white matter hyperintensity load in the pravastatin arm (P=0.046).

123 ciation of high vs nonhigh deep white matter hyperintensity load with change in cognitive scores (-3.

124 erebral blood flow, and greater white matter hyperintensity load.

125 Hippocampal T2 hyperintensity, maximum in Sommer's sector, occurred acu

126 These hyperintensities may represent the structural correlate

127 agnetic resonance imaging, with white matter hyperintensities, microbleeds, and brain atrophy reflect

128 nts, who consistently have more white matter hyperintensities, microbleeds, microinfarctions and cere

129 o the latest classification, is white matter hyperintensity - morphological findings of small blood v

130 imaging data and other sources: white matter hyperintensities (N = 42,310), fractional anisotropy (N

131 h cerebral atrophy or dentate and pontine T2 hyperintensities observed in 28%.

132 Persistent T2 hyperintensity occurs in two thirds of STEMI patients.

133 Nine patients (47.4%) developed T1 hyperintensities of the basal ganglia, corresponding to

134 Rate of iso-or hyperintensity of HCA on HPB phase MR images was variabl

135 Fifty-six patients had T2 hyperintensity of spinal gray matter on magnetic resonan

136 fuse callosal signal change, and atrophy and hyperintensity of the corticospinal tracts.

137 ntradictory results have been reported about hyperintensity of the globus pallidus and/or dentate nuc

138 bral lesions, including microhemorrhages and hyperintensities on fluid-attenuated inversion recovery

139 of Fabry disease, visualized as white matter hyperintensities on MRI in 42-81% of patients.

140 re (OR = 4.2, 95% CI = 3.0-5.9) white matter hyperintensities on MRI were independently associated wi

141 Hyperintensities on short-tau inversion recovery sequenc

142 irect effect of periventricular white matter hyperintensities on WAB-AQ (P > 0.05); (iii) significant

143 total effect of periventricular white matter hyperintensities on WAB-AQ (standardized beta = -0.348,

144 of more severe periventricular white matter hyperintensities on worse aphasia severity mediated in p

145 luding delayed myelination with white matter hyperintensity on brain magnetic resonance imaging in on

146 An acute ACE lesion was defined by a new hyperintensity on diffusion-weighted and fluid-attenuate

147 Hyperintensity on diffusion-weighted images and involvem

148 ar disease represented by brain white matter hyperintensity on magnetic resonance imaging is associat

149 Marked hyperintensity on T2-weighted images was seen in 12 of 1

150 arkers of small vessel disease (white matter hyperintensities or lacune volume)?

151 s, hypointensity was more common compared to hyperintensity or heterogeneous intensity.

152 s also associated with cerebral white matter hyperintensities (OR [95% CI] = 1.10 [1.05-1.16]; p = 5.

153 : OR, 1.58; 95% CI, 1.28-1.96), white matter hyperintensities (OR, 1.29; 95% CI, 1.19-1.39), cerebral

154 dividuals with higher volume of white matter hyperintensities (P value for interaction=0.019).

155 lated with overall volume of white matter T2 hyperintensity (Pearson correlation, 0.53; p = 0.007).

156 subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and

157 At 6 months, T2 hyperintensity persisted in 189 (67%) patients, who were

158 ationships between the rates of white matter hyperintensity progression and cortical grey matter atro

159 P < 0.05), we show the rate of white matter hyperintensity progression is associated with increases

160 ral white matter in the rate of white matter hyperintensity progression?

161 in Scale scores differed across white matter hyperintensity quintiles (P < 0.001).

162 szel test), and the upper three white matter hyperintensity quintiles (versus the first quintile) had

163 ion analysis showed that higher white matter hyperintensity quintiles were independently associated w

164 ration (19.4%), and the top two white matter hyperintensity quintiles were more vulnerable still: 23.

165 positively correlated with deep white matter hyperintensities (R(2) = 0.928, p < 0.01).

166 Fabry disease, extending beyond white matter hyperintensities seen on conventional MRI.

167 ranges from lacunar infarcts to white matter hyperintensities seen on magnetic resonance imaging.

168 ast, follow-up of 116 children without acute hyperintensity showed abnormal T2 signal in only 1 (foll

169 p MRI obtained on 14 of the 22 with acute T2 hyperintensity showed HS in 10 and reduced hippocampal v

170 Only white matter hyperintensities significantly mediated the age effect o

171 s) and large-scale alterations (white matter hyperintensities, structural connectivity, cortical thic

172 igate a possibly causal role of white matter hyperintensities, structural equation modelling was used

173 ssive symptoms with presence of white matter hyperintensities, suggesting future studies may focus on

174 rostrocaudal midpoint of a spindle-shaped T2 hyperintensity suggests that spondylosis is the cause of

175 In conventional neonatal MRI, the T2 hyperintensity (T2h) in cerebral white matter (WM) at te

176 ween LLD, vascular risk factors and cerebral hyperintensities, the radiological hallmark of vascular

177 sible CAA-ri (not requiring the white matter hyperintensities to be asymmetric).

178 rlying pathophysiology relating white matter hyperintensities to chronic aphasia severity.

179 es mellitus, hyperlipidemia and white matter hyperintensities to predict poorer cognitive performance

180 We quantified white matter hyperintensities using automated segmentation and summar

181 attenuated inversion recovery (FLAIR) signal hyperintensities, ventricular size increases, prominent

182 imed at reducing progression of white matter hyperintensities via end-arteriole damage may protect ag

183 netic resonance imaging-defined white matter hyperintensities volume and cerebral microbleeds.

184 ignificant relationship between white matter hyperintensities volume and hypertension (P = 0.001), di

185 GLS was associated with greater white matter hyperintensity volume (adjusted beta=0.11, P<0.05), unli

186 lead level and log-transformed white matter hyperintensity volume (b = 0.05 log mm3; 95% CI, -0.02 t

187 hemorrhage, and an increase in white matter hyperintensity volume (beta = 0.11, 95% CI = 0.01-0.21).

188 sel disease including increased white matter hyperintensity volume (P < 0.001), lower total brain vol

189 sis (39.0%), outcomes varied by white matter hyperintensity volume (P = 0.01, Cochran-Mantel-Haenszel

190 s did not vary significantly by white matter hyperintensity volume (P = 0.19, Cochran-Mantel-Haenszel

191 t with covert brain infarcts or white-matter hyperintensity volume (P>0.05).

192 White matter hyperintensity volume (p<0.0001) and cognitive performan

193 Primary outcome measures were white matter hyperintensity volume (WMHV) quantified from multimodal

194 ity (gait speed) and accrual of white matter hyperintensity volume after 3 years.

195 White matter hyperintensity volume and ECV were entered as predictors

196 rmance, cortical thickness, and white matter hyperintensity volume at baseline, and the rate of subse

197 This was also true for white matter hyperintensity volume but not after removal of an outlyi

198 D group brain volume was lower, white matter hyperintensity volume higher and all diffusion character

199 In conclusion, white matter hyperintensity volume independently correlates with stro

200 White matter hyperintensity volume modified the effect of ECV on aggr

201 brain volume abnormalities and white matter hyperintensity volume on term MRI in extremely low birth

202 standard deviation increase in white matter hyperintensity volume over time, new subcortical infarct

203 lities (gray matter atrophy and white matter hyperintensity volume via magnetic resonance imaging), a

204 ected in 53 participants (12%), white matter hyperintensity volume was 0.63+/-0.86%.

205 ical superficial siderosis, and white matter hyperintensity volume were assessed on MRI.

206 MR regional brain volumetrics, white matter hyperintensity volume, and number of infarcts.

207 onventional MRI markers of SVD (white matter hyperintensity volume, brain volume, and lacunes), and d

208 allele, CSF total-tau (t-tau), white matter hyperintensity volume, depression, diabetes, hypertensio

209 n vivo beta-amyloid deposition, white matter hyperintensity volume, hippocampal volume or Alzheimer's

210 cerebrospinal fluid (CSF), and white matter hyperintensity volume, lacunar infarcts, and cerebral mi

211 d conventional imaging markers (white matter hyperintensity volume, lacune volume, and brain volume)

212 Conclusion White matter hyperintensity volume, local network efficiency, and inf

213 follow-up (2007-2011), included white matter hyperintensity volume, subcortical infarcts, cerebral mi

214 Measurements were obtained for white matter hyperintensity volume, total brain volume, gray matter v

215 a greater 5-year progression of white matter hyperintensity volume.

216 ss and the progression of total white matter hyperintensity volume.

217 overt brain infarcts, and large white-matter hyperintensity volume.

218 f the right VIIIa cerebellum and elevated WM hyperintensity volume.

219 o had exhibited greater frontal white matter hyperintensities volumes that predicted shorter time to

220 htly underestimated compared with DW imaging hyperintensity volumes (33.0 vs 41.6 mL, P=.01; ratio=0.

221 We investigated how white matter hyperintensity volumes affect stroke outcomes, generally

222 The white matter hyperintensity volumes were not associated with either h

223 hereas changes from baseline in white matter hyperintensity volumes were smaller (0.29%) in the inten

224 White matter hyperintensity volumes were stratified into quintiles.

225 Persistent T2 hyperintensity was associated with all-cause death and h

226 Persistent T2 hyperintensity was associated with NT-proBNP (N-terminal

227 er volume of supratentorial MRI white matter hyperintensity was associated with slower timed gait and

228 Persistent T2 hyperintensity was associated with the initial STEMI sev

229 Persisting T2 hyperintensity was defined as infarct T2 >2 SDs from rem

230 A central area of T2 hyperintensity was identifiable in 26 of the 27 astronau

231 T2-mesiotemporal hyperintensity was more common in LGI1-IgG-positive (41%

232 n subjects with high burdens of white matter hyperintensities, we performed clinicopathological studi

233 SBIs and white matter hyperintensities were assessed by brain MRI.

234 Moreover, higher white matter hyperintensities were associated with poor modified Rank

235 In this subtype, worse white matter hyperintensities were associated with worse National Ins

236 Regardless of stroke subtype, white matter hyperintensities were not associated with stroke recurre

237 that harboured periventricular white matter hyperintensities were selected and the molecular organiz

238 White matter hyperintensities were semi-automatically segmented using

239 OND and central optic nerve T2 hyperintensity were quantified at mid orbit.

240 s of 16 patients, revealed characteristic T2 hyperintensities with a predilection for the head of the

241 ed a significant association of white matter hyperintensities with incident depression (OR, 1.19; 95%

242 results link the progression of white matter hyperintensities with increasing rates of regional grey

243 her with increasing severity of white matter hyperintensities (with severe white matter hyperintensit

244 facies, myopathy, and cerebral white matter hyperintensities, with cardiac systolic dysfunction pres

245 Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephal

246 itions presenting with T1 weighted spin echo hyperintensity within the central nervous system in gene

247 either appeared normal or showed T2-weighted hyperintensities without fascicular enlargement (reader

248 th higher odds of having severe white matter hyperintensities (WMH) (odds ratio [OR]: 1.32; 95% confi

249 the group into mild-to-moderate white matter hyperintensities (WMH) and severe WMH group based on med

250 White matter hyperintensities (WMH) are a common radiographic finding

251 White matter hyperintensities (WMH) are the most common brain-imaging

252 Amyloid burden and white matter hyperintensities (WMH) are two common markers of neurode

253 The burden of cerebral white matter hyperintensities (WMH) is associated with an increased r

254 White matter hyperintensities (WMH) observed on neuroimaging of elder

255 ing imaging biomarkers, such as white matter hyperintensities (WMH) on MRI and amyloid-beta (Abeta) P

256 ring brain tissue (NABT) and in white matter hyperintensities (WMH) predict longitudinal cognitive de

257 White matter hyperintensities (WMH) volume, lacunar infarcts, and gra

258 d magnetic resonance imaging of white matter hyperintensities (WMH), and their addresses were geocode

259 ated scales were used to assess white matter hyperintensities (WMH), cerebral microbleeds (CMB) and l

260 is characterised by progressive white matter hyperintensities (WMH), cognitive decline and loss of fu

261 To quantify SVD, we assessed white matter hyperintensities (WMH), enlarged perivascular spaces, ce

262 and rs12255372) with volumes of white matter hyperintensities (WMH), gray matter, and regional volume

263 rovascular pathology, including white matter hyperintensities (WMH), infarcts, cerebral microbleeds,

264 e CSVD burden was assessed with white matter hyperintensities (WMH), lacunes, and microbleeds (MBs) o

265 ease burdens were assessed with white matter hyperintensities (WMH), lacunes, and microbleeds.

266 s of magnetic resonance imaging white matter hyperintensities (WMH), lacunes, microbleeds with CSF be

267 ficity and if it is mediated by white matter hyperintensities (WMH).

268 otal cerebral volume (TCV), and white matter hyperintensities (WMH).

269 11 710 cases, 287 067 controls; white matter hyperintensities (WMH): 10 597 individuals; intracerebra

270 agnetic resonance imaging (MRI) white matter hyperintensities (WMH; or leukoaraiosis) in patients wit

271 High white matter hyperintensity (WMH) burden is commonly found on brain M

272 tions were modified by cerebral white matter hyperintensity (WMH) burden.

273 etabolic risk factors influence white matter hyperintensity (WMH) development: in metabolic syndrome

274 easures of infarct, hemorrhage, white matter hyperintensity (WMH) grade, brain and hippocampal volume

275 onship to the presence of brain white matter hyperintensity (WMH) in older adults, a type of white ma

276 ned its associations with brain white matter hyperintensity (WMH) in older adults.

277 disease (SCeVD) demonstrated by white matter hyperintensity (WMH) on MRI contributes to the developme

278 Among SVD markers white matter hyperintensity (WMH) score or volume were additional sig

279 ng phenotype consisted of total white matter hyperintensity (WMH) volumes quantified using combined T

280 pact of individual SVD markers (white matter hyperintensity - WMH, microbleeds, lacunes, enlarged per

281 of small vessel disease (SVD) (white matter hyperintensities [WMH] on structural MRI, visual scores

282 ciations of 25(OH)D levels with white matter hyperintensities (WMHs) and MRI-defined infarcts were in

283 MRI arterial spin labeling, white matter hyperintensities (WMHs) and transcranial doppler (TCD) w

284 White matter hyperintensities (WMHs) are a common manifestation of ce

285 White matter hyperintensities (WMHs) are areas of increased signal on

286 Although white matter hyperintensities (WMHs) are associated with the risk for

287 White matter hyperintensities (WMHs) are associated with vascular cog

288 White matter hyperintensities (WMHs) are linked to vascular risk fact

289 White matter hyperintensities (WMHs) have been shown to be associated

290 l small vessel disease, such as white matter hyperintensities (WMHs) in individuals with cardiometabo

291 White matter hyperintensities (WMHs) of the brain are important marke

292 is associated with subcortical white matter hyperintensities (WMHs) on fluid-attenuated inversion re

293 vascular disease, visualized as white matter hyperintensities (WMHs) on magnetic resonance imaging sc

294 Quantified white matter hyperintensities (WMHs) represented cerebrovascular dise

295 even years later, the volume of white matter hyperintensities (WMHs) was determined from brain MR ima

296 distribution of microbleeds and white matter hyperintensities (WMHs) were assessed.

297 maging (MRI) to assess atrophy, white matter hyperintensities (WMHs), and diffusion parameters, and t

298 sel and cardiovascular disease (white matter hyperintensities [WMHs] on MRI, blood pressure, and body

299 the aura effect, the effect of white matter hyperintensities [WMHs]) and the correlations between co

300 GM volume, hippocampal volume, white matter hyperintensities, years of education, and APOE epsilon4