ライフサイエンスコーパス: hyperintensity

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

2 hich is significantly correlated with MBH T2 hyperintensity.

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

4 wed global brain atrophy and white matter T2 hyperintensities.

5 iated with increasing volume of white matter hyperintensities.

6 no association between MeDi and white matter hyperintensities.

7 luding cerebral microbleeds and white matter hyperintensities.

8 .79; P = 2 x 10(-5)) but not periventricular hyperintensities.

9 odified by baseline severity of white matter hyperintensities.

10 f 16.2% of the variance in deep white matter hyperintensities.

11 matter hyperintensities and periventricular hyperintensities.

12 iovale perivascular spaces, and white matter hyperintensities.

13 iovale perivascular spaces, 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 rgement (29/32), T1 isointensity (27/32), T2 hyperintensity (25/32) and contrast enhancement (20/20).

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

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

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

20 Hippocampal T2 hyperintensity after FSE represents acute injury often e

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

22 White matter hyperintensities also contribute to brain atrophy patter

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

24 regression weights of -0.14 for white matter hyperintensities and -0.20 for hippocampal atrophy.

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

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

27 White matter hyperintensities and brain infarcts were measured using

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

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

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

31 with the volumes of whole brain white matter hyperintensities and gray and white matter in depressed

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

33 red semiquantitatively for deep white matter hyperintensities and periventricular hyperintensities.

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

35 mance and whole brain-segmented white matter hyperintensities and white and gray matter volumes were

36 T2-weighted hyperintensity and contrast enhancement both yielded 100

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

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

39 2-weighted imaging for atrophy, white matter hyperintensities, and infarcts.

40 ter volume, hippocampal volume, white matter hyperintensities, and lacunes.

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

42 e globus pallidus, confluent T2 white matter hyperintensities, and profound pontocerebellar atrophy i

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

44 es for deep white matter and periventricular hyperintensities, and stepwise multiple linear regressio

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

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

47 White matter hyperintensities are associated with elevated levels of

48 White matter hyperintensities are associated with increased risk of d

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

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

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

52 Hyperintensity around the injection tracts on T2-weighte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 ression effects for both white matter signal hyperintensity burden (t = 2.0, beta = 0.22, P = 0.045)

69 robust association with white matter signal hyperintensity burden (t = 4.0, beta = 0.43, P =0.0001)

70 White matter hyperintensity burden and ECV predict rapid cognitive de

71 nalysis with measures of white matter signal hyperintensity burden and nigrostriatal denervation as i

72 re the total brain and regional white matter hyperintensity burden between depressed patients and com

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

74 No significant white matter signal hyperintensity burden effects were found for rigidity or

75 indicate that increased white matter signal hyperintensity burden is associated with worse motor per

76 White matter signal hyperintensity burden regression effects for bradykinesi

77 Individuals with severe white matter hyperintensity burden showed a significant reduction in

78 Conversely, those with severe white matter hyperintensity burden showed greater activity in rostral

79 Additionally, those with severe white matter hyperintensity burden showed reduced functional connecti

80 White matter signal hyperintensity burden was log-transformed and normalized

81 White matter signal hyperintensity burden was significantly higher in the su

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

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

84 subjects and those with minimal white matter hyperintensity burden.

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

86 were present in 15, and included multifocal hyperintensities, cerebral atrophy, and confluent cortic

87 A prominent ring of T2-weighted image hyperintensity, characteristic of edema, surrounded the

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

89 d increased rates of subcortical gray matter hyperintensities compared with healthy controls.

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

91 White matter hyperintensities contribute to the presentation of AD an

92 executive function; whole brain white matter hyperintensities correlated with executive function; who

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

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

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

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

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

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

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

100 esterol (r = 0.20), and with periventricular hyperintensities for glycated hemoglobin level (r = 0.28

101 Hyperintensity from gadopentetate dimeglumine enabled vi

102 e condition relative to the low white matter hyperintensity group and young individuals.

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

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

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

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

107 ) if there was a high burden of white matter hyperintensity; however, this risk increased to 14.5 (95

108 equency of cortical and subcortical cerebral hyperintensities in 100 children and adolescents with To

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

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

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

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

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

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

115 on, and mood; the role of brain white matter hyperintensities in mediating this association; and the

116 he principal predictors of deep white matter hyperintensities in nondiabetic subjects.

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

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

119 ypertension after adjusting for white matter hyperintensities in the model, 21% hazard ratio change).

120 groups, the likelihood of detecting cerebral hyperintensities in the subcortex (primarily the basal g

121 multiple gadolinium-enhancing T(1) -weighted hyperintensities in the white matter of the cerebral hem

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

123 aken from regions that exhibited GCI-induced hyperintensity in diffusion-weighted imaging, and a sign

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

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

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

127 l dropout with surrounding cortical areas of hyperintensity in the middle cerebral artery borderzone

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

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

130 h MDD had reduced rates of deep white matter hyperintensities, increased corpus callosum cross-sectio

131 ancement (LGE) in 17 patients, and T2 signal hyperintensity indicating edema in 9 additional patients

132 resence and severity of linear and reticular hyperintensities, indicating SOS-type liver injury, usin

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

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

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

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

137 s rating was conducted to grade white matter hyperintensity lesions.

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

139 1 and P=0.050) and with greater white matter hyperintensity load in the pravastatin arm (P=0.046).

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

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

142 ts had seven regions of greater white matter hyperintensities located in the following white matter t

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

144 that the strategic location of white matter hyperintensities may be critical in late-life depression

145 These hyperintensities may represent the structural correlate

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

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

148 7)) and increased rates of deep white matter hyperintensities (odds ratio = 2.49; 95% confidence inte

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

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

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

152 s quantified by measuring brain white matter hyperintensities on fluid attenuation inversion recovery

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

154 he perivascular distribution of white matter hyperintensities on magnetic resonance imaging.

155 Most patients have white matter hyperintensities on MRI but these are of similar appeara

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

157 tive cognitive complaints, more white matter hyperintensities on MRI, and an expanded spatial extent

158 Hyperintensities on short-tau inversion recovery sequenc

159 ta1-42 and vascular disease via white matter hyperintensities on T2/proton density magnetic resonance

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

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

162 Hyperintensity on diffusion-weighted images and involvem

163 Regions of interest localized to areas of hyperintensity on DW images were drawn on postcontrast i

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

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

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

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

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

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

170 creased the likelihood of detecting cerebral hyperintensities, particularly in the subcortex, support

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

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

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

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

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

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

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

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

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

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

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

182 protons, Vp) of 15 out of 18 animals showed hyperintensity regions in gross or microscopic HT areas

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

184 neuropsychological function and white matter hyperintensity severity predicted MADRS scores prospecti

185 sed on executive dysfunction or white matter hyperintensity severity.

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

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

188 Only white matter hyperintensities significantly mediated the age effect o

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

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

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

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

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

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

195 We quantified white matter hyperintensities using automated segmentation and summar

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

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

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

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

200 city was associated with higher white matter hyperintensity volume (0.108 +/- 0.045 SD/SD, P = 0.018)

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

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

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

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

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

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

207 V), temporal horn volume (THV), white matter hyperintensity volume (WMHV), and MRI-defined brain infa

208 White matter hyperintensity volume and ECV were entered as predictors

209 BP in the progression of brain white matter hyperintensity volume burden associated with impairment

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

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

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

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

214 p was associated with increased white matter hyperintensity volume over that same period, as well as

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

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

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

218 hite matter and T2-hyperintense white matter hyperintensity volume was performed with semiautomated s

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

220 ns among vascular risk factors, white matter hyperintensity volume, and functional status.

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

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

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

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

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

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

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

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

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

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

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

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

233 (grey and white matter volumes, white matter hyperintensity volumes and prevalent subcortical infarct

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

235 White matter hyperintensity volumes were stratified into quintiles.

236 A greater degree of white matter hyperintensities was associated with impairments in the

237 The frequency of cerebral hyperintensities was significantly higher in subjects wi

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

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

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

241 Persistent T2 hyperintensity was associated with the initial STEMI sev

242 infrequent with plaque disruption, T2 signal hyperintensity was common with plaque disruption.

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

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

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

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

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

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

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

250 Segmented brain white matter hyperintensities were compared between subjects with lat

251 Pearson correlations with deep white matter hyperintensities were found for glycated hemoglobin leve

252 Cerebral white matter hyperintensities were measured for each group using magn

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

254 In contrast, white matter hyperintensities were only correlated with Boston naming

255 White matter hyperintensities were related to age and to white matter

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

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

258 hypertension, or the volume of white matter hyperintensities; which were not detectably higher in FT

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 Brain atrophy and white-matter hyperintensity (WMH) are also associated with impaired c

280 nctional MRI was used to assess white matter hyperintensity (WMH) burden and functional magnetic reso

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

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

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

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

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

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

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

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

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

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

291 White matter hyperintensities (WMHs) detectable by magnetic resonance

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

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

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

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

296 Quantified white matter hyperintensities (WMHs) represented cerebrovascular dise

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

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

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

300 ents with stroke, the volume of white matter hyperintensity (WMHV).