ライフサイエンスコーパス: post-stroke

1 and (ii) at a chronic stage (after 9 months post stroke).

2 onths following stroke (on average <3 months post-stroke).

3 with lacunar stroke; 24% had MCI or dementia post stroke.

4 er-extremity (UE) motor function in patients post stroke.

5 as at 24 h, confirmed histologically at 48 h post stroke.

6 ith HT, had MRI indices of hemorrhage at 3 h post stroke.

7 P<0.01) to neuroprotection seen up to 7 days post stroke.

8 ays, in addition to the corticospinal tract, post stroke.

9 ar thrombectomy improves outcomes at 90 days post stroke.

10 available for measuring upper limb function post-stroke.

11 igated the effects of tDCS on motor learning post-stroke.

12 ents with heterogeneous lesions at 1-2 weeks post-stroke.

13 e improves functional outcome up to 2 months post-stroke.

14 ety and quality of life (QoL), up to 5 years post-stroke.

15 gesterone was given starting at 3, 6 or 24 h post-stroke.

16 urogenesis were performed for up to 3 months post-stroke.

17 e plasma and brains at different time points post-stroke.

18 ioneurogenesis when given no later than 12 h post-stroke.

19 tions between arm function and use in humans post-stroke.

20 lind fields, but they disappear by ~6 months post-stroke.

21 not enhance motor recovery in patients early post-stroke.

22 received treatment via a femoral vein at 4 h post-stroke.

23 hemic cell damage analyzed at 6, 24 and 48 h post-stroke.

24 mals at 1 day, 2 days and weekly for 6 weeks post-stroke.

25 These rats were sacrificed at 24, or 48, h post-stroke.

26 equires further study at earlier time points post-stroke.

27 that this representation is mostly preserved post-stroke.

28 tes of severe disability or death at 90 days post-stroke.

29 matory cell death and DNA damage at 12 weeks post-stroke.

30 65 years) at admission and days 7, 30 and 90 post-stroke.

31 rward progression during gait in individuals post-stroke.

32 erity and worse functional outcome at day 90 post-stroke.

33 ognitive functioning between 90 and 365 days post-stroke.

34 ction in these muscles after injury, such as post-stroke.

35 s a major contributor to physical disability post-stroke.

36 nversation for patients with chronic aphasia post-stroke.

37 ed improved behavioral recovery at one month post-stroke.

38 ation and non-leaky blood vessels by 10 days post-stroke.

39 70% of their initial impairment by 3 months post-stroke.

40 static resting state functional MRI studies post-stroke.

41 important role in the recovery of movements post-stroke.

42 earning effects with tDCS and motor practise post-stroke.

43 ears; 7 female; 3 multiple sclerosis [MS]; 6 post-stroke; 1 post-traumatic).

44 224 patients (median time post-stroke 18 months) completed the 6-month programme.

45 s fugax and transient ischemic attack (45%), post-stroke (7%), global ischemia (10%), and asymptomati

46 ors (mean age 61 +/- 14 years, 5 +/- 5 years post-stroke, 89 males) and 60 controls (mean age 57 +/-

47 A post-stroke ABC pathway is proposed, as a more holistic

48 sults suggest enhanced sensorimotor recovery post-stroke after CMR.

49 12 hemiparetic patients (7.3 +/- 4.0 months post-stroke, age 26-75 years, six male/six female) acros

50 nd DMS D1-neurons, contributing to increased post-stroke alcohol-seeking and relapse.

51 (i.e. contralesional) secondary motor areas post-stroke, although with no apparent capacity to suppo

52 , produces similar effects on motor recovery post stroke and cognitive decline post TBI.

53 Rats were killed at 22 days post-stroke and brains extracted for evaluation of infar

54 an age 68.4 years) were scanned three months post-stroke and compared to 40 age- and sex-matched cont

55 ns of acute stroke care on one year survival post-stroke and determined the size of the effect across

56 onal measurement of grip strength at 4 weeks post-stroke and haemorrhagic stroke explained the undere

57 ical activity levels are reduced immediately post-stroke and remain below recommended levels for heal

58 etic resonance images were obtained 12-weeks post-stroke and tissue was collected for immunohistochem

59 d V in the dorsolateral prefrontal cortex of post-stroke and vascular dementia and, of mixed and Alzh

60 tein SMI31 immunoreactivity was increased in post-stroke and vascular dementia compared with post-str

61 etermine their temporal course up to 90 days post-stroke, and explore their utility as an early diagn

62 The molecular signals for post-stroke angiogenesis begin within hours of initial c

63 on of the miR-15a/16-1 cluster also enhances post-stroke angiogenesis by promoting vascular remodelin

64 had neuroprotective properties and enhanced post-stroke angiogenesis, a key component of brain repai

65 The overlap in molecular signaling between post-stroke angiogenesis, neurogenesis and axonal sprout

66 The Continue or Stop Post-Stroke Antihypertensives Collaborative Study (COSSA

67 = 0.04), poor cognitive outcome (P = 0.03), post-stroke anxiety (P = 0.04) and post-stroke depressio

68 were collected from 46 patients with chronic post-stroke aphasia and 20 neurotypical adults.

69 as 'goath') are commonly seen in persisting post-stroke aphasia and are thought to signal impairment

70 The clinical profiles of individuals with post-stroke aphasia demonstrate considerable variation i

71 Post-stroke aphasia might improve over many years with s

72 In this study, 17 patients with chronic post-stroke aphasia performed inner speech tasks (rhyme

73 clear evidence that the language profile in post-stroke aphasia reflects graded variations along mul

74 en white matter hyperintensities and chronic post-stroke aphasia severity.

75 administered to 38 individuals with chronic post-stroke aphasia, in addition to detailed language te

76 Language impairments caused by stroke (post-stroke aphasia, PSA) and neurodegeneration (primary

77 rrors were obtained from 64 individuals with post-stroke aphasia, who also underwent high-resolution

78 battery, to identify fundamental domains of post-stroke aphasia.

79 and neuroimaging data from individuals with post-stroke aphasia.

80 twork, with residual language performance in post-stroke aphasia.

81 EG) are sensitive to cortical dysfunction in post-stroke aphasia.

82 g the diverse, graded variations observed in post-stroke aphasia.

83 sions of language and cognition variation in post-stroke aphasia.

84 matter fibres in 48 individuals with chronic post-stroke aphasia.

85 ech is one of the most common impairments in post-stroke aphasia.

86 Post-stroke arthritic changes that may compromise rehabi

87 or older and had been diagnosed with aphasia post-stroke at least 4 months before randomisation; they

88 rd of all ischaemic strokes, even more after post-stroke atrial fibrillation monitoring.

89 e mechanisms aimed at mitigating the risk of post-stroke autoimmune complications driven by adaptive

90 inical utility as a prognostic biomarker for post-stroke BBB complications, and are likely elevated e

91 elevated early in patients who later develop post-stroke BBB disruption due to the presence of an inv

92 rrelations between connectivity measures and post-stroke behavioural status, either cross-sectionally

93 of any of these 16 genes are predictive for post-stroke blood brain barrier (BBB) disruption.

94 At day 7 post-stroke, both immediate and delayed intracerebral tr

95 R-15a/16-1 cluster in endothelium attenuates post-stroke brain infarction and atrophy and improves th

96 he acute and sub-acute/chronic phases in the post-stroke brain.

97 es phagocytosis during the recovery phase in post-stroke brains and suggests that CD36 plays a repara

98 occur spontaneously in the first few months post-stroke, by 6 months post-stroke, the deficit is con

99 The brain-heart axis is implicated in post-stroke cardiovascular complications known as the st

100 cal trials may be further refined to advance post-stroke cell therapy to the clinic.

101 Because lesions at this site can produce the post-stroke central pain syndrome, this finding supports

102 o predict the course and severity of chronic post-stroke cognitive and motor outcomes, as the ability

103 d dementia, but the mechanisms that underlie post-stroke cognitive decline are not well understood.

104 Post-stroke cognitive impairment (PSCI) is a major sourc

105 e physical impairments and reduced mobility, post-stroke cognitive impairment is often not prioritize

106 tory phase Elastic Net model correlated with post-stroke cognitive trajectories (r = -0.692, Bonferro

107 ADE levels were elevated 5, 15, and 30 days post-stroke compared to controls (p = 0.002, p = 0.002,

108 tory substances may be beneficial in chronic post-stroke conditions, while multimodal imaging can be

109 possibility that asymmetric walking patterns post-stroke could be remediated utilizing the split-belt

110 of crossbridge force generation and faster (post-stroke) crossbridge detachment by negative strain.

111 grees before reaching the orientation in the post-stroke crystal structure, consistent with previous

112 can be combined to improve the prediction of post-stroke deficits at 12-months.

113 es was increased by >2-fold in subjects with post-stroke demented compared to post-stroke non-demente

114 s in the white matter that would distinguish post-stroke demented from post-stroke non-demented subje

115 ed Cambridge Cognition Examination scores in post-stroke demented subjects.

116 nd temporal white matter were not greater in post-stroke demented versus post-stroke non-demented sub

117 or Alzheimer pathology in the development of post stroke dementia.

118 significantly changed between patients with post-stroke dementia and post-stroke patients with no de

119 Post-mortem brain tissues from post-stroke dementia and post-stroke patients with no de

120 decreased neuronal volumes in subjects with post-stroke dementia and vascular dementia.

121 d with dementia and executive dysfunction in post-stroke dementia and vascular dementia.

122 evalence and risk factors for pre-stroke and post-stroke dementia are conflicting.

123 ble data on the prevalence and predictors of post-stroke dementia are needed to inform patients and c

124 risk factors may be of benefit in preventing post-stroke dementia in the general population.

125 The strong association of post-stroke dementia with multiple strokes and the progn

126 who survive stroke develop delayed dementia (post-stroke dementia), with most cases being diagnosed a

127 vascular dementias, multi-infarct dementia, post-stroke dementia, subcortical ischaemic vascular dis

128 and place were more strongly associated with post-stroke dementia.

129 d for factors associated with pre-stroke and post-stroke dementia.

130 to identify risk factors for pre-stroke and post-stroke dementia.

131 Post stroke depression (PSD) is one of the most common c

132 = 0.03), post-stroke anxiety (P = 0.04) and post-stroke depression (P = 0.02).

133 as been thought to be effective for treating post-stroke depression (PSD).

134 Recent investigations indicate that post-stroke depression and social impairment are cross-c

135 model replicates multiple features of human post-stroke depression and thus provides a new model for

136 Clinical correlates of post-stroke depression include severity of physical and

137 Post-stroke depression is a frequent chronic and recurre

138 rhaps the most compelling reason to identify post-stroke depression, however, is its substantial impa

139 broadly overactive immune system in chronic post-stroke depression.

140 ted with mood we produced a model of chronic post-stroke depression.

141 ed impairment in long-term memory at 4-weeks post-stroke despite recovery from motor deficits, with h

142 ollow-up, neurovascular thrombectomy reduced post-stroke disability and improved health-related quali

143 triever thrombectomy reduced the severity of post-stroke disability and increased the rate of functio

144 Post-stroke domain V administration increased VEGF level

145 Post stroke dysphagia (PSD) is common and associated wit

146 ty of swallowing impairment in patients with post stroke dysphagia and is appropriate for use in clin

147 Such proposed therapies for post-stroke dysphagia have required confirmation of phys

148 Based on evidence from the post-stroke dysphagia neurostimulation literature, these

149 ion have demonstrated therapeutic promise in post-stroke dysphagia when applied contralaterally.

150 ulate cortical swallowing neurophysiology in post-stroke dysphagia with therapeutic effects which are

151 eloping cerebellar rTMS into a treatment for post-stroke dysphagia.

152 Other post-stroke emotional/behavioral disorders include mania

153 nd to antidepressant drug therapy, the other post-stroke emotional/behavioral disorders need to be ev

154 6% developed post-stroke epilepsy.

155 ot independently associated with the risk of post-stroke epilepsy.

156 outcomes are common in young adults 6 months post-stroke, even in those with an mRS score of 0-1 (ind

157 d, whereas C3a receptor deficiency decreased post-stroke expression of GAP43 (P < 0.01), a marker of

158 Our current findings suggest that post-stroke fatigue (1) is a problem of movement speed (

159 we investigated the long-term prevalence of post-stroke fatigue in patients with a young transient i

160 The pathophysiology of post-stroke fatigue is poorly understood although it is

161 Post-stroke fatigue negatively influences short-term fun

162 citability is associated with high levels of post-stroke fatigue.

163 excitability is lower in patients with high post-stroke fatigue.

164 both would be influenced by the presence of post-stroke fatigue.

165 hemisphere is a viable therapeutic target in post-stroke fatigue.

166 The post-stroke free-energy minimum is higher and is formed

167 to improve the accuracy of predictability in post-stroke functional impairment.

168 eflects the tension loss due to the original post-stroke heads executing a reverse power stroke.

169 ing gait training of individuals affected by post-stroke hemiparesis.

170 ts and 17 subjects with chronic (> 6 months) post-stroke hemiplegia participated in the study.

171 dy was performed to sonographically evaluate post-stroke hemiplegic shoulders and explore possible re

172 y after major stroke, resulting in so-called post-stroke hypertension.

173 to regulate acute and chronic phases of the post-stroke immune response, and their influence is subs

174 d accurately from baseline measures of acute post-stroke impairment alone.

175 a novel multivariate approach of predicting post-stroke impairment of speech and language from the i

176 Characterizing post-stroke impairments in the sensorimotor control of a

177 reate localized infarcts useful for modeling post-stroke impairments.

178 BSc2118 was intrastriatally injected 12 h post-stroke in mice that had received normal saline or r

179 ADEs were increased 15 days post-stroke in patients with hemorrhagic transformation

180 According to kinematic and kinetic raw data, post-stroke individuals showed reduced functional perfor

181 on preserved NK cell function and restrained post-stroke infection.

182 inhibition of neurogenic innervation limits post-stroke infection.

183 0 +/- 17 years, range 28-87 years) underwent post stroke language assessment with the Revised Western

184 Although ED1(+) cells decreased by 7-14 days post-stroke, large numbers of Iba1(+) cells persisted in

185 seline and having AF first diagnosed >7 days post-stroke (late AF) was highly associated with recurre

186 Greater post-stroke left hemisphere network fragmentation and hi

187 Univariate post-stroke lesion-behavior mapping is a particularly po

188 ice were associated with greater deficits in post-stroke locomotor functions.

189 Although post-stroke (<or=1 year) dementia rates were heterogeneo

190 ntrol groups, and negatively associated with post-stroke lymphocyte counts.

191 itative findings suggest that motor recovery post-stroke may exhibit some characteristics of proporti

192 Circulating extracellular vesicles (EVs) post-stroke may help brain endothelial cells (BECs) coun

193 = 13.2 years, range = 23.1-77.0 years; time post-stroke: mean = 49.2 months, standard deviation = 55

194 = 12.2 years, range = 17.2-80.1 years; time post-stroke: mean = 55.6 months, standard deviation = 62

195 he type of task used in motor rehabilitation post-stroke might be less relevant, as long as it is int

196 ke (IS), prior studies of IV-tPA's impact on post-stroke mortality did not have sufficient representa

197 Post-stroke mortality is higher among residents of disad

198 The forward (pre-stroke to post-stroke) motion has an approximately 4.5 k(B)T (wher

199 Post-stroke movement disorders can manifest in parkinson

200 healthy controls (n = 5), and patients with post-stroke muscle stiffness (n = 5) were recruited (Mar

201 les to quantify GAG content in patients with post-stroke muscle stiffness before and after hyaluronid

202 GAG content in the muscles of patients with post-stroke muscle stiffness, and that muscle hyaluronan

203 osaminoglycan (GAG) content in patients with post-stroke muscle stiffness; and to determine the effec

204 ution of structural brain damage, defined as post-stroke necrosis or cortical disconnection.

205 Furthermore, SDF1 and Ang1 promote post-stroke neuroblast migration and behavioral recovery

206 , we report here critical check-points about post-stroke neurogenesis after cortical infarcts, import

207 nal knockdown leads to a specific deficit in post-stroke neurogenesis through impaired migration of n

208 tion in the subventricular zone and impaired post-stroke neurogenesis.

209 ata can improve mechanistic understanding of post-stroke neurological impairments and guide future bi

210 Post-stroke neuronal knockdown of CCR5 in pre-motor cort

211 bjects with post-stroke demented compared to post-stroke non-demented subjects (P = 0.026) and by 11-

212 would distinguish post-stroke demented from post-stroke non-demented subjects.

213 e not greater in post-stroke demented versus post-stroke non-demented subjects.

214 hese, 6/28 (21%) were continent at six weeks post-stroke or discharge.

215 hite matter changes, which may contribute to post-stroke or small vessel disease dementia.

216 The pathological substrates associated with post-stroke or vascular dementia are poorly understood,

217 h, and it develops a 24 degrees twist in the post-stroke orientation.

218 how its alpha-helical neck in either pre- or post-stroke orientations, little is known about the tran

219 ographics, and vascular risks, and improving post-stroke outcome prediction, this subtyping-staging m

220 ically as a tool for the control for central post-stroke pain and neuropathic facial pain.

221 Lesions of 10 patients with central post-stroke pain of thalamic origin and 10 control patie

222 fying patients at risk of developing central post-stroke pain of thalamic origin early after thalamic

223 Central post-stroke pain of thalamic origin is an extremely dist

224 ally implicated in the generation of central post-stroke pain of thalamic origin.

225 s put patients at risk of developing central post-stroke pain of thalamic origin.

226 o three additional lesion syndromes: central post-stroke pain, auditory hallucinosis, and subcortical

227 Conversely, post-stroke paretic-leg rotary stiffness mechanisms incr

228 Sixteen individuals post-stroke participated in 40 minutes of HISTT for four

229 Using a representative post-stroke patient as an example, this article reviews

230 or posterior inferior frontal gyrus (IFG) in post-stroke patients with left temporo-parietal lesions

231 subjects to be reduced by 30-40% compared to post-stroke patients with no dementia and controls.

232 t-stroke and vascular dementia compared with post-stroke patients with no dementia and correlated wit

233 tween patients with post-stroke dementia and post-stroke patients with no dementia groups or ageing c

234 brain tissues from post-stroke dementia and post-stroke patients with no dementia were derived from

235 In post-stroke patients with spasticity of the biceps brach

236 , in cortically-induced blindness, the early post-stroke period appears characterized by gradual-rath

237 ent should be continued during the immediate post-stroke period is unclear.

238 as sensitized to MBP but did not survive the post-stroke period.

239 elevant changes are possible after the early post-stroke phase.

240 s in patients and healthy controls to assess post-stroke plasticity.

241 ot affect the incidence of algorithm-defined post-stroke pneumonia (71 [13%] of 564 patients in antib

242 adverse events were infections unrelated to post-stroke pneumonia (mainly urinary tract infections),

243 noted no differences in physician-diagnosed post-stroke pneumonia between groups (101 [16%] of 615 p

244 Algorithm-defined post-stroke pneumonia could not be established in 129 (1

245 axis cannot be recommended for prevention of post-stroke pneumonia in patients with dysphagia after s

246 The primary outcome was post-stroke pneumonia in the first 14 days, assessed wit

247 Post-stroke pneumonia is associated with increased morta

248 Post-stroke prognoses are usually inductive, generalizin

249 Here, we sought to establish how applicable post-stroke prognostic models, trained with monolingual

250 At 3 days post-stroke (PSD3), slight microgliosis (IBA-1) and astr

251 ge 5-112) and ending at a mean of 426.6 days post-stroke (range 170-917).

252 collection beginning at a mean of 36.9 days post-stroke (range 5-112) and ending at a mean of 426.6

253 presence in the affected regions, suggesting post-stroke reactivation that magnifies pro-inflammatory

254 een shown to be necessary and sufficient for post-stroke recovery in rodents.

255 uture studies addressing key elements of the post-stroke recovery process, with the goal to improve n

256 mising therapeutic target, but their role in post-stroke recovery remains controversial.

257 ndition tended to have the greatest relative post-stroke recovery.

258 may have important clinical implications for post-stroke recovery.

259 shment of causality between connectivity and post-stroke recovery.

260 l connectivity may also prove informative in post-stroke recovery.

261 t in limiting tissue injury and accelerating post-stroke recovery.

262 een proposed as a possible backup system for post-stroke rehabilitation even for the hand.

263 Post-stroke rehabilitation has also, naturally, focused

264 right or left hemisphere lesions to enhance post-stroke rehabilitation interventions.

265 icipation in society is an important goal of post-stroke rehabilitation.

266 ms that drive perturbation of the microbiota post-stroke remain poorly understood.

267 ould be consistent with their involvement in post-stroke reorganization.

268 ts suggest the involvement of these areas in post-stroke reorganization.

269 glia migration that may have implications in post stroke repair.

270 e and reduced brain atrophy at 3 and 35 days post-stroke, respectively.

271 y ECG monitoring in the 7 days and 12 months post-stroke, respectively.

272 Histological analysis at 3 days post-stroke revealed that only those ischemic animals tr

273 of the primary somatosensory (S1) cortex in post-stroke sensory discrimination and 2) To determine t

274 and 2) To determine the relationship between post-stroke sensory discrimination and structural integr

275 however, the neural structures that support post-stroke sensory function have not been described.

276 icity genes were differentially expressed in post-stroke SI mice.

277 One day post-stroke, slight increases in both ED1(+) and Iba1(+)

278 Due to the significant post-stroke sNfL increase, several months are needed for

279 thy older adults (HOA, n = 9), and subjects' post-stroke (SPS, n = 8participated in a telehealth phys

280 ributed pattern of activation was evident in post-stroke subjects with a positive correlation between

281 ethods for improving social participation in post-stroke survivors, however it is unclear what the mo

282 we performed clinicopathological studies in post-stroke survivors, who had exhibited greater frontal

283 e matter and cognitive impairment in elderly post-stroke survivors.

284 At 4 months post stroke the DVR group showed a higher rate of change

285 At 6 months post stroke, the EuroQol was moderately correlated with

286 he first few months post-stroke, by 6 months post-stroke, the deficit is considered chronic and perma

287 Three days post-stroke, there was marked infiltration and aggregate

288 up had significantly better behavior at 6/10 post-stroke time points as compared to Saline+Saline.

289 jects had a cognitive assessment at 3 months post stroke to exclude dementia, and had an MRI scan (n=

290 successfully predicted behavioural deficits post-stroke to a level comparable to lesion information.

291 We jointly analysed 385 post-stroke trajectories from six separate studies-one o

292 Importantly, post-stroke treatment (3 h after MCAo) was still effecti

293 ifferent anatomical structures in supporting post-stroke upper limb motor recovery and points towards

294 e little data on whether functional recovery post-stroke varies among hospitals.

295 known about the functional properties of the post-stroke visual system in the subacute period, nor do

296 Z image analysis took into account potential post-stroke volume loss.

297 ICP from pre-stroke to 24 h post-stroke was measured, and infarct volumes were calcu

298 phere stroke patients, each more than a year post-stroke when first assessed-testing each patient's s

299 late the deficient perception of step length post-stroke, which may contribute to gait asymmetries im

300 12.4 years, 20 females, 56.81 +/- 63 months post-stroke) with minimal motor and cognitive impairment