ライフサイエンスコーパス: aphasia

1 concepts from sensory inputs (in Wernicke's aphasia).

2 curring with a generalized language deficit (aphasia).

3 identify fundamental domains of post-stroke aphasia.

4 P35 and SERPINA1 with progressive non-fluent aphasia.

5 twork in each variant of primary progressive aphasia.

6 be crucial for speech recovery in poststroke aphasia.

7 tern in semantic variant primary progressive aphasia.

8 nt/agrammatic variant of primary progressive aphasia.

9 y undergo hypertrophy after a stroke causing aphasia.

10 able in individuals with primary progressive aphasia.

11 aphasia compared to those without history of aphasia.

12 aging data from individuals with post-stroke aphasia.

13 rent from the lesion pattern associated with aphasia.

14 in recovery from word production deficits in aphasia.

15 ts with semantic variant primary progressive aphasia.

16 reorganization even in patients with chronic aphasia.

17 pain, auditory hallucinosis, and subcortical aphasia.

18 residual language performance in post-stroke aphasia.

19 to the study of mechanisms of recovery from aphasia.

20 nctions interfere with the rehabilitation of aphasia.

21 itive to cortical dysfunction in post-stroke aphasia.

22 istently led to semantic primary progressive aphasia.

23 theses about how to improve the treatment of aphasia.

24 neuroimaging features of primary progressive aphasia.

25 nd grammar impairment in primary progressive aphasia.

26 y influences speech fluency in patients with aphasia.

27 isolated syndrome of music agraphia without aphasia.

28 ork in logopenic variant primary progressive aphasia.

29 icit in semantic variant primary progressive aphasia.

30 rity of overall cognitive impairment but not aphasia.

31 ts with semantic variant primary progressive aphasia.

32 sia, the two most common kinds of non-fluent aphasia.

33 e, graded variations observed in post-stroke aphasia.

34 guage and cognition variation in post-stroke aphasia.

35 e classification of patients with agrammatic aphasia.

36 ent (n = 39) variants of primary progressive aphasia.

37 h we will refer to as progressive agrammatic aphasia.

38 s in 48 individuals with chronic post-stroke aphasia.

39 le in the abilities of patients with chronic aphasia.

40 ific atrophy patterns in primary progressive aphasia.

41 f the most common impairments in post-stroke aphasia.

42 entrainment for rehabilitation of non-fluent aphasia.

43 ute for Health Research, Tavistock Trust for Aphasia.

44 ent varies among individuals with non-fluent aphasia.

45 ht for logopenic variant primary progressive aphasia.

46 emantic (n = 96) variant primary progressive aphasias.

47 cohort (eg, visual agnosia [5.6%, 3.9-7.2], aphasia [23.0%, 20.0-26.0], and behavioural changes [31.

48 se (45% of cases) and progressive non-fluent aphasia (25% of cases).

49 ts with semantic variant primary progressive aphasia, 25 patients with Alzheimer's disease (as diseas

50 ments, respectively), most frequently due to aphasia (32% of patients).

51 lopathy (57%), headache (42%), tremor (38%), aphasia (35%) and focal weakness (11%).

52 ng visual agnosia (55.1%, 95% CI 45.7-64.6), aphasia (57.9%, 48.6-67.3), and behavioural changes (61.

53 the logopenic variant of primary progressive aphasia, 6 age-matched patients with AD, and 6 control s

54 study used patients with primary progressive aphasia, a clinical dementia syndrome characterized by p

55 the nonfluent variant of primary progressive aphasia, a neurodegenerative disorder with tau accumulat

56 Agrammatic aphasia affects grammatical language production and can

57 of language in healthy participants, chronic aphasia after left rather than right hemisphere lesions,

58 rial, patients aged 70 years or younger with aphasia after stroke lasting for 6 months or more were r

59 d language therapy for chronic (>/=6 months) aphasia after stroke, but large-scale, class 1 randomise

60 people aged 70 years or younger with chronic aphasia after stroke, providing an effective evidence-ba

61 daily-life situations in people with chronic aphasia after stroke.

62 the nonfluent variant of primary progressive aphasia (age, 67.0 +/- 7.4 y; 4 women) and 8 healthy con

63 The patients with progressive agrammatic aphasia also showed different neuroimaging abnormalities

64 s with logopenic variant primary progressive aphasia also showed significant hypersynchrony of delta-

65 tia and semantic variant primary progressive aphasia (also called semantic dementia) are two clinical

66 the semantic variant of primary progressive aphasia, also known as semantic dementia, and Alzheimer'

67 rom the semantic variant primary progressive aphasia analysis was strongly connected with a large-sca

68 Twelve participants with chronic Wernicke's aphasia and 12 control participants performed semantic a

69 s with logopenic variant primary progressive aphasia and 13 patients with posterior cortical atrophy

70 ed from 46 patients with chronic post-stroke aphasia and 20 neurotypical adults.

71 hirty-five patients with primary progressive aphasia and 29 control subjects were recruited.

72 at both semantic variant primary progressive aphasia and Alzheimer's disease are significantly impair

73 Both semantic variant primary progressive aphasia and Alzheimer's disease had atrophy that include

74 nd both semantic variant primary progressive aphasia and behavioural variant frontotemporal dementia

75 nd region of interest analysis in Wernicke's aphasia and control participants found that semantic jud

76 Logopenic variant primary progressive aphasia and developmental dyslexia both manifest with ph

77 ts the distinction of progressive agrammatic aphasia and has implications for the classification of p

78 into the mechanisms of non-fluent speech in aphasia and has potential implications for future resear

79 left temporal lobe for logopenic progressive aphasia and medial and lateral temporal lobe for typical

80 However, recent primary progressive aphasia and normal neurophysiological studies have chall

81 olleague John Hughlings Jackson, his work on aphasia and paralysis was highly regarded by contemporar

82 al phenotypes, such as logopenic progressive aphasia and posterior cortical atrophy.

83 Patients with Wernicke's aphasia and semantic aphasia were distinguished accordin

84 luent/agrammatic variant primary progressive aphasia and semantic variant PPA.

85 Participants with chronic poststroke aphasia and spoken language comprehension impairments co

86 ever, approximately 30-40% sustain permanent aphasia and the factors determining incomplete recovery

87 deficits in human participants with chronic aphasia and the topological distribution of structural b

88 s design to compare patients with Wernicke's aphasia and those with semantic aphasia on Warrington's

89 Both semantic aphasia and Wernicke's aphasia cases showed multimodal s

90 Therefore, patients with semantic aphasia and Wernicke's aphasia have partially distinct i

91 d at age 54 years with logopenic progressive aphasia and, at autopsy, showed both frontotemporal loba

92 y than logopenic variant primary progressive aphasia) and higher-order visual network (lower in poste

93 have speech repetition deficits (conduction aphasia) and studies using covert speech and haemodynami

94 with semantic variant of primary progressive aphasia, and 30 patients with Huntington disease.

95 t and non-fluent variant primary progressive aphasia, and 46 healthy controls) described themselves o

96 with semantic variant of primary progressive aphasia, and 6 of 30 patients (20%) with Huntington dise

97 rophy, logopenic variant primary progressive aphasia, and corticobasal syndrome).

98 D, semantic dementia, progressive non-fluent aphasia, and FTD overlapping with motor neuron disease [

99 ability, developmental delay, short stature, aphasia, and hypotonia in which homozygous non-synonymou

100 drocephalus, severe intellectual disability, aphasia, and motor symptoms.

101 egions of the left hemisphere and expressive aphasia; and (iv) bilateral precentral/left posterior su

102 acted neural networks in primary progressive aphasia are lacking.

103 uch as logopenic variant primary progressive aphasia are more commonly associated with Alzheimer's di

104 f criteria for logopenic primary progressive aphasia are proposed to address these challenges.

105 topsies of patients with primary progressive aphasia are reported.

106 ve (dys)functions in individuals with stroke aphasia are still scarce and the relationship to underly

107 ilesional tissue in recovery from poststroke aphasia are unclear.

108 to the development of standardized clinical aphasia assessment is reassessed through detailed analys

109 d non-verbal modalities; and (ii) Wernicke's aphasia, associated with poor auditory-verbal comprehens

110 eutics; for example, in stroke patients with aphasia attempting to reacquire a vocabulary.SIGNIFICANC

111 applicable language scores from the Western Aphasia Battery (WAB).

112 language assessment with the Revised Western Aphasia Battery and neuroimaging scanning within a fortn

113 ted by clinical judgements using the Western Aphasia Battery speech fluency scale, diadochokinetic ra

114 red with the aphasia quotient of the Western Aphasia Battery-Revised (WAB-AQ).

115 derwent language assessment with the Western Aphasia Battery-Revised and tests of other cognitive dom

116 lative to neurotypical adults, patients with aphasia, both fluent and non-fluent, showed reduction in

117 sion is significantly impaired in Wernicke's aphasia but the capacity to comprehend visually presente

118 n in semantic variant of primary progressive aphasia', by Bertoux et al. (doi:10.1093/brain/awaa313).

119 Individuals with chronic aphasia can improve their spoken word comprehension many

120 Both semantic aphasia and Wernicke's aphasia cases showed multimodal semantic impairment, alt

121 nted with EAS, accounting for 9% of epilepsy-aphasia cases.

122 phasia, including in cases with (i) semantic aphasia, characterized by poor executive control of sema

123 ence comprehension impairments in Wernicke's aphasia come almost exclusively from patients with cereb

124 ased in semantic variant primary progressive aphasia compared to controls in the temporal regions, an

125 usters were greater in stroke survivors with aphasia compared to those without history of aphasia.

126 n in 51 individuals with primary progressive aphasia, composed of all clinical variants and a range o

127 dex were associated with more severe chronic aphasia, controlling for the size of the stroke lesion.

128 cal profiles of individuals with post-stroke aphasia demonstrate considerable variation in the presen

129 Patients with semantic variant aphasia did not overestimate functioning on any domain.

130 the logopenic variant of primary progressive aphasia, differ from amnestic AD in distributions of tau

131 ts with semantic variant primary progressive aphasia discounted delayed rewards more steeply than con

132 r's disease pathology in primary progressive aphasia displayed multiple atypical features.

133 ross-sectional study of 42 participants with aphasia due to unilateral left hemisphere stroke.

134 with stepwise dosing were encephalopathy and aphasia (each 9%) and tremor, speech disorder, dizziness

135 ries of 18 patients with primary progressive aphasia (eight with semantic variant, six with non-fluen

136 tanding of the multidimensionality of stroke aphasia, emphasize the importance of assessing non-verba

137 with non-fluent variant primary progressive aphasia [five female; 67.4 (8.1) years] and 22 healthy c

138 There is growing awareness that aphasia following a stroke can include deficits in other

139 ory impairment exists in primary progressive aphasia for non-linguistic stimuli.

140 12 with semantic variant primary progressive aphasia [four female; 66.9 (7.0) years], nine with non-f

141 system may be a better conceptualization of aphasia from both causes; and (ii) despite the very diff

142 The Wernicke's aphasia group displayed an 'over-activation' in comparis

143 irment, although as expected, the Wernicke's aphasia group showed greater deficits on auditory-verbal

144 icipants with non-fluent primary progressive aphasia had evolved either corticobasal degeneration (n

145 ults demonstrate that progressive agrammatic aphasia has a different clinical disease course and diff

146 t types of pathology, these broad classes of aphasia have considerable features in common.

147 ions in semantic variant primary progressive aphasia have inspired an alternative model featuring the

148 atients with semantic aphasia and Wernicke's aphasia have partially distinct impairment of semantic '

149 esion-based studies of stroke survivors with aphasia have suggested that neocortical regions adjacent

150 superior-/middle-temporal gyri and receptive aphasia; (iii) widespread temporal/frontal lobe regions

151 Non-fluent aphasia implies a relatively straightforward neurologica

152 th syntactic deficits in primary progressive aphasia in a number of structural and functional neuroim

153 Many stroke survivors with aphasia in the acute period experience spontaneous recov

154 The estimated prevalence of aphasia in the UK and the USA is 250 000 and 1 000 000,

155 d to 38 individuals with chronic post-stroke aphasia, in addition to detailed language testing and MR

156 xamined 39 patients with primary progressive aphasia including logopenic variant (n = 14, age = 61 +/

157 Comprehension deficits are common in stroke aphasia, including in cases with (i) semantic aphasia, c

158 ain several challenging phenomena in frontal aphasias, including agrammatism and subjective difficult

159 g with logopenic variant primary progressive aphasia initially thought to be due to Alzheimer disease

160 Aphasia is a heterogeneous syndrome, and the simple clas

161 Stroke aphasia is a multidimensional disorder in which patient

162 Primary progressive aphasia is a neurodegenerative clinical syndrome that pr

163 Primary progressive aphasia is a syndrome characterized by progressive loss

164 Stroke-induced aphasia is associated with adverse effects on quality of

165 Wernicke's aphasia is characterized by severe word and sentence com

166 to the phenomenology of primary progressive aphasia is not established.

167 INTRODUCTION: Aphasia is one of the most disabling sequelae after stro

168 The rehabilitation of non-fluent speech in aphasia is particularly challenging as patients are rare

169 uage processing revealed that non-fluency in aphasia is primarily predicted by damage to the anterior

170 The syndrome of Wernicke's aphasia is thus likely to reflect damage not only to the

171 Language impairment, or aphasia, is a disabling symptom that affects at least on

172 cits), logopenic variant primary progressive aphasia (language deficits), and posterior cortical atro

173 s with logopenic variant primary progressive aphasia ('language variant of Alzheimer's disease', n =

174 cobasal syndrome, and progressive non-fluent aphasia) localize to different disease-specific brain ne

175 , seven patients with logopenic/phonological aphasia (LPA) and 18 age matched healthy participants co

176 ith logopenic variant of primary progressive aphasia (lvPPA) have beta-amyloid (Abeta) deposition on

177 ophy (PCA), 12 logopenic primary progressive aphasia (lvPPA), 20 behavioural variant FTD (bvFTD), 7 n

178 ophy in semantic variant primary progressive aphasia may follow connectional pathways within a large-

179 Post-stroke aphasia might improve over many years with speech and la

180 luding logopenic-variant primary progressive aphasia (n = 25), posterior cortical atrophy (n = 20), a

181 vioural variant, n = 14; primary progressive aphasias, n = 21) and 27 control subjects.

182 nt/agrammatic variant of primary progressive aphasia (naPPA), but well-controlled clinical measures o

183 impact of language impairment after stroke (aphasia), neuroplasticity research is garnering consider

184 ith nonfluent/agrammatic primary progressive aphasia (nfvPPA) and progressive supranuclear palsy (PSP

185 , (4) non-fluent variant primary progressive aphasia (nfvPPA) or (5) early onset Alzheimer's disease

186 Wernicke's aphasia occurs after a stroke to classical language comp

187 mance of 31 participants with chronic stroke aphasia on a large, detailed battery of behavioural asse

188 h Wernicke's aphasia and those with semantic aphasia on Warrington's paradigmatic assessment of seman

189 addition, patients with CBD may present with aphasia or behavioural change.

190 unlikely whereas the presence of a logopenic aphasia or word comprehension impairment made FTLD-tau u

191 ight hemisphere independently contributes to aphasia outcomes after chronic left hemisphere stroke.

192 al functioning, and patients with non-fluent aphasia overestimated emotional and interpersonal functi

193 al. disregard attested knowledge concerning aphasia, Parkinson disease, cortical-to-striatal circuit

194 community structure had significantly worse aphasia, particularly when key temporal lobe regions wer

195 tia and semantic variant primary progressive aphasia patients alone confirmed this result.

196 solution T1-weighted images were obtained in aphasia patients and 30 demographically matched healthy

197 The progressive agrammatic aphasia patients performed abnormally on tests of langua

198 extent or not at all in primary progressive aphasia patients whose syntax was relatively impaired.

199 sm, the patients with progressive agrammatic aphasia performed better on tests of motor speech and pa

200 l dementia [bvFTD], 18 progressive nonfluent aphasia [PNFA], 16 semantic dementia [SD]), 22 progressi

201 P35 and SERPINA1 with progressive non-fluent aphasia point towards a potential role of the stress-sig

202 8 years or older and had been diagnosed with aphasia post-stroke at least 4 months before randomisati

203 ry to conversation for patients with chronic aphasia post-stroke.

204 mporal dementia (bvFTD), primary progressive aphasia (PPA) and corticobasal syndrome (CBS).

205 The dementia syndrome of primary progressive aphasia (PPA) can be caused by 1 of several neuropatholo

206 Primary progressive aphasia (PPA) is a progressive language disorder associa

207 ive brain stimulation in primary progressive aphasia (PPA) is a promising approach.

208 Primary progressive aphasia (PPA) refers to a disorder of declining language

209 cohort of patients with primary progressive aphasia (PPA) variants defined by current diagnostic cla

210 and semantic variants of primary progressive aphasia (PPA), progressive supranuclear palsy and cortic

211 In primary progressive aphasia (PPA), speech and language difficulties are caus

212 ons and often damaged in primary progressive aphasia (PPA).

213 pattern of deposition in primary progressive aphasia (PPA).

214 ) and neurodegeneration (primary progressive aphasia, PPA) have overlapping symptomatology, nomenclat

215 ge impairments caused by stroke (post-stroke aphasia, PSA) and neurodegeneration (primary progressive

216 es and aphasia severity as measured with the aphasia quotient of the Western Aphasia Battery-Revised

217 Eight participants with chronic aphasia received intensive speech therapy for 3 weeks, w

218 Treatment guidelines for aphasia recommend intensive speech and language therapy

219 The role of the right hemisphere in aphasia recovery after left hemisphere damage remains un

220 re language network seems to be important in aphasia recovery after left hemispheric stroke.

221 omprehension deficits in primary progressive aphasia reflect not only structural and functional chang

222 nt/agrammatic variant of primary progressive aphasia relates to the strength of connectivity in pre-d

223 age comprehension therapies for persons with aphasia remains equivocal.

224 had grade 3 neurologic events, one of which (aphasia) required temporary treatment interruption.

225 in both semantic variant primary progressive aphasia samples.

226 ht executive-control networks, the logopenic aphasia seed connectivity map and the language network,

227 ion of words and pictures, while in semantic aphasia, semantic access was initially good but declined

228 sities, connectome fibre-length measures and aphasia severity as measured with the aphasia quotient o

229 gression was conducted with the longitudinal aphasia severity as the dependent variable.

230 e only independent predictor of longitudinal aphasia severity in the left hemisphere [beta = -0.630,

231 cular white matter hyperintensities on worse aphasia severity mediated in parallel by fewer long-rang

232 vessel brain disease seems to affect chronic aphasia severity through a change of the proportions of

233 clined faster over time, on tests of general aphasia severity, agrammatism, and naming.

234 s could be important determinants of chronic aphasia severity.

235 lowing in these patients was correlated with aphasia severity.

236 , P = 0.020] were predictors of longitudinal aphasia severity.

237 s relationship with brain health and chronic aphasia severity.

238 ing white matter hyperintensities to chronic aphasia severity.

239 ter hyperintensities and chronic post-stroke aphasia severity.

240 f stimulus repetition: cases with Wernicke's aphasia showed initial improvement with repetition of wo

241 ic encephalopathy, often within the epilepsy-aphasia spectrum.

242 luent/agrammatic variant primary progressive aphasia spreads over time from a syndrome-specific epice

243 n age and gender to each primary progressive aphasia subgroup (n = 20, age = 65 +/- 5 years).

244 n for one or more of the primary progressive aphasia subtypes.

245 Individual features of the aphasia, such as agrammatism and comprehension impairmen

246 n areas typically associated with non-fluent aphasia, such as the superior longitudinal fasciculus, p

247 In eleven chronic aphasia survivors, we devised a method to localize peril

248 The semantic variant of primary progressive aphasia (svPPA) is a clinical syndrome characterized by

249 The semantic variant of primary progressive aphasia (svPPA) is typically associated with frontotempo

250 (3) semantic variant of primary progressive aphasia (svPPA), (4) non-fluent variant primary progress

251 the semantic variant of primary progressive aphasia (svPPA), is strongly associated with TAR-DNA bin

252 iant of semantic variant primary progressive aphasia (svPPA).

253 with semantic variant of primary progressive aphasia (svPPA).

254 TD) and semantic variant primary progressive aphasia (svPPA).

255 receptor (NMDAR) gene GRIN2A cause epilepsy-aphasia syndrome (EAS), a spectrum of epileptic, cogniti

256 Epilepsy-aphasia syndromes (EAS) are a group of rare, severe epil

257 ts disorders while complementing traditional aphasia syndromes that follow stroke.

258 onal synchronizations in primary progressive aphasia syndromes.

259 ech comprehension score on the comprehensive aphasia test.

260 andardised co-primary outcome (Comprehensive Aphasia Test: Spoken Words and Sentences).

261 and semantic variant of primary progressive aphasia than in those with AD and is more likely to be a

262 al atrophy and 22 with logopenic progressive aphasia) that had undergone baseline and 1-year follow-u

263 Within semantic variant primary progressive aphasia the right-handed and non-right-handed cohorts ap

264 te nucleus in non-fluent primary progressive aphasia (the corticobasal degeneration/progressive supra

265 rer picture of cortical damage in non-fluent aphasia, the current study examined brain damage that ne

266 standing of lesion-symptom mapping in stroke aphasia, the same approach could be used to clarify brai

267 culus adjudicated between Broca's and global aphasia, the two most common kinds of non-fluent aphasia

268 pand the differential of primary progressive aphasia to include prion disease.

269 t of 11 patients with progressive agrammatic aphasia to provide a complete picture of this syndrome.

270 encephalopathy range from mild confusion and aphasia to somnolence, obtundation, and in some cases se

271 hnique that enables patients with non-fluent aphasia to speak fluently.

272 ance in semantic variant primary progressive aphasia to ventral and medial portions of the left tempo

273 select optimal paradigms for individualised aphasia treatment are needed.

274 suppression of specific cortices can improve aphasia treatment outcomes.

275 rsonalized variable for clinical staging and aphasia treatment planning.

276 attention as means for eventually improving aphasia treatments and how they are delivered.

277 tructural neuroimaging studies indicate that aphasia treatments can recruit both residual and new neu

278 ty-two left hemisphere stroke survivors with aphasia underwent language assessment with the Western A

279 ophy in semantic variant primary progressive aphasia using cortical thickness analysis in two indepen

280 al power changes in each primary progressive aphasia variant, compared to age-matched controls.

281 cant differences between primary progressive aphasia variants themselves.

282 neuronal dysfunction in primary progressive aphasia variants.

283 ifficulty resolving competition (in semantic aphasia) versus initial activation of concepts from sens

284 ic processing of written words in Wernicke's aphasia was additionally supported by recruitment of the

285 nt/agrammatic variant of primary progressive aphasia was derived in a group of 10 mildly affected pat

286 hologies associated with primary progressive aphasia was the asymmetric prominence of atrophy, neuron

287 ontotemporal dementia or primary progressive aphasia, we included 70 subjects with a negative amyloid

288 Amusia and aphasia were behaviorally assessed at acute and 3 month

289 atients with Wernicke's aphasia and semantic aphasia were distinguished according to lesion location

290 misphere stroke survivors with no history of aphasia were identified.

291 tia and semantic variant primary progressive aphasia were most likely to exhibit disgusting behaviors

292 ts in the context of his 'Friday Lessons' on aphasia, which took place at the Salpetriere Hospital in

293 ssed in 72 patients with primary progressive aphasia who collectively displayed a wide spectrum of co

294 association of logopenic primary progressive aphasia with Alzheimer's disease pathology was much more

295 ociated semantic variant primary progressive aphasia with distributed cortical atrophy that is most p

296 ols and in patients with primary progressive aphasia with relatively spared syntax, but they were mod

297 m movements at the age of 11 and a transient aphasia with right-sided weakness at the age of 30.

298 nt interventions in 20 patients with chronic aphasia with speech comprehension impairment following l

299 se and logopenic variant primary progressive aphasia), with a trend towards lower (18)F-labelled fluo

300 nd picture semantic processing in Wernicke's aphasia, with the wider aim of examining how the semanti