ライフサイエンスコーパス: aphasia

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

2 viduals with poststroke language impairment (aphasia).

3 in recovery from word production deficits in aphasia.

4 ts with semantic variant primary progressive aphasia.

5 P35 and SERPINA1 with progressive non-fluent aphasia.

6 reorganization even in patients with chronic aphasia.

7 pain, auditory hallucinosis, and subcortical aphasia.

8 residual language performance in post-stroke aphasia.

9 to the study of mechanisms of recovery from aphasia.

10 nctions interfere with the rehabilitation of aphasia.

11 istently led to semantic primary progressive aphasia.

12 theses about how to improve the treatment of aphasia.

13 neuroimaging features of primary progressive aphasia.

14 nd grammar impairment in primary progressive aphasia.

15 y influences speech fluency in patients with aphasia.

16 isolated syndrome of music agraphia without aphasia.

17 ork in logopenic variant primary progressive aphasia.

18 icit in semantic variant primary progressive aphasia.

19 rity of overall cognitive impairment but not aphasia.

20 ts with semantic variant primary progressive aphasia.

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

22 esion location that gives rise to non-fluent aphasia.

23 mentia), and none with progressive nonfluent aphasia.

24 ons in logopenic variant primary progressive aphasia.

25 twork in each variant of primary progressive aphasia.

26 ourth variant of 'mixed' primary progressive aphasia.

27 s syndrome distinct from primary progressive aphasia.

28 eatures and three had progressive non-fluent aphasia.

29 rom 106 individuals with diverse profiles of aphasia.

30 a treatment for speech production in Broca's aphasia.

31 e, none met criteria for primary progressive aphasia.

32 occur in the variants of primary progressive aphasia.

33 diagnostic evaluation of primary progressive aphasia.

34 syndrome from other variants of progressive aphasia.

35 be crucial for speech recovery in poststroke aphasia.

36 tern in semantic variant primary progressive aphasia.

37 nt/agrammatic variant of primary progressive aphasia.

38 y undergo hypertrophy after a stroke causing aphasia.

39 ht for logopenic variant primary progressive aphasia.

40 able in individuals with primary progressive aphasia.

41 aphasia compared to those without history of aphasia.

42 aging data from individuals with post-stroke aphasia.

43 rent from the lesion pattern associated with aphasia.

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

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

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

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

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

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

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

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

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

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

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

55 les for 50 patients with primary progressive aphasia, along with neurodegenerative and normal control

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

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

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

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

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

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

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

63 ts with semantic variant primary progressive aphasia and 57 patients with Alzheimer's disease to judg

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

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

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

67 are commonly seen in persisting post-stroke aphasia and are thought to signal impairment in retrieva

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

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

70 cognitive rehabilitation and strategies for aphasia and dysarthria is scarce.

71 /or programming that is distinguishable from aphasia and dysarthria.

72 rbal fluency deficits in primary progressive aphasia and further confirm the role of the uncinate fas

73 d with C9orf72 expansion carriers, nonfluent aphasia and limb apraxia were significantly more common

74 n potential sources of speech dysfunction in aphasia and neuropsychiatric disorders, identifying anat

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

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

77 modality specific in progressive non-fluent aphasia and part of a more severe generic semantic defic

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

79 sing occurred in both progressive non-fluent aphasia and semantic dementia, and deficits of semantic

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

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

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

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

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

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

86 s designed to be inclusive for patients with aphasia and/or spatial neglect.

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

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

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

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

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

92 encephalopathy, focal neurological findings, aphasia, and abnormal electroencephalographic findings.

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

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

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

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

97 acted neural networks in primary progressive aphasia are lacking.

98 arly and mild disease in primary progressive aphasia are poorly understood.

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

100 topsies of patients with primary progressive aphasia are reported.

101 the logopenic variant of primary progressive aphasia as a distinct clinical entity and to outline rec

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

103 Characterising and quantifying the aphasia associated with PCA is important for clarifying

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

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

106 aving apraxia of speech without any signs of aphasia based on a comprehensive battery of language tes

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

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

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

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

111 asymmetry for tangles in primary progressive aphasia but not in the amnestic Alzheimer-type dementia

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

113 ction in each variant of primary progressive aphasia, by quantifying speech output along a number of

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

115 rsal and that individual primary progressive aphasia cases with Alzheimer pathology exist where distr

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

117 e-treatment outcome in patients with chronic aphasia caused by stroke.

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

119 neurological disorders and his research into aphasia, Charcot's ideas about how the brain processes m

120 emory and Aging Center's primary progressive aphasia cohort (n = 198) for history of language-related

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

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

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

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

125 s were more common in progressive non-fluent aphasia, deficits of apperceptive processing occurred in

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

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

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

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

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

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

132 torhinal tangle ratio in primary progressive aphasia establishes clinical concordance of Alzheimer pa

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

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

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

136 ts with semantic variant primary progressive aphasia had a significantly more prominent deficit for n

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

138 l learning disability in primary progressive aphasia has been reported.

139 speech of patients with primary progressive aphasia has often been dichotomized simply as 'fluent' o

140 definitive diagnosis of primary progressive aphasia has promoted diagnostic specificity, but has als

141 epetition, the primary symptom of conduction aphasia, has been associated with involvement of the lef

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

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

144 logopenic and nonfluent primary progressive aphasia have some deficits recognizing emotional prosody

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

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

147 Non-fluent aphasia implies a relatively straightforward neurologica

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

149 tionships in subtypes of primary progressive aphasia in hopes of utilizing language phenotype as a ma

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

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

152 In 1898 his Treatise on Aphasia included a list of 34 questions that were to be

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

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

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

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

157 Primary progressive aphasia is a clinical syndrome defined by progressive de

158 Primary progressive aphasia is a clinical syndrome that encompasses three ma

159 Aphasia is a heterogeneous syndrome, and the simple clas

160 Stroke aphasia is a multidimensional disorder in which patient

161 Primary progressive aphasia is a neurodegenerative clinical syndrome that pr

162 Primary progressive aphasia is a neurodegenerative syndrome characterized by

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 A distinguishing feature of Broca's aphasia is non-fluent halting speech typically involving

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

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

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

170 inds in semantic variant primary progressive aphasia is related in part to disease in visual associat

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

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

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

176 the logopenic variant of primary progressive aphasia (lvPPA) performed a recognition task on words wi

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 4 clinical syndromes: progressive nonfluent aphasia (n = 5), behavioral variant frontotemporal demen

180 dementia and non-fluent primary progressive aphasia (n = 9 each) were contrasted with control subjec

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

182 nt/agrammatic variant of primary progressive aphasia (naPPA) is a young-onset neurodegenerative disor

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

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 with non-fluent variant primary progressive aphasia (nfvPPA)) and 17 healthy control subjects, using

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

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

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

190 of patients with either primary progressive aphasia or a typical amnestic dementia.

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

192 Cases with predominant primary progressive aphasia or extra-pyramidal syndromes were excluded.

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

194 s where it has typically been subsumed under aphasia, or it occurs in the context of more widespread

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

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

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

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

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

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

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

202 study, 17 patients with chronic post-stroke aphasia performed inner speech tasks (rhyme and homophon

203 tric pathology cause the primary progressive aphasia phenotype, characterized by relative preservatio

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

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

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

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

208 Primary progressive aphasia (PPA) is a clinical dementia syndrome characteri

209 Primary progressive aphasia (PPA) is a clinical syndrome characterised by pr

210 Primary progressive aphasia (PPA) is a neurodegenerative syndrome that cause

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

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

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

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

215 the nonfluent variant of primary progressive aphasia (PPA), degeneration of the posterior IFC is asso

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

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

218 inment improves speech production in Broca's aphasia providing a potential therapeutic method for a d

219 This report is based on 25 patients with aphasia quotients >85%, 13 of whom were within 2 years o

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

221 Treatment guidelines for aphasia recommend intensive speech and language therapy

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

223 f homologous right hemisphere areas supports aphasia recovery after left hemisphere damage.

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

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

226 or the logopenic variant primary progressive aphasia region of interest, and the higher visual networ

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

228 ated with improved naming ability in chronic aphasia rely on preservation and recruitment of eloquent

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

230 asic speech; when they are undamaged, fluent aphasias result.

231 ould not have been surmised in patients with aphasia resulting from cerebrovascular lesions.

232 in both semantic variant primary progressive aphasia samples.

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

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

235 ntotemporal dementia, progressive non-fluent aphasia, semantic dementia or mixture of these syndromes

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

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

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

239 esting, but the two groups did not differ in aphasia severity.

240 s could be important determinants of chronic aphasia severity.

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

242 hydrocephalus and MASA (Mental retardation, Aphasia, Shuffling gait, Adducted thumbs) syndrome.

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

244 ble clinical correlates including conduction aphasia, stuttering, and aspects of schizophrenia.

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

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

247 tracts in the different primary progressive aphasia subtypes.

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

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 ht with semantic variant primary progressive aphasia (svPPA), five with non-fluent variant primary pr

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

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

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

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

256 onal synchronizations in primary progressive aphasia syndromes.

257 ech comprehension score on the comprehensive aphasia test.

258 ition among 45 stroke patients who underwent aphasia testing and MRI examination.

259 can be seen in the approach to standardized aphasia testing developed in the latter 20th century thr

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

261 variant is a distinct subtype of progressive aphasia that may hold value as a predictor of underlying

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

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

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

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

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

267 ech entrainment allows patients with Broca's aphasia to double their speech output compared with spon

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

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

270 rsonalized variable for clinical staging and aphasia treatment planning.

271 ltiple MRI sessions before and after 30 h of aphasia treatment targeting anomia, an impairment in the

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

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

274 eficits in patients with primary progressive aphasia, using multimodal neuroimaging and neurolinguist

275 with left hemisphere damage and concomitant aphasia usually have difficulty repeating others' speech

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

277 Each of the primary progressive aphasia variants showed different patterns of diffusion

278 cant differences between primary progressive aphasia variants themselves.

279 neuronal dysfunction in primary progressive aphasia variants.

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

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

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

283 ject with a diagnosis of primary progressive aphasia was identified with this mutation.

284 Progressive non-fluent aphasia was most commonly associated with tau pathology.

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

286 , with one exception, progressive non-fluent aphasia were associated with transactive response DNA bi

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

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

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

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

291 In Experiment 1, 13 patients with Broca's aphasia were tested in three conditions: (i) speech entr

292 the semantic subtype of primary progressive aphasia, which is associated with marked temporopolar at

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

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

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

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

297 viourally, patients with primary progressive aphasia with non-semantic subtypes were severely impaire

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

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

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

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

302 atypical distribution in primary progressive aphasia yielded inconclusive results.