ライフサイエンスコーパス: left hemisphere

1 ly with presentation to the right hemifield (left hemisphere).

2 here), and fast profiles (all but one in the left hemisphere).

3 onses in temporal-perisylvian areas of their left hemisphere.

4 ls in the region responsive to words, in the left hemisphere.

5 en Broca's and Wernicke's territories in the left hemisphere.

6 as lateral temporal-parietal regions in the left hemisphere.

7 face and tongue are greatly expanded in the left hemisphere.

8 ctural and resting state connectivity in the left hemisphere.

9 se to the Broca's or Wernicke's areas of the left hemisphere.

10 ponding locations in the structurally intact left hemisphere.

11 hey are also specifically lateralized to the left hemisphere.

12 in the right hemisphere and semantics in the left hemisphere.

13 on and recruitment of eloquent cortex in the left hemisphere.

14 ented on the right producing activity in the left hemisphere.

15 sual analysis, which performed better in the left hemisphere.

16 of which were unilaterally activated in the left hemisphere.

17 nd revealed TOJ activation in the TPJ of the left hemisphere.

18 citation of neural pathways in the undamaged left hemisphere.

19 icits observed after posterior damage to the left hemisphere.

20 Activations were more extensive in the left hemisphere.

21 mporal features (20-50 Hz) lateralize to the left hemisphere.

22 ile following the envelope compared with the left hemisphere.

23 reflecting recruitment of the nonspecialized left hemisphere.

24 differs from that with a functionally normal left hemisphere.

25 ctivated in the right hemisphere than in the left hemisphere.

26 t majority of behavioral effects seen on the left hemisphere.

27 cingulum and uncinate--predominantly in the left hemisphere.

28 tric gene expression assigns language to the left hemisphere.

29 gions of the fronto-thalamic circuits in the left hemisphere.

30 nal connectivity of these regions within the left hemisphere.

31 terior parietal cortex, predominantly in the left hemisphere.

32 rain activation is mostly lateralised to the left hemisphere.

33 eserved contralateral representations in the left hemisphere.

34 illions of cells distributed over the entire left hemisphere.

35 n learning, with a transient bias toward the left hemisphere.

36 d or enhanced contralateral dominance in the left hemisphere.

37 ed to be computed in the dominant, typically left hemisphere.

38 4-year follow-up period in the right but not left hemisphere.

39 cerebral commissure connecting the right and left hemispheres.

40 ditory cortical activation in both right and left hemispheres.

41 anopia, with no difference between right and left hemispheres.

42 oteinopathy in the language-dominant (mostly left) hemisphere.

43 irectly introduced to the language-dominant (left) hemisphere.

44 ferential permeability between the right and left hemispheres; (2) altered social behavior with incre

45 eir breadth of semantic activation, with the left hemisphere activating a narrow, focused semantic fi

46 , stronger lateralization resulted from more left hemisphere activation in both regions as well as re

47 In contrast to strongly lateralized left hemisphere activations for language in neurotypical

48 n contrast, in the later stages after stroke left hemisphere activations predict chronic aphasia; spe

49 Subjects with BDD showed greater left hemisphere activity relative to controls, particula

50 l fusion elicited activity biased toward the left hemisphere, although failed cross-modal binding rec

51 , usually consistent with a reduction in the left hemisphere and a relative increase in the right hem

52 nates of right NAc pcore and pshell onto the left hemisphere and examined structural and resting stat

53 espread temporal/frontal lobe regions of the left hemisphere and expressive aphasia; and (iv) bilater

54 in December or May/June, lateralized to the left hemisphere and specific to behaviorally relevant st

55 al, middle temporal, and angular gyri of the left hemisphere and the lingual and inferior temporal gy

56 d to identify critical language areas in the left hemisphere and then to quantify each stroke survivo

57 ry inputs (the right visual hemifield in the left hemisphere and vice versa) is a fundamental feature

58 ft hemispheres, hippocampus in the right and left hemispheres and cerebellum.

59 he same linguistic functions as those in the left-hemisphere and only indirectly contribute to preser

60 e effect of lesion location (in the affected left hemisphere) and grey matter density (in the unaffec

61 insula, and extending into occipital cortex (left hemisphere) and orbitofrontal cortex (right hemisph

62 cortex (9 out of 10 Brodmann's areas in the left hemisphere) and temporal lobe (10 out of 11 Brodman

63 (three tasks selected to probe the right or left hemisphere), and (11)C-flumazenil positron emission

64 er parieto-frontal network in the right than left hemisphere, and a significant correlation between t

65 ly, Broca's area is most often larger in the left hemisphere, and functional imaging studies in human

66 The P1 and N1 latencies were shorter in the left hemisphere, and the N1 and P2 amplitudes were large

67 s of interhemispheric inhibition, we applied left hemisphere anodal-excitatory and right hemisphere c

68 lation between attentional control and FA in left hemisphere anterior corona radiata, as well as the

69 tentional control and FA within a ROI in the left hemisphere anterior corona radiata.

70 articipants showed greater activation in the left hemisphere anterior extent of MT/V5 when motion wor

71 In addition, we found over the left hemisphere, anterior to primary auditory cortex, a

72 The integrity of the left hemisphere appears predictive of a better clinical

73 1 subjects with focal hemisphere lesions (15 left hemisphere) as well as 16 normal controls on a batt

74 There was a left-hemisphere association of motor ability in the cont

75 Paired-pulse TMS was delivered to the left hemisphere at the following interstimulus intervals

76 hree characteristics: greater atrophy of the left hemisphere; atrophy of anterior components of the p

77 In the left hemisphere, attending to the stimulus also resulted

78 peech has long been considered the domain of left-hemisphere auditory areas.

79 es by rate-specialized neurons in right- and left-hemisphere auditory cortex.

80 ctor of longitudinal aphasia severity in the left hemisphere [beta = -0.630, t(-3.129), P = 0.011].

81 lly specific relationships, primarily in the left hemisphere, between atrophy and impairments in lang

82 Individuals suffering from posterior left hemisphere brain injury often exhibit temporal proc

83 reorganize to the right-hemisphere following left-hemisphere brain damage.

84 case of the high grade glioma (HGG) only the left hemisphere Broca's area was activated (LI=1).

85 controls, syntactic processing co-activated left hemisphere Brodmann areas 45/47 and posterior middl

86 real-life narrative is not localized to the left hemisphere but recruits an extensive bilateral netw

87 network and language-related regions in the left hemisphere but to attention networks in the right h

88 this specific error type in 45 patients with left hemisphere chronic stroke.

89 Dendritic length measurements in the left hemisphere confirm that males have greater overall

90 he control sample demonstrating rapid within-left hemisphere connectivity increases and the traumatic

91 Here, we show that mPFC neurons in the left hemisphere control stress effects on social behavio

92 eached levels of smoothness (associated with left hemisphere control), acceleration time (associated

93 sal premotor cortex (PMd) of the nondominant left hemisphere correlated with the left-to-right shift

94 and found the amount of FOXP2 protein in the left hemisphere cortex of 4-year-old boys was significan

95 f different, but overlapping, regions of the left hemisphere cortex, such that the distribution of ti

96 Patients with left hemisphere damage and concomitant aphasia usually h

97 r integrity and performance in patients with left hemisphere damage and healthy participants to ask w

98 in differentiating between individuals with left hemisphere damage and right hemisphere damage where

99 amage produce different effects on movement: Left hemisphere damage produces deficits in specifying f

100 e right hemisphere in aphasia recovery after left hemisphere damage remains unclear.

101 ts indicated a double dissociation; although left hemisphere damage was associated with greater error

102 the right hemisphere has been observed after left hemisphere damage.

103 sphere areas supports aphasia recovery after left hemisphere damage.

104 l neglect syndrome), but only for right (not left) hemisphere damage.

105 However, patients with right, but not left, hemisphere damage showed significantly larger erro

106 onger in patients with right- as compared to left-hemisphere damage and were independent of lesion vo

107 We predicted that left-hemisphere damage would produce deficits in specifi

108 ity and lesion size are properly controlled, left-hemisphere-damaged patients and control participant

109 ues, whereas average volume elsewhere in the left hemisphere deviated from control values by only 8%.

110 In the left hemisphere, differential visual processing occurred

111 sistently suggest that the normal pattern of left hemisphere dominance of language processing is sign

112 e right middle cerebral arteries, indicating left hemisphere dominance.

113 s for auditory recognition and that there is left-hemisphere dominance for processing information der

114 The left-hemisphere dominance for S-R mapping could be relat

115 ns, the approximately 0.5 Hz coupling became left-hemisphere dominant, compared with bilateral coupli

116 raphy imaging shows a clinically concordant, left-hemisphere-dominant pattern of deposition in primar

117 maging showed that microstructural damage to left hemisphere dorsal tracts--the superior longitudinal

118 identify a structural brain marker-volume of left hemisphere dorsolateral prefrontal cortex-associate

119 ith right-side onset of motor symptoms (RPD, left hemisphere dysfunction) would be impaired at local

120 ght-hemisphere dysfunction; RPD, predominant left-hemisphere dysfunction) would display distinct patt

121 a common network strongly lateralized to the left hemisphere especially during planning but also acti

122 erior temporal atrophy, predominantly in the left hemisphere, especially along the superior temporal

123 The left hemisphere exhibited load-dependent activity only f

124 ocampal and fusiform gyri, and predominantly left hemisphere extra-temporal activations within the in

125 nts with schizophrenia by a reduction in the left hemisphere (F = 7.7, df 1,32, P < 0.01).

126 span (right hemisphere: F = 7.69, P < 0.001; left hemisphere: F = 8.69, P < 0.001).

127 zure onset with temporal lateralization, and left hemisphere focus with a unilateral right pattern.

128 and must subsequently be transferred to the left hemisphere for language processing than when it is

129 for different aspects of motor control: the left hemisphere for predicting and accounting for limb d

130 misphere, affording it an advantage over the left hemisphere for the activation of distantly related

131 200 ms, ISI and this difference was over the left-hemisphere for linguistic probes and over the right

132 may prevent fronto-parietal networks in the left hemisphere from resolving the activity imbalance wi

133 Recovery of left hemisphere frontoparietal metabolic activity was fu

134 rrelated with chunk concatenation, whereas a left-hemisphere frontoparietal network was correlated wi

135 tegrated from signs using the same classical left hemisphere frontotemporal network used for speech i

136 is is a failure of segregation of right from left hemisphere functions.

137 c problems have abnormal volume of posterior left hemisphere grey matter.

138 etry was attributable to a right slower than left hemisphere growth rate mapped in COS patients (P =

139 responses, suggesting that most ACFs in the left hemisphere had greater resilience against reduced c

140 spitalization for schizophrenia, MMN indexed left hemisphere Heschl gyrus gray matter volume, consist

141 Only schizophrenia evinced longitudinal left hemisphere Heschl gyrus reduction (P=.003), highly

142 ispheres, the basal ganglia in the right and left hemispheres, hippocampus in the right and left hemi

143 ht-hemisphere tangle density despite greater left-hemisphere hypoperfusion and atrophy during life.

144 sities in another and frontal atrophy of the left hemisphere in a third patient.

145 indings challenge consensus that because the left hemisphere in neglect is pathologically over-excite

146 ally depends on posterior brain areas of the left hemisphere in proficient adult readers.

147 This establishes the unique role of the left hemisphere in syntax, a core component in human lan

148 n important role for anterior regions of the left hemisphere in the selection of semantic information

149 significant difference between the right and left hemispheres in the overall size of the dorsolateral

150 Broca's area was present- in 2 cases in the left hemisphere, in 1 case in the right hemisphere and i

151 p, particularly along the mesial wall of the left hemisphere, in the same region where we previously

152 ht temporal cortex, (2) increased HFA in the left hemisphere including the medial temporal lobe (MTL)

153 es of human brain functions in the right and left hemispheres, including sensory, motor, and language

154 isphere, and the cuneus and precuneus in the left hemisphere, independent of familial risk.

155 athways to all calculated PFC regions in the left hemisphere, indicating stronger pathways for person

156 ession abilities associated with blurring in left hemisphere inferior frontal cortex and temporal pol

157 that better language outcome following early left hemisphere injury relies on the contribution of the

158 ch is typically more severe after right than left hemisphere injury, includes deficits of spatial att

159 This suggests that, following left hemisphere injury, language-related processing in t

160 ntral tegmental areas and nucleus accumbens, left-hemisphere insula, orbitofrontal cortex, and ventro

161 Lateralization of language to the left hemisphere is considered a key aspect of human brai

162 n contrast to adults and older children, the left hemisphere is larger than the right hemisphere, and

163 characteristics support a model in which the left hemisphere is more sensitive to temporal and the ri

164 ory, which predicts that the right-eye (i.e. left-hemisphere) is used to categorize stimuli while the

165 We evaluated 331 patients with left hemisphere ischemic stroke with various spelling te

166 o controls before training comprised damaged left hemisphere language areas, right precentral and sup

167 language homologues compensate for damage in left hemisphere language areas, the current prevailing t

168 epsy (n = 21, 5-12 years, nine females) with left hemisphere language dominance.

169 iform network (resulting in agnosia) and the left hemisphere language network (resulting in profound

170 s characterised by dysfunction of the normal left hemisphere language network and also implicates abn

171 yndrome that causes a gradual atrophy of the left hemisphere language network, leading to impairments

172 tional MR hemisphere activation and definite left-hemisphere language dominance.

173 tional MR hemisphere activation and definite left-hemisphere language dominance.

174 tional MR hemisphere activation and definite left-hemisphere language dominance.

175 These findings suggest that left-hemisphere language processing emerges from early b

176 s associated with activation of a network of left-hemisphere language regions, such as the angular gy

177 Moreover, the left hemisphere lateralization of this operation remains

178 Asymmetry in the form of left-hemisphere lateralization is a striking characteris

179 Finally, we show that the more left hemisphere-lateralized the pedunculopontine nucleus

180 MRI study, we assessed the hypothesis that a left-hemisphere-lateralized system including the inferio

181 ontribute to language function after a focal left hemisphere lesion.

182 Both right and left hemisphere lesioned patients were significantly imp

183 he differential deficits induced by right or left hemisphere lesions to enhance post-stroke rehabilit

184 Thirty-eight stroke patients (16 with left-hemisphere lesions) underwent MRI anatomical brain

185 ioral data in 21 human patients with chronic left hemisphere (LH) lesions and a range of language imp

186 ablished that in human speech perception the left hemisphere (LH) of the brain is specialized for pro

187 of the unambiguous conditions; however, the left hemisphere (LH) showed less facilitation for the we

188 onal targets across the visual field; in the left hemisphere (LH), IPS0-2 codes primarily contralater

189 In adults, color CP is lateralized to the left hemisphere (LH), whereas in infants, it is laterali

190 ior temporal white matter connections of the left hemisphere likely involved in semantic and lexical

191 rior-posterior topography of P3 amplitude at left hemisphere, midline, and right hemisphere scalp loc

192 ion with perceiving actions in videos, while left-hemisphere MNS showed a supramodal association with

193 at asymmetric NPTN expression may render the left hemisphere more sensitive to the effects of NPTN mu

194 f 1.53 x 10(5) neurons/mm(3) (greater in the left hemisphere), more glia (72% of all cells) than neur

195 features of human hand movements within the left-hemisphere motor network.

196 Largely left-hemisphere MZS showed a supramodal association with

197 Greater post-stroke left hemisphere network fragmentation and higher modular

198 posed to rely on areas outside the classical left-hemisphere network for alphabetic reading.

199 While healthy controls activated a left-hemisphere network of correlated activity including

200 together, and the degree of fragmentation of left hemisphere networks.

201 al regions of the right hemisphere (with the left hemisphere not analyzed given artifacts arising fro

202 th normally developing controls, significant left-hemisphere occipitotemporal deficits in cortical th

203 Compared with controls, left-hemisphere occipitotemporal thickness correlations

204 edial prefrontal cortex of the right but not left hemisphere of CVT-performing animals.

205 r synaptic activity in the right than in the left hemisphere of females, mediating timely neuroendocr

206 , neocortical NFTs were more numerous in the left hemisphere of PPA/AD.

207 that were confined almost exclusively to the left hemisphere of the brain and that involved almost it

208 , language is processed predominantly by the left hemisphere of the brain, but we do not know how or

209 The left hemisphere of the human cerebral cortex is dominant

210 In the left hemispheres of PSCs we found a negative correlation

211 sphere was not correlated with damage in the left-hemisphere or with performance.

212 only a 1.3% per year trend for growth in the left hemisphere (P = 0.066).

213 1755, associating with thinner cortex in the left hemisphere (P=1.12 x 10(-)(7)), particularly in the

214 Second, regions in the left hemisphere (particularly within temporal and subcor

215 As expected, deaf signers engaged left-hemisphere perisylvian language areas during the pe

216 Neural connectivity was reduced in a left-hemisphere pre-language region, and the degree to w

217 under both movement conditions namely in the left hemisphere precentral gyrus (BA 4), the left hemisp

218 e correlation between total PANESS score and left hemisphere primary motor and premotor white matter

219 triking pattern of underconnectivity between left-hemisphere pSTS and distributed nodes of the dopami

220 Lesion-symptom mapping showed that specific left hemisphere regions related to different language ab

221 n these two groups occurred in homologues of left hemisphere regions that sustained task activation.

222 o 15-year-olds) in effective connectivity in left hemisphere regions were examined using dynamic caus

223 g a model language network consisting of six left hemisphere regions, the DCM analysis demonstrated r

224 ho stutter exhibited deactivation over these left hemisphere regions.

225 In two left-hemisphere regions (pars opercularis, planum polare

226 re activation in homologous regions to those left-hemisphere regions typically involved in the young.

227 symmetry in the brain's coding of space: the left hemisphere represents the right side, whereas the r

228 In the left hemisphere, residual noise variance strongly correl

229 nd processed in the right hemisphere and the left hemisphere, respectively.

230 ater diagnosed as autistic display deficient left hemisphere response to speech sounds and have abnor

231 ust responses than the American listeners at left hemisphere scalp sites that probably index activity

232 nvoluntary orienting were more frequent with left-hemisphere seeds.

233 The left hemisphere seems to perform faster processing to re

234 We studied 45 patients, all with a left hemisphere seizure focus (mean age 22.8, seizure on

235 t, only patients with parietal damage in the left hemisphere showed a clear deficit in movement adapt

236 vs. the right cerebral hemisphere, with the left hemisphere showing a preference to interact more ex

237 calization judgments of two individuals with left hemisphere somatosensory damage subsequent to strok

238 thermore, our lateralization results suggest left hemisphere specificity for the processing of phonol

239 that the recovery of speech production after left hemisphere stroke not only depends on the integrity

240 sed lesion-symptom mapping with data from 71 left hemisphere stroke participants to assess the critic

241 10 healthy adults and 10 individuals with left hemisphere stroke participated.

242 We report data from 43 left hemisphere stroke patients in two action recognitio

243 lesion-symptom mapping (VLSM) in a series of left hemisphere stroke patients to identify brain region

244 miliar and novel objects was assessed in six left hemisphere stroke patients, two of whom exhibited d

245 s, 27 patients (aged 59 +/- 11 years) with a left hemisphere stroke performed behavioural assessments

246 anisms underlying recovery of language after left hemisphere stroke remain elusive.

247 l anatomical whole-brain connectomes from 90 left hemisphere stroke survivors using diffusion MR imag

248 Thirty-two left hemisphere stroke survivors with aphasia underwent

249 To confirm this result, 10 chronic left hemisphere stroke survivors with no history of apha

250 ognition tests were obtained from 67 chronic left hemisphere stroke survivors.

251 to language production abilities in chronic left hemisphere stroke, and that these areas may undergo

252 reasoning test) in 64 patients with chronic left hemisphere stroke.

253 o receptive language outcome following early left hemisphere stroke.

254 he sSTR support sensory discrimination after left hemisphere stroke.

255 comprehension in patients with aphasia after left hemisphere stroke.

256 ontributes to aphasia outcomes after chronic left hemisphere stroke.

257 th speech comprehension impairment following left hemisphere stroke: (1) phonological training using

258 Here, we analysed longitudinal change in 28 left-hemisphere stroke patients, each more than a year p

259 ho were investigated at least 1 year after a left-hemisphere stroke.

260 f the disorder following right compared with left hemisphere strokes.

261 cessing is considered to be dominated by the left hemisphere, studies have indicated that both left a

262 d 8 right-handed patients who had suffered a left-hemisphere subcortical ischemic stroke with paresis

263 ex white matter volume in both the right and left hemispheres, such that increased white matter volum

264 left hemisphere precentral gyrus (BA 4), the left hemisphere superior parietal lobe (BA 7), and the b

265 ng early inferential processing, whereas the left hemisphere superior temporal gyrus is particularly

266 The left hemisphere superiority for language, then, must be

267 The left hemisphere temporal and parietal regions remained s

268 ned present in a large cluster involving the left hemisphere temporal and precuneus regions.

269 rived from a steeper decline with age in the left hemisphere than in the right on the mesial surface.

270 and PFt and this cluster was greater in the left hemisphere than in the right.

271 reveal a frontal-subcortical circuit in the left hemisphere that is simultaneously associated with e

272 There are several regions in the left hemisphere that show greater activation to one's ow

273 dorsal and ventral processing streams in the left hemisphere that underlie core linguistic abilities

274 ionally defined visual word form area in the left hemisphere that was activated for words relative to

275 In the left hemisphere, the supramarginal gyrus was thinner in

276 locations: the frontal lobe in the right and left hemispheres, the basal ganglia in the right and lef

277 Reduced neural integrity in the left-hemisphere through brain damage or healthy ageing r

278 o stutter that were found primarily in major left hemisphere tracts (e.g. superior longitudinal fasci

279 Patients with left hemisphere tumors generally performed worse than th

280 ical surface area of planum temporale in the left hemisphere (usually asymmetrically larger) was posi

281 ns by supporting disrupted processing in the left hemisphere via interhemispheric connections.

282 predictors including preinjury intelligence, left hemisphere volume loss, and dorsolateral PFC volume

283 T (r = 0.541, P = 0.005), and the larger the left hemisphere volume, the faster the switching attenti

284 Higher Abeta load in the left hemisphere was associated with reduced glucose meta

285 on, hypothalamus, and septum/striatum of the left hemisphere was correlated with social status.

286 For each subject, the SLF of the left hemisphere was reconstructed from diffusion tensor

287 Even when the left hemisphere was relatively spared, subjects with dis

288 volume of the thalamus (including right and left hemispheres) was measured (in cubic centimeters) an

289 s, FD values of the lesion-free areas of the left hemisphere were associated with better FM scores; w

290 the nonspecialized right to the specialized left hemisphere when the latter did not have direct acce

291 in the anterior and posterior regions of the left hemisphere, whereas damage to the posterior portion

292 language is predominantly lateralized to the left hemisphere, whereas the degree of lateralization of

293 onal connectivity is better preserved in the left hemisphere while prefrontal DTI fiber pathways are

294 l lobe (10 out of 11 Brodmann's areas in the left hemisphere) while the pulvinar correlated only with

295 The magnitude of left hemisphere white matter disturbances mediated the s

296 Reduced left hemisphere white matter was associated with slower

297 urban youth by disrupting the development of left hemisphere white matter, whereas postnatal PAH expo

298 l delta brushes which were associated in the left hemisphere with ipsilateral BOLD activation in the

299 dic Creutzfeldt-Jakob disease, mainly in the left hemisphere, with a strong trend (P=0.06) towards re

300 an elicit larger responses in the right than left hemisphere within these areas, depending on task de