ライフサイエンスコーパス: dyslexic

1 ilar to those identified postmortem in human dyslexics.

2 y impairment, as demonstrated by five of the dyslexics.

3 zed that implicit memory decays faster among dyslexics.

4 r controls who read at the same level as the dyslexics.

5 on of the MGB is critical for performance in dyslexics.

6 this study, we examined the neuroanatomy of dyslexic (14 males, four females) and control (19 males,

7 ile the other group ('Magnocellular-Typical' dyslexics; 46.3%) had comparable thresholds to neurotypi

8 cals (referred to as 'Magnocellular-Deficit' dyslexics; 53.7%), while the other group ('Magnocellular

9 rweighting the stimulus statistics decreased dyslexics' ability to compensate for noisy observations.

10 ter morphology by voxel-based morphometry in dyslexic adolescents in comparison with (i) an age-match

11 lated (FM) tones at 5, 20 and 240 Hz between dyslexic adults and controls.

12 emission tomography in matched groups of six dyslexic adults and six control adults as they carried o

13 infrequent tone omissions in a group of six dyslexic adults and six IQ and age-matched controls.

14 monstrate that behavioral changes in tutored dyslexic adults are associated with (1) increased activi

15 netics study are discussed with reference to dyslexic adults from a prior study, who were ascertained

16 ion was significantly lower (p<0.01) for the dyslexic adults than for the controls in the right cereb

17 her there was abnormal brain activation when dyslexic adults undertook tasks known normally to involv

18 chophysical tasks, the MMN responses of some dyslexic adults were found to be abnormal.

19 left inferior frontal gyrus in both deaf and dyslexic adults when contrasted with hearing non-dyslexi

20 ided direct evidence that, for this group of dyslexic adults, the behavioural signs of cerebellar abn

21 By using functional MRI, we found that, in dyslexic adults, the MGB responded abnormally when the t

22 Sixteen dyslexic and 16 control university students were adminis

23 ere, we used event-related potentials whilst dyslexic and control adults performed a pseudoword-word

24 onfound of reading level, we also contrasted dyslexic and control children matched for reading perfor

25 ifferences in cognitive function between the dyslexic and control groups were performed by using the

26 We tested voice-recognition abilities of dyslexic and control listeners for voices speaking liste

27 locations for structural differences between dyslexic and control participants in imaging studies.

28 al neural patterns between the two tasks for dyslexic and control participants.

29 maging was used to measure brain activity in dyslexic and control subjects in conditions designed to

30 a learning disabilities clinic if they were dyslexic and had unstable binocular control.

31 equency or tone duration were recorded in 10 dyslexic and matched control subjects.

32 igh (75%) temporal contrast were compared in dyslexic and neurotypical children individually matched

33 Both dyslexic and non-dyslexic groups consisted of 17(53.1%)

34 areas in primary visual cortex (area 17) in dyslexic and nondyslexic autopsy specimens.

35 e differences in reading acquisition between dyslexic and nonimpaired readers and provide further evi

36 ging to compare brain activation patterns in dyslexic and nonimpaired subjects as they performed task

37 as uncued search results were equivalent for dyslexic and normal adult readers, the majority of dysle

38 of the cueing task at discriminating between dyslexic and normal readers surpasses that of a range of

39 holds, and reading performance in a group of dyslexic and normal readers to test the hypothesis that

40 There were high correlations, for both dyslexic and normal readers, between their sensitivity t

41 We show significant differences between dyslexic and normally reading children, and between youn

42 study examines the Visual Word Form Area in dyslexic and typical readers, exploring how this key com

43 pace so that reading accuracy was equal for dyslexics and controls.

44 %) in dissociating the Magnocellular-Deficit dyslexics and neurotypicals.

45 Hearing developmental dyslexics and profoundly deaf individuals both have diff

46 provements in tutored compared to nontutored dyslexics, and these gains were associated with signal i

47 -large letter spacing helps reading, because dyslexics are abnormally affected by crowding, a percept

48 Dyslexics are diagnosed for their poor reading skills, y

49 dyslexic children as a case group and 32 non-dyslexics as a control group.

50 between plastic and persistent traits in the dyslexic brain is critical for developing effective inte

51 rences in the functional architecture of the dyslexic brain.

52 Dyslexic brains exhibit histologic changes in the magnoc

53 rger neurons in the left hemisphere, whereas dyslexic brains had no asymmetry.

54 ual cortex in nondyslexics that is absent in dyslexic brains.

55 e nucleus did not show consistent changes in dyslexic brains.

56 s not associated with faster RANln scores in dyslexics, but was in neurotypical readers.

57 We show that dyslexics cannot compensate for their perceptual noise b

58 ated by reading more--a vicious circle for a dyslexic child).

59 The dyslexic children also exhibited reduced activation bila

60 eural systems for reading in nonimpaired and dyslexic children and adolescents.

61 Surprisingly, the problems faced by many dyslexic children are by no means confined to reading an

62 ing suggest that white matter differences in dyslexic children are not limited to the portion of the

63 Dyslexic children are unaware of the position of their a

64 tched case-control study was conducted on 32 dyslexic children as a case group and 32 non-dyslexics a

65 that the activation differences seen in the dyslexic children cannot be accounted for by either curr

66 xpected, also found lower V5/MT activity for dyslexic children compared to age-matched controls.

67 datasets showed a reduction in thickness in dyslexic children compared with controls in the region r

68 Dyslexic children exhibited decreased contrast sensitivi

69 Dyslexic children exhibited reduced activation relative

70 Nine of the 10 dyslexic children exhibited reduced left parietotemporal

71 Results for the dyslexic children from the family genetics study are dis

72 Dyslexic children had elevated contrast thresholds when

73 Most dyslexic children have deficient phonological awareness

74 heir impairments in literacy-related skills, dyslexic children show characteristic difficulties in ph

75 A recent study found that dyslexic children trained on action video games show sig

76 using a reading level-matched design, where dyslexic children were contrasted not only with age-matc

77 in high noise, but performed as well as non-dyslexic children when either type was displayed without

78 he binocular control and reading progress of dyslexic children with initially unstable binocular cont

79 a rhyme judgment task, in which we compared dyslexic children with two control groups: age-matched c

80 To evaluate dyslexic children's learning abilities with graphemic ma

81 eading ability or scanner-performance to the dyslexic children).

82 d approach on a total of 76 participants (31 dyslexic children).

83 rge, unselected sample of Italian and French dyslexic children.

84 ese two special populations to a hearing non-dyslexic control group.

85 nucleus, and consistent with these changes, dyslexics demonstrate abnormal visually evoked potential

86 These results suggest that dyslexics distribute their crossmodal attention resource

87 exic adults when contrasted with hearing non-dyslexics during reading or phonological tasks.

88 ellation to compare connectivity profiles of dyslexic (DYS) versus non-impaired (NI) readers in the f

89 ietal cortex has been directly implicated in dyslexic dysfunction, and substantial indirect evidence

90 ence of the involvement of the cerebellum in dyslexic dysfunction.

91 athway; so, we postulated that developmental dyslexics ("dyslexics" hereafter) would show differences

92 We found that unlike their peers, dyslexics' ERP responses are not sensitive to the relati

93 The dyslexics exhibited significantly smaller right anterior

94 nterior lobe of the cerebellum distinguished dyslexic from control participants in both studies.

95 analysis did not adequately distinguish the dyslexics from neurotypicals, on the basis of flicker th

96 -matched group (n = 12; mean 9.8 years), the dyslexic group (n = 12; mean 14.5 years) also exhibited

97 matched group (n = 19; mean 14.4 years), the dyslexic group (n = 19; mean 14.4 years) exhibited hypoa

98 and dyslexic groups than in the hearing non-dyslexic group across a large portion of the left inferi

99 ii) a reading-matched group younger than the dyslexic group but equal to the dyslexic group in readin

100 Compared to neurotypicals, the dyslexic group displayed significantly lower ability to

101 ger than the dyslexic group but equal to the dyslexic group in reading performance.

102 ot emerge until the P600 range, in which the dyslexic group showed significantly attenuated priming.

103 The dyslexic group showed significantly smaller MMNs in the

104 ocesses are absent (deaf group) or impaired (dyslexic group).

105 ns that exhibited atypical activation in the dyslexic group, only the left parietal region exhibited

106 ions observed in controls were absent in the dyslexic group.

107 rformance were often superior to that of the dyslexic group.

108 Relative to rest, both normal and dyslexic groups activated the same peri- and extra-sylvi

109 Both dyslexic and non-dyslexic groups consisted of 17(53.1%) boys and 15(46.9%

110 indicate greater activation in the deaf and dyslexic groups than in the hearing non-dyslexic group a

111 The dyslexics had specific deficits in word reading relative

112 This view on task-related MGB dysfunction in dyslexics has the potential to reconcile influential the

113 It is widely accepted that dyslexics have deficits in reading and phonological awar

114 Many dyslexics have impaired development of the magnocellular

115 In addition, in the visual modality, dyslexics have reduced structural connectivity between t

116 First, we tested the hypothesis that dyslexics have reduced structural connectivity between t

117 we postulated that developmental dyslexics ("dyslexics" hereafter) would show differences in audiovis

118 We show that dyslexic individuals are less sensitive both to particul

119 ic and normal adult readers, the majority of dyslexic individuals failed to display a comparable bene

120 dissociation observed in the performance of dyslexic individuals on different auditory tasks suggest

121 , this remains controversial because not all dyslexic individuals show psychophysical deficits on aud

122 Dyslexic individuals show subtle impairments in naming p

123 A recent proposal suggests that dyslexic individuals suffer from attentional deficiencie

124 oach, based on magnetoencephalography, in 10 dyslexic individuals who all share the same rare, weakly

125 on activity and improve reading abilities in dyslexic individuals.

126 ay contribute to the reading difficulties of dyslexic individuals.

127 ng and change as being dysfunctional in many dyslexic individuals.

128 Developmental dyslexics, individuals with an unexplained difficulty re

129 diffusion tensor imaging, we here show that dyslexic male adults have reduced white matter connectiv

130 In hearing dyslexics, many argue, auditory processes may be impaire

131 Dyslexics may be unable to process fast incoming sensory

132 tal cortex and cerebellum of 14 well-defined dyslexic men and 15 control men of similar age.

133 We found biochemical differences between dyslexic men and controls in the left temporo-parietal l

134 We found lateral biochemical differences in dyslexic men in both these brain regions (Cho/NA in temp

135 he cerebellum is biochemically asymmetric in dyslexic men, indicating altered development of this org

136 study visual motion processing in normal and dyslexic men.

137 However, in all conditions, dyslexic observers were two to three times less sensitiv

138 Developmental dyslexics often complain that small letters appear to bl

139 ateral chemical difference and handedness in dyslexic or control men.

140 impact of sound regularities in benefitting dyslexics' oral reading rate.

141 Relative to the control group, the dyslexic participants showed reduced activation in a lef

142 evidence of a striking dissociation between dyslexic participants' performance in cued and uncued co

143 s activated to a greater extent by deaf than dyslexic participants, whereas the superior posterior po

144 ited an MMNm response in only one of the six dyslexic participants.

145 minicolumnar abnormalities in the brain of a dyslexic patient.

146 ipants watched a silent movie indicated that dyslexics' perceptual deficiency may stem from poor auto

147 Our findings show that dyslexics' perceptual deficit can be accounted for by in

148 attempt to specify the mechanisms underlying dyslexics' perceptual difficulties computationally by ap

149 The dyslexics performed less well than their peers on a rang

150 Dyslexic persons, however, often report both somatic sym

151 etic mechanisms causing heterogeneity in the dyslexic population.

152 r indicate auditory grouping deficits in the dyslexic population.

153 ory processing abilities in neurotypical and dyslexic populations.

154 In all dyslexics, presentation of moving stimuli failed to prod

155 amilies that were selected on the basis of a dyslexic proband.

156 e are well-documented differences in the way dyslexics process low-level visual and auditory stimuli,

157 of left mPT-MGB connectivity correlates with dyslexics RANln scores.

158 ht-handed children 7 to 18 years of age (113 dyslexic readers and 119 nonimpaired readers) as they re

159 ed to reveal reduced phonological priming in dyslexic readers from 250 ms after target word onset.

160 Two dyslexic readers participated in a remediation program a

161 The results confirm previous findings that dyslexic readers process written stimuli atypically, bas

162 However, the dyslexic readers showed less activation than controls in

163 Dyslexic readers showed no differential left frontal res

164 The dyslexic readers showed reduced activation in BA 37 rela

165 ffered significantly between the groups with dyslexic readers showing relative underactivation in pos

166 c awareness is characteristically lacking in dyslexic readers who, therefore, have difficulty mapping

167 ve to the difference between such stimuli in dyslexic readers, and plastic enough in adulthood to dev

168 In contrast, in dyslexic readers, systems in the left posterior medial o

169 d to discover the status of that response in dyslexic readers.

170 rence in asymmetry between younger and older dyslexic readers.

171 only, there was increased activation for the dyslexics relative to the controls in a pre-motor region

172 unsteady vision; this could explain why many dyslexics report that letters appear to move around, cau

173 s and specific strengths in exploration that dyslexic researchers bring to their disciplines.

174 ic community can address the challenges that dyslexic researchers face, and how science stands to ben

175 attention shifting" (SAS) appeared only when dyslexics shifted their attention from the visual to the

176 We propose that dyslexics' shorter neural adaptation paradoxically accou

177 In addition, dyslexics show a disruption in white matter connectivity

178 Dyslexics showed a faster decay of implicit memory effec

179 Dyslexics showed difficulty shifting their attention bet

180 Consistent with previous reports, dyslexics showed less GMV in multiple left and right hem

181 Dyslexics showed reduced activity compared with controls

182 Dyslexics showed reduced brain activity compared with co

183 points toward sensory thalamus dysfunctions: dyslexics showed reduced responses in the left auditory

184 n of the critical role of accommodations for dyslexic students and the recent neurobiological evidenc

185 Rather, two distinct dyslexic subgroups were identified by cluster analysis -

186 The two dyslexic subgroups were not differentially associated wi

187 triangularis correctly classified 72% of the dyslexic subjects (94% of whom had a rapid automatic nam

188 The hypothesis that dyslexic subjects are impaired in auditory frequency dis

189 rious temporal regions have been reported in dyslexic subjects compared with controls.

190 Recent work with dyslexic subjects provides the first empirical evidence

191 Eight dyslexic subjects, impaired on measures of reading, spel

192 In the dyslexic subjects, the age-related increases in FA in th

193 to changes in tone duration were abnormal in dyslexic subjects.

194 ottom-up processing and top-down strategies, dyslexics' successful coping strategies may positively i

195 Individual data reveal that all 16 dyslexics suffer from a phonological deficit, 10 from an

196 ularis, was activated to a greater extent by dyslexic than deaf participants.

197 To further test for causality, dyslexics underwent a phonological-based reading interve

198 Notably, stereoacuity was increased in dyslexics versus controls (94.2 +/- 73.6 vs. 60.94 +/- 1

199 itivity (CS) was decreased and aggravated in dyslexics versus controls.

200 le of contrast sensitivity and its impact on dyslexic vision.

201 Higher LGN-V5/MT connectivity in dyslexics was associated with the faster rapid naming of

202 r, not all of these differences emerged when dyslexics were compared with controls matched on reading

203 However, when dyslexics were matched to younger controls on reading ab

204 One hundred and forty-three dyslexics were studied.

205 ontrol subjects of similar age and IQ to the dyslexics, were scanned whilst reading aloud and during

206 niversity students who had been diagnosed as dyslexic when younger, and two groups of control subject

207 Therefore we have studied whether dyslexics who perform adequately on auditory psychophysi

208 Thus, even among compensated dyslexics with above-average cognitive abilities and ade

209 measured motion perception in two groups of dyslexics, with and without a deletion within the DCDC2

210 rk adaptation was shown to be impaired in 10 dyslexic young adults when compared with a similar contr