ライフサイエンスコーパス: dyslexic

1 zed that implicit memory decays faster among dyslexics.

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

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

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

5 ilar to those identified postmortem in human dyslexics.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

20 Sixteen dyslexic and 16 control university students were adminis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 Hearing developmental dyslexics and profoundly deaf individuals both have diff

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

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

42 Dyslexics are diagnosed for their poor reading skills, y

43 Dyslexic brains exhibit histologic changes in the magnoc

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

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

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

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

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

49 The dyslexic children also exhibited reduced activation bila

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

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

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

53 Dyslexic children are unaware of the position of their a

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

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

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

57 Dyslexic children exhibited reduced activation relative

58 Nine of the 10 dyslexic children exhibited reduced left parietotemporal

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

60 Dyslexic children had elevated contrast thresholds when

61 Most dyslexic children have deficient phonological awareness

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

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

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

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

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

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

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

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

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

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

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

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

74 These results suggest that dyslexics distribute their crossmodal attention resource

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

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

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

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

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

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

81 The dyslexics exhibited significantly smaller right anterior

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

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

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

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

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

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

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

89 The dyslexic group showed significantly smaller MMNs in the

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

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

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

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

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

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

96 The dyslexics had specific deficits in word reading relative

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

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

99 Many dyslexics have impaired development of the magnocellular

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

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

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

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

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

105 Dyslexic individuals show subtle impairments in naming p

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

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

108 ay contribute to the reading difficulties of dyslexic individuals.

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

110 Developmental dyslexics, individuals with an unexplained difficulty re

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

112 Dyslexics may be unable to process fast incoming sensory

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

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

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

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

117 study visual motion processing in normal and dyslexic men.

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

119 Developmental dyslexics often complain that small letters appear to bl

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

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

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

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

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

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

126 minicolumnar abnormalities in the brain of a dyslexic patient.

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

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

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

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

131 Dyslexic persons, however, often report both somatic sym

132 etic mechanisms causing heterogeneity in the dyslexic population.

133 r indicate auditory grouping deficits in the dyslexic population.

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

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

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

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

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

139 Two dyslexic readers participated in a remediation program a

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

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

142 Dyslexic readers showed no differential left frontal res

143 The dyslexic readers showed reduced activation in BA 37 rela

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

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

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

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

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

149 rence in asymmetry between younger and older dyslexic readers.

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

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

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

153 We propose that dyslexics' shorter neural adaptation paradoxically accou

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

155 Dyslexics showed a faster decay of implicit memory effec

156 Dyslexics showed difficulty shifting their attention bet

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

158 Dyslexics showed reduced activity compared with controls

159 Dyslexics showed reduced brain activity compared with co

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

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

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

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

164 Recent work with dyslexic subjects provides the first empirical evidence

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

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

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

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

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

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

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

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

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

174 One hundred and forty-three dyslexics were studied.

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

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

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

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

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

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