ライフサイエンスコーパス: scotoma

1 apillofoveal horizontal step ("pistol barrel scotoma").

2 within the central 10 degrees ("Amsler grid scotoma").

3 egion of the contralateral visual hemifield (scotoma).

4 ocessing, introducing central vision loss (a scotoma).

5 m adjust to a loss of foveal vision (central scotoma)?

6 xation, with marked reduction of the central scotoma.

7 l targets presented in a foveal, TMS-induced scotoma.

8 ubjects with and without a simulated central scotoma.

9 ta were used to draw a map of the developing scotoma.

10 imulus was larger, but still confined to the scotoma.

11 localize bright targets within the resultant scotoma.

12 responses to visual stimuli presented in the scotoma.

13 because this would cause a blinding central scotoma.

14 usually at the fovea or just outside a dense scotoma.

15 lue flashes presented within and outside the scotoma.

16 oss of vision in the left eye with a central scotoma.

17 fixation sparing and supero-temporal central scotoma.

18 tegorized as "normal," "relative," or "deep" scotoma.

19 e central vision is blocked by an artificial scotoma.

20 d over weeks in the absence of the simulated scotoma.

21 tion task, using a gaze-contingent simulated scotoma.

22 by others for real or artificial peripheral scotomas.

23 al islands or extensive central rod and cone scotomas.

24 he RPE melanin; laminopathy was found in the scotomas.

25 on over pathologic and physiological retinal scotomas.

26 ence of physiological and pathologic retinal scotomas.

27 ital cortex can produce visual phosphenes or scotomas.

28 lthy females with acute onset of paracentral scotomas.

29 and presented with complaints of paracentral scotomas.

30 er nuclear layer atrophy with persistence of scotomas.

31 s with normal sensitivity, relative, or deep scotomas.

32 d grids is warranted in eyes with parafoveal scotomas.

33 erented by a contralateral retinal lesion (a scotoma) 8 d earlier.

34 Holmes combined observations of visual-field scotomas across brain-lesioned soldiers to produce a sch

35 For nine subjects with retinal scotomas, alignment thresholds were measured over the ma

36 to detect or discriminate motion within the scotoma, although they could discriminate moving from st

37 gressive loss of visual acuity, centrocoecal scotoma and bilateral temporal atrophy of the optic nerv

38 analyzed to produce retinal maps showing the scotoma and bivariate ellipses of fPRL and fingertip ret

39 patients presented with an acute paracentral scotoma and demonstrated a classic dark gray paracentral

40 reduced BOLD response in patients reporting scotoma and increased response in patients who only expe

41 ting the percentage of absolute and relative scotoma and mean central retinal sensitivity weighted by

42 34-year-old man had sudden onset of central scotoma and photopsia in the left eye.

43 l infarction that explained the visual field scotoma and the retinal nerve fibre layer defect in the

44 individuals with CN, VI adults with central scotomas and children with CVI.

45 Retinal locations and sizes of subjects' scotomas and PRLs were mapped with a scanning laser opht

46 were recorded while subjects with bilateral scotomas and subjects with normal vision reached for and

47 y seen with visual symptoms of photopsia and scotoma, and most had a detectable lesion in the fundus

48 cientists who have recorded and analysed the scotomas, and in particular the expanding fortification

49 e observed centrally but not in regions with scotomas, and retinal pigment epithelial cells were visi

50 s of subjects' preferred retinal loci (PRL), scotomas, and visual acuities.

51 ar; retinal detachment; retinal hemorrhages; scotomas; and an increased number of floaters.

52 Filling in across pathologic scotomas appears to involve higher level image processin

53 in reach-to-grasp movement caused by macular scotomas are greater in degree than those reported by ot

54 esion size influenced the course of absolute scotoma area (P = .0015), while lesion type had no effec

55 lyses were performed between the Amsler grid scotoma area and the 10-2 VF parameters (mean deviation

56 The Amsler grid scotoma area had the strongest relationship with 10-2 MD

57 ivity, mean central retinal sensitivity, and scotoma area in dependence of age, lesion type, lesion s

58 al to or more than a doubling of the central scotoma area in response to a II2e test stimulus in the

59 Decrease of absolute scotoma area missed statistical significance over time (

60 ting characteristic curve of the Amsler grid scotoma area was 0.810 (95% confidence interval, 0.723-0

61 egative predictive values of the Amsler grid scotoma area were calculated with the 10-2 VF as the cli

62 ual stimulation in one quadrant ["artificial scotoma" (AS)].

63 Possible effects on a relative scotoma at the edge of a lesion have not been adequately

64 sual acuity ranged from 20/16 to 20/40, with scotomas beginning at 3 degrees eccentricity.

65 in spared-V1 was shifted slightly toward the scotoma border in 2 of 5 patients compared with AS contr

66 was slightly increased in patients near the scotoma border; and (iii) pRF size in the contralesional

67 iseases had their dense and relative macular scotoma borders mapped with the scanning laser ophthalmo

68 be used to generate an improved estimate of scotoma boundaries.

69 ision region, typically near the edge of the scotoma boundary, for all subjects except one.

70 se with HCQ toxicity who had parafoveal ring scotomas but a normal-appearing SD-OCT.

71 The depth of scotomas caused by major vessels varied in all subjects

72 t is likely that factors other than fPRL and scotoma characteristics contribute to poorer maze-tracin

73 ity to improve the accuracy and precision of scotoma characterization relative to standard methods.

74 a new foveated ideal observer with a central scotoma correctly predicts that the human optimal point

75 r, laser treatment itself causes an absolute scotoma correlating with the site of the laser photocoag

76 Absolute scotoma, defined as 0 dB retinal sensitivity, correspond

77 he influence of two different wavelengths on scotoma depth.

78 of the fovea, consistent with the ring-like scotoma described by the patient.

79 visual impairment confronted with a central scotoma develop a preferred retinal locus to replace the

80 Participants with binocular CFL (scotoma diameter, 7 degrees -25 degrees ; visual acuity,

81 lation of the RF surround with an artificial scotoma did not have any additional aftereffects over th

82 n patients affected by central or peripheral scotoma due to retinal diseases.

83 Visual scotomas due to post-chiasmal lesions were associated wi

84 er a high-contrast stimulus or an artificial scotoma [equivalent to the stimulation of the receptive

85 of Stargardt disease, likelihood of central scotoma expansion, and visual acuity deterioration.

86 MD (quadratic R(2)=0.681), followed by 10-2 scotoma extent (quadratic R(2)=0.611) and 10-2 scotoma m

87 the 10-2 VF parameters (mean deviation [MD], scotoma extent [number of test points with P < 0.01 in t

88 the INL, resulting in persistent paracentral scotomas for the patient.

89 Persons with central scotomas frequently use a preferred retinal locus (PRL)

90 Consequently, bilateral macular scotomas from age-related macular degeneration (AMD) may

91 Macular scotomas from age-related macular degeneration (AMD) may

92 Subjects with bilateral macular scotomas from AMD and normally sighted controls traced a

93 ed subjects, subjects with bilateral macular scotomas from AMD have reach-to-grasp movements with lon

94 sual islands were separated by midperipheral scotomas from far temporal peripheral islands.

95 this study: 30 patients affected by central scotoma, group 1, and 30 affected by peripheral scotoma,

96 toma, group 1, and 30 affected by peripheral scotoma, group 2.

97 conditions to measure the effects of the rod scotoma in human early visual cortex.

98 er the maximum vertical extent of the larger scotoma in one eye and at an equal separation and eccent

99 At 28 days, there was a scotoma in the area of the SC that represents the centra

100 teers (80%) successfully simulated a central scotoma in the first field and all 10 (100%) did so on i

101 as evaluated within a week of the onset of a scotoma in the nasal field of his left eye.

102 shape and location of the aura wavefront or scotoma in the visual field at one minute intervals.

103 macular schisis with small relative central scotomas in each eye.

104 Red fields often showed more prominent scotomas in early retinopathy but sometimes showed irreg

105 the topographic organization of suppression scotomas in humans with exotropia.

106 f the visual cortex corresponding to central scotomas in subjects with macular degeneration (MD) is c

107 lism that can be correlated with suppression scotomas in subjects with strabismus.

108 of retinal thinning were also matching with scotomas in the automated visual fields.

109 adaptation, and produce dense, irreversible scotomas in the visual field, the initial decline in VA

110 ore peripheral eccentricities outside of rod scotoma influence in coherence, eccentricity representat

111 manual tasks and how the fingers, fPRL, and scotomas interacted in task performance.

112 esults suggest that motion processing in the scotoma is severely impaired, and that the puzzling disc

113 As a naturally occurring central scotoma, it has a large cortical representation, is free

114 Microperimetry demonstrated relative scotomas mapping to the area of middle retinal hyperrefl

115 ere was a correspondence between suppression scotoma maps and the eye used to acquire peripheral targ

116 otoma extent (quadratic R(2)=0.611) and 10-2 scotoma mean depth (quadratic R(2)=0.299) (all P < 0.001

117 ts with P < 0.01 in total deviation map] and scotoma mean depth [mean sensitivity of test points with

118 = 12), nasal steps (n = 11) and paracentral scotomas (n = 16).

119 ovea that corresponded with a dense relative scotoma noted on light-adapted static perimetry in the l

120 We demonstrate the importance of a visible scotoma on the speed of the adjustment and suggest a pos

121 ith early HCQ toxicity showed prominent ring scotomas on field testing without obvious SD-OCT abnorma

122 ry flow loss on OCT angiography and with the scotomas on visual fields.

123 measured using a novel method for projecting scotomas onto the flattened cortical representation.

124 al-field testing on the locations of present scotomas or using frequency doubling technology may prov

125 fore symptomic night blindness, visual-field scotomas, or decreased visual acuity arise.

126 showed a doubling in the size of the central scotoma over this duration.

127 sitivity loss (mean deviation) and localized scotomas (pattern standard deviation) were worse in pati

128 y and contrast sensitivity loss, the central scotoma per se delayed hazard detection even though smal

129 P < .001), and with a higher number of deep scotoma points (beta = -0.70; P < .001).

130 mulation during the period of gray screen or scotoma presentation was associated with an increase in

131 esented to the lesion-affected visual field (scotoma) produced significant V1-independent fMRI activa

132 ve amplitudes) a higher mean rate of central scotoma progression compared with those patients with no

133 l field data, 8 patients with faster central scotoma progression rates had significantly worse scotop

134 and receptive field (RF) scaling in cortical scotoma projection zones (SPZs) the result of long-term

135 Relative and dense scotoma rates were calculated in the GA areas.

136 We created an artificial scotoma (region missing from a visual pattern) to direct

137 und that some patients with relative central scotomas reliably used two different preferred retinal l

138 CO levels in cortical scotomas remained severely depressed for months after re

139 stimulation over the visual cortex induced a scotoma, responses nonetheless were delayed significantl

140 eccentricity in the eye with a smaller or no scotoma RESULTS: In control subjects, alignment threshol

141 The scotoma shifted with coil position according to known to

142 Scotoma simulation was achieved electronically with a cl

143 ors for normalized search duration including scotoma size and acuity, as well as interactions among s

144 Scotoma size and contrast sensitivity predicted outcomes

145 Scotoma size and ERG parameters differed significantly b

146 Scotoma size and specific eye pathology do not influence

147 visual acuity was 20/200, and median central scotoma size was 20.0 degrees.

148 ze and acuity, as well as interactions among scotoma size, age, acuity, and contrast (P < 0.05).

149 dimming the stimulus increased the relative scotoma size.

150 ribute to poorer maze-tracing performance by scotoma subjects in comparison with controls.

151 ock width at a significantly higher rate for scotoma subjects than for control subjects.

152 Scotoma subjects' hand trajectories had longer movement

153 positively correlated with saccade rate for scotoma subjects.

154 icantly with dense regions of the perimetric scotoma, suggesting that pRF analysis may help identify

155 r its immediate afferents results in a dense scotoma, termed cortical blindness (CB).

156 holds were no better over pathologic retinal scotomas than more intact, equally eccentric retina (P =

157 dus-related microperimetry results indicated scotomas that corresponded to the locations where RPE ce

158 The scotoma then elongated toward the physiologic blind spot

159 nge of macular VF defects from clear arcuate scotomas to a papillofoveal horizontal step ("pistol bar

160 om full kinetic fields with relative central scotomas to remnant peripheral islands; from reduced ERG

161 ology (flash, zig-zag, strobe, scintillating scotoma, twinkling, other); (3) color (white, silver, ye

162 This subject had a PRL within the simulated scotoma under two conditions, but the percentage of tota

163 as always located within an area of relative scotoma, usually at the fovea or just outside a dense sc

164 The scotoma was centrally located and had defined horizontal

165 ted in pattern-dependent distortion, and the scotoma was filled in with temporally adjacent stimuli,

166 Mean (SD) rate of relative scotoma was significantly higher in the GA area imaged a

167 A possible laser-induced central scotoma was suspected in only 1 patient who had undergon

168 sented with declining visual acuity, central scotomas, waxy disc pallor, attenuated vasculature, smal

169 lso, synaptic current frequencies within the scotoma were not affected after the P11 lesions.

170 rgic synaptic currents on neurons within the scotoma were significantly reduced.

171 tinal granulomatous mass/scar, vitritis, and scotoma were the most common ophthalmologic signs found

172 range, 0-68); abnormal sensitivity and deep scotomas were more prevalent in the central macula.

173 lished macular disease and bilateral central scotomas were recruited.

174 graphic) were found only within visual field scotomas, whereas changes of the log sensitivity paramet

175 idered "abnormal" if there was any perceived scotoma with missing or blurry grid lines within the cen

176 tre because of a deep unilateral paracentral scotoma with the presumptive diagnosis of a normal tensi

177 erimetry revealed a reduction in the central scotoma with three patients recovering normal foveal sen

178 acuity was 20/60, and she had midperipheral scotomas with retained function centrally and in the far

179 e completion of pathologic and physiological scotomas would be consistent with large-scale reorganiza