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 ocessing, introducing central vision loss (a scotoma).

4 ubretinally in the area of atrophy (absolute scotoma).

5 egion of the contralateral visual hemifield (scotoma).

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

7 xation, with marked reduction of the central scotoma.

8 ween angle alpha and the presence of central scotoma.

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

10 ubjects with and without a simulated central scotoma.

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

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

13 localize bright targets within the resultant scotoma.

14 responses to visual stimuli presented in the scotoma.

15 because this would cause a blinding central scotoma.

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

17 lue flashes presented within and outside the scotoma.

18 e prosthetic visual perception in the former scotoma.

19 resented with a persistent bilateral central scotoma.

20 twork is modified following the onset of the scotoma.

21 presumably with receptive fields within the scotoma.

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

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

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

25 fixation sparing and supero-temporal central scotoma.

26 e central vision is blocked by an artificial scotoma.

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

28 by others for real or artificial peripheral scotomas.

29 al islands or extensive central rod and cone scotomas.

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

31 on over pathologic and physiological retinal scotomas.

32 ence of physiological and pathologic retinal scotomas.

33 testing) to further characterize the visual scotomas.

34 ital cortex can produce visual phosphenes or scotomas.

35 in both eyes, often associated with central scotomas.

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

37 lthy females with acute onset of paracentral scotomas.

38 and presented with complaints of paracentral scotomas.

39 er nuclear layer atrophy with persistence of scotomas.

40 d grids is warranted in eyes with parafoveal scotomas.

41 set of reduced visual acuity and paracentral scotomas 2 weeks after their first infusion of atezolizu

42 d visual distortions (32.4% versus 13.3%) or scotomas (29.4% versus 6.7%), compared with a less speci

43 ting symptoms included blurred vision (82%), scotomas (56%), photopsias (43%), and floaters (23%).

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

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

46 e review of all patients who reported visual scotomas after 23- or 25-gauge PPV (Constellation Vision

47 Nine patients reported visual scotomas after PPV for RRD from January 2013 to December

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

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

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

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

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

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

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

55 a 26-year old male patient presenting acute scotoma and metamorphopsia in OD.

56 34-year-old man had sudden onset of central scotoma and photopsia in the left eye.

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

58 angle beta (+c) with the presence of central scotoma and visual field defect parameters, respectively

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 atients had symptomatic visual loss from the scotoma because it involved the center of fixation.

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

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

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

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

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

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

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

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

88 who suffered from acute onset of paracentral scotoma, caused by branch retinal artery occlusion (BRAO

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

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

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

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

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

94 he influence of two different wavelengths on scotoma depth.

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

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

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

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

99 l participant was masked using an artificial scotoma directly derived from clinical measurements in t

100 d HFMD, a 31-year old male noticed a central scotoma, distorted lines and loss of visual acuity (Snel

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

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

103 l decline is faster at the edge of the dense scotoma (eMS) than by using the overall MS.

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

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

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

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

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

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

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

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

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

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

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

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

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

117 it restored visual sensitivity in the former scotoma in each of the 5 patients.

118 He complained about acute onset of central scotoma in his left eye.

119 tient initially presented with a paracentral scotoma in his right eye persisting for 7 days and scatt

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

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

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

123 orted improved colour vision and a decreased scotoma in the centre of her visual field.

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

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

126 There was a central scotoma in the perimetry of the right eye and peripheral

127 artment with headaches and new onset central scotoma in the right eye.

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

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

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

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

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

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

134 included the time to development of absolute scotomas in the 4 and 16 central macular points.

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

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

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

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

139 noted paracentral or cecocentral location of scotomas involving the inferior temporal visual field.

140 itial nasal defect (IND), initial parafoveal scotoma (IPFS), and combined nasal and parafoveal defect

141 The paracentral scotoma is located inferotemporally and correlates anato

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

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

144 oss, superior peripheral defect, and central scotoma (listed in order of decreasing statistical signi

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

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

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

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

149 Symptoms included central scotoma, metamorphopsia, and mild to moderate visual los

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

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

152 ment delayed time to development of absolute scotomas of all 16 central points (PM: HR: 0.57 [43% ris

153 plan delayed time to development of absolute scotomas of all 4 central macular points compared to sha

154 ble visual sensitivity on one side and dense scotoma on the other.

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

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

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

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

159 m strategies to remap spared inputs around a scotoma or a cortical infarct.

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

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

162 Thresholds measured along ORTs showed dense scotoma over the tubule in all 4 participants, despite t

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

164 Cases had more dense scotomas (P = 0.03) than controls with a positive correl

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

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

167 nterdevice correlation, the repeatability of scotoma point detection, and any potential effects on fi

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

169 e test points directly adjacent to the dense scotoma points and to calculate their mean sensitivity (

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

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

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

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

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

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

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

177 but 3 eyes (23.1%) demonstrated paracentral scotomas related to the atrophy.

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

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

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

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

182 The scotoma shifted with coil position according to known to

183 Scotoma simulation was achieved electronically with a cl

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

185 Scotoma size and contrast sensitivity predicted outcomes

186 Scotoma size and ERG parameters differed significantly b

187 Scotoma size and specific eye pathology do not influence

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

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

190 dimming the stimulus increased the relative scotoma size.

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

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

193 Scotoma subjects' hand trajectories had longer movement

194 positively correlated with saccade rate for scotoma subjects.

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

196 field testing confirmed an inferior-temporal scotoma.Systemic work-up revealed elevated inflammatory

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

198 ignificantly faster at the edge of the dense scotoma than in the overall test grid.

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

200 3-year-old male presented with a paracentral scotoma that began several days ago.

201 eptive fields within or at the border of the scotoma that responded consistently to drifting sinusoid

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

203 The scotoma then elongated toward the physiologic blind spot

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

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

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

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

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

209 The scotoma was centrally located and had defined horizontal

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

211 A central scotoma was noted on the Amsler chart and a loss of pigm

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

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

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

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

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

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

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

219 lished macular disease and bilateral central scotomas were recruited.

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

221 All eyes showed large central scotomas, which were associated with visual field constr

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

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

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

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

226 Seven of 9 patients reported the central scotoma within the first week after surgery.

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