ライフサイエンスコーパス: visual loss

1 ptly to minimize the risk for ulceration and visual loss.

2 aging technology can prevent progression and visual loss.

3 l approach in FMNS with infantile unilateral visual loss.

4 nsiderable morbidity and may cause permanent visual loss.

5 ool age group and are associated with severe visual loss.

6 patients with FMNS with infantile unilateral visual loss.

7 dative retinopathy, vitreous hemorrhage, and visual loss.

8 It can lead to significant visual loss.

9 Only 32% reported visual loss.

10 toreceptor cell death associated with severe visual loss.

11 ese patients often have non-diabetes related visual loss.

12 entional treatment and can lead to permanent visual loss.

13 cterial keratitis remains a leading cause of visual loss.

14 nal detachment remains an important cause of visual loss.

15 aucomatous optic nerve damage and subsequent visual loss.

16 immunosuppressive drugs lowered the risk of visual loss.

17 e were independent prognostic parameters for visual loss.

18 neuroretinal tissue, scarring, and permanent visual loss.

19 ly and tended to cause progressive, profound visual loss.

20 ath, which contributes to the persistence of visual loss.

21 r syndrome type 1B, which causes hearing and visual loss.

22 itudinal changes in RNFL thickness relate to visual loss.

23 nd is associated with clinically significant visual loss.

24 tional impairments as a consequence of their visual loss.

25 strategy to prevent further progression and visual loss.

26 ase characterized by a progressive bilateral visual loss.

27 be important in the management of nonorganic visual loss.

28 r syndrome type 1B, which causes hearing and visual loss.

29 essential in diagnosing a cerebral cause for visual loss.

30 L) in individuals with untreatable causes of visual loss.

31 inable transitions to severe laminopathy and visual loss.

32 this may progress to microbial keratitis and visual loss.

33 ive accumulation of droplets in CDK leads to visual loss.

34 to headache, seizure, confusion and frequent visual loss.

35 be required in an attempt to avoid permanent visual loss.

36 death from six adult subjects with monocular visual loss.

37 for progression to advanced AMD and related visual loss.

38 nd can be useful in ascertaining reasons for visual loss.

39 intraocular inflammation is a major cause of visual loss.

40 d their degeneration results in irreversible visual loss.

41 s, pigmentary retinopathy, and retrochiasmal visual loss.

42 ptions are available to prevent irreversible visual loss.

43 ervative treatment and may develop permanent visual loss.

44 dysfunction, photoreceptor death and severe visual loss.

45 ages alone, since it does not correlate with visual loss.

46 mulus contrast (M(y) cells) in patients with visual loss.

47 eron retinopathy and to subsequent permanent visual loss.

48 canal, but that in itself does not result in visual loss.

49 rvention may help prevent or mitigate severe visual loss.

50 angiography in a 66 years old man suffering visual loss.

51 age caused by diabetes is a leading cause of visual loss.

52 ith underlying heterogeneity of mechanism of visual loss.

53 s of the retina and choroid can cause severe visual loss.

54 uspect optic nerve pathology as the cause of visual loss.

55 rovides evidence of ischemia as the cause of visual loss.

56 of choroidal neovascular membrane (CNVM) and visual loss.

57 tive-day, she presented with sudden painful, visual loss.

58 order and the most leading cause of lifelong visual loss.

59 sted, except for the subject with nonorganic visual loss.

60 ng to secondary glaucoma which may result in visual loss.

61 ease, intraocular pressure is raised without visual loss.

62 fully establish, the diagnosis of nonorganic visual loss.

63 with 63.6% achieving visual success and 8.2% visual loss.

64 Retinal detachment is an important cause of visual loss.

65 , although at a slower pace than the rate of visual loss.

66 fects of acetazolamide in patients with mild visual loss.

67 h basketball-related injury may cause severe visual loss.

68 valuating patients with suspected nonorganic visual loss.

69 derate risk for malignant transformation and visual loss.

70 in the differential diagnosis of nonorganic visual loss.

71 ctasis, associated with a medical history of visual loss.

72 ith 62.8% achieving visual success and 14.9% visual loss.

73 ccidental Closantel use is related to severe visual loss.

74 acuity (VA) in the evaluation of nonorganic visual loss.

75 ny RPE loss) is important to prevent central visual loss.

76 ay correlate and possibly predict functional visual loss.

77 sive subfoveal exudates and severe permanent visual loss.

78 involved in many ocular diseases that cause visual loss.

79 d avoid complications and further peripheral visual loss.

80 ly minimize late progression and the risk of visual loss.

81 change on OCT at increased risk of worsening visual losses.

82 diseases such as glaucoma with irreversible visual losses.

83 ord recognition speed for people with severe visual loss (101 +/- 25%), while for those with moderate

84 tion in BEST1 and is associated with central visual loss, a characteristic retinopathy, an absent ele

85 diated disorder characterized by progressive visual loss, abnormal electroretinographic and visual fi

86 macular degeneration and a leading cause of visual loss after age 55.

87 criteria, biopsy results, and progression of visual loss after diagnosis.

88 The patients' severe visual loss after the injection was associated with ocul

89 Six patients with severe visual loss (ages 62-93) were examined clinically, and 1

90 e could significantly decrease the burden of visual loss among Mexican Americans.

91 educed visual acuity secondary to nonorganic visual loss and bilateral ametropic amblyopia with strab

92 Uveitis is an important cause of functional visual loss and blindness in the developed world.

93 Rates of visual loss and complications among patients with RV wer

94 To describe factors that predict visual loss and complications in intermediate uveitis.

95 tal eye anomalies that can cause significant visual loss and cosmetic disfigurement in children.

96 etic counseling for prognostic estimation of visual loss and disease progression.

97 Fourteen patients with visual loss and mutated G11778A mitochondrial DNA.

98 h NF1-associated optic gliomas often develop visual loss and Nf1 genetically engineered mice with opt

99 To describe the incidence rates of visual loss and ocular complications in patients with re

100 Visual loss and ocular complications were common among H

101 Main outcome measures included rates of visual loss and ocular complications.

102 nner retinal neurons, and it also suppressed visual loss and optic atrophy induced by a mutant ND4 ho

103 id to correlate with the severity of initial visual loss and recovery.

104 In such cases, there is an increased risk of visual loss and severe systemic complications requiring

105 a strong and consistent association between visual loss and smoking, independent of gender and alcoh

106 ritic pruning precedes the onset of clinical visual loss and structural changes in the optic nerve in

107 improved estimate of the prospective time of visual loss and to a better timing of emerging therapies

108 ections may be associated with high rates of visual loss and/or mortality.

109 receptor disease with rod- and cone-mediated visual losses and thinning of the outer nuclear layer.

110 t presentation (median 16 days from onset of visual loss) and after 3, 6, 12 and 18 months.

111 in diagnosing optic neuropathies, nonorganic visual loss, and assessing visual function in infants or

112 thies) are some of the most common causes of visual loss, and can present in isolation or with associ

113 findings include headache, jaw claudication, visual loss, and constitutional symptoms (malaise, fever

114 corneal decompensation, endophthalmitis, and visual loss are all important and some have recently bee

115 The development of CNV and visual loss are associated with lower choroidal circulat

116 a correct diagnosis may lead to irreversible visual loss as well as inappropriate evaluation and trea

117 do not like the term 'medically unexplained visual loss' as a diagnostic label.

118 xamined by an ophthalmologist and a cause of visual loss assigned to eyes with uncorrected acuity < o

119 anti-VEGF therapeutic approach may limit the visual loss associated with conjunctivalization of the c

120 incidence that presents with abrupt onset of visual loss associated with retinal vasculitis, retinal

121 achieved in 81%, although 38.5% had profound visual loss, associated with age older than 50 years and

122 to 33.7% at 1 year, and 92% avoided moderate visual loss at 1 year.

123 t remained stable, and 2 patients had severe visual loss at presentation that precluded assessment of

124 ent, and approximately 2 lines of additional visual loss at the conclusion follow-up.

125 Macular edema is a common cause of visual loss at uveitic patients.

126 In one subject, monocular visual loss began at age 4 months, causing shrinkage of

127 psing course suggested an increased risk for visual loss but was not statistically significant, perha

128 male presented with predominantly unilateral visual loss, but extensive bilateral visual field defect

129 drome of blunt force to the forehead causing visual loss, but iatrogenic injury is increasingly recog

130 cted patients present in infancy with severe visual loss, but may have some preservation of the photo

131 f affected patients so that those at risk of visual loss can be identified early and treated more agg

132 Cortical visual loss can be mistaken for FVL.

133 Overall, permanent visual loss can be observed and worse refractive outcome

134 ted controls to determine whether peripheral visual loss can lead to changes in gray matter volume.

135 nal detachment (RD) is associated with acute visual loss caused by anatomic displacement of the photo

136 Visual loss caused by giant cell arteritis is a medical

137 l loss of accommodation (2-3 D), and no near visual loss compared with higher doses.

138 d in all studies" included visual acuity and visual loss, death of participants, and intraocular pres

139 Clinical features of NMO include visual loss, decreased coordination, widespread asthenia

140 come was undertaken, with visual success and visual loss defined as a gain or reduction of 0.3 logMAR

141 ated three patients in whom severe bilateral visual loss developed after they received intravitreal i

142 ement of the photoreceptors and with chronic visual loss/disturbance caused by retinal remodeling and

143 nto 4 groups based on increasing severity of visual loss (DOA1 to DOA4) and were stratified by OPA1 m

144 Thus, visual loss does pose a problem for a composer accustome

145 lar edema (DME), is the most common cause of visual loss due to diabetes mellitus.

146 Corneal endotheliitis may cause permanent visual loss due to endothelial decompensation.

147 Fixational eye movements prevent and restore visual loss during fixation, yet the relative impact of

148 f pathologic RPE changes in the evolution of visual loss during long-term treatment with DFO.

149 ressively controlling known risk factors for visual loss, ensuring adherence to ophthalmologic treatm

150 ery which leads to high ocular morbidity and visual loss even with antibiotic treatment.

151 hy (TON) is a devastating cause of permanent visual loss following blunt injury to the head.

152 The fifth participant with visual loss for less than 12 months received the low dos

153 The fifth participant had visual loss for less than 12 months.

154 Four participants with visual loss for more than 12 months were treated.

155 ssionist painter Edgar Degas had progressive visual loss from a type of maculopathy during the last 4

156 ial proportion of the population at risk for visual loss from age-related macular degeneration consum

157 ntion that consistently prevents or reverses visual loss from diabetic macular edema in all patients.

158 recovery of visual function in patients with visual loss from GCA is poor.

159 risk for axonal degeneration and persistent visual loss from optic neuritis and multiple sclerosis.

160 Visual loss from optic neuropathy and ophthalmoplegia in

161 important, and the subsequent prevention of visual loss from PACG depends on an accurate assessment

162 s the standard treatment for reducing severe visual loss from proliferative diabetic retinopathy.

163 l have eye-related manifestations, including visual loss from the optic nerve and retinal disease, vi

164 luded and a positive diagnosis of functional visual loss (FVL) can be established.

165 group 2), and 2 participants with unilateral visual loss (group 3) were treated.

166 ter gain, final VA >/=20/40 or >/=20/25) and visual loss (>/=1 ETDRS line loss, >/=2 ETDRS line loss,

167 relationship between OCT characteristics and visual loss has not been well documented.

168 Patients with IIH with mild visual loss have typical symptoms, may have mild acuity

169 With visual loss, however, lamination was coarse and there wa

170 Personalized treatment reversed the visual loss, illustrating how proteomic tools may indivi

171 Visual loss impacted significantly on the lives of peopl

172 grade was associated with increased rates of visual loss in a dose-dependent fashion.

173 ent study evaluates the causes and extent of visual loss in a group of patients with OFNF.

174 hthalmologist may be called upon to evaluate visual loss in a patient with posterior reversible encep

175 ention of angiogenesis, vascular leakage and visual loss in age-related macular degeneration.

176 rment is rapidly becoming a leading cause of visual loss in children in developed countries predomina

177 visual impairment (CVI) is a major cause of visual loss in children worldwide.

178 ion of these disorders can lead to long-term visual loss in children.

179 urofibroma [OPPN]) can result in significant visual loss in children.

180 al visual impairment is a prevalent cause of visual loss in children.

181 ng, are major causes of ocular morbidity and visual loss in diabetes.

182 X-linked retinoschisis results in visual loss in early life with splitting within the inne

183 se dyes can significantly reduce the risk of visual loss in eyes with subfoveal choroidal neovascular

184 appears to decrease likelihood of stroke or visual loss in giant-cell arteritis without increasing b

185 d is at least as good as FT for detection of visual loss in individual examinations.

186 cular degeneration (AMD), a leading cause of visual loss in older adults, has limited therapeutic opt

187 thought to contribute to the persistence of visual loss in optic neuritis and multiple sclerosis (MS

188 Severe visual loss in patients with age-related macular degener

189 py has been shown to halt the progression of visual loss in patients with age-related macular degener

190 tachment (NSD) remains an important cause of visual loss in patients with diabetes.

191 Photoreceptor apoptosis is a major cause of visual loss in retinal detachment (RD) and several other

192 We tested for rescue of visual loss in rodent eyes also injected with a mutant G

193 sible for the photoreceptor death and severe visual loss in Stargardt's patients.

194 cin accumulation and thus delay the onset of visual loss in Stargardt's patients.

195 vent ischemic damage and halt progression of visual loss in the affected eye and prevent involvement

196 collectively the most common cause of severe visual loss in the developed world.

197 n (AMD) is the leading cause of irreversible visual loss in the elderly in developed countries and ty

198 ular degeneration (AMD) is a common cause of visual loss in the elderly, with increasing prevalence d

199 mmon form of systemic vasculitis that causes visual loss in the elderly.

200 lateral NAION event based on the severity of visual loss in the first affected eye.

201 ERMs are a cause of significant visual loss in the general, especially elderly, populati

202 He complained of sudden painless profound visual loss in the left eye (LE) two hours after emboliz

203 Improved function of the amblyopic eye after visual loss in the non-amblyopic eye could be a model fo

204 y macular involvement and associated central visual loss in the third or fourth decade of life.

205 Because visual loss in these patients often has a psychosocial b

206 he finding of different regional patterns of visual loss in these patients suggests that the optimal

207 retinitis in the macula were associated with visual loss in these patients.

208 Visual loss in this condition is often due to changes in

209 gene therapy as a means of preventing severe visual loss in this condition.

210 Visual loss in this Mexican-American population is highe

211 Visual loss in this OFNF cohort was common, typically pr

212 a and reduced the rate of sustained moderate visual loss in those with moderately severe to very seve

213 We observed no significant visual loss in treated abcr(-/-) mice by electroretinogr

214 among the most common causes of irreversible visual loss in uveitis.

215 lar degeneration (AMD) is a leading cause of visual loss in Western populations.

216 c atrophy, exudative disease, or AMD causing visual loss) in one or both eyes during the course of th

217 Some causes of visual loss (including congenital glaucoma with buphthal

218 Determination of the mechanisms by which visual loss increases mortality risk is important for de

219 of the retina is involved the risk of RD and visual loss increases significantly.

220 suppressive drug therapy lowered the risk of visual loss, independent of relapsing disease course (OR

221 Visual loss is common in bacterial or fungal endophthalm

222 Visual loss is common in subjects with PIC, predominantl

223 ns with amblyopia suggest that much of their visual loss is due to active suppression of their amblyo

224 treatment with anti-VEGF therapies; although visual loss is modified in a portion of these cases, no

225 Acute visual loss is most often due to hemorrhage from new ves

226 on and clinical management is imperative, as visual loss is often reversible with prompt treatment di

227 Visual loss is often the initial manifestation of disord

228 'Unexplained visual loss' is a useful working diagnosis until occult

229 ths (group 1), 6 participants with bilateral visual loss lasting less than 12 months (group 2), and 2

230 Six participants with chronic bilateral visual loss lasting more than 12 months (group 1), 6 par

231 way to decrease the risk of three causes of visual loss: macular edema, neovascularization, and reti

232 Visual loss may be the result of orbital hemorrhage or d

233 Our data suggest that visual loss may occur during a preoccult phase of choroi

234 ing identified early-onset (aged </=3 years) visual loss (mean [SD] best-corrected visual acuity, +0.

235 cular necrotizing fasciitis may cause severe visual loss more often than previously recognized.

236 Development of CNVM, moderate visual loss (MVL) (</=20/50), and severe visual loss (SV

237 est-corrected visual acuity (BCVA), moderate visual loss (MVL; </=20/50), severe visual loss (SVL; </

238 xible pro re nata (PRN) regimen, progressive visual loss occurred exclusively in the group with prima

239 ity of the study group eyes (71%); permanent visual loss occurred in 4 eyes (1.7%).

240 Moderate visual loss occurred in 40 eyes (12.6%), with an inciden

241 Secondary visual loss occurs in millions of patients due to a woun

242 before disappearing, at which stage central visual loss occurs.

243 ous sinuses, and may result in more profound visual loss, ocular motor deficits, and hypopituitarism.

244 Visual loss of >2 Snellen lines occurred in 24 of 428 pa

245 442 incident cases of neovascular AMD with a visual loss of 20/30 or worse due primarily to AMD.

246 We accrued 567 patients with AMD with a visual loss of 20/30 or worse.

247 on initial presentation and to compare mean visual loss of firstly versus secondly affected eyes.

248 ted imaging (DWI) in patients with monocular visual loss of presumed ischemic origin (MVL).

249 isk ratio = 3.47, 95% CI: 1.24-8.70) to show visual loss of three or more lines than were eyes with a

250 resulting in diplopia, oscillopsia, blurred visual, loss of stereopsis, and reading fatigue.

251 and symptoms often include severe headache, visual loss, ophthalmoplegia, altered consciousness, and

252 Transient monocular visual loss or complex visual hallucinations may lead to

253 ociated with a high morbidity from potential visual loss or rapid progression of latent systemic dise

254 were associated with >/= 2 Snellen lines of visual loss (P < .01) and visual acuity loss to 20/50 or

255 drugs was associated with a reduced risk of visual loss, particularly for the </=20/50 outcome (haza

256 acceptable, and most subjects with profound visual loss perform better on visual tasks with system t

257 ecovery usually follows the acute episode of visual loss, persistent visual deficits are common and a

258 Perioperative visual loss (POVL) is an uncommon complication primarily

259 Symptoms can include headaches, visual loss, pulsatile tinnitus, and back and neck pain,

260 our understanding of the natural history of visual loss, recovery, and recurrence in these disorders

261 adenosine triphosphate synthesis, suppressed visual loss, reduced apoptosis of retinal ganglion cells

262 Anesthesiologists developed a Postoperative Visual Loss Registry in an effort to better understand a

263 ge and lowering of intraocular pressure, the visual loss remained.

264 eyes) with >or=6 months follow-up, eyes with visual loss showed greater RNFL thinning compared to eye

265 hen stratifying by mean deviation, with mild visual loss, size V was most sensitive, followed by STP;

266 Sustained moderate visual loss (SMVL) was defined as a 15-letter or more re

267 in different patients and in detecting other visual losses such as those associated with glaucoma.

268 inal appearance and a similar early onset of visual loss, suggesting both impaired retinal developmen

269 n loss has occurred may reduce the amount of visual loss sustained with anti-vascular endothelial gro

270 ate visual loss (MVL) (</=20/50), and severe visual loss (SVL) (</=20/200).

271 moderate visual loss (MVL; </=20/50), severe visual loss (SVL; </=20/200).

272 y visual pathways have different patterns of visual loss than patients with glaucoma.

273 Early visual loss that began at 3 mo and progressed to blindne

274 nvestigation and management of patients with visual loss that cannot be accounted for by organic path

275 kinetic fields revealed regional patterns of visual loss that suggested a disease sequence.

276 ly important, including the mode of onset of visual loss, the presence of pain with eye movements, th

277 In patients with IIH and mild visual loss, the use of acetazolamide with a low-sodium

278 In 1 patient with progressive, idiopathic visual loss, this last-line analysis implicated retinal

279 ng and health care productivity and reducing visual loss through early treatment.

280 ange: 1-6) appeared to have greater risk for visual loss to 20/50 (odds ratio [OR] = 2.07; 95% CI, 0.

281 44 months (range: 1-153 months), the rate of visual loss to 20/50 or worse was 0.13 per eye-year (/EY

282 patients with FMNS with infantile unilateral visual loss underwent strabismus surgery to correct an A

283 l amblyopes, even those with the most severe visual loss, veridically matched all blurred edges, incl

284 p = 0.04), in MVL characterized by permanent visual loss versus transient symptoms (33 vs 18%, p = 0.

285 Visual loss was associated with a marked impact on healt

286 ersus without lens), no selective functional visual loss was demonstrated with any of the tasks used.

287 e damage to Meyer's loop was determined, and visual loss was quantified using Goldmann perimetry.

288 Causes of visual loss were classified using the World Health Organ

289 Regional patterns of visual loss were evident using dark-adapted static thres

290 Visual losses were predictably related to a decline in O

291 racterized by severe and rapidly progressive visual loss when caused by a mutation in the mitochondri

292 ent therapy against the background of severe visual loss, whereas it may be harder to detect incremen

293 assist in clarifying how drusen give rise to visual loss, which is currently not known.

294 lamide in 165 participants with IIH and mild visual loss who received a low-sodium weight-reduction d

295 l relatives in this Chinese family developed visual loss with a wide range of severity, ranging from

296 typical presentation is sudden and painless visual loss with examination features of an optic neurop

297 Patients were also more likely to experience visual loss with laser than with ranibizumab treatment.

298 amely visual disability (permanent bilateral visual loss with visual acuity of <6/36 in the best eye)

299 People with ESCS also suffer visual loss, with night blindness occurring from early i

300 ign bodies (IOFBs) are an important cause of visual loss within the group of working age population.