ライフサイエンスコーパス: glaucomatous

1 ous eyes into nine axes (VF patterns): seven glaucomatous.

2 Hundred and fifty five subjects were glaucomatous: (67 PXG, 42 Primary Open Angle Glaucoma (P

3 imicking the stiffness of normal (5 kPa) and glaucomatous (75 kPa) HTM.

4 sociated with maculopathy and different from glaucomatous acquired pits of the optic nerve, which rep

5 e observed decreased MMP-3 activity in human glaucomatous AH compared to age-matched normotensive con

6 Treatment with glaucomatous AH resulted in significantly increased tran

7 eneration after trauma or disease, including glaucomatous and mitochondrial optic neuropathies, are l

8 ocystoid macular changes was similar between glaucomatous and nonglaucomatous eyes.

9 ults at 1 and 6 months were compared between glaucomatous and nonglaucomatous eyes.

10 sent on automated perimetry in patients with glaucomatous and nonglaucomatous optic neuropathies.

11 udy was to determine whether IOP lowering in glaucomatous and ocular hypertensive (OHT) eyes leads to

12 One hundred and twelve normal, glaucomatous, and glaucoma suspect eyes (99 patients) we

13 he presence of significant levels of CCL2 in glaucomatous aqueous is a new finding.

14 levels of these cytokines were higher in the glaucomatous aqueous, but not significantly so.

15 the well documented presence of TGF-beta2 in glaucomatous aqueous.

16 provide useful therapeutic entry points into glaucomatous axon degeneration.

17 VT in the prelamina has been associated with glaucomatous axonal death, our results suggest that the

18 As the abnormal model is based on glaucomatous behaviour this algorithm has not been valid

19 Eyes were classified as glaucomatous by repeatable abnormal standard automated p

20 s of 42 patients had evidence of progressive glaucomatous change and were included in the preperimetr

21 patients without any evidence of progressive glaucomatous change followed untreated for an average of

22 d stereophotographic evidence of progressive glaucomatous change in the appearance of the optic nerve

23 G did not develop represents normal aging or glaucomatous change not detected by conventional methods

24 of RGC alone in the identification of early glaucomatous change.

25 ard automated perimetry (SAP) or progressive glaucomatous changes on stereophotographs.

26 ral and functional abnormalities from 'true' glaucomatous changes.

27 ssure and plays a neuroprotective role under glaucomatous conditions, while voriconazole, an antifung

28 es together may improve our understanding of glaucomatous damage and aid in the management of patient

29 our eyes without any evidence of progressive glaucomatous damage and followed untreated for 12.8 +/-

30 ay contribute to the increased prevalence of glaucomatous damage associated with these regions of the

31 chosen a priori and included at least 2 with glaucomatous damage but a sensitivity of >/= 6 dB.

32 CT performed well in detecting preperimetric glaucomatous damage in a cohort of glaucoma suspects and

33 lar measurements for detecting preperimetric glaucomatous damage in a cohort of glaucoma suspects.

34 tive and specific method for detecting early glaucomatous damage in eyes with OH, and together with O

35 t sensitive and specific for detecting early glaucomatous damage in ocular hypertension (OH).

36 Together, these data support a model of glaucomatous damage involving monocyte entry into the op

37 Detecting progression of glaucomatous damage is often challenging.

38 Eyes with preperimetric and perimetric glaucomatous damage were included in the glaucoma group.

39 Forty-eight eyes with progressive glaucomatous damage were included in the preperimetric g

40 findings suggest that C3 protects from early glaucomatous damage, a process that may involve EGFR sig

41 nning of the inferior quadrant suggests that glaucomatous damage, more than uveitic ocular hypertensi

42 eactive (IR) cells were highly vulnerable to glaucomatous damage, whereas choline acetyltransferase (

43 cal role for non-NMDA glutamate receptors in glaucomatous damage.

44 ng results in lower IOP and prevents further glaucomatous damage.

45 the potential to improve early detection of glaucomatous damage.

46 as sensitive as the actual VF for detecting glaucomatous damage.

47 th normal intraocular pressure could lead to glaucomatous damage.

48 can provide early and sensitive detection of glaucomatous damage.

49 flectance was the most robust correlate with glaucomatous damage.

50 ment prevented monocyte entry and subsequent glaucomatous damage.

51 unctional measures for detecting progressive glaucomatous damage.

52 erve fiber bundles with different degrees of glaucomatous damage.

53 l advantage in terms of reducing the risk of glaucomatous damage.

54 he study and represented the entire range of glaucomatous damage.

55 on of the number of ganglion cells lost in a glaucomatous defect.

56 ompanied by any detectable clinical signs of glaucomatous deterioration.

57 laucoma, and variability in IOP might herald glaucomatous development or progression.

58 l field (Uv-H) (n = 233), and raised IOP and glaucomatous disc and/or visual field (Uv-G) (n = 88).

59 B-scan, the endoscope helped in detecting a glaucomatous disc in 10 of those eyes; 7 of them had gla

60 up than those patients with mild or moderate glaucomatous disease (adjusted OR 1.89, 95% CI 1.21-2.94

61 ay explain the occurrence and progression of glaucomatous disease in the setting of seemingly control

62 These findings may help shed light on the glaucomatous disease process and aid efforts to reduce t

63 confounding variables, subjects with severe glaucomatous disease were found to have been less adhere

64 g epidemiologic evidence linking myopia with glaucomatous disease, but a myopic optic nerve can pose

65 t improvement of patient knowledge regarding glaucomatous disease, follow-up rates were poor for all

66 ere significantly more likely to have severe glaucomatous disease, suggesting that poor follow-up may

67 ng medication regimen than those with milder glaucomatous disease.

68 , or may be characteristics that result from glaucomatous disease.

69 se positive referrals with more diagnosis of glaucomatous disease.

70 hin the optic nerve were also protected from glaucomatous disruption in the transgenic mice.

71 ng of LC3-II in ONH sections from normal and glaucomatous donor eyes was performed.

72 ed retinal proteins previously identified in glaucomatous donors (or that exhibited increased methion

73 dings suggest the possibility of reversal of glaucomatous dysfunction of retinal ganglion cells and t

74 In the glaucomatous eye, this process becomes impaired.

75 in sectors without a visible RNFL defect in glaucomatous eyes (15 +/- 29%; P < .001) and higher than

76 Totals of 47 glaucomatous eyes (47 patients; VF mean deviation, -12.7

77 udy of 198 normal eyes (138 subjects) and 66 glaucomatous eyes (55 subjects) recruited from the Diagn

78 [OR], 0.49; 95% CI, 0.22-1.10) or enucleated glaucomatous eyes (OR, 0.66; 95% CI, 0.15-2.89).

79 002, respectively) and remained unchanged in glaucomatous eyes (P = .400 and P = .700, respectively).

80 ficity in discriminating between healthy and glaucomatous eyes across the glaucoma continuum.

81 in 33 of 125 (26.4%) longitudinally followed glaucomatous eyes and 2 of 33 (6%) same-day control pati

82 ty occurs after surgical reduction of IOP in glaucomatous eyes and may represent a potential biomarke

83 loss was significantly faster in progressing glaucomatous eyes compared with healthy eyes for both ri

84 e density of RPCs was significantly lower in glaucomatous eyes compared with matched-peripapillary re

85 phere with apparently normal visual field in glaucomatous eyes compared with the mean hemispheric val

86 C activity, were significantly attenuated in glaucomatous eyes following a time course that matched t

87 A total of 199 randomly selected glaucomatous eyes from 199 patients aged 18 years and ab

88 potential therapeutic targets for protecting glaucomatous eyes from pressure-induced injuries.

89 average number of RGCs in the healthy group, glaucomatous eyes had an average RGC loss of 28.4%, rang

90 eported excellent compliance but only 56% of glaucomatous eyes had IOPs less than 21 mmHg.

91 hm (SITA) VFs from a set of 2,085 normal and glaucomatous eyes into nine axes (VF patterns): seven gl

92 A total of 112 preperimetric glaucomatous eyes of 92 patients were examined to obtain

93 relationship may need further exploration in glaucomatous eyes prior to its application in clinical s

94 l group, which consisted of 32 contralateral glaucomatous eyes receiving antiglaucoma medications wit

95 In glaucomatous eyes the mean Retinal Response Density (RRD

96 optic disc photographs of 40 healthy and 48 glaucomatous eyes to a visual field chosen from 4 option

97 , these correlations need to be evaluated in glaucomatous eyes to better understand normal and abnorm

98 Normal and glaucomatous eyes underwent spectral-domain optical cohe

99 found that the CRVT in glaucoma suspect and glaucomatous eyes was located significantly more nasally

100 Glaucomatous eyes were classified as normal or high-tens

101 age rim area loss in healthy and progressing glaucomatous eyes were compared using multivariate, nest

102 Glaucomatous eyes were included if localized RNFL defect

103 scopic optic disc photographs of healthy and glaucomatous eyes were presented to clinicians using the

104 In glaucomatous eyes with both quiescent and active uveitis

105 observations indicate that MPOD is lower in glaucomatous eyes with foveal GCC involvement relative t

106 Glaucomatous eyes with GCC loss involving the foveal zon

107 defects of the LC were frequently visible in glaucomatous eyes with localized RNFL defects.

108 indicators of RNFL defects in preperimetric glaucomatous eyes with normal cpRNFL.

109 A total of 62 eyes, comprising 38 glaucomatous eyes with open angle glaucoma and 24 health

110 In glaucomatous eyes with single-hemifield damage, the RBF

111 Glaucomatous eyes with the earliest detectable visual fi

112 f 152 eyes of 83 subjects (96 healthy and 56 glaucomatous eyes) underwent peripapillary RNFL imaging

113 ects (44 healthy, 59 glaucoma suspect and 89 glaucomatous eyes) were scanned with SD-OCT.

114 nction and discriminated between healthy and glaucomatous eyes, and also showed good differentiation

115 te the prevalence of visual field defects in glaucomatous eyes, glaucoma suspects, and ocular hyperte

116 In glaucomatous eyes, pars plana vitrectomy with epiretinal

117 In glaucomatous eyes, reduced pupillary responses to high-i

118 In glaucomatous eyes, there were 136 sectors with visible R

119 ored in the tissue with minimal variation in glaucomatous eyes.

120 c nerve head findings frequently observed in glaucomatous eyes.

121 1.7%) eye bank eyes, and 2 (1.3%) enucleated glaucomatous eyes.

122 d in the perimetrically normal hemisphere of glaucomatous eyes.

123 eyes, 517 eye bank eyes, and 155 enucleated glaucomatous eyes.

124 redict contrast sensitivity (CS) outcomes in glaucomatous eyes.

125 al CDR of 0.45 +/- 0.15 vs. 0.80 +/- 0.16 in glaucomatous eyes.

126 and prelaminar tissue in living healthy and glaucomatous eyes.

127 nctional progression in glaucoma suspect and glaucomatous eyes.

128 TIMP4 elevation is a novel finding in glaucomatous eyes.

129 e difference was detected between health and glaucomatous eyes.

130 or RTVue measurements in healthy compared to glaucomatous eyes.

131 ized in the SVC, but not the ICP and DVP, in glaucomatous eyes.

132 y reported values in age-matched healthy and glaucomatous eyes.

133 ho did not with that in the same healthy and glaucomatous eyes.

134 rate of visual field progression in treated glaucomatous eyes.

135 epleted from RGC axons in the optic nerve of glaucomatous eyes.

136 PA receptor (CP-AMPAR) expression in RGCs of glaucomatous eyes.

137 that influence cataract surgery outcomes in glaucomatous eyes.

138 efined glaucoma" if either disc demonstrated glaucomatous features, and VF data were combined with op

139 ge angle, glaucomatous optic neuropathy, and glaucomatous field defect), glaucoma suspect, ocular hyp

140 ith pre-existing glaucoma had progression of glaucomatous field defect.

141 ALK, 3 of 71 cases (4.48%) developed de novo glaucomatous field defects, and 1 case with pre-existing

142 al-evoked potentials metrics to discriminate glaucomatous from healthy eyes were compared with global

143 e RNFL thickness parameter in discriminating glaucomatous from healthy eyes with receiver operating c

144 ion, it is often not possible to distinguish glaucomatous from nonglaucomatous disease based on a sin

145 greater CCT (576.33 +/- 49.32 mum) than the glaucomatous groups (p = 0.004).

146 ing is contrary to TM stiffening reported in glaucomatous human eyes.

147 ted from the inner wall of SC of healthy and glaucomatous human eyes.

148 A patient was considered glaucomatous if at least 2 of the 3 RNFL or GCIPL scans

149 retinal ganglion cell (RGC) survival during glaucomatous injury in a chronic ocular hypertensive rat

150 PERG amplitudes and rate of RGC loss during glaucomatous injury.

151 mprovement in PERG and RGC integrity against glaucomatous injury.

152 n of one or more opioid receptors can reduce glaucomatous-injury via suppression of TNF-alpha and cas

153 dual-function mechanism to effectively treat glaucomatous intraocular pressure (IOP) dysregulation.

154 Glaucomatous LC cells possessed significantly higher lev

155 41.01 +/- 3.9, p = 0.02, n = 3) was found in glaucomatous LC cells relative to normal LC cells.

156 PD patients may demonstrate glaucomatous-like perimetric defects even in the absence

157 robustly protected against both ischemic and glaucomatous loss of RGC axonal integrity, as well as lo

158 Clinically, our only method of slowing glaucomatous loss of vision is to reduce intraocular pre

159 The frequency of TTF increased with stage of glaucomatous loss: 28.3% in eyes with mean deviation (MD

160 mimicking those found in normal (5 kPa) and glaucomatous meshworks (75 kPa), or tissue culture polys

161 V4 antagonist prodrug analogs lowered IOP in glaucomatous mouse eyes and protected retinal neurons fr

162 lso describe the use of OCTA to detect early glaucomatous nerve damage, associated with focal reducti

163 rtant role in diseases and injuries, such as glaucomatous neuro-degeneration and retinal detachment.

164 ort the hypothesis that during the course of glaucomatous neurodegeneration, axonal cytoskeletal and

165 Conversely, 11.9% of the glaucomatous neuropathies were misdiagnosed as neurophth

166 The device discriminated eyes with glaucomatous neuropathy from healthy eyes in a clinicall

167 c Perimetry is the gold standard to evaluate glaucomatous neuropathy, the joint use of mfVEP and OCT

168 to both intraocular pressure regulation and glaucomatous neuropathy.

169 = 30 months of follow-up with no evidence of glaucomatous neuropathy.

170 ve head (ONH) are believed to play a role in glaucomatous neuropathy.

171 bjects) with a central ODP had glaucoma with glaucomatous neuroretinal rim thinning, RNFL loss, and c

172 pendently evaluated 140 image pairs from 100 glaucomatous/ocular hypertensive patient eyes using a ha

173 tous disc in 10 of those eyes; 7 of them had glaucomatous optic atrophy.

174 differences between CG and the suspects with glaucomatous optic disc appearance (GODA).

175 yes of a control group (CG), patients having glaucomatous optic disc appearance or ocular hypertensio

176 nd the spatial relationship between them and glaucomatous optic disc changes such as neuroretinal rim

177 OMPARED WITH PATIENTS WITHOUT PROGRESSION IN GLAUCOMATOUS OPTIC DISC CHANGES.

178 tous visual field abnormality or evidence of glaucomatous optic disc damage, or both when not present

179 ophotograph review determined progression of glaucomatous optic disc damage.

180 traction, optic or scleral pit, or advanced glaucomatous optic nerve changes.

181 ction during hemodialysis (HD) could lead to glaucomatous optic nerve damage and subsequent visual lo

182 Glaucomatous optic nerve damage developed in 23% versus

183 east one of the following: darkened choroid, glaucomatous optic nerve damage, or conjunctival hyperem

184 onally CD94 status had no detected effect on glaucomatous optic nerve damage.

185 set of IOP elevation accompanied by advanced glaucomatous optic nerve damage.

186 ar pressure and hence to prevent progressive glaucomatous optic nerve head damage.

187 The astrocytes in severely glaucomatous optic nerves also showed simplification of

188 sults after optic nerve crush, astrocytes in glaucomatous optic nerves had thickened and simplified p

189 tion, proliferative diabetic retinopathy and glaucomatous optic neuropathies (GONs).

190 nto 3 groups on the basis of the presence of glaucomatous optic neuropathy (GON) and 24-2 visual fiel

191 isc photographs of subjects with and without glaucomatous optic neuropathy (GON) followed during the

192 valuation Study (ADAGES) with a diagnosis of glaucomatous optic neuropathy (GON) or ocular hypertensi

193 to determine the feasibility of identifying glaucomatous optic neuropathy (GON) using IOP corrected

194 d stereophotographic evidence of progressive glaucomatous optic neuropathy (PGON).

195 One hundred eyes from 74 patients with glaucomatous optic neuropathy and a 24-2 VF with mean de

196 urophthalmological conditions that may mimic glaucomatous optic neuropathy and to determine which mos

197 Eyes affected by glaucomatous optic neuropathy at presentation were exclu

198 promise optic nerve head perfusion and cause glaucomatous optic neuropathy by creating transient hypo

199 ucoma was based on clinical examination with glaucomatous optic neuropathy defined by the presence of

200 years, the patient also developed bilateral glaucomatous optic neuropathy despite a well-controlled

201 rom 22 countries who self-registered for the Glaucomatous Optic Neuropathy Evaluation (GONE) Project

202 etinal vascular geometry are associated with glaucomatous optic neuropathy independently of vascular

203 ng IOP elevation of >/= 10 mmHg and incident glaucomatous optic neuropathy over the first 2 years com

204 Patients with OHT or glaucomatous optic neuropathy were recruited, and photop

205 Early POAG subjects had glaucomatous optic neuropathy with mild, reproducible vi

206 ere classified as POAG (open drainage angle, glaucomatous optic neuropathy, and glaucomatous field de

207 nds on the signs of chronic angle damage and glaucomatous optic neuropathy.

208 yes with concomitant epiretinal membrane and glaucomatous optic neuropathy.

209 lar pressure, can lead to the development of glaucomatous optic neuropathy.

210 ay lead to the development or progression of glaucomatous optic neuropathy.

211 ribute to the development and progression of glaucomatous optic neuropathy.

212 athic epiretinal membranes, with and without glaucomatous optic neuropathy.

213 and to the chronic development of bilateral glaucomatous optic neuropathy.

214 lary retinal perfusion, which suggests early glaucomatous optic neuropathy.

215 door allergen exposure in the development of glaucomatous optic neuropathy.

216 Classification accuracy (as glaucomatous or healthy) was compared with EODAT data.

217 re should be taken while classifying them as glaucomatous or not based solely on these characteristic

218 may be applicable to treatments directed at glaucomatous pathology.

219 ntify rapid progression in a newly diagnosed glaucomatous patient over 2 years.

220 es were mixed with tests from 21 consecutive glaucomatous patients (42 eyes with normal tension glauc

221 e Cambridge Face Memory Test was assessed in glaucomatous patients (n = 54; mean age = 69) with a ran

222 DA (p = 0.005) concentration was observed in glaucomatous patients as compared with controls.

223 ping behaviours and techniques may help some glaucomatous patients to adapt to their condition.

224 with age-similar people with healthy vision, glaucomatous patients with advanced bilateral 24-2 VF lo

225 ttern in OHTN patients is similar to that in glaucomatous patients.

226 Topical ocular PBA reduces glaucomatous phenotypes in Tg-MYOC(Y437H) mice, most lik

227 ction of a suitable method for assessment of glaucomatous progression and estimation of rates of chan

228 y will lead to an enhanced ability to detect glaucomatous progression and will allow for more timely

229 om the fitted exponential model, the rate of glaucomatous progression for an average subject of age 7

230 The goal of this study was to determine if glaucomatous progression in suspect eyes can be predicte

231 Timely detection of glaucomatous progression is crucial in the delivery of g

232 Trend analysis techniques to detect glaucomatous progression typically assume a constant rat

233 ments could identify eyes that showed future glaucomatous progression with a higher accuracy than the

234 Additional treatments, glaucomatous progression, intraocular pressure, visual a

235 ral data that enhances our ability to detect glaucomatous progression.

236 are limitations in visual field analysis for glaucomatous progression.

237 evalence of betaPPA affect the likelihood of glaucomatous progression.

238 as development of repeatable abnormal SAP or glaucomatous progressive optic disc changes.

239 t-functionalized biodegradable thermogels in glaucomatous rabbits.

240 ation of retinal ganglion cells (RGC) in the glaucomatous retina is accompanied by activation of the

241 activation of the complement cascade in the glaucomatous retina requires the presence of immunoglobu

242 ater immunoreactivity of the patient sera to glaucomatous retinal proteins (or to oxidatively stresse

243 Bundles in 30 control retinas and 41 glaucomatous retinas were examined.

244 In glaucomatous retinas, reflectance spectra changed along

245 ated with the appearance of tau oligomers in glaucomatous retinas.

246 Screening for glaucomatous RNFL changes in uveitis must be performed d

247 used alone or in combination for identifying glaucomatous RNFL thinning.

248 m IgG was eluted from five randomly selected glaucomatous samples and analyzed by linear ion trap mas

249 proteins, including those detectable only in glaucomatous samples.

250 a reduced tendency for pore formation in the glaucomatous SC cell--likely accounting for increased ou

251 neurodegeneration, transport-intact areas of glaucomatous SC exhibited larger retinal terminals and a

252 ingtin) exhibited higher ELISA titers in the glaucomatous sera.

253 to aid in differentiating between normal and glaucomatous states of the ONH and RNFL - typically by e

254 yes, despite the continued presence of other glaucomatous stresses and signaling pathways.

255 nto irradiated eyes, combined with the other glaucomatous stresses, restored neural damage with a top

256 A total of 758 normal and 58 glaucomatous subjects underwent complete eye examination

257 (myopic subjects), and 7.6 +/- 4.2 degrees (glaucomatous subjects) (all P > .05).

258 , 46 nonglaucomatous myopic subjects, and 86 glaucomatous subjects.

259 We examined the ultrastructure of the glaucomatous superior colliculus (SC) with three-dimensi

260 peripheral LC is located more posteriorly in glaucomatous than in normal eyes, as well as in eyes wit

261 LC depths were significantly greater in the glaucomatous than in the normal eyes in all 11 scans (al

262 he change and rate of change were greater in glaucomatous than normal eyes, and were greater than des

263 Act A protein levels in normal TM (NTM) and glaucomatous TM (GTM) cells.

264 be uniquely present in control but absent in glaucomatous TM and vice versa.

265 Glaucomatous TM cell strains have a lower GRbeta-GRalpha

266 vivo demonstration that regeneration of the glaucomatous TM is possible and points toward novel appr

267 and phosphatidylinositol between control and glaucomatous TM showed several species common between th

268 Glaucomatous TM tissue is stiffer than age-matched contr

269 ss markers was observed in human post-mortem glaucomatous TM tissues.

270 ncreased ECM accumulation in mouse and human glaucomatous TM tissues.

271 tion of IOP and increased strain observed in glaucomatous TM.

272 ship between relative optic nerve axon loss (glaucomatous-to-control eye) and relative RNFLT at the f

273 the Wnt signaling pathway inhibitor, in the glaucomatous trabecular meshwork (GTM), and found that k

274 hosphatidylinositol) profiles of control and glaucomatous trabecular meshwork (TM) derived from human

275 Objective: To model the process of glaucomatous VF decay over the entire perimetric range f

276 Glaucoma and glaucomatous VF loss are associated with greater likelih

277 GCC thickness can predict the development of glaucomatous VF loss in glaucoma suspects and preperimet

278 te visual field (VF) progression and rate of glaucomatous VF loss in patients with primary angle-clos

279 rt the concept that the measured behavior of glaucomatous VF loss to perimetric blindness is nonlinea

280 ocal LC defects are strongly associated with glaucomatous VF progression, and eyes with focal LC defe

281 t in the context of depicting the effects of glaucomatous vision loss and raising awareness for glauc

282 benefit from therapy to prevent progressive glaucomatous vision loss.

283 s was glaucoma (12/31, 39%), and the risk of glaucomatous visual acuity loss was 15% at 2 years and 2

284 (mean age: 67 [SD: 9] years) with a range of glaucomatous visual field (VF) defects in both eyes (mea

285 ) for its ability to identify progression of glaucomatous visual field (VF) defects.

286 f this study is to determine if glaucoma and glaucomatous visual field (VF) loss are associated with

287 Importance: Identifying the course of glaucomatous visual field (VF) loss that progresses from

288 fined as the presence of an open angle and a glaucomatous visual field abnormality or evidence of gla

289 SITA uses prior distributions of normal and glaucomatous visual field behaviour to estimate threshol

290 Most eyes had early (35%) or moderate (31%) glaucomatous visual field defects, but 134 subjects (33%

291 AG was defined as the development of typical glaucomatous visual field loss combined with matching op

292 Rates of glaucomatous visual field loss did not significantly cha

293 tients with glaucoma with moderate to severe glaucomatous visual field loss.

294 , severity, and functional impact of central glaucomatous visual field loss.

295 sk factor information into the estimation of glaucomatous visual field progression resulted in more a

296 al feature in glaucoma and a risk factor for glaucomatous visual field progression, it may be helpful

297 hich a prognostic factor was associated with glaucomatous visual field progression.

298 which may significantly increase the risk of glaucomatous visual field progression.

299 llowing factors were clearly associated with glaucomatous visual field progression: age, disc hemorrh

300 into 2 groups according to TTF in the first glaucomatous visual field: (1) eyes with TTF, defined as