ライフサイエンスコーパス: glaucoma

1 (for AMD) to 24 of 89 outcomes (27.0%) (for glaucoma).

2 y and surgically treated patients (21%) with glaucoma.

3 VF for the detection of progression in early glaucoma.

4 egarding the preferred primary operation for glaucoma.

5 ents with ocular hypertension and open-angle glaucoma.

6 1 kinase may have a role in the pathology of glaucoma.

7 ropia was greater in patients that developed glaucoma.

8 n between discordant IOP values and stage of glaucoma.

9 structural changes can be detected in severe glaucoma.

10 development of vision-related disability in glaucoma.

11 pect, 28% had glaucoma, and 28% had advanced glaucoma.

12 ility of predictive genetic testing for MYOC glaucoma.

13 odel of the common neurodegenerative disease glaucoma.

14 fits those eyes relatively more than in mild glaucoma.

15 reement for each camera for the diagnosis of glaucoma.

16 r tissues may have a protective role against glaucoma.

17 ith glaucoma and/or likelihood of developing glaucoma.

18 cestrally-related index patient with ASD and glaucoma.

19 is not appropriate as a screening metric for glaucoma.

20 01) in the normal hemisphere of the eye with glaucoma.

21 tflow, is a major risk factor for open-angle glaucoma.

22 May 31, 2016, among 112 white patients with glaucoma.

23 ssess the association between statin use and glaucoma.

24 to optic neuropathies such as normal tension glaucoma.

25 ed States and had newly diagnosed open-angle glaucoma.

26 changes that otherwise occur early in DBA/2J glaucoma.

27 and intraocular pressure (IOP) elevation in glaucoma.

28 -invasive gel/microsphere (GMS) eye drop for glaucoma.

29 provide insight into the pathophysiology of glaucoma.

30 rdant in eyes with thin corneas and advanced glaucoma.

31 ome neurophthalmological disorders can mimic glaucoma.

32 a protein associated with primary open-angle glaucoma.

33 that indicates a clinically more challenging glaucoma.

34 tility of vCDR asymmetry in the diagnosis of glaucoma.

35 mouse model of hereditary primary open-angle glaucoma.

36 cellent diagnostic performance for detecting glaucoma.

37 (19.7%), of which 28 (55.0%) had concomitant glaucoma.

38 r segment neovascularization, or neovascular glaucoma.

39 n, may be more applicable for treating human glaucoma.

40 self-reported visual function of people with glaucoma.

41 crucial for the diagnosis and management of glaucoma.

42 prevention and novel treatment approaches to glaucoma.

43 ereas blindness and vision impairment due to glaucoma (0.71 [0.57-0.86]) and corneal opacity (0.54 [0

44 Exclusions included 11 patients with glaucoma, 1 patient with Stickler syndrome, and 1 patien

45 n-Meier], respectively) and less neovascular glaucoma (11.6% and 21.3% after 5 years, P = .001 and P

46 sterior synechiae (34%), cataract (32%), and glaucoma (15%).

47 Among the 33 participants with glaucoma, 19 (58%) were white, 12 (36%) were black, and

48 A total of 364 eyes had early glaucoma, 303 eyes were glaucoma suspects, and 108 eyes

49 (8.4 million [0.9 million to 29.5 million]), glaucoma (4.0 million [0.6 million to 13.3 million]), an

50 6, 100%), neurotrophic keratitis (2/26, 8%), glaucoma (5/26, 19%), and tortuous retinal vessels (4/26

51 Twenty-one eyes from 21 patients with glaucoma (7 men and 14 women; mean [SD] age, 63.7 [9.9]

52 ne is associated with 1-2% of normal tension glaucoma, a common cause of vision loss and blindness th

53 ulation are important to prevent neovascular glaucoma, a common complication.

54 ar pressure (IOP) is a major risk factor for glaucoma, a leading cause of blindness.

55 Long-term treatment of glaucoma, a major leading cause of blindness, is challen

56 Tg-TBK1 mice exhibit the cardinal sign of glaucoma, a progressive loss of RGCs.

57 fected, glaucoma suspect, glaucoma, advanced glaucoma) according to the severity of disease at the ti

58 into 4 groups (unaffected, glaucoma suspect, glaucoma, advanced glaucoma) according to the severity o

59 radiation retinopathy and 57.8% neovascular glaucoma after 5 years).

60 rt the incidence of, and factors related to, glaucoma after lens-sparing vitrectomy (LSV) surgery in

61 th more severe ROP had a higher incidence of glaucoma after lens-sparing vitrectomy.

62 need to increase awareness of the impact of glaucoma among clinicians, patients and their families,

63 yes of 909 subjects with suspect or manifest glaucoma and >/=5 VF examinations.

64 A total of 30 perimetric glaucoma and 30 age-matched normal participants were inc

65 All patients had been diagnosed with glaucoma and 6 eyes had glaucoma drainage devices (GDDs)

66 A total of 195 eyes (116 glaucoma and 79 glaucoma suspect) of 99 patients with st

67 ed in patients with common eye diseases like glaucoma and age-related macular degeneration.

68 heritable risk factor for primary open angle glaucoma and currently the only target for glaucoma ther

69 carpine is a prototypical drug used to treat glaucoma and dry mouth and is classified as either a ful

70 tatistically significant association between glaucoma and each of anxiety and depression.

71 chesani-like syndrome and primary open angle glaucoma and ectopia lentis in dogs.

72 ystoid macular changes increased at advanced glaucoma and epiretinal membrane stages.

73 iple functional tests for early detection of glaucoma and for circuit-specific therapeutic targets in

74 ne-type diterpenoid used in the treatment of glaucoma and heart failure based on its activity as a cy

75 orter inhibitor, in patients with open-angle glaucoma and ocular hypertension.

76 d screening intervention designed to improve glaucoma and other eye disease detection and follow-up c

77 hes for cell replacement-based therapies for glaucoma and other optic neuropathies.SIGNIFICANCE STATE

78 onged GC therapy that can lead to iatrogenic glaucoma and permanent vision loss.

79 ding age-related macular degeneration (AMD), glaucoma and refractive error.

80 nicity of the TBK1 gene duplication in human glaucoma and suggest that excess production of TBK1 kina

81 the awareness and knowledge of adults about glaucoma and the factors affecting it in Gondar town, No

82 derstand structure-function relationships in glaucoma and their application to improve glaucoma diagn

83 s; standard deviation [SD], 4.56 years) with glaucoma and their parents.

84 mary congenital glaucoma (PCG), as judged by glaucoma and visual outcomes.

85 terval, from 45 eyes of 23 participants with glaucoma and/or likelihood of developing glaucoma.

86 ly than change in neuroretinal parameters in glaucoma, and (2) Bruch's membrane or anterior sclera sh

87 cal cases 44% were glaucoma suspect, 28% had glaucoma, and 28% had advanced glaucoma.

88 a better understanding of diseases, such as glaucoma, and accelerate the development of therapeutic

89 ss loss was detectable in early and moderate glaucoma, and average macular GCIPL thickness loss was d

90 s, such as age-related macular degeneration, glaucoma, and diabetic retinopathy, are ideal candidates

91 generation, cataracts, diabetic retinopathy, glaucoma, and intraocular cancers.

92 patterns vary in the surgical management of glaucoma, and opinions differ among surgeons regarding t

93 symmetry >/=0.20 for disc plus field defined glaucoma are 22.7% and 97.7%, respectively, whereas the

94 c membranes, keratoprosthesis retention, and glaucoma are major challenges in the postoperative perio

95 dy confirmed that elevated IOP and secondary glaucoma are major complications in herpetic AU.

96 Chronic forms of glaucoma are painless and symptomatic visual-field defec

97 ls at an early stage or even before signs of glaucoma are present.

98 Glaucomas are neurodegenerative diseases that cause visi

99 discordant IOP measurements and the stage of glaucoma, as assessed by the Glaucoma Severity Score.

100 Two glaucoma-associated mutants of OPTN, E50K and M98K, but

101 worse) mean (SD) scores than those with mild glaucoma at baseline on the Local Eye (4.68 [6.62] vs 3.

102 c targets for some patients with early-onset glaucoma based on the molecular and cellular events caus

103 d resulting visual deficits are hallmarks of glaucoma, but the underlying mechanisms remain unclear.

104 is the most common genetic mutation causing glaucoma by increasing intraocular pressure (IOP).

105 Glaucoma can occur at all ages, with Mendelian inheritan

106 To examine whether patients with glaucoma can perform self-tonometry using a rebound tono

107 measured CDR and noted possible evidence of glaucoma (CDR >/= 0.7 or the presence of a notch or disc

108 s included differences in RNFL thickness and glaucoma classification (i.e., normal, borderline, or ou

109 This study was conducted at a glaucoma clinic at a university hospital from March 1, 2

110 t patients were consecutively recruited from glaucoma clinics at the University of California, San Fr

111 uously for 2 years had a 21% reduced risk of glaucoma compared with nonusers (adjusted HR, 0.79; 95%

112 an-Meier method estimated the probability of glaucoma control vs time postoperatively, and values wer

113 omy, cataract extraction, or a procedure for glaucoma control.

114 ucoma (interval between LSV and the onset of glaucoma), date of lensectomy (if performed), and retina

115 Neovascular glaucoma developed in 20 of 36 eyes (56%).

116 ibuting, and the only preventable, factor in glaucoma development.

117 ioxidant biodegradable thermogels to prevent glaucoma development.

118 awareness of four ocular diseases; cataract, glaucoma, diabetic retinopathy (DR) and dry eye disease

119 in glaucoma and their application to improve glaucoma diagnosis and monitoring.

120 structure-function relationships to improve glaucoma diagnosis first are discussed.

121 for change over time also may be useful for glaucoma diagnosis, with advantages over classifying eye

122 nd retinal ganglion cells is the hallmark of glaucoma diagnosis.

123 s more likely to develop rapidly progressive glaucoma disease despite significantly lower mean and ba

124 nt Boston type I keratoprosthesis (KPro) and glaucoma drainage device (GDD) implantation.

125 trabeculectomy, complicated trabeculectomy, glaucoma drainage device, and cycloablative procedure.

126 -penetrating keratoplasty), bleb-associated, glaucoma drainage device-associated, and open globe inju

127 been diagnosed with glaucoma and 6 eyes had glaucoma drainage devices (GDDs) inserted before KPro im

128 in was detected in human tissues relevant to glaucoma (e.g., ciliary body).

129 e should be enhanced through public oriented glaucoma education via mass media and incorporating eye

130 ociated central visual field (VF) defects in glaucoma, even in early stages.

131 Laser-induced experimental glaucoma (ExGl) in non-human primates (NHPs) is a common

132 significantly different between healthy and glaucoma eyes during this relatively short follow-up per

133 early and moderate glaucoma eyes; in severe glaucoma eyes, rates of average macular GCIPL loss were

134 compared global change over time in advanced glaucoma eyes.

135 ckness were detectable in early and moderate glaucoma eyes; in severe glaucoma eyes, rates of average

136 rabbit model of scar tissue formation after glaucoma filtration surgery increased the long-term succ

137 Two hundred thirty-six patients with glaucoma followed up for an average of 4.3+/-1.5 years.

138 ven patients with newly diagnosed open-angle glaucoma from the CIGTS.

139 hile the utility of NFL declines in advanced glaucoma, GCC remains a sensitive progression detector f

140 Diagnostic genetic tests using early-onset glaucoma genes are also proving useful for pre-symptomat

141 06 subjects (411 eyes): 210 normal (NL), 183 glaucoma (GL), and 18 diabetic retinopathy (DR) at Tilga

142 In the glaucoma group, 16 of the 26 eyes (61.5%) classified as

143 In the glaucoma group, the SVC and all-plexus retinal VD (mean

144 d DCP VD were not significantly lower in the glaucoma group.

145 Participants with more severe glaucoma had higher (worse) mean (SD) scores than those

146 An experimental model of glaucoma has been established by elevating the intraocul

147 Congenital and childhood glaucomas have strong genetic bases and disease-causing

148 t independent factor associated with time to glaucoma (hazard ratio = 2.76, 95% confidence interval =

149 ered during early, predegenerative stages of glaucoma; however, whether the early immune responses oc

150 data on visual field testing/a diagnosis of glaucoma (if available).

151 End stage glaucoma in patient 2 resulted in the enucleation of the

152 Patients with glaucoma in the treated eye (n = 9) had greater anisomet

153 igher level of awareness and knowledge about glaucoma in urban communities than previous studies.

154 How microRNAs (miRs) regulate IOP and glaucoma in vivo is largely unknown.

155 rs74315329 for ocular hypertension (and thus glaucoma), in comparison with that reported previously.

156 elopment of certain ocular diseases, such as glaucoma, in these patients.

157 The risk of developing glaucoma increases with age; therefore, understanding me

158 nal surgeries, presence of glaucoma, time to glaucoma (interval between LSV and the onset of glaucoma

159 ABSTARCT: Glaucoma is a chronic disease that shares many similarit

160 Glaucoma is a heterogeneous group of diseases characteri

161 Glaucoma is a leading cause of blindness that leads to c

162 Glaucoma is a leading cause of blindness worldwide, and

163 Glaucoma is a leading cause of blindness, with an estima

164 Glaucoma is a major cause of irreversible blindness worl

165 Glaucoma is the leading cause of irreversible blindness

166 er optic neuropathies.SIGNIFICANCE STATEMENT Glaucoma is the most common cause of blindness worldwide

167 However, awareness and knowledge about glaucoma is unknown at community level, making provision

168 r imaging has been heavily incorporated into glaucoma management and provides important information t

169 Optimal glaucoma management requires information from imaging an

170 Our findings indicate that patients with glaucoma may potentially be at risk of higher or lower I

171 CH significantly higher for GLD compared to glaucoma (mean difference 1.83, p < 0.001), and signific

172 and significantly higher for OHT compared to glaucoma (mean difference 2.35, p < 0.001).

173 found in the normal hemisphere of eyes with glaucoma, measured by mean [SE] differences in blood flu

174 a, median -8.25 D; IQR -11.38, -5.25 D vs no glaucoma median -2.75; IQR -6.38, -0.75 D; P = .005).

175 eated eye (n = 9) had greater anisometropia (glaucoma, median -8.25 D; IQR -11.38, -5.25 D vs no glau

176 Secondary outcome measures include IOP, glaucoma medical therapy, visual acuity, visual fields,

177 per bottle and drops per milliliter (mL) of glaucoma medication.

178 tively, required IOP-lowering treatment with glaucoma medications added, adjunctive laser trabeculopl

179 ributable to eye care providers is driven by glaucoma medications, accounting for $1.2 billion (54% o

180 r bottle of a variety of commonly prescribed glaucoma medications.

181 In advanced glaucoma, more GC-IPL tissue remains above the measureme

182 39) or high IOP (>/=22 mm Hg) with suspected glaucoma (n = 23), of whom several required preoperative

183 surgery, 62 patients had either preexisting glaucoma (n = 39) or high IOP (>/=22 mm Hg) with suspect

184 gher than 35 mm Hg, and 1 with angle-closure glaucoma not attributed to the study drug or procedure.

185 intraocular pressure (IOP) in Normal Tension Glaucoma (NTG) patients.

186 ated with POAG (including the normal tension glaucoma (NTG) subgroup), 8 with PACG and 2 with XFS.

187 To evaluate the effect of glaucoma on functional vision and on vision-related (VR)

188 aPPA) has been reported as a risk factor for glaucoma onset and progression.

189 Eyes with glaucoma or glaucoma suspect were excluded from primary

190 variability in patients diagnosed as having glaucoma or glaucoma suspects.

191 There were no reports of neovascular glaucoma or iris neovascularization.

192 and included both eyes of 100 patients with glaucoma or ocular hypertension.

193 if each set of exams was from a patient with glaucoma or with a neurophthalmologic condition.

194 line, IOP of 5 mmHg or less, reoperation for glaucoma, or loss of light perception vision.

195 loss in patients with primary angle-closure glaucoma (PACG) using pointwise linear regression (PLR)

196 ght the importance of ANGPT/TEK signaling in glaucoma pathogenesis and identify a candidate target fo

197 nterpret NEI VFQ-25 scores in their advanced glaucoma patient cohort.

198 One hundred fifty-five glaucoma patients and 35 healthy controls.

199 mated RGC density, and cone-to-RGC ratios in glaucoma patients and healthy controls.

200 Glaucoma patients and healthy participants underwent in

201 sess the character and degree of concerns of glaucoma patients and identify demographic/clinical fact

202 s found between healthy control subjects and glaucoma patients in the mean rate of PCT change (P = .2

203 Glaucoma patients reported varied degrees of concern reg

204 At baseline, 67 of 236 (28%) glaucoma patients were classified as disabled based on N

205 Glaucoma patients were followed up for a mean of 3.90 ye

206 Glaucoma patients, in comparison to non-glaucoma patients, had a higher number of IOP peaks duri

207 Glaucoma patients, in comparison to non-glaucoma patient

208 ts' concerns was administered to consecutive glaucoma patients.

209 ally invasive surgical option for refractory glaucoma patients.

210 n summary indices were extracted from 11,449 glaucoma patients.

211 Primary congenital glaucoma (PCG) is a leading cause of blindness in childr

212 tional angle surgeries in primary congenital glaucoma (PCG), as judged by glaucoma and visual outcome

213 l trabeculotomy (CPT) for primary congenital glaucoma (PCG).

214 dy included patients with primary open angle glaucoma (POAG group, n = 30) and controls (non POAG gro

215 (SLT) as sole therapy for primary open-angle glaucoma (POAG) in an Afro-Caribbean population.

216 fibrosis of the TM as in primary open-angle glaucoma (POAG) patients, and is characterized by increa

217 so occur in patients with primary open angle glaucoma (POAG), in which there is specific RGC loss.

218 Primary open-angle glaucoma (POAG), the most common optic neuropathy, is a

219 and after development of primary open-angle glaucoma (POAG); determine the prognostic significance o

220 GFCS and JOAG in a single-surgeon pediatric glaucoma practice who underwent illuminated microcathete

221 On the basis of PR-OCTA, glaucoma preferentially affects perfusion in the SVC in

222 Diagnosed glaucoma prevalence increased by 9.4% (P = .03) from 6.7

223 a mouse model of glucocorticoid (GC)-induced glaucoma, primary human TM cells and human post-mortem T

224 agreement was fair regarding questions about glaucoma progression (kappa, 0.39; 95% CI, 0.32-0.48) an

225 tion (P = 0.049) and less vision loss due to glaucoma progression (P = 0.046).

226 These data suggest that these glaucoma progression software packages are insufficient

227 Characteristic patterns of glaucoma-related macular RGC+IPL loss appeared to be mor

228 h missing data (n = 4) and those requiring a glaucoma-related secondary surgical intervention (n = 9)

229 Children with glaucoma report HR QoL scores similar to those described

230 bserved eyes (in decade 2) developed painful glaucoma requiring enucleation.

231 ay associated proteins were activated in the glaucoma samples suggesting an innate inflammatory respo

232 ine were calculated in 87 eyes with advanced glaucoma (SAP MD </=-12 dB).

233 cular degeneration, diabetic retinopathy and glaucoma) segments of the eye.

234 sensitivity was not a reliable surrogate for glaucoma severity in this cross-sectional study.

235 combined with trabectome surgery using a new glaucoma severity index.

236 OPGAT showed a positive correlation with the Glaucoma Severity Score (rs = 0.33; P < .001) and a nega

237 The mean (SD) Glaucoma Severity Score was 4.7 (3.4) (95% CI, 4.1-5.4).

238 nd the stage of glaucoma, as assessed by the Glaucoma Severity Score.

239 ield (VF) reliability at different stages of glaucoma severity.

240 e of lens opacity, then the hazard of having glaucoma significantly increased compared with those wit

241 hese images were mixed randomly and a masked glaucoma specialist was asked to distinguish if each set

242 e eyes were misdiagnosed when evaluated by a glaucoma specialist, which can lead to inadequate manage

243 Optic disc photographs were read by 2 masked glaucoma specialists for VCDR and HCDR estimation.

244 The collaborative consisted of 13 glaucoma specialists from 3 practices in Michigan.

245 Interobserver agreement among the 5 glaucoma specialists with the VF progression software wa

246 ereoscopic optic disc photograph readings by glaucoma specialists.

247 e (2013-2015) data from the ongoing Falls in Glaucoma Study (FIGS).

248 ths) in the multicenter Advanced Imaging for Glaucoma Study.

249 tion was seen in subjects with more advanced glaucoma suggesting that the trabecular meshwork is the

250 as detectable in early, moderate, and severe glaucoma, suggesting that structural changes can be dete

251 Higher CH in GLD and OHT compared to glaucoma suggests increased viscoelasticity of ocular ti

252 participants (67%) had previously undergone glaucoma surgery (fibrotic group) (mean [SD] age, 43.8 [

253 ticipants (33%) had not previously undergone glaucoma surgery (nonfibrotic group) (mean [SD] age, 47.

254 The adjusted rate ratio of glaucoma surgery among those who received 7 or more inje

255 Risk of glaucoma surgery compared with the number of intravitreo

256 2 mm Hg and 20% reduction without additional glaucoma surgery or devastating complication.

257 cular pressure could lead to higher rates of glaucoma surgery to lower this pressure.

258 us associated with binocular diplopia due to glaucoma surgery was hypertropia (10/11 GDD cases, 2/2 t

259 of patients with conjunctival fibrosis after glaucoma surgery with candidate gene expression tissue b

260 a lower failure rate, lower rate of de novo glaucoma surgery, and lower mean IOP on fewer medication

261 ines from patients with and without previous glaucoma surgery, respectively.

262 OP lowering medications and without need for glaucoma surgery.

263 and prognosis in conjunctival fibrosis after glaucoma surgery.

264 Nineteen percent of the patients needed glaucoma surgery.

265 Cases were identified using glaucoma surgical codes for trabeculectomy, complicated

266 Eyes with glaucoma or glaucoma suspect were excluded from primary analysis but

267 A total of 195 eyes (116 glaucoma and 79 glaucoma suspect) of 99 patients with stereoscopic photo

268 spect, whereas among Clinical cases 44% were glaucoma suspect, 28% had glaucoma, and 28% had advanced

269 en sub-classified into 4 groups (unaffected, glaucoma suspect, glaucoma, advanced glaucoma) according

270 f Genetic cases were unaffected and 17% were glaucoma suspect, whereas among Clinical cases 44% were

271 f 364 eyes had early glaucoma, 303 eyes were glaucoma suspects, and 108 eyes were ocular hypertensive

272 f visual field defects in glaucomatous eyes, glaucoma suspects, and ocular hypertensives with 24-2 an

273 in patients diagnosed as having glaucoma or glaucoma suspects.

274 To develop a shortened glaucoma symptom measure based on the Collaborative Init

275 sing Ocular Surface Disease Index (OSDI) and Glaucoma Symptoms Scale (GSS) questionnaires.

276 Patients with or suspected glaucoma tested with 24-2 and 10-2.

277 .91; 95% CI, 3.40-4.49) of not receiving any glaucoma testing compared with blacks with commercial he

278 ts with OAG are receiving substantially less glaucoma testing compared with persons with commercial h

279 edicaid had 198% higher odds of receiving no glaucoma testing compared with whites possessing commerc

280 nts were 234% more likely to not receive any glaucoma testing in the 15 months after initial diagnosi

281 ave therapeutic potential for those cases of glaucoma that are sub-optimally responsive to convention

282 rated the discovery of genes contributing to glaucoma, the leading cause of irreversible blindness wo

283 e glaucoma and currently the only target for glaucoma therapy.

284 ), subsequent retinal surgeries, presence of glaucoma, time to glaucoma (interval between LSV and the

285 2.5 million to 16.3 million), and because of glaucoma to 3.2 million (0.4 million to 11.0 million).

286 .8 million (0.8 million to 32.1 million), by glaucoma to 4.5 million (0.5 million to 15.4 million), a

287 m measure based on the Collaborative Initial Glaucoma Treatment Study (CIGTS) Symptom and Health Prob

288 HVF tests, 25% of these were misdiagnosed as glaucoma (two ischemic optic neuropathies and two congen

289 Consecutive eyes with uncontrolled glaucoma underwent microstent or trabeculectomy surgery

290 To detect macular perfusion defects in glaucoma using projection-resolved optical coherence tom

291 protective effect of statins on the risk of glaucoma varies depending on the daily dosage or type of

292 nt can play a significant role in preventing glaucoma vision loss and blindness in people of African

293 edical and ocular history, family history of glaucoma, visual acuity, and intraocular pressure measur

294 area under the curve (AUC) to differentiate glaucoma was 0.873 for BMO-MRA, compared to 0.866 for BM

295 Glaucoma was diagnosed based on a masked grading of opti

296 was noted in 22 patients (44%), neovascular glaucoma was noted in 1 patient (2%), and there were no

297 Preexisting glaucoma was present in 72.9% (35 of 48 eyes).

298 eviews that addressed AMD, cataract, DR, and glaucoma; were published as of July 20, 2016; and includ

299 (RNFL) between the hemispheres in eyes with glaucoma with single-hemifield visual field (VF) defects

300 ymmetry should initiate a more comprehensive glaucoma workup, especially in individuals with addition