What is the main cause of the atrophy of the retina?

This atrophy leads to an overall thickness reduction which is counterbalanced by increased water content and thus is associated with concurrent atrophy and swelling.

What is the meaning of retrograde maculopathy in glaucoma?

The authors suggest that the term retrograde maculopathy in glaucoma suitably describes the structural findings of thinning of the GCL, thickening of theunderlying inner nuclear and outer plexiform layers, and/or MME in advanced glaucoma cases.

What was the thickness of the peripapillary nerve fiber layer?

For the measurement of the peripapillary retinal nerve fiber layer (pRNFL) thickness an OCT section along a ring of 3.6mm diameter centered on the disc was used.

(Open Access) Retrograde Maculopathy in Patients With Glaucoma. (2017) | Jacqueline Brazerol

Q: What are the contributions in "Retrograde maculopathy in patients with glaucoma" ?

In this study the authors systematically investigated glaucoma-induced changes in macular layers to evaluate whether glaucoma-associated damage extends beyond the macular ganglion cell layer.

Q: How much thinner was mINL/OPL in PEXG patients?

mINL/OPL was about 3 mm thinner in PEXG patients as compared with POAG patients (INL/OPL thickness in PEXG patients=66± 0.4mm, mINL/OPL thickness in POAG patients=69± 0.5mm, P=0.001).

Q: What is the mean value of mGCL/IPL?

1.2±0.3 6.2±0.5 16±1.9 0.001 <0.001 <0.001 pRNFL 117±2.5 80±1.5 50±3.1 <0.001 <0.001 <0.001 mGCL/IPL 91±1.3 73±1.0 51±4.0 <0.001 <0.001 <0.001 mINL/OPL 68±0.9 68±0.3 81±2.6 0.9 <0.001 <0.001 mORT 152±1.9 154±0.6 161±3.0 0.2 0.03 0.04

source: https://doi.org/10.7892/boris.108241 | downloaded: 10.8.2022

Retrograde Maculopathy in Patients With Glaucoma

Jacqueline Brazerol, BSc,* Milko E. Iliev, MD,* Rene

hn, MD,*

Stephan Fra

nkl, MD,* Hilary Grabe, MD,* and Mathias Abegg, MD, PhD*

Purpose: Macular optical coherence tomography (OCT) analysis

can be used for quantitative measures of optic nerve atrophy at a

location far from the optic nerve head. This recently led to the

ﬁnding of microcystic macular edema (MME), that is vacuolar

inclusions in the macular inner n uclear layer, in some glaucoma

patients. The involvement of individual retinal layers is yet

unclear in glaucoma. In this study we systematically investigated

gla ucoma-induc ed changes in macular layers to evaluate whether

gla ucoma-associated damage extends beyond the macular g an-

glion cell layer.

Patients and Methods: We included 218 consecutive patients and

282 eyes with conﬁrmed primary open-angle glaucoma or pseu-

doexfoliation glaucoma, and macular OCT in a cross-sectional

observational study. Eyes were screened for presence of MME.

Thickness of individual retinal layers was determined using a

semiautomatic segmentation algorithm. Peripapillary nerve ﬁber

layer thickness and mean defect in visual ﬁeld testing were

extracted from OCT and medical records, respectively. Results

were compared with a small group of eyes with no apparent

glaucoma.

Results: We found MME in 5 eyes from 5 primary open-angle

gla ucoma patients and 3 eyes of 3 pseudoexfolia tion glaucoma

patients (2.8%). MME was conﬁned to the inner nuclear layer

in a perifoveal ring and was associated wit h thinning of the

ganglion cell layer and thickening of the macular inner nuclear

layer. Glaucoma eyes without MME showed a signiﬁcant inverse

correlation of inner nuclear layer thickness with glaucoma

severity.

Conclusions: Glaucomatous damage leads to a gradual thickening

of the inner nuclear layer, which leads to MME in more severe

glaucoma cases. These changes, along with nerve ﬁber loss and

ganglion cell loss, may be summarized as glaucoma-associated

retrograde maculopathy.

Key Words: retina, maculopathy, glaucoma, segmentation, macular

edema

(J Glaucoma 2017;26:423–429)

reliable determination of glaucoma severity and pro-

gression rate is key to the successful management of

this common disease, which imposes a considerable bur-

den of disease both on aﬀected patients and society.

Traditionally, the glaucoma-associated nerve ﬁber loss is

assessed at the level of the optic disc, where it causes

increased disc cupping and thinning of the retinal nerve

ﬁber layer (RNFL). The latter may be measured using

spectral-domain optical coherence tomography, w hich

provides reproducible imaging at high spatial resolution.

RNFL measurements have brought great advances in

objective quantitative assessment of glaucoma pro-

gression

1,2

outperforming every other imaging device so

far.

Given that all nerve ﬁbers pass through the optic

nerve head, it is logical to measure ﬁber loss at this level.

However, there are numerous situations in which RNFL

measures are diﬃcult or impossible to use: advanced

glaucomatous disc damage, optic disc drusen, concurrent

intracranial hypertension, dysplastic discs, myopic disc

alterations, etc. Thus a measure o f g lauc oma-associated

retinal nerve ﬁber loss distant to the optic disc is useful

and has inspired research in the recent past. Most research

has focused, with good reason, on the analysis of the

macular ganglion cel l layer (mGCL) complex representing

the area with the highest density of retinal ganglion cells in

the retina ( about 50%).

Studies found that the mGCL

and inner plexiform layer (IPL), the macular ganglion cell

complex (mGCC = RNFL + GCL + IPL), and the total

macular thickness can be used to detect glaucoma pro-

gression.

5,6

Less ex plor ed is the eﬀect of glaucoma on

deeper retinal layers. It was found that glaucoma might be

associated with changes at the level of photoreceptors.

7,8

The involvement of the inner nuclear layer is not clear:

Some have reported that outer retinal layer thickness and

inner nuclear layer thickness is not changed from glau-

coma

5,9

while others have found a thinning of the inner

nuclear layer.

Recent works from nonglaucoma-

associated optic neuropathies showed that optic neuro-

pathy may lead to thickening and edema in the inner

nuclear layer, which was termed microcystic macular

edema (MME).

Nerve ﬁber damage and the subsequent

retrograde loss of ganglion cells is thought to cause a

dysfunction of Muller c ells, which impairs retinal water

clearance and results in edema.

12–15

Muller cell gliosis is

indeed a common ﬁnding in animal models of optic

neuropathy

16,17

and in humans.

MME has been found in

all types of optic neuropathy including glaucoma,

with a

reported prevalence of 4% in the latter and 9% in non-

glaucoma optic neuropathies.

It is unclear, however,

why some but not other patients develop this edema. On

the basis of the Muller cell dysfunction hypothesis one

would predict a thickness change, with or without

microcysts, in most cases with pronounced optic neuro-

pathy. Given the potential of macular layer analysis for

future assessment of glaucoma damage and the observa-

tion of MME in glaucoma, we believe that the analysis of

the macular anatomy, inner and outer layers, is important

in glaucoma.

Received for publication June 29, 2016; accepted December 30, 2016.

From the *Department of Ophthalmology, Inselspital, Bern University

Hospital, University of Bern, Bern, Switzerland; and wDepartment

of Ophthalmology, University Medical Center Mainz, Mainz,

Germany.

Disclosure: The authors declare no conﬂict of interest.

Reprints: Mathias Abegg, MD, PhD, Department of Ophthalmology,

Bern University Hospital, University of Bern, Inselspital, CH-3010

Bern, Switzerland (e-mail: mathias.abegg@insel.ch).

DOI: 10.1097/IJG.0000000000000633

ORIGINAL STUDY

J Glaucoma



Volume 26, Number 5, May 2017 www.glaucomajournal.com

423

In this work we systematically explored individual

retinal layers in the macula of patients with primary open-

angle glaucoma (POAG) and pseudoexfoliation glaucoma

(PEXG) to determine thickness in and below the GCL and

to correlate these parameters with the severity of glaucoma.

We determined the frequency of MME in POAG and

PEXG and explored changes in the deeper layers associated

with glaucoma damage.

PATIENTS AND MET HODS

Study Design and Patients

All medical re cords of patients seen between Ja nuary

2010 and January 2015 at the Department of Oph-

thalmology, Inselspital, University Hospital, University of

Bern, were retrospectively screened for the German

translation of the keywords “open-angle glaucoma”

(POAG) and “pseudoexfoliation glaucoma” (PEXG).

Inclusion criteria were (1) conﬁrmed diagnosis of either

POAG or PEXG by a glaucoma specialist and (2) presence

of high resolution macular OCT. The diagnosis of glau-

coma was based on standard clinical criteria, that is

presence of optic neuropathy, elevated intraocular pres-

sure in the present or the past, and visua l ﬁeld defects.

Glaucoma suspects or normal tension glaucoma were thus

not included. Exclusion criteria were the following:

Known history of retinal disease (eg, diabetic retinopathy,

age-related macular degeneration, retinal detachment,

etc.), optic nerve abnormalities other than glaucoma, and

poor image quality. The study was approved by the local

ethics committee.

Demographics and Clinical Characteristi cs

For each patient we determined age and sex. If avail-

able we also collected the best-corrected visual acuity,

intraocular pressure on the last visit, and mean defect (MD)

in visual ﬁeld determined by the “glaucoma program” of

the Octopus Perimeter (Haag-Streit, Switzerland). Visual

acuity was converted from Snellen values into logMAR

values according to a previously published conversion

table

to allow averaging and statistical analysis.

Imaging, Segmentation, and Analysis

For imaging, a high-resolution OCT with a scanning

laser ophthalmoscope (Spectralis HRA + OCT; Heidelberg

Engineering, Heidelberg, Germany) was used. This allows

for simultaneous OCT scans with infrared imaging. The

OCT scans included a volume scan (30 20 degrees) using

61 line scans, each consisting of 9 averaged line scans.

Macular line scans were screened manually for presence of

MME which was deﬁned by the presence of vertical

vacuoles in the inner nuclear layer.

For the analysis of retinal layers we used a custom-

built segmentation software as described previously.

13,21

The segmentation algorithm determined the border

between (1) the internal limiting membrane; (2) GCL; (3)

inner nuclear layer; (4) outer nuclear layer; (5) junction of

the inner and the outer segments; (6) outer segment of

photoreceptors/pigment epithelium complex; and (7) Bruch

membrane. From this we determined the thickness of the

combined mGCL and the IPL, macular inner nuclear layer

thickness and outer plexiform layer (mINL/OPL) and

macular outer retinal thickness (mORT). The latter was

deﬁned as the thickness from the inner border of the outer

nuclear layer down to Bruch membrane. The automatic

segmentation was veriﬁed by an examiner (J.B.) and, when

necessary, manually adapted. To obtain layer thickness

values an “Early Treatment Diabetic Retinopathy Study

(ETDRS)”—grid was centered on the fovea and the average

thickness value for each sector of the grid was exported. To

simplify the further analysis of the macular layers, we cal-

culated the mean thickness of the superior, temporal, and

inferior sectors of the inner ring of the Early Treatment

Diabetic Retinopathy Study-grid for each layer and each

patient. This resulted in a single value per layer per patient.

For the measurement of the peripapillary retinal nerve ﬁber

layer (pRNFL) thickness an OCT section along a ring of

3.6 mm diameter centered on the disc was used. pRNFL

values were automatically provided by standard Spectralis

software and yielded values from 6 sectors around the disc:

superotemporal, superonasal, inferotemporal, inferonasal,

temporal, and nasal. For this analysis, too, the mean of the

superotemporal, the temporal and the inferotemporal sec-

tor of the pRNFL was calculated for each patient to sim-

plify statistical analysis. If only 1 eye fulﬁlled the diagnostic

criteria for glaucoma, we used the contralateral eye as

control, provided the pRNFL was within normal limits of

the Heidelberg system. Given that an apparently normal

contralateral eye of a glaucoma patient may not be con-

sidered as “healthy” we refer to this group as “normal-

RNFL” group. To enlarge the normal-RNFL group we

additionally included 9 eyes from 9 healthy age-matched

subjects that were found in our database. This resulted in 3

groups, glaucoma without MME, glaucoma with MME,

and normal-RNFL eyes. For quantitative analysis we

excluded the left eye of those patients that had data for

TABLE 1. Summary of Clinical Findings in Glaucoma Patients With MME

Patient ID Age (y) Sex Eye Diagnosis BCVA (logMAR) MD (dB) pRNFL ( lm) mGCL/IPL (lm) mINL/OPL (lm)

25 81 F OS POAG 0.0 6.8 59 69 66

72 68 M OD POAG 0.1 17.9 50 49 86

81 60 M OS POAG 0.2 19.6 34 38 87

92 56 M OD POAG 0.2 51 58 86

100 48 F OD POAG 0.05 20.3 56 64 79

198 75 F OS PEXG 0.0 15.5 59 43 75

203 72 F OD PEXG 0.3 19.2 41 43 88

212 67 M OD PEXG 0.0 11.8 52 46 83

BCVA indicates best-corrected visual acuity; F, female; M, male; MD, mean visual ﬁeld defect; mGCL/IPL, macular ganglion cell layer/inner nuclear layer;

mINL/OPL, macular inner nuclear layer/outer plexiform layer; MME, microcystic macular edema; OD, right eye; OS, left eye; PEXG, pseudoexfoliation

glaucoma; POAG, primary open-angle glaucoma; pRNFL, peripapillary retinal nerve ﬁber layer.

Brazerol et al J Glaucoma



Volume 26, Number 5, May 2017

424

www.glaucomajournal.com Copyright

FIGURE 1. Anatomic characteristics of microcystic macular edema in a glaucoma patient. The infrared image of the right eye is shown.

The location of the optical coherence tomography (OCT) section is indicated with a white line. The OCT section shows vertical vacuolar

inclusions in the inner nuclear layer. Ganglion cell layer (GCL) thickness map of that patient shows marked ganglion cell loss that

respects the temporal raphe thus consistent with a nerve fiber bundle loss. Thickness map of the inner nuclear layer, shows macular

inner nuclear layer thickness and outer plexiform layer thickening in areas that are most affected by ganglion cell loss. The corre-

sponding thickness maps of a normal-retinal nerve fiber layer eye without apparent glaucoma are shown to allow visual comparison.

Figure 1 can be viewed in color online at www.glaucomajournal.com.

TABLE 2. Layer Thickness, MD and pRNFL in Normal-RNFLs (Ctrl), Glaucoma Patients (Glauc), and Glaucoma Patients With MME

Ctrl Glaucoma MME Glauc. vs. Ctrl MME vs. Ctrl MME vs. Glauc.

Eyes (patients) 25 210 8 Sig. Sig. Sig.

Age 69 ± 2 72 ± 0.8 66 ± 3.7 0.2 0.5 0.2

MD 1.2 ± 0.3 6.2 ± 0.5 16 ± 1.9 0.001 < 0.001 < 0.001

pRNFL 117 ± 2.5 80 ± 1.5 50 ± 3.1 < 0.001 < 0.001 < 0.001

mGCL/IPL 91 ± 1.3 73 ± 1.0 51 ± 4.0 < 0.001 < 0.001 < 0.001

mINL/OPL 68 ± 0.9 68 ± 0.3 81 ± 2.6 0.9 < 0.001 < 0.001

mORT 152 ± 1.9 154 ± 0.6 161 ± 3.0 0.2 0.03 0.04

Mean values are reported with SE of the mean. Mean values were compared between the 3 groups and signiﬁcance levels (sig.) are reported for each

comparison.

MD indicates mean defects; mGCL/IPL, macular ganglion cell layer/inner nuclear layer; mINL/OPL, macular inner nuclear layer thickness and outer

plexiform layer; MME, microcystic macular edema; mORT, macular outer retinal thickness; pRNFL, peripapillary retinal nerve ﬁber layer.

J Glaucoma

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Volume 26, Number 5, May 2017 Retrograde Maculopathy in Patients With Glaucoma

425

both eyes, such that only 1 eye per patient was included in

the statistical analysis. Mean values were compared with

analysis of variance. Correlation of parameters were com-

puted with the Pearson test (IBM, SPSS Statistics, Version

21). Values are reported as mean ± SE of the mean.

RESULTS

We identiﬁed 282 eyes from 218 patients with con-

ﬁrmed high-tension glaucoma a nd good quality macular

OCT. One hundred ﬁfty-nine eyes (56%) were from

patient s with POAG and 123 eyes (44%) were f rom

patients with PEXG. From 282 glaucoma eyes a total of 8

eyes (2.8%) from 8 patients (3.7%) showed MME, 3 eyes

were from the PEXG group and 5 eyes were from the

POAG group (Table 1). The normal-RNFL group was

composed of 16 contralateral eyes of patients that did not

fulﬁll the diagnostic criteria for glauc oma and 9 eyes from

9 healthy nonrelated subjects. This normal-RNFL group

was comparable in age to the glaucoma patients

(P = 0.18). No MME was found in the normal-RNFL

group.

For quantitative and statistical analysis only a single

eye per patient was used to prevent bias. This left us with 98

eyes with PEXG and 112 eyes with POAG. In our cohort

patients with PEXG were signiﬁcantly older than POAG

patients (77 ± 0.8 and 68 ± 1.2 y for PEXG and POAG

patients, respectively, P < 0.001). mINL/OPL was about

3 mm thinner in PEXG patients as compared with POAG

patients (INL/OPL thickness in PEXG patients = 66 ±

0.4 mm, mINL/OPL thickness in POAG patients = 69 ±

0.5 mm, P = 0.001). All other parameters, that is MD in

visual ﬁeld, mGCL (mGCL/IPL), mINL/OPL, mORT, and

temporal pRNFL thickness were not statistically diﬀerent

between the 2 glaucoma groups (P > 0.35 for all). Owing to

missing data the sample size of mean visual ﬁeld defect was

FIGURE 2. Macular optical coherence tomography section of a patient with advanced glaucoma but without microcystic macular

edema. Ganglion cell layer (GCL) thickness map (top left) shows severe atrophy in the perifoveal GCL. The corresponding inner nuclear

layer (INR) thickness map (top right) shows a thickening, indicating presence of retrograde maculopathy in the absence of microcystic

macular edema. Scatter plots of peripapillary retinal nerve fiber layer (RNFL) and macular GCL/inner plexiform layer (IPL) show an

excellent correlation of these 2 parameters. Scatter plot of pRNFL and macular inner nuclear layer thickness and outer plexiform layer

(mINL/OPL) thickness of all patients shows a significant inverse correlation of mINL/OPL thickness with glaucoma severity, thus

predicting cases of retrograde maculopathy without microcystic macular edema. Figure 2 can be viewed in color online at www.

glaucomajournal.com.

Brazerol et al J Glaucoma



Volume 26, Number 5, May 2017

426

www.glaucomajournal.com Copyright

n = 166 instead of 210, which reduced statistical power for

this parameter. We combined the PEXG group and the

POAG group into a single glaucoma group for the

remainder of the analysis. Compared with the non-MME

glaucoma group the patients with MME had more

advanced glaucoma with more visual ﬁeld defect, reduced

pRNFL, and reduced mGCL/IPL thickness (P < 0.001 for

each comparison, Table 2). We found a signiﬁcantly thicker

mINL/OPL in MME patients compared with the glaucoma

group or normal RNFLs (P < 0.001). The vertical micro-

cysts were exclusively present in the inner nuclear layer and

were located in a perifoveal ring sparing the fovea itself

(Fig. 1).

We next investigated the deeper retinal layers in those

patients that did not show MME. As MME patients show

obvious involvement of deeper retinal layers, eyes with

MME were excluded from the following analysis. We found

that our glaucoma group had a signiﬁcant visual ﬁeld loss

(MD in glaucoma group = 6.2 ± 0.5, MD in normal-

RNFL group = 1.2 ± 0.3, P < 0.001). This ﬁeld loss was

associated with a thinning of the papillary nerve ﬁber layer

(pRNFL = 80 ± 1.5 and 117 ± 2.5 mm in glaucoma and

normal-RNFL patients, respectively) and with a thinning

of the mGCL (mGCL/IPL = 73 ± 1 mm in glaucoma and

91 ± 1 mm in normal RNFL, P < 0.001). Of note, we found

no diﬀerence of the mean mINL/OPL thickness and mORT

between glaucoma patients and the normal-RNFL group

(PZ0.2 for both). Thus, average retinal layers beneath

GCL are not diﬀerent between the normal-RNFL group

and the glaucoma group. Next we tested whether there is a

correlation of glaucoma severity and individual retinal

layers. We found a strong inverse correlation of visual ﬁeld

defect with both pRNFL and mGCL/IPL thickness

(P < 0.001 for both, Fig. 2 and Table 3). A positive

correlation was found between the visual ﬁeld defect and

mINL/OPL (P = 0.016). Similarly we found a signiﬁcant

correlation of pRNFL with mGCL/IPL (P < 0.001) and an

inverse correlation with mINL/OPL (P < 0.001, Table 3

and Fig. 2). No signiﬁcant correlation was found for the

deeper retinal layers (P = 0.37, Table 3).

DISCUSSION

In this study we found that glaucoma-associated

macular layer chan ges are not limited to the ganglion cell

level: First, we found MME in about 3% of glaucoma

eyes. Second, we found a signiﬁcant correlation of mINL/

OPL thickness with glaucoma severity, that is an inverse

correlation of mGCL/IPL thickness a nd mINL/OPL

thickness. This correlation may explain why only some

cases of optic neuropathy develop MME: ganglion cell

lossmayleadtoagradualthickeningofmINL/OPL,

which in advanced cases may result in clinically visible

MME. Consistent with this hypothesis we found that

glaucoma was signiﬁcantly worse in patients with MME as

compared with the remaining glaucoma group. The cor-

relation with severity may a lso help to understand the

variable MME prevalence previously reported in diﬀerent

types of optic neuropathies. Some optic neuropathies,

including neuromyelitis optica, cause more severe optic

atrophy and have a prevalence of MME up to 30%,

14,22

while m ore moderate optic neuropathies, such as those in

MS, have a lower prevalence of about 4%.

We found a

frequency of MME of 3% in the glaucoma group, while

we previously found a prevalence of 8% in nonglaucoma-

associated optic neuropathy.

Hasegawa et al

found a

higher MME frequency of 6% in POAG eyes. The latter

diﬀerence in frequency may be explained by the higher

TABLE 3. Cross Correlations of Macular Layer Thickness, pRNFL, and MD

MD pRNFL mGCL/IPL mINL/OPL mORT

Corr.coeﬀ.  0.622w  0.705w 0.187* 0.029

Sig. 0.000 0.000 0.016 0.715

n 166 166 166 166

pRNFL

Corr.coeﬀ.  0.622w 0.791w  0.272w  0.062

Sig. 0.000 0.000 0.000 0.372

n 166 210 210 210

mGCL/IPL

Corr.coeﬀ.  0.705w 0.791w  0.158*  0.011

Sig. 0.000 0.000 0.022 0.879

n 166 210 210 210

mINL/OPL

Corr.coeﬀ. 0.187*  0.272w  0.158* 0.023

Sig. 0.016 0.000 0.022 0.739

n 166 210 210 210

mORT

Corr.coeﬀ. 0.029  0.062  0.011 0.023

Sig. 0.715 0.372 0.879 0.739

n 166 210 210 210

Pearson correlation coeﬃcients (corr.coeﬀ.), statistical signiﬁcance (sig.), and number of eyes (n) are reported. Except for outer retinal thickness all

parameters show correlation with each other. Patients with MME were excluded for this analysis.

*Correlation is signiﬁcant at the 0.05 level.

wCorrelation is signiﬁcant at the 0.01 level.

MD indicates mean defects; mGCL/IPL, macular ganglion cell layer/inner nuclear layer; mINL/OPL, macular inner nuclear layer thickness and outer

plexiform layer; MME, microcystic macular edema; mORT, macular outer retinal thickness; pRNFL, peripapillary retinal nerve ﬁber layer.

J Glaucoma



Volume 26, Number 5, May 2017 Retrograde Maculopathy in Patients With Glaucoma

427

Retrograde Maculopathy in Patients With Glaucoma.

Figures

Citations

Detection of Macular Ganglion Cell Loss in Glaucoma by Fourier-Domain Optical Coherence Tomography

Retinal and Epiretinal Glia???An Immunohistochemical Study

Microcystoid Macular Changes in Association With Idiopathic Epiretinal Membranes in Eyes With and Without Glaucoma: Clinical Insights.

Macular imaging with optical coherence tomography in glaucoma.

Differentiation of Underlying Pathologies of Macular Edema Using Spectral Domain Optical Coherence Tomography (SD-OCT).

References

Topography of ganglion cells in human retina.

Visual acuities "hand motion" and "counting fingers" can be quantified with the freiburg visual acuity test.

Detection of macular ganglion cell loss in glaucoma by Fourier-domain optical coherence tomography.

Retinal nerve fiber layer imaging with spectral-domain optical coherence tomography: a variability and diagnostic performance study.

Optical Coherence Tomography Longitudinal Evaluation of Retinal Nerve Fiber Layer Thickness in Glaucoma

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Frequently Asked Questions (6)

Q1. What are the contributions in "Retrograde maculopathy in patients with glaucoma" ?

Q2. What is the main cause of the atrophy of the retina?

Q3. How much thinner was mINL/OPL in PEXG patients?

Q4. What is the mean value of mGCL/IPL?

Q5. What is the meaning of retrograde maculopathy in glaucoma?

Q6. What was the thickness of the peripapillary nerve fiber layer?