REVIEW

CURRENT
OPINION Myopic optic disc changes and its role
in glaucoma
Nicholas Y.Q. Tan a,b, Chelvin C.A. Sng a,c,d, and Marcus Ang a,b,d,e

Purpose of review
Optic nerve head (ONH) changes such as tilt and torsion are associated with the progression of myopia,
and may in turn predispose toward glaucoma. At the same time, these ONH deformations also make the
structural assessment for glaucoma difficult. Here, we review the mechanisms and changes to the myopic
optic disc, and the advances in structural imaging to better evaluate the ONH in myopia.
Recent findings
The distance, depth, and angle between the optic disc and the deepest point of the elongated eyeball may be
related to the degree and direction of optic disc tilt and torsion. It is hypothesized that as the eyeball grows
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axially, the disc is pulled toward its most protruded point. These ONH deformations in myopia are thought to
induce strain on the lamina cribrosa and the axons passing through it. Recent studies have shown unique
characteristics of the lamina cribrosa in myopia that may account for susceptibility toward glaucoma. New
developments in imaging the ONH in myopia, including the use of optical coherence tomography-
angiography may also further our understanding of the relationship between myopia and glaucoma.
Summary
Optic disc changes in myopia are secondary to the configuration of the posterior globe. These ONH
deformations may predispose toward glaucoma, although the causative relationship between myopia and
glaucoma remains to be further clarified.
Keywords
glaucoma, lamina cribrosa defect, myopia, optic disc tilt, optic disc torsion

INTRODUCTION factor for the development of glaucoma [9–12].

Myopia is increasing in prevalence worldwide. A
recent meta-analysis has estimated that by 2050,
up to 50% of the world’s population will be myopic
[1]. This represents a significant public health issue
for a number of reasons. First, uncorrected refractive
However, myopia does not appear to contribute
to the risk of further glaucomatous progression
[13–16]. As a result, some authors have postulated
that some forms of optic neuropathy in myopia may
be related to myopia itself, rather than glaucoma
&

error is currently a leading cause of visual [17,18,19 ].

impairment worldwide [2]. This is especially true
in communities where access to refractive correc-
tion is limited [3]. Second, in contrast to refractive
error that is correctable, pathological myopia may
cause irreversible visual loss [4]. Third, and of direct
interest to this review, apart from affecting the
retina, it is now better recognized that myopia
may also adversely affect the optic nerve.
The appearance of the optic nerve head (ONH)
is known to be altered with myopia [5–8]. Such
optic discs may appear tilted, cyclotorted, stretched
in the vertical and/or horizontal dimension, with
larger and shallower cups, or larger cup-to-disc
ratios that may appear glaucomatous (Fig. 1). In
fact, many population-based epidemiological stud-
ies have strongly suggested myopia as an associated
A further problem that is commonly encountered
in studying the ONH in myopia is that its ophthal-
moscopic appearance may often be confused with
glaucoma [20]. Thus, quantitative parameters on
a
Singapore Eye Research Institute, bSingapore National Eye Centre,
c
Ophthalmology Department, National University Hospital, Singapore,
d
Moorfields Eye Hospital, London, UK and eOphthalmology and Visual
Sciences Academic Clinical Program, Duke-NUS Medical School,
Singapore
Correspondence to Marcus Ang, MBBS, Singapore National Eye
Centre, 11 Third Hospital Avenue, Singapore 168751, Singapore.
Tel: +(65) 62277255; fax: +(65) 6323 1903;
e-mail: marcus.ang@snec.com.sg
Curr Opin Ophthalmol 2019, 30:89–96
DOI:10.1097/ICU.0000000000000548

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Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.

Glaucoma
KEY POINTS
 Optic disc changes in myopia are secondary to the
configuration of the posterior globe.
 The optic nerve head deformations secondary to myopia
may induce strain on the lamina cribrosa and the axons
passing through it, potentially leading to glaucoma.
 Lamina cribrosa in myopia shows unique characteristics
that might be related to the development of glaucoma.
 Alterations to the microvasculature of the ONH are
associated with myopia, although the pathophysiological
significance of these changes is yet to be determined.
 Diagnosis of glaucoma is challenging in a myopic eye,
and serial structural imaging of the optic nerve should
be combined with serial optic disc photographs and
visual field assessment.
structural imaging of the ONH for glaucoma assess-
ment take on an even greater importance in the
context of myopia [20]. However, imaging a distorted
ONH that is structurally different from that in a
nonhighly myopic population (used as the reference
normative database in imaging software) may also
lead to misdiagnoses [21,22].
Thus, the aim of this review is to describe the
changes to the optic disc that are associated with
myopia, and how these deformations to the ONH
FIGURE 1. Color photograph of the optic disc in a myopic
left eye. The optic disc is vertically tilted and
inferotemporally cyclotorted, with an increased vertical cup-
to-disc ratio, and temporal peripapillary atrophy-b.
90 www.co-ophthalmology.com
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
may potentially lead to glaucoma. Additionally, we
will also discuss some of the challenges in structur-
ally assessing the myopic optic disc.
HOW OPTIC NERVE HEAD
DEFORMATIONS MAY ARISE IN MYOPIA
As early as the 19th century, ophthalmologists have
postulated that acquired myopic changes to the
optic disc may be caused by a progressive mechani-
cal stretching of the posterior globe [23,24]. They
hypothesized that a temporal crescent of choriore-
tinal atrophy, which was recognized to be correlated
with axial length, may be caused by a disparity in the
area between the scleral shell and the lamina vitrea
complex [23]. Furthermore, it was thought that the
shifting tissue planes of the peripapillary retina may
result in a nasal elevation (‘supertraction’) and tem-
poral flattening (‘dystraction’) of the disc, causing
the appearance of disc tilt [24]. Recent studies have
supported this theory.
In a retrospective study of 118 Korean children
(aged 7.3  3.7 years) using serial disc photographs, it
was demonstrated that there was progressive tilting
of the ONH and the development/enlargement of
peripapillary atrophy (PPA) in children with incipi-
ent myopic shift [25]. Their results were further cor-
roborated by another Korean study of children aged
<14 years [26]. On serial disc photographs, it was
found that a myopic change in spherical equivalent
was independently associated with the presence of
either ONH or PPA changes [26]. The authors there-
fore postulated that in myopic shift, with axial elon-
gation of the eye, the temporal sclera moves back and
pulls the optic nerve temporally, resulting in the
aforementioned disc changes [25]. Recent studies
&
by Kim et al. [27 ] have examined this hypothesis—
that a myopic disc configuration is caused by the disc
being pulled toward the deepest point of the eyeball
(DPE)—in greater detail.
Using an en face mode on optical coherence
tomography (OCT) that provided a coronal view
of the posterior segment at different depths, Kim
&
et al. [27 ]defined the DPE as the deepest interface
between Bruch’s membrane and the choroid. With
the DPE as an anatomical landmark, the distance
between the optic disc and the DPE (Disc–DPE
distance) was used as a surrogate for scleral stretch-
ing in the xy plane, and the depth between the DPE
and the temporal border of the optic disc (Disc–DPE
depth) was used as a surrogate for scleral stretching
in the z-axis. Disc–DPE angle was used as an addi-
tional coordinate to specify the location of the DPE
in the coronal sections. Both Disc–DPE distance and
Disc–DPE depth were found to be significantly
larger in myopic compared to emmetropic eyes,
Volume 30  Number 2  March 2019

and both parameters were related to disc tilt. As
Disc–DPE distance elongated, the horizontal tilt
angle significantly enlarged; similarly, as Disc–
DPE depth grew larger, the degree of disc ovality
&
also increased [27 ]. On the other hand, Disc–DPE
angle had a strong relationship with disc torsion
angle. This geometric relationship, in fact, could be
represented by an equation: Disc–DPE angle ¼ optic
disc torsion þ disc–foveal angle [27 ]. These find-
&
ings strongly imply that optic disc configuration is
the result of variation in the posterior pole contour.
These results also agree with a previous report that
inferior disc tilt and torsion were related to the
thinning of the inferior region of the posterior sclera
in eyes with high myopia [28]. Thus, in this schema,
disc tilt may arise from both horizontal and vertical
strains as the DPE migrates horizontally and/or pos-
teriorly during axial elongation. However, retroe-
quatorial elongation of the sclera may be
asymmetric, which can lead to disc torsion.
The concept of the optic disc being pulled toward
the DPE was also found to explain the phenomenon
of tilted disc syndrome (TDS) [29]. The TDS is defined
clinically as an inferonasal tilting of the optic disc,
with an inferior or inferonasal crescent, an ectasia of
the lower fundus or inferior staphyloma, and the
presence of myopic and astigmatic refractive errors
[24,30,31]. It is commonly thought to be a congenital
malformation with improper closure of the embry-
onic ocular fissure [24]. However, using DPE-related
parameters, Kim et al. [29] were able to demonstrate
that similar to myopic eyes, in eyes with TDS, optic
disc configuration is explicable by the location of the
DPE. Namely, TDS appeared to be secondary to the
downward sloping of the posterior sclera. An mag-
netic resonance imaging study by Shinohara et al. [32]
also supports this hypothesis. In all eyes with TDS, the
lower part of the posterior globe was found to be
protruded, and the optic nerve was attached to the
upper nasal edge of the protrusion [32]. However, in
eyes without TDS, eyes were either emmetropic, of
symmetrical shape without any posterior protrusion,
or if there was a protrusion in the myopic eyes, the site
of attachment of the optic nerve was within the
protrusion [32]. Thus, it appears that the contour
of the posterior globe determines the eventual shape
of the ONH.
Other features of the ONH in myopic eyes may
therefore also be explained by the elongation and
stretching of posterior globe. The ONH may be
regarded as a three-layered hole, with the Bruch’s
membrane hole forming the inner layer, the hole in
the choroid forming the middle layer, and the
scleral canal forming the outer layer. As the eye
elongates with myopia, the shift in the position of
the outer hole may not be followed by the opening
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Myopic optic disc changes and its role in glaucoma Tan et al.
in Bruch’s membrane. Thus, this may lead to an
overhanging of Bruch’s membrane at the nasal disc,
and an absence of Bruch’s membrane at the tempo-
ral disc [33]. This area without Bruch’s membrane
(labeled ‘PPA-gamma’) has been demonstrated his-
tologically as well as in vivo on OCT imaging [33–
35]. The area of the gamma zone is significantly
associated with longer axial length [34,35], and
the prevalence of the gamma zone steeply increases
at a cutoff value of 26.5 mm [33]. The location of the
PPA may also be explained by the direction of elon-
gation of the globe. In a study of 134 myopic eyes
with normal tension glaucoma, Park et al. [36] found
that in eyes with posterior staphylomas located
temporal to the disc, the disc was small, tilted,
and torted, with temporal PPA. However, when
the staphyloma involved the disc itself, the optic
disc was extensively enlarged (i.e., a macrodisc) with
circumferential PPA [36].
THE PATHOPHYSIOLOGICAL
SIGNIFICANCE OF OPTIC NERVE HEAD
DEFORMATIONS IN MYOPIA
As opposed to the remodeling of the ONH secondary
to intraocular pressure (IOP)-related mechanical
stresses that occur in glaucoma [37], structural
changes to the ONH in myopia may result from
the elongation of the posterior segment itself. It is
possible that these IOP-independent changes to the
myopic ONH predisposes toward glaucoma. This is
suggested by studies that have shown glaucoma to
be more common in myopia [9–12], and that the
direction of disc tilt or torsion may correspond to
the location of retinal nerve fiber layer (RNFL) loss or
visual field defects [38–42].
It is likely that the lamina cribrosa plays a key role
in explaining the association between myopia and
resultant optic neuropathy. The lamina cribrosa has
long been identified as the main site of retinal gan-
glion cell (RGC) axonal injury in glaucoma [43,44]. It
is a sieve-like structure that fills the posterior scleral
foramen, which unmyelinated RGC axons pass
through before converging as the optic nerve. In
myopia, the lamina cribrosa may also be thinned,
concurrent with the stretching and thinning of the
peripapillary sclera [45–47]. This is important
because a thinner lamina cribrosa translates to a
higher translaminar pressure gradient across it (as
the translaminar pressure difference , which is the
difference between IOP and the retrobulbar cerebro-
spinal fluid pressure, is spread across a shorter dis-
tance) [48,49]. The higher translaminar pressure
gradient may exert greater stress on the RGC axons
as they pass through the lamina cribrosa. Accord-
ingly, a thinner lamina cribrosa has been shown to be
www.co-ophthalmology.com 91
Glaucoma
associated with a faster rate of RNFL thinning in
glaucoma [50]. Thus, this may be one mechanism
by which myopia predisposes toward glaucoma.
However, apart from the translaminar pressure
difference that generates an anterior-posterior stress
across the lamina cribrosa, IOP also causes an in-wall
circumferential hoop stress that tends to stretch the
scleral canal open [51]. This, in turn, transmits a
strain on the lamina cribrosa. Although this in-wall
hoop stress is normally borne by the stiff peripapil-
lary sclera and Bruch’s membrane [52–54], both of
these tissues may be deficient in glaucoma. As dis-
cussed, PPA-gamma, which is more common in
myopia, represents an area lacking in Bruch’s mem-
brane [33–35]. Furthermore, the peripapillary
scleral flange may also be significantly thinned
out in myopia [55,56]. With the loss of these support
structures to the ONH, the structural stability of the
lamina cribrosa, and the passageway of RCG axons
across it, may be further compromised.
The weakening of the support structure of the
lamina cribrosa and the deformations induced on
the ONH because of elongation and stretching of the
posterior globe may therefore also explain why lam-
ina cribrosa defects are more common in myopia
[57,58]. Lamina cribrosa defects are related to glau-
comatous damage to the ONH as the location of
these defects generally shows good correspondence
to the location of Drance hemorrhages, focal RNFL
loss, and visual field deficits [59–64]. It is postulated
that in lamina cribrosa defects, the collapse of lami-
nar beams (whose intrabeam capillaries perfuse the
intralaminar optic nerve [65,66]) results in a Drance
hemorrhage, and the loss of support cells that line
the laminar beams (which provides structural and
functional support to the RGC axons [65,67]) con-
tributes toward RGC axonal damage.
Although lamina cribrosa defects may be found
in both myopia and glaucoma, those found in myo-
pia show slightly different characteristics: they are
often temporally located, and are spatially related to
the torsion or tilt of the optic disc; in addition, they
are often of a larger size (compared to lamina cribrosa
defects in nonmyopic eyes), and are more common
&
and larger in the presence of glaucoma [19 ,57,68]. In
contrast, in nonmyopic glaucoma, lamina cribrosa
defects do not show any specific tendency toward the
temporal periphery, and are often of a smaller size
&
[19 ]. As such, one might hypothesize that the cause
of lamina cribrosa defects might be different in myo-
pic-glaucoma (a consequence of strains on the lamina
cribrosa because of myopic deformations of the
ONH) versus nonmyopic-glaucoma (a consequence
of IOP-related mechanical strains on the ONH). How-
ever, in the presence of high IOP, existing lamina
cribrosa defects may be a foci of strain on the lamina
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cribrosa, which may lead to further glaucomatous
&
progression [19 ,69].
OPTIC NERVE HEAD MICROCIRCULATION
IN MYOPIA
In addition to the macroscopic structural changes to
the ONH in myopia as discussed above, various lines
of evidence also suggest that the blood supply to the
ONH is additionally altered with myopia. For
instance, Jonas et al. [70] showed on histology that
the distance of the peripapillary arterial circle of
Zinn–Haller to the optic disc border markedly
increased with longer axial lengths. As the circle
of Zinn–Haller is the main arterial source for the
lamina cribrosa blood supply [71–73], this may
potentially contribute to increased glaucoma sus-
ceptibility in highly myopic eyes. Using OCT angi-
ography [74,75], the peripapillary vessel density in
highly myopic eyes was also found to be signifi-
cantly lower compared to normal eyes [76–78]. As
radial peripapillary capillaries compose a unique
capillary plexus within the RNFL that supplies the
RGC axons [79], reduced perfusion in the peripapil-
lary region may be linked to glaucomatous change.
In addition, myopic eyes have also shown a reduced
central retinal artery blood velocity and ocular pul-
satility [80,81]; furthermore, the reduction in pulsa-
tile ocular blood flow was found to be related to
decreased ocular rigidity with axial elongation [81].
Lastly, peripapillary choroidal thickness is also
demonstrably reduced in myopic eyes on both
OCT [82] and OCT angiography [83].
However, despite these alterations to the micro-
vasculature of the ONH in myopia, its pathophysio-
logical significance is unproven. Similar to myopia,
in glaucoma, reduced blood flow has been reported
to occur at or around the ONH [76,84–87] and
retrobulbar vessels [88,89]. However, whether these
vascular changes are a cause or consequence of
glaucoma remains hotly debated [76,90,91]. Fur-
thermore, ocular blood flow does not seem to be a
modifiable risk factor for glaucoma or a therapeutic
target [92]. Thus, the role of measuring of ocular
blood flow in myopia – and how best to do so [93] –
remains to be established.
STRUCTURAL ASSESSMENT OF THE
OPTIC NERVE HEAD IN MYOPIA
The structural evaluation of the ONH and peripapil-
lary structures can be challenging in myopia. Thus, it
may often be difficult to diagnose glaucoma (which
myopia may predispose toward) in a myopic eye.
In modern clinical practice, OCT imaging of the
peripapillary RNFL (Fig. 2) is often used to detect and
Volume 30  Number 2  March 2019
 Myopic optic disc changes and its role in glaucoma Tan et al.

FIGURE 2. Print-out of the optical coherence tomography examination (Cirrus-HD software version 6.0; Carl Zeiss Meditec,
Inc., Dublin, California, USA) of the optic nerve head and peripapillary retinal nerve fiber layer (RNFL). The myopic right eye
(spherical equivalent: 8.5 diopters; axial length: 27.99 mm) without glaucoma is used for illustration. The RNFL thickness
map shows temporalization of the superotemporal and inferotemporal RNFL bundles. This is also shown graphically on the
RNFL thickness profile. The superior RNFL hump is temporally displaced such that it lies above the 95th percentile of thickness
in that location; accordingly, on the four quadrant and 12 clock hour sector maps, there is apparent supranormal thickness in
the temporal sector(s). At the same time, the temporalization of the nasal trough of the superior RNFL hump results in it skirting
across the lowest 10th percentile of thickness in that location. The RNFL deviation map correspondingly shows apparent RNFL
thinning superiorly, nasal to the superotemporal RNFL bundle. There is also (false negative) borderline superior RNFL thinning
reported in the superior sector and clock hour thickness maps. A similar process involves the temporalized inferior RNFL
bundle of the right eye, resulting in false negative signals of RNFL thinning on the deviation map.

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Glaucoma
monitor glaucoma [94]. However, the in-built nor-
mative databases of commonly available OCT
machines often do not incorporate highly myopic
eyes into their reference ranges. This is problematic
as it has been shown that with increasing axial
elongation, the peak locations of the RNFL thickness
profile (i.e., the superotemporal and inferotemporal
RNFL ‘humps’’) are skewed temporally toward each
other [21,22]. A mismatch in RNFL thickness pro-
files between myopic and nonmyopic eyes may
therefore lead to false positive findings of RNFL
thinning (superiorly and inferiorly) in nonglaucom-
atous but myopic eyes [21,22]. Conversely, the
thickening of the RNFL temporally may lead to
underdiagnosing papillomacular bundle defects,
which are known to be more common in myopia
[95,96]. The interpretation of RNFL measurements is
further complicated by myopic optic disc tilt. Shin
et al. [97] showed that with optic disc tilt, the
temporal RNFL thickness parameter had a reduced
diagnostic capability in detecting glaucoma.
In addition to peripapillary RNFL assessment,
OCT also has the ability to measure the neuroretinal
rim thickness, which is also thinned out in glau-
coma [98]. As opposed to neuroretinal rim param-
eters based on the identifiable optic disc margin
(which are known to be anatomically imprecise)
on confocal scanning laser tomography, neuroreti-
nal rim measurements on OCT are based on the
clinically invisible, but OCT-detected Bruch’s mem-
brane opening (BMO) [98]. The BMO-minimum rim
width (BMO-MRW), defined as the minimum dis-
tance between the BMO and the internal limiting
membrane, has been shown to have a higher sensi-
tivity (at 95% specificity) than RNFL thickness meas-
urements in detecting early glaucoma [98]. When
BMO-MRW is applied to the diagnosis of glaucoma
in myopic eyes, various studies have reported similar
sensitivities [99] or higher specificities [100,101]
compared to RNFL parameters. However, as areas
of PPA-gamma (which lack Bruch’s membrane) are
more common in myopia [33–35], the use of BMO-
MRW may be less applicable in highly myopic eyes.
Zheng et al. [102] showed that in high myopia,
around 30% of eyes may have indiscernible BMO
in at least 1 meridian, and that BMO was indistinct
most frequently at common areas of glaucomatous
neuroretinal rim thinning (i.e., the superotemporal,
temporal, and superotemporal meridians). Thus,
similar to the OCT assessment of the peripapillary
RNFL, the evaluation of the neuroretinal rim thick-
ness on OCT may also be confounded by myopia.
In the face of these difficulties, a multimodal
approach may be advantageous in the assessment of
the myopic optic disc. In the study by Shin et al. [97]
that showed how the interpretation of RNFL
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Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
thickness may be affected by disc tilt, the authors
also showed that macular ganglion cell inner plexi-
form layer measurement provided reliable parame-
ters for diagnosing glaucoma, regardless of the
extent of optic disc tilt. Thus, assessment of the
macula may potentially complement the assess-
ment of the ONH, especially in myopia. In addition
to newer OCT technologies, older strategies such as
serial disc photographs may retain lasting value in
monitoring for structural glaucomatous changes
over the years (especially as newer machines/imag-
ing modalities are succeeded by one another).
Lastly, the detection of glaucomatous visual field
changes that corresponds to structural defects in a
myopic disc remains paramount in managing glau-
coma [103]. In myopic patients with a suspicious
optic disc and visual field defects (that may also be
the consequence of myopic maculopathy), the diag-
nosis of glaucoma may in some cases only be made
reliably if there are both visual field and structural
progression. Thus, some patients with mild visual
field defects may choose to be monitored for defini-
tive progression before starting glaucoma treatment.
On the other hand, clinicians may be prudent to
start treatment early in eyes with extensive visual
field loss and a markedly cupped optic disc, even
before evidence of progression, as such cases cannot
risk further visual loss.
CONCLUSION
In recent years, we have come to better understand
the mechanisms behind the optic disc changes in
myopia. Namely, with the asymmetric elongation of
the posterior globe in axial myopia, the ONH may be
pulled toward the DPE, resulting in typical optic disc
features such as tilt or torsion. The mechanical
strains across the lamina cribrosa that arise from
myopic deformations of the ONH may injure the
RGC axons as they pass through it. Ultimately, this
may lead to glaucoma (or possibly a distinct form of
optic neuropathy). In this regard, the clinical impli-
cation is that accurate diagnostic structural imaging
of the ONH will be important in enabling clinicians
to distinguish between diseased and healthy discs.
Future directions may include the use of multitopo-
graphic imaging [104,105] or artificial intelligence
[105–107] for identifying glaucoma. Additionally,
the question of whether or not myopia truly pre-
disposes toward glaucomatous progression still
remains to be conclusively answered. Future pro-
spective studies that include updated technologies
to monitor glaucoma progression in myopic eyes
may be more appropriately posed to answer this
clinical conundrum. As myopia becomes even more
prevalent in the near future, clinicians will
Volume 30  Number 2  March 2019

increasingly encounter the dilemma of diagnosing
and prognosticating glaucoma in myopia. Thus, the
study of myopia and optic disc changes has never
been as pertinent as it is currently.
Acknowledgements
None.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
REFERENCES AND RECOMMENDED
READING
Papers of particular interest, published within the annual period of review, have
been highlighted as:
& of special interest
&& of outstanding interest
1. Holden BA, Fricke TR, Wilson DA, et al. Global prevalence of myopia and
high myopia and temporal trends from 2000 through 2050. Ophthalmology
2016; 123:1036–1042.
2. Naidoo KS, Leasher J, Bourne RR, et al. Global vision impairment and
blindness due to uncorrected refractive error, 1990–2010. Optom Vis
Sci 2016; 93:227–234.
3. Holden BA, Sulaiman S, Knox K. The challenge of providing spectacles in the
developing world. Community eye Heal 2000; 13:9–10.
4. Wong TY, Ferreira A, Hughes R, et al. Epidemiology and disease burden of
pathologic myopia and myopic choroidal neovascularization: an evidence-
based systematic review. Am J Ophthalmol 2014; 157:9.e12–25.e12.
5. Jonas JB, Gusek GC, Naumann GO. Optic disk morphometry in high myopia.
Graefes Arch Clin Exp Ophthalmol 1988; 226:587–590.
6. Jonas JB, Dichtl A. Optic disc morphology in myopic primary open-angle
glaucoma. Graefe’s Arch Clin Exp Ophthalmol 1997; 235:627–633.
7. Savatovsky E, Mwanza JC, Budenz DL, et al. Longitudinal changes in
peripapillary atrophy in the ocular hypertension treatment study: A case-
control assessment. Ophthalmology 2015; 122:79–86.
8. Samarawickrama C, Mitchell P, Tong L, et al. Myopia-related optic disc and
retinal changes in adolescent children from Singapore. Ophthalmology
2011; 118:2050–2057.
9. Mitchell P, Hourihan F, Sandbach J, Wang JJ. The relationship between
glaucoma and myopia: the Blue Mountains Eye study. Ophthalmology 1999;
106:2010–2015.
10. Xu L, Wang Y, Wang S, et al. High myopia and glaucoma susceptibility.
Ophthalmology 2007; 114:216–220.
11. Suzuki Y, Iwase A, Araie M, et al. Risk Factors for open-angle glaucoma in a
Japanese population: the Tajimi study. Ophthalmology 2006; 113:1613–1617.
12. Shen L, Melles RB, Metlapally R, et al. The association of refractive error with
glaucoma in a multiethnic population. Ophthalmology 2016; 123:92–101.
13. Sohn SW, Song JS, Kee C. Influence of the extent of myopia on the
progression of normal-tension glaucoma. Am J Ophthalmol 2010;
149:831–838.
14. Lee JR, Kim S, Lee JY, et al. Is myopic optic disc appearance a risk factor for
rapid progression in medically treated glaucomatous eyes with confirmed
visual field progression? J Glaucoma 2016; 25:330–337.
15. Park HY, Hong KE, Park CK. Impact of age and myopia on the rate of visual
field progression in glaucoma patients. Med (United States) 2016; 95:1–7.
16. Ernest PJ, Schouten JS, Beckers HJ, et al. An evidence-based review of
prognostic factors for glaucomatous visual field progression. Ophthalmology
2013; 120:512–519.
17. Doshi A, Kreidl KO, Lombardi L, et al. Nonprogressive glaucomatous cupping
and visual field abnormalities in young Chinese males. Ophthalmology 2007;
114:472–479.
18. Ohno-Matsui K, Shimada N, Yasuzumi K, et al. Long-term development of
significant visual field defects in highly myopic eyes. Am J Ophthalmol 2011;
152:256.e1–265.e1.
19. Sawada Y, Araie M, Kasuga H, et al. Focal lamina cribrosa defect in myopic
& eyes with nonprogressive glaucomatous visual field defect. Am J Ophthalmol
2018; 190:34–49.
The authors found that in myopic eyes with nonprogressive visual field loss, there
were specific patterns of lamina cribrosa defects characteristic to the myopic
deformation of the optic disc.
1040-8738 Copyright ß 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Myopic optic disc changes and its role in glaucoma Tan et al.
20. Chang RT, Singh K. Myopia and glaucoma: diagnostic and therapeutic
challenges. Curr Opin Ophthalmol 2013; 24:96–101.
21. Leung CK, Yu M, Weinreb RN, et al. Retinal nerve fiber layer imaging with
spectral-domain optical coherence tomography: interpreting the RNFL maps
in healthy myopic eyes. Investig Ophthalmol Vis Sci 2012; 53:7194–7200.
22. Yamashita T, Kii Y, Tanaka M, et al. Relationship between supernormal
sectors of retinal nerve fibre layer and axial length in normal eyes. Acta
Ophthalmol 2014; 92:481–487.
23. Curtin BJ, Karlin DB. Axial length measurements and fundus changes of the myopic
eye. I. The posterior fundus. Trans Am Ophthalmol Soc 1970; 68:312–334.
24. Apple DJ, Rabb MF, Walsh PM. Congenital anomalies of the optic disc. Surv
Ophthalmol 1982; 27:3–41.
25. Kim TW, Kim M, Weinreb RN, et al. Optic disc change with incipient myopia
of childhood. Ophthalmology 2012; 119:21–26.
26. Park HY, Kim SE, Park CK. Optic disc change during childhood myopic shift:
comparison between eyes with an enlarged cup-to-disc ratio and childhood
glaucoma compared to normal myopic eyes. PLoS One 2015; 10:1–11.
27. Kim YC, Jung Y, Park HY, Park CK. The location of the deepest point of the
& eyeball determines the optic disc configuration. Sci Rep 2017; 7:1–13.
This study first reported the use of the DPE as a reference parameter, and
demonstrated that posterior pole profile plays a major role in understanding the
optic disc alterations found in myopic study participants.
28. Park HY, Choi S Il, Choi JA, Park CK. Disc torsion and vertical disc tilt are
related to subfoveal scleral thickness in open-angle glaucoma patients with
myopia. Investig Opthalmol Vis Sci 2015; 56:4927.
29. Kim YC, Moon JS, Park HY, Park CK. Three dimensional evaluation of
posterior pole and optic nerve head in tilted disc. Sci Rep 2018; 8:1–11.
30. Alexander LJ. The tilted disc syndrome. J Am Optom Assoc 1978; 49:1060–1062.
31. Sowka J, Aoun P. Tilted disc syndrome. Optom Vis Sci 1999; 76:618–623.
32. Shinohara K, Moriyama M, Shimada N, et al. Analyses of shape of eyes and
structure of optic nerves in eyes with tilted disc syndrome by swept-source
optical coherence tomography and three-dimensional magnetic resonance
imaging. Eye 2013; 27:1233–1242.
33. Jonas JB, Jonas SB, Jonas RA, et al. Parapapillary atrophy: histological
gamma zone and delta zone. PLoS One 2012; 7:1–7.
34. Dai Y, Jonas JB, Huang H, et al. Microstructure of parapapillary atrophy: beta
zone and gamma zone. Investig Ophthalmol Vis Sci 2013; 54:2013–2018.
35. Kim M, Kim TW, Weinreb RN, Lee EJ. Differentiation of parapapillary atrophy
using spectral-domain optical coherence tomography. Ophthalmology 2013;
120:1790–1797.
36. Park H-Y, Jung Y, Park CK. Posterior staphyloma is related to optic disc
morphology and the location of visual field defect in normal tension glaucoma
patients with myopia. Eye (Lond) 2014; 29:1–9.
37. Crawford Downs J, Roberts MD, Sigal IA. Glaucomatous cupping of the
lamina cribrosa: a review of the evidence for active progressive remodeling as
a mechanism. Exp Eye Res 2011; 93:133–140.
38. Choi JA, Park HY, Shin HY, Park CK. Optic disc tilt direction determines the
location of initial glaucomatous damage. Investig Ophthalmol Vis Sci 2014;
55:4991–4998.
39. Park HY, Lee K, Park CK. Optic disc torsion direction predicts the location of
glaucomatous damage in normal-tension glaucoma patients with myopia.
Ophthalmology 2012; 119:1844–1851.
40. Sung MS, Kang YS, Heo H, Park SW. Optic disc rotation as a clue for
predicting visual field progression in myopic normal-tension glaucoma.
Ophthalmology 2016; 123:1484–1493.
41. Lee KS, Lee JR, Kook MS. Optic disc torsion presenting as unilateral
glaucomatous-appearing visual field defect in young myopic Korean eyes.
Ophthalmology 2014; 121:1013–1019.
42. Lee KM, Lee EJ, Kim T-W. Lamina cribrosa configuration in tilted optic discs
with different tilt axes: a new hypothesis regarding optic disc tilt and torsion.
Investig Opthalmol Vis Sci 2015; 56:2958.
43. Quigley H, Anderson DR. The dynamics and location of axonal transport
blockade by acute intraocular pressure elevation in primate optic nerve.
Invest Ophthalmol 1976; 15:606–616.
44. Quigley HA, Addicks EM, Green WR, Maumenee AE. Optic nerve damage in
human glaucoma. II. The site of injury and susceptibility to damage. Arch
Ophthalmol (Chicago Ill 1960) 1981; 99:635–649.
45. Ren R, Wang N, Li B, et al. Lamina cribrosa and peripapillary sclera
histomorphometry in normal and advanced glaucomatous Chinese eyes with
various axial length. Investig Ophthalmol Vis Sci 2009; 50:2175–2184.
46. Jonas JB, Berenshtein E, Holbach L. Lamina cribrosa thickness and spatial
relationships between intraocular space and cerebrospinal fluid space in
highly myopic eyes. Investig Ophthalmol Vis Sci 2004; 45:2660–2665.
47. Park HY, Park CK. Diagnostic capability of lamina cribrosa thickness by
enhanced depth imaging and factors affecting thickness in patients with
glaucoma. Ophthalmology 2013; 120:745–752.
48. Balaratnasingam C, Morgan WH, Johnstone V, et al. Histomorphometric
measurements in human and dog optic nerve and an estimation of optic nerve
pressure gradients in human. Exp Eye Res 2009; 89:618–628.
49. Tan NY, Koh V, Girard MJ, Cheng CY. Imaging of the lamina cribrosa and its
role in glaucoma: a review. Clin Exp Ophthalmol 2018; 46:177–188.
50. Lee EJ, Kim TW, Kim M, Kim H. Influence of lamina cribrosa thickness and
depth on the rate of progressive retinal nerve fiber layer thinning. Ophthal-
mology 2015; 122:721–729.
www.co-ophthalmology.com 95
Glaucoma
51. Sigal IA, Yang H, Roberts MD, et al. IOP-induced lamina cribrosa deformation
and scleral canal expansion: independent or related? Investig Ophthalmol Vis
Sci 2011; 52:9023–9032.
52. Coudrillier B, Pijanka JK, Jefferys JL, et al. Glaucoma-related changes in the
mechanical properties and collagen micro-architecture of the human sclera.
PLoS One 2015; 10:e0131396.
53. Jia X, Yu J, Liao SH, Duan XC. Biomechanics of the sclera and effects on
intraocular pressure. Int J Ophthalmol 2016; 9:1824–1831.
54. Wang X, Teoh CK, Chan AS, et al. Biomechanical properties of Bruch’s
membrane: choroid complex and their influence on optic nerve head bio-
mechanics. Invest Ophthalmol Vis Sci 2018; 59:2808–2817.
55. Ohno-Matsui K, Akiba M, Moriyama M, et al. Imaging retrobulbar subarach-
noid space around optic nerve by swept-source optical coherence tomo-
graphy in eyes with pathologic myopia. Investig Ophthalmol Vis Sci 2011;
52:9644–9650.
56. Jonas JB, Jonas SB, Jonas RA, et al. Histology of the parapapillary region in
high myopia. Am J Ophthalmol 2011; 152:1021–1029.
57. Han JC, Cho SH, Sohn DY, Kee C. The characteristics of lamina cribrosa
defects in myopic eyes with and without open-angle glaucoma. Investig
Ophthalmol Vis Sci 2016; 57:486–494.
58. Kimura Y, Akagi T, Hangai M, et al. Lamina cribrosa defects and optic disc
morphology in primary open angle glaucoma with high myopia. PLoS One
2014; 9:1–18.
59. Kiumehr S, Park SC, Dorairaj S, et al. In vivo evaluation of focal lamina
cribrosa defects in glaucoma. Arch Ophthalmol 2012; 130:443–445.
60. Takayama K, Hangai M, Kimura Y, et al. Three-dimensional imaging of lamina
cribrosa defects in glaucoma using swept-source optical coherence tomo-
graphy. Investig Opthalmol Vis Sci 2013; 54:4798.
61. Tatham AJ, Miki A, Weinreb RN, et al. Defects of the lamina cribrosa in eyes
with localized retinal nerve fiber layer loss. Ophthalmology 2014;
121:110–118.
62. Faridi OS, Park SC, Kabadi R, et al. Effect of focal lamina cribrosa defect on
glaucomatous visual field progression. Ophthalmology 2014; 121:1524–1530.
63. Sharpe GP, Danthurebandara VM, Vianna JR, et al. Optic disc hemorrhages
and laminar disinsertions in glaucoma. Ophthalmology 2016;
123:1949–1956.
64. Kim YK, Jeoung JW, Park KH. Effect of focal lamina cribrosa defect on disc
hemorrhage area in glaucoma. Investig Ophthalmol Vis Sci 2016; 57:899–907.
65. Downs JC, Roberts MD, Burgoyne CF. Mechanical environment of the optic
nerve head in glaucoma. Optom Vis Sci 2008; 85:425–435.
66. Mackenzie PJ, Cioffi GA. Vascular anatomy of the optic nerve head. Can J
Ophthalmol 2008; 43:308–312.
67. Hernandez MR. The optic nerve head in glaucoma: role of astrocytes in tissue
remodeling. Prog Retin Eye Res 2000; 19:297–321.
68. Sawada Y, Araie M, Ishikawa M, Yoshitomi T. Multiple temporal lamina
cribrosa defects in myopic eyes with glaucoma and their association with
visual field defects. Ophthalmology 2017; 124:1600–1611.
69. Tham YC, Aung T, Fan Q, et al. Joint effects of intraocular pressure and
myopia on risk of primary open-angle glaucoma: the Singapore epidemiology
of eye diseases study. Sci Rep 2016; 6:19320.
70. Jonas JB, Holbach L, Panda-Jonas S. Peripapillary arterial circle of Zinn-
Haller: location and spatial relationships with myopia. PLoS One 2013;
8:e78867.
71. Henkind P, Levitzky M. Angioarchitecture of the optic nerve: I. the papilla. Am
J Ophthalmol 1969; 68:979–986.
72. Hayreh SS. Blood supply of the optic nerve head and its role in optic atrophy,
glaucoma, and oedema of the optic disc. Br J Ophthalmol 1969;
53:721–748.
73. Anderson DR, Braverman S. Reevaluation of the optic disk vasculature. Am J
Ophthalmol 1976; 82:165–174.
74. Ang M, Tan AC, Cheung CM, et al. Optical coherence tomography angio-
graphy: a review of current and future clinical applications. Graefe’s Arch Clin
Exp Ophthalmol 2018; 256:237–245.
75. Sharma S, Ang M, Najjar RP, et al. Optical coherence tomography angio-
graphy in acute nonarteritic anterior ischaemic optic neuropathy. Br J
Ophthalmol 2017; 101:1045–1051.
76. Suwan Y, Aghsaei Fard M, Geyman LS, et al. Association of myopia with
peripapillary perfused capillary density in patients with glaucoma an optical
coherence tomography angiography study. JAMA Ophthalmol 2018;
136:507–513.
77. Sung MS, Lee TH, Heo H, Park SW. Association between optic nerve head
deformation and retinal microvasculature in high myopia. Am J Ophthalmol
2018; 188:81–90.
78. Chen Q, He J, Hua Y, Fan Y. Exploration of peripapillary vessel density in
highly myopic eyes with peripapillary intrachoroidal cavitation and its relation-
ship with ocular parameters using optical coherence tomography angiogra-
phy. Clin Exp Ophthalmol 2017; 45:884–893.
79. Yu D-Y, Cringle SJ, Balaratnasingam C, et al. Retinal ganglion cells: ener-
getics, compartmentation, axonal transport, cytoskeletons and vulnerability.
Prog Retin Eye Res 2013; 36:217–246.
80. Benavente-Pérez A, Hosking SL, Logan NS, Broadway DC. Ocular blood
flow measurements in healthy human myopic eyes. Graefe’s Arch Clin Exp
Ophthalmol 2010; 248:1587–1594.
96 www.co-ophthalmology.com
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
81. Dastiridou AI, Ginis H, Tsilimbaris M, et al. Ocular rigidity, ocular pulse
amplitude, and pulsatile ocular blood flow: the effect of axial length. Investig
Ophthalmol Vis Sci 2013; 54:2087–2092.
82. Gupta P, Cheung CY, Saw SM, et al. Peripapillary choroidal thickness in
young Asians with high myopia. Investig Ophthalmol Vis Sci 2015;
56:1475–1481.
83. Yokoi T, Zhu D, Bi HS, et al. Parapapillary diffuse choroidal atrophy in children
is associated with extreme thinning of parapapillary choroid. Investig Opthal-
mol Vis Sci 2017; 58:901.
84. Chen HS, Liu CH, Wu WC, et al. Optical coherence tomography angio-
graphy of the superficial microvasculature in the macular and peripapillary
areas in glaucomatous and healthy eyes. Investig Ophthalmol Vis Sci 2017;
58:3637–3645.
85. Jia Y, Wei E, Wang X, et al. Optical coherence tomography angiography of
optic disc perfusion in glaucoma. Ophthalmology 2014; 121:1322–1332.
86. Wang X, Jiang C, Ko T, et al. Correlation between optic disc perfusion and
glaucomatous severity in patients with open-angle glaucoma: an optical
coherence tomography angiography study. Graefe’s Arch Clin Exp Ophthal-
mol 2015; 253:1557–1564.
87. Yokoyama Y, Aizawa N, Chiba N, et al. Significant correlations between optic
nerve head microcirculation and visual field defects and nerve fiber layer loss
in glaucoma patients with myopic glaucomatous disk. Clin Ophthalmol 2011;
5:1721–1727.
88. Yamazaki Y, Drance SM. The relationship between progression of visual field
defects and retrobulbar circulation in patients with glaucoma. Am J Ophthal-
mol 1997; 124:287–295.
89. Galassi F, Sodi A, Ucci F, et al. Ocular hemodynamics and glaucoma
prognosis. Arch Ophthalmol 2003; 121:1711.
90. Nakazawa T. Ocular blood flow and influencing factors for glaucoma. Asia-
Pacific J Ophthalmol (Philadelphia, Pa) 2016; 5:38–44.
91. Grieshaber MC, Mozaffarieh M, Flammer J. What is the link between vascular
dysregulation and glaucoma? Surv Ophthalmol 2007; 52:S144–S154.
92. Hecht I, Achiron A, Man V, Burgansky-Eliash Z. Modifiable factors in the
management of glaucoma: a systematic review of current evidence. Graefe’s
Arch Clin Exp Ophthalmol 2017; 255:789–796.
93. Grudzinska E, Modrzejewska M. Modern diagnostic techniques for the
assessment of ocular blood flow in myopia: current state of knowledge. J
Ophthalmol 2018; 2018:4694789.
94. Medeiros FA, Zangwill LM, Bowd C, et al. Evaluation of retinal nerve fiber
layer, optic nerve head, and macular thickness measurements for glaucoma
detection using optical coherence tomography. Am J Ophthalmol 2005;
139:44–55.
95. Chihara E, Tanihara H. Parameters associated with papillomacular bundle
defects in glaucoma. Graefe’s Arch Clin Exp Ophthalmol 1992;
230:511–517.
96. Kimura Y, Hangai M, Morooka S, et al. Retinal nerve fiber layer defects in
highly myopic eyes with early glaucoma. Investig Ophthalmol Vis Sci 2012;
53:6472–6478.
97. Shin HY, Park HY, Park CK. The effect of myopic optic disc tilt on measure-
ment of spectral-domain optical coherence tomography parameters. Br J
Ophthalmol 2015; 99:69–74.
98. Chauhan BC, O’Leary N, Almobarak FA, et al. Enhanced detection of open-
angle glaucoma with an anatomically accurate optical coherence tomogra-
phy-derived neuroretinal rim parameter. Ophthalmology 2013;
120:535–543.
99. Malik R, Belliveau AC, Sharpe GP, et al. Diagnostic accuracy of optical
coherence tomography and scanning laser tomography for identifying glau-
coma in myopic eyes. Ophthalmology 2016; 123:1181–1189.
100. Rebolleda G, Casado A, Oblanca N, Muñoz-Negrete FJ. The new Bruch’s
membrane opening: minimum rim width classification improves optical
coherence tomography specificity in tilted discs. Clin Ophthalmol 2016;
10:2417–2425.
101. Sastre-Ibañez M, Martinez-de-la-Casa JM, Rebolleda G, et al. Utility of Bruch
membrane opening-based optic nerve head parameters in myopic subjects.
Eur J Ophthalmol 2018; 28:42–46.
102. Zheng F, Wu Z, Leung CK. Detection of Bruch’s membrane opening in
healthy individuals and glaucoma patients with and without high myopia.
Ophthalmology 2018; 125:1537–1546.
103. Hood DC, Kardon RH. A framework for comparing structural and functional
measures of glaucomatous damage. Prog Retin Eye Res 2007;
26:688–710.
104. Baek SU, Kim KE, Kim YK, Park KH, Jeoung JW. Development of topographic
scoring system for identifying glaucoma in myopic eyes: a spectral-domain
OCT study. Ophthalmology 2018, In Press
105. Park K, Kim J, Lee J. Macular vessel density and ganglion cell/inner plexiform
layer thickness and their combinational index using artificial intelligence. J
Glaucoma 2018; 27:750–760.
106. Li Z, He Y, Keel S, et al. Efficacy of a deep learning system for detecting
glaucomatous optic neuropathy based on color fundus photographs.
Ophthalmology 2018; 125:1199–1206.
107. Muhammad H, Fuchs TJ, De Cuir N, et al. Hybrid deep learning on single
wide-field optical coherence tomography scans accurately classifies glau-
coma suspects. J Glaucoma 2017; 26:1.
Volume 30  Number 2  March 2019