C L I N I C A L A N D E X P E R I M E N T A L

OPTOMETRY
CLINICAL COMMUNICATION

Progressive adult antimetropia

Clin Exp Optom 2014; 97: 375–378 DOI:10.1111/cxo.12129

Stephen J Vincent PhD
Scott A Read PhD
Contact Lens and Visual Optics Laboratory, School of
Optometry and Vision Science, Queensland
University of Technology, Brisbane, Queensland,
Australia
E-mail: sj.vincent@qut.edu.au
Antimetropia, a sub-classification of anisometropia, is a rare refractive condition in which
one eye is myopic and the fellow eye is hyperopic. This case report describes the ocular
characteristics and atypical refractive progression in an adult male with a moderate degree
of non-amblyopic antimetropia over a 20-year period. The potential mechanisms under-
lying unilateral axial elongation, anisometropia and myopia progression in adulthood are
discussed.

Submitted: 12 August 2013

Revised: 1 October 2013
Accepted for publication: 7 November
2013

Key words: adult, antimetropia, anisometropia, unilateral myopia progression

Anisometropia is an asymmetry in refractive
error between the fellow eyes of an indi-
vidual, typically due to an interocular differ-
ence in axial lengths.1 The prevalence of
anisometropia varies with age, the magni-
tude of refractive error and the criteria used
to define the condition (for example, spheri-
cal component or spherical equivalent
refraction and the magnitude of the inter-
ocular difference considered anisometro-
pic). Typically, a between-eye difference of
at least one dioptre is considered clinically
relevant and using this criterion the preva-
lence of non-amblyopic anisometropia has
been reported to range between one and six
per cent in children (six months to 15 years)2
and 15 to 20 per cent in adults (40 to 80
years).3,4 The term antimetropia describes a
rare subset of anisometropia, in which one
eye is hyperopic and the fellow eye is myopic.
The prevalence of naturally occurring anti-
metropia (excluding surgically induced
cases, such as aphakia) is extremely low, up
to 0.1 per cent in large student populations5,6
and is typically associated with amblyopia in
the hyperopic eye.7
Anisometropic eye growth in the absence
of amblyopia or ocular pathology is an inter-
esting anomaly, since two eyes within the one
visual system, presumably exposed to similar
genetic and environmental influences, have
developed different refractive errors. The
mechanisms underlying anisometropic eye
growth in humans, in particular anisometro-
pia associated with late-onset myopia (that is,
developing in adulthood) are poorly under-
stood. This report describes the refractive
progression of an initially mild anisome-
tropic Caucasian man, who developed a
substantial degree of antimetropia (greater
than 5.00 D interocular difference in sphe-
rical refraction) over a 20-year period
throughout adult life in the absence of
ocular injury, pathology, amblyopia or an
anomaly of binocular vision. The clinical
findings are presented along with a discus-
sion of the potential mechanisms underlying
the development of anisometropia and
antimetropia.
CASE REPORT
A 58-year-old Caucasian man presented to
the optometric clinic at the Queensland
University of Technology for a routine
review. He had attended our clinic for over
20 years. Past ocular history was negative for
injury or surgery; however, he reported a
positive family history of primary open angle
glaucoma. He was currently taking Lipex
(simvastatin) for hypercholesterolaemia but
otherwise reported good general health.
Pupil reactions were normal with no relative
afferent pupil defect. Ocular motility was full
and cover testing revealed no ocular mis-
alignment (heterotropia or heterophoria)
during distance or near fixation. Non-cyclo-
plegic subjective refraction revealed marked
antimetropia of 5.50 D: R -4.00 DS (6/6) and
L +1.50 DS (6/6). A +2.25 D near addition
enabled N4 print to be read binocularly at a
comfortable working distance.
Examination of the anterior segment
and ocular adnexae was unremarkable
except for bilateral Hudson-Stähli lines
and mild nuclear sclerosis of the crystalline
lens in each eye. Indirect ophthalmoscopy
revealed healthy maculae and optic discs in
both eyes; however, peripapillary atrophy
was visible surrounding the entire right optic
nerve head. The right fundus had the typical
appearance of a moderate to highly myopic
eye8 (circumferential peripapillary atrophy
and prominent choroidal vasculature),
while the posterior pole of the left hypero-
pic eye was unremarkable (Figure 1). While
there was no posterior staphyloma in the
myopic right eye, obvious interocular differ-
ences in retinal curvature and choroidal
thickness were evident in cross-sectional
images (Figure 2) obtained with optical
coherence tomography (Cirrus HD-OCT,
Carl Zeiss Meditec, Inc, Jena, Germany).
The right eye displayed the typical retinal
curvature of a moderate to highly myopic
eye, while the curvature of the left retina
appeared relatively flat.
Axial length measurements obtained
using the IOLMaster (Carl Zeiss Meditec,

© 2014 The Authors Clinical and Experimental Optometry 97.4 July 2014
Clinical and Experimental Optometry © 2014 Optometrists Association Australia 375
Progressive adult antimetropia Vincent and Read

Inc, Jena, Germany) confirmed the antime-

tropia was axial in nature (R 25.68 mm and L
23.45 mm). Scheimpflug imaging (Pentacam
HR system, Oculus Inc, Wetzlar, Germany)
of the anterior segment revealed; central
corneal thicknesses of R 497 μm and L
491 μm, anterior chamber depths of R
3.04 mm and L 2.92 mm and mean simu-
lated keratometry readings of R 43.7 D and L
44.2 D. The anterior corneal higher-order
aberration (third- to fourth-order Zernike
terms) root mean square error (derived
from an 8.0 mm corneal diameter) was
similar between the fellow eyes (R 0.015 μm
and L 0.017 μm). Quantitative lens densi-
tometry analysis (a linear densitogram
through the crystalline lens centred on the
visual axis) revealed a similar mild degree of
crystalline lens opacification in each eye (R
7.6 ± 1.6 per cent and L 8.6 ± 1.9 per cent).
Intraocular pressures (IOP) were R 12 and
L 12 mmHg at 10:00 am using a non-contact
tonometer (Topcon CT80, Topcon Corp,
Tokyo, Japan). Visual fields were full in each
eye using static white on white computerised
perimetry (SITA standard 24-2, Humphrey
Visual Field Analyzer, Carl Zeiss Meditec,
Inc, Jena, Germany). Fundus examination
through dilated pupils revealed no periph-
eral retinal abnormalities in either eye. Con-
sequently, routine annual eye examinations
Figure 1. Retinal photographs and optical coherence tomography (OCT) images of the were recommended to monitor the myopia
and antimetropic progression and screen
right myopic (top panel) and left hyperopic (bottom panel) eyes. Left inset: scanning laser
forglaucomagiventhepositivefamily history.
ophthalmoscopic image of the fundus. Right inset: line scan through the deepest point of
Retrospective analysis of the previous con-
the optic nerve. sultations revealed a gradual increase in the
degree of antimetropia throughout adult-
hood (age 38 to 58 years) (Figure 2). The
subjective refraction and IOP measure-
2.00 ments from each examination are summa-
rised in Table 1. Based on the spherical
1.00 equivalent refractive error obtained from
Spherical equivalent refraction (D)

L non-cycloplegic subjective refractions, over

0.00 20 years the right eye underwent a 3.00 D
myopic shift, while the left eye experienced a
R
-1.00 1.50 D hyperopic shift. Visual acuities were
6/6 or better in each eye at all examinations.
-2.00 There was no clinically significant change
in binocular visual status over the 20-year
-3.00 review period. The mean dissociated hori-
zontal heterophoria during distance fixa-
-4.00 tion was 0.5 ± 1.5Δ esophoria (range: 3Δ
esophoria to 2Δ exophoria) averaged across
-5.00 all consultations.
35 40 45 50 55 60
Age (years)
DISCUSSION
Figure 2. Change in spherical equivalent refraction between the This report describes the refractive changes
fellow eyes over a 20-year period. in an adult male with a moderate degree of

Clinical and Experimental Optometry 97.4 July 2014 © 2014 The Authors
376 Clinical and Experimental Optometry © 2014 Optometrists Association Australia
 Progressive adult antimetropia Vincent and Read
Age Subjective refraction (D) IOP (mmHg)
(years) Right eye Left eye Right eye Left eye
38 -1.00 +0.50/-0.75 × 5 11 12.5
40 -1.50 +0.50/-0.50 × 3 13 12.5
42 -2.25 +0.50/-0.50 × 180 14 13.5
44 -2.00/-0.25 × 90 +0.50/-0.50 × 180 11 10
46 -2.75/-0.25 × 85 +0.50/-0.25 × 180 12 10
48 -3.50/-0.25 × 28 +1.00 20 20
52 -3.50/-0.50 × 95 +1.00/-0.50 × 5 15 15
55 -3.50/-1.00 × 96 +1.25/-0.25 × 147 12 13
57 -3.75/-0.50 × 65 +1.25/-0.25 × 115 15 14
58 -4.00 +1.50 12 12
Table 1. Non-cycloplegic subjective refraction and intraocular pressure (IOP) measured
with non-contact tonometry at each consultation over a 20-year period.
antimetropia in the absence of any obvious increase in prevalence every seven years).
potential causative ocular abnormalities. To A decrease in binocular co-ordination later
our knowledge, this is the first documented in life (a regression of accommodation and
longitudinal retrospective examination of binocular visual development during older
a naturally occurring, non-amblyopic case adulthood), which in turn affects accommo-
of antimetropia. Of particular interest is not dation and refractive status has been sug-
only the magnitude of divergent refractive gested as a potential mechanism underlying
errors but the age at which the refractive anisometropia development in older age.10
changes progressed, namely, well into adult- More recently, larger clinical studies have
hood, beyond the plastic period of ocular also reported a significant increase in the
development (eight to 12 years) and the age prevalence of anisometropia during adult
at which early-onset myopia usually stabilises life;11,12 however, the reported magnitude
(15 to 18 years). Kuo, Shen and Shen9 exam- of change in anisometropia is typically
ined various ocular biometrics in a small small (0.25 to 0.75 D), unlike the increase
cohort of male Taiwanese antimetropes observed in this case (over 4.00 D).
(19 to 30 years old, mean spherical equiva- In our patient, we observed no change in
lent refractive antimetropia 5.28 D) and binocular vision status with age and during
found no clinically meaningful differences the most recent examination cover and
between the fellow eyes for measures of motility testing were within normal limits.
corneal thickness (mean interocular differ- The left eye underwent a gradual increase in
ence of 3.6 μm), anterior chamber depth hyperopia, which is not uncommon between
(0.06 mm) or IOP (0.1 mmHg). While ages 40 and 60. Non-cycloplegic retinoscopy
the visual acuity of these patients was not at the initial consultation 20 years earlier
reported, the biometric basis of the between (age 38 years) was R -1.00 DS, L +1.50/-0.50
eye difference in refraction was due primar- × 5. Consequently, in this particular case, the
ily to an asymmetry in axial length, as increase in antimetropia appears to be a
observed in our patient. result of a combination of unilateral myopia
The development of anisometropia in progression in the right eye and the gradual
older age groups in the absence of obvious manifestation of latent hyperopia in the left
pathology (for example, unilateral cataract) eye.
is poorly understood. Weale10 observed that Both early- (youth) and late- (adult) onset
the prevalence of non-amblyopic anisome- myopia result from axial (vitreous chamber)
tropia decreases in early life in conjunction elongation; however, the former is thought
with the development of binocular vision, to have a significant hereditary component
increases during the teenage years associ- and the latter to be a result of environmental
ated with myopia development and contin- influences.13,14 A two-year longitudinal study
ues to increase throughout adulthood of myopia progression in adult microsco-
into older age (approximately one per cent pists15 revealed that adult-onset myopes (age
© 2014 The Authors
Clinical and Experimental Optometry © 2014 Optometrists Association Australia
of onset approximately 26 years) progressed
at a rate of 0.29 D per year. This is slightly
higher than the overall rate of myopia pro-
gression in our patient over a 20-year period
(0.15 D per year) but similar to the progres-
sion observed between ages 38 and 42 years
(0.31 D per year). Considering each eye of
our patient separately, it could be argued
that the amount of refractive progression
observed in each eye is not uncommonly
encountered in clinical practice; however,
myopic or hyperopic refractive changes
during adulthood typically progress in the
same direction bilaterally (that is, both
eyes progress towards myopia or hypero-
pia), although sometimes in an asymmetric
manner. While the structural cause of adult-
onset myopia has been identified, it is
difficult to explain why vitreous chamber
expansion might differ so markedly between
the fellow eyes of an adult individual.
Potential mechanisms underlying
unilateral myopia progression
While no studies have examined the genetic
contribution to the development of antime-
tropia, there is some evidence to suggest that
genetics may play a role in the aetiology of
severe myopic anisometropia. Mirror or
directly symmetric severe anisometropia
has been observed in both monozygotic
twins16–18 and non-twin siblings;19 however,
such cases are typically associated with
abnormal ocular development, reduced
visual acuity and an apparent structural
abnormality in the affected (more myopic)
eye such as optic nerve or macular hypo-
plasia typically present from an early age. In
our patient, as anisometropia developed
much later in life and visual acuity remained
unaffected throughout the antimetropic
progression, it is unlikely there was a signifi-
cant genetic influence; however, we cannot
rule out the possibility of a delayed response
to genetically pre-programmed asymmetric
axial elongation.
Unilateral image degradation in humans
has been associated with the development
of anisometropia. Alteration of the visual
image during ocular development due
to eyelid ptosis20 or media opacities (that
is, corneal scarring,21 cataract22 or vitreous
haemorrhage23) typically results in axial
elongation and myopic development (often
with astigmatism) in the affected eye. It has
been hypothesised that more subtle inter-
ocular differences in optical quality may
also promote asymmetric axial elongation.
Higher-order aberrations, arising from the
Clinical and Experimental Optometry 97.4 July 2014
377
Progressive adult antimetropia Vincent and Read
cornea or crystalline lens, may degrade
retinal image quality but cross-sectional
studies of adult myopic anisometropes do
not support this theory.24,25 In our patient,
corneal higher-order aberrations and
crystalline lens opacification were similar
between the fellow eyes, although slightly
greater in the hyperopic eye compared to
the myopic eye.
Asymmetric IOP has been suggested as a
potential mechanical mechanism for inter-
ocular differences in axial elongation due to
unequal pressure-induced globe expansion;
however, cross-sectional studies24,26 examin-
ing IOP in anisometropic eyes have failed to
observe clinically or statistically significantly
higher IOP in the more myopic/less hyper-
opic eye compared to the fellow eye. In
our patient, IOP was largely symmetrical
between the two eyes over the 20-year review
period (mean absolute interocular differ-
ence 0.75 mmHg). The possibility remains
that an interocular difference in diurnal vari-
ations of IOP (or IOP spikes)27 may contrib-
ute to asymmetric axial elongation, or that
anisometropia may develop with symme-
trical IOP, if scleral biomechanics differ
between the more and less myopic eyes. A
previous case of unilateral chronic angle-
closure glaucoma was associated with a
marked myopic shift in the affected eye;
however, the anisometropia in that particu-
lar case was due to a change in corneal cur-
vature rather than axial elongation.28
Recently, several cross-sectional studies
have examined the association between
ocular sighting dominance and non-
amblyopic anisometropia with conflicting
results. Studies of Asian adults24,29 suggest
that for anisometropia of 1.75 D or greater,
the more myopic eye is typically the domi-
nant sighting eye. Various theories have
been proposed to explain this association,
typically suggesting that the dominant eye
may be the ‘preferred eye’ for near work
during binocular viewing, resulting in more
exposure to myopiagenic stimuli compared
to the fellow non-dominant eye; however, a
large study of European adults11 observed
the opposite trend; on average the dominant
eye was significantly less myopic compared
to the non-dominant eye. Although ocular
dominance was not assessed in our patient,
future studies investigating the differences
between dominant and non-dominant eyes
during myopia progression may help to elicit
the influence of ocular dominance, if any,
upon the development of anisometropic
refractive errors.
Clinical and Experimental Optometry 97.4 July 2014
378
While a specific stimulus underlying the
unilateral myopic development in our pati-
ent was not readily identified, the inter-
ocular difference in the direction and
magnitude of the refractive progression
observed throughout adult life supports
existing evidence (in both children30 and
various animal models31) for a local mecha-
nism of ocular growth regulation with mini-
mal cross talk between the fellow eyes. The
strength of this case report is the long-term
follow-up period; however, a limitation is a
lack of serial biometric measurements such
as corneal and crystalline lens thickness,
vitreous chamber depth and axial length,
which would provide further insight into
the specific ocular components associated
with asymmetric eye growth. In our patient,
antimetropia progressed throughout adult
life and appeared to be due to a combination
of unilateral myopia progression and mani-
festation of latent hyperopia in the fellow
eye. This case highlights that substantial
asymmetric myopic refractive change can
occur well into adulthood; however, further
longitudinal research is required to better
understand the mechanisms underlying
asymmetric refractive development.
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© 2014 The Authors