C L I N I C A L A N D E X P E R I M E N T A L
OPTOMETRY
A review of astigmatism and its possible genesis
Clin Exp Optom 2007; 90: 1: 5–19
Scott A Read PhD
Michael J Collins PhD
Leo G Carney DSc
Contact Lens and Visual Optics
Laboratory, School of Optometry,
Queensland University of Technology,
Brisbane, Queensland, Australia
E-mail: sa.read@qut.edu.au
Submitted: 7 September 2006
Revised: 3 October 2006
Accepted for publication: 10 October
2006
Key words: aberrations, astigmatism, cornea, corneal topography, refractive error
Astigmatism is a commonly encountered
refractive error, accounting for about 13
per cent of the refractive errors of the
human eye.1 Our knowledge of astigma-
tism appears to have begun in the early
1800s when Thomas Young reported on
his own astigmatism but it was not until
1825 that the first cylindrical lens was used
by George Airy for the purpose of correct-
ing his own astigmatic refractive error.2
Since these early explorations, there has
been a great deal of research carried out
into various aspects of astigmatism. One
reason for this research interest is the fact
that the presence of astigmatism appears
to have the potential to influence normal
visual development. The presence of high
© 2007 The Authors
Journal compilation © 2007 Optometrists Association Australia
INVITED REVIEW
DOI:10.1111/j.1444-0938.2007.00112.x
Astigmatism is a refractive condition encountered commonly in clinical practice. This
review presents an overview of research that has been carried out examining various
aspects of this refractive error. We examine the components of astigmatism and the
research into the prevalence and natural course of astigmatic refractive errors through-
out life. The prevalence of astigmatism in various ethnic groups and diseases and syn-
dromes is also discussed. We highlight the extensive investigations that have been
conducted into the possible aetiology of astigmatism, however, no single model or theory
of the development of astigmatism has been proven conclusively. Theories of the devel-
opment of astigmatism based on genetics, extraocular muscle tension, visual feedback
and eyelid pressure are considered. Observations and evidence from the literature
supporting and contradicting these hypotheses are presented. Recent advances in tech-
nology such as wavefront sensors and videokeratoscopes have led to an increased under-
standing of ocular astigmatism and with continued improvements in technology, our
knowledge of astigmatism and its genesis should continue to grow.
degrees of astigmatism is associated with a visual feedback model in which astigma-
the development of amblyopia3–5 and tism develops in response to visual cues.
some associations have also been noted In this review we will consider the various
between astigmatism and the develop- hypotheses regarding the aetiology of
ment of myopia.6–10 Advances in technol- astigmatism and examine the evidence in
ogy and instrumentation mean that our the literature for these theories. We will
ability to measure, define and analyse the also present some new evidence from
eye’s optical and shape properties (includ- recent research in our laboratory that has
ing astigmatism) have improved markedly investigated the role of near work and eye-
in recent years. lid forces on corneal shape and refractive
Despite extensive research, the exact error development.
cause of astigmatism is still not known.
One possible reason for astigmatic devel-
COMPONENTS OF ASTIGMATISM
opment would be a genetic aetiology.
Other possible causes include mechanical Ocular astigmatism can occur as a result
interactions between the cornea and the of unequal curvature along the two prin-
eyelids and/or the extraocular muscles or cipal meridia of the anterior cornea
Clinical and Experimental Optometry 90.1 January 2007
5
Astigmatism and its genesis Read, Collins and Carney

(known as corneal astigmatism) and/or it

may be due to the posterior cornea,
unequal curvatures of the front and back
surfaces of the crystalline lens, decentra-
tion or tilting of the lens or unequal refrac-
tive indices across the crystalline lens
(known as internal or residual astigma-
tism). The combination of the corneal and
the internal astigmatism gives the eye’s
total astigmatism (that is, total astigmatism
equals corneal astigmatism plus internal
astigmatism). Corneal astigmatism is often
classified according to the axis of asti- Figure 1. Example of the classification of corneal astigmatism according to the axis.
gmatism as being either with-the rule Astigmatism can be classified as either with-the-rule (WTR) (where the steepest corneal
(WTR), oblique or against-the-rule (ATR) meridian is oriented approximately vertically) (left), against-the-rule (ATR) (where the
(Figure 1). In the past, astigmatism has steepest corneal meridian is oriented close to horizontal) (right) or as oblique (where
been defined as ‘regular’ or ‘irregular’. the steepest corneal meridian is oriented at an oblique angle) (centre). Axial curvature
Typically, irregular astigmatism is used to corneal topography maps are shown here for three different subjects.
describe a variety of asymmetric aberra-
tions such as coma, trefoil and quadrafoil.
The widely adopted use of Zernike poly-
nomials to describe the detailed compo-
nents of the eye’s optics has made the use
of the term ‘irregular’ astigmatism largely
redundant.
A recent study investigating corneal
topography has classified astigmatism
according to the changes occurring in the
astigmatism of the peripheral cornea.11
Corneal astigmatism was classified as
being stable, reducing or increasing in
the peripheral cornea. Of the subjects
with significant corneal astigmatism tested
in this study, astigmatism was found most
commonly to be reducing (47 per cent
of astigmatic subjects) or stable (44 per
cent) in the peripheral cornea. Figure
2 illustrates these forms of corneal
astigmatism.

CORNEAL AND INTERNAL

ASTIGMATISM

It is well accepted that there is some rela-

tionship between the eye’s corneal and
internal astigmatism. In 1890, Javal pro-
posed a rule that predicted the total astig-
matism of the eye based on the corneal
astigmatism.12 Javal’s rule states:
At = k + p( Ac )
where At is the total astigmatism and Ac is
the corneal astigmatism. The terms k and
Figure 2. Examples of two forms of corneal astigmatism. The maps on the left illus-
trate corneal astigmatism that is stable in the peripheral cornea (or astigmatism that
extends out into the peripheral cornea). The maps on the right illustrate corneal
astigmatism that reduces in the peripheral cornea (or astigmatism that is primarily
confined to the central cornea). Axial power maps are displayed at the top and only
the cylinder power is plotted in the lower maps (for both the central and peripheral
cornea).

Clinical and Experimental Optometry 90.1 January 2007 © 2007 The Authors
6 Journal compilation © 2007 Optometrists Association Australia

Early childhood
Birth to 4 years
· Cornea steep
· High degrees of
corneal astigmatism
· Most
ATR?
common axis
Figure 3. The typical changes that occur in astigmatism throughout life
p are constants approximated by 0.5 and
1.25, respectively. This rule relies on the
fact that residual astigmatism is thought to
be constant and ATR in most people (that
is, -0.50 D ATR).
Grosvenor, Quintero and Perrigin13 sug-
gested a simplification of Javal’s rule.
Regression analysis was carried out to
investigate the relationship between cor-
neal and total astigmatism. The slope of
this regression line is equivalent to the
constant ‘p’ (from Javal’s rule), and the y
intercept is equivalent to constant ‘k’. The
slope of the regression line was found to
be slightly less than one, and the y inter-
cept close to 0.5. Based on these results,
the authors proposed a simplified Javal’s
rule of At = Ac - 0.5. This simplified rule
was found to fit their data more closely
than the original Javal’s rule, which sug-
gests that an internal astigmatism of mag-
nitude 0.5 D is relatively constant across
subjects with different amounts of corneal
astigmatism.
Keller and colleagues14 investigated the
relationship between corneal and total
astigmatism by measuring corneal astig-
matism with a computer-assisted videok-
eratoscope. The corneal topographical
data were converted into a best fit sphero-
cylinder for a number of different pupil
sizes and subjective refraction was mea-
sured using the same pupil sizes. Corneal
astigmatism was plotted against total astig-
matism for the different pupil sizes and
the relationship between corneal and
total astigmatism was found to be inde-
pendent of pupil size. The results from
this study supported Javal’s rule as simpli-
© 2007 The Authors
Journal compilation © 2007 Optometrists Association Australia
Astigmatism and its genesis Read, Collins and Carney
Childhood Adulthood
4 to 18 years 18 to 40 years
· Cornea flattens · Cornea remains
· Astigmatism stable
reduces · Small degrees of
· Small degrees of
WTR astigmatism
WTR astigmatism
most common
most common
fied by Grosvenor, Quintero and Perrigin
(1988).
Kelly, Mihashi and Howland15 used an
instrument that allowed simultaneous cap-
ture of corneal and total eye aberrations
on a population of young subjects. They
found that some corneal aberrations are
compensated by the internal optics of the
eye, including horizontal/vertical astigma-
tism, lateral coma and spherical aberra-
tion. They suggested that the horizontal/
vertical astigmatism compensation is an
active process determined through a
fine-tuning, emmetropisation process. No
significant compensation was found for
oblique astigmatism in this population.
Dunne, Elawad and Barnes16 investi-
gated residual astigmatism, by measuring
the difference between ocular and total
astigmatism (by cylindrical decomposi-
tion). The average residual astigmatism
was found to be -0.46 × 98.2° for right
eyes and -0.50 × 99.4° for left eyes. In ap-
proximately two-thirds of eyes, the axis
of the residual astigmatism was found to
be perpendicular to the axis of corneal
astigmatism.
Several studies have investigated the
astigmatism contributed by the posterior
corneal surface.17–20 These studies have
found levels of astigmatism for the poste-
rior cornea ranging from 0.18–0.31 D.
The curvature of the posterior cornea
combined with the refractive index differ-
ence between the cornea and the aqueous
means that the posterior corneal astigma-
tism is of opposite sign to that of the ante-
rior cornea. Therefore, the compensation
of corneal astigmatism by the eye’s inter-
Clinical and Experimental Optometry 90.1 January 2007
Older adulthood
40+ years
· Cornea steepens
(more in horizontal
meridian)
· Shift
in corneal
astigmatism axis
towards ATR being
most common
nal optics can be attributed, in part, to the
astigmatism of the posterior cornea.
The compensation of corneal astigma-
tism by the internal optics of the eye has
been known for many years.12,15,16 The
numerous studies into Javal’s rule tend to
indicate that this compensation is a pas-
sive process (that is, the majority of the
population has approximately 0.5 D of
internal astigmatism, opposite in sign to
the corneal astigmatism). Some authors15
have suggested the possibility of an
active ‘feedback driven’ process operat-
ing to reduce the total astigmatism of
the eye (particularly horizontal/vertical
astigmatism).
PREVALENCE OF ASTIGMATISM AND
CHANGES WITH AGE
There have been many studies that have
attempted to define the prevalence of
astigmatism in the population and to illus-
trate the typical changes that occur in
astigmatism throughout life. These inves-
tigations provide some clues to the pos-
sible causes of astigmatism. Figure 3
illustrates the typical changes that occur in
astigmatism throughout life.
Astigmatism in early life (infancy
and early childhood)
Generally, studies have shown that in the
first months of life, infants exhibit a high
prevalence of significant degrees of astig-
matism,21–30 which appears to be corneal
in origin.24,27,29 The cornea of newborns is
steep and exhibits large degrees of astig-
matism.27,29,31 Isenberg and co-workers29
7
Astigmatism and its genesis Read, Collins and Carney
used videokeratoscopy to measure the cor-
neal curvature of newborns (up to eight
days after birth) and found an average of
six dioptres of corneal astigmatism. Stud-
ies have also shown that the steepest, most
astigmatic corneas occur in the newborns
with the lowest birth weight and lowest
post-conceptional age.27 While studies
have consistently found high degrees of
corneal astigmatism to be present in
infancy, there is some conflicting evidence
of the most common axis of astigmatism.
Perhaps indicating the difficulties of
obtaining accurate measurements on new-
born infants or suggesting a large amount
of variability in the corneal shape of
infants, some studies have found a pre-
dominance of WTR corneal astigma-
tism,26,29,30 while others have shown a
predominance of ATR corneal astigma-
tism in infants.22–25,27
As infants grow older, the prevalence
of high degrees of astigmatism typically
reduces or, in other words, an emmetropi-
sation of the astigmatic refractive error
occurs.21–29 Dobson, Fulton and Sebris22
and Gwiazda and colleagues23 found a
shift in astigmatism from a predominance
of higher degrees of ATR astigmatism in
children younger than four years, to a pre-
dominance of low levels of WTR astigma-
tism in children older than four years.
Gwiazda and colleagues23 postulated that
pressure from the eyelids on the cornea
over time may be causing the shift in astig-
matic axis from ATR to WTR in children.
Studies of preschool-age children gen-
erally show a relatively low prevalence of
high degrees of astigmatism (that is,
greater than one dioptre) that is predom-
inantly WTR in nature.32–34 Huynh and
associates34 investigated a large population
of six-year-old children and found that
only 4.8 per cent of children exhibited
greater than one dioptre of ocular astig-
matism and 75 per cent of subjects exhib-
ited WTR corneal astigmatism.
In summary, at birth children exhibit a
high incidence of astigmatism that is cor-
neal in origin. As children grow older,
the cornea flattens with significantly
reduced astigmatism. Over the age of
four years, the prevalence of large
amounts of astigmatism is low, with small
Clinical and Experimental Optometry 90.1 January 2007
8 Journal compilation © 2007 Optometrists Association Australia
amounts of WTR astigmatism being
found most commonly.
Astigmatism in adults
Astigmatism in young adults (younger
than 40 years) occurs commonly but in
relatively low amounts.35,36 In an investiga-
tion of young adults aged 20 to 30 years,
Satterfield36 found that 63 per cent of sub-
jects exhibited 0.25 D or more of ocular
astigmatism, however, the majority of sub-
jects with measurable astigmatism exhib-
ited less than one dioptre. In a cross-
sectional study, Fledelius and Stubgaard37
found that 46 per cent of the total popu-
lation had corneal astigmatism of greater
than 0.5 D but only 4.7 per cent of the
population exhibited greater than 1.5 D
of corneal astigmatism. Generally, studies
have shown that in young adults, WTR
astigmatism occurs most commonly.35,37–42
With increasing age, a general shift in
the axis of astigmatism is found from a
predominance of WTR astigmatism (in
adults younger than 40 years) to a pre-
dominance of ATR astigmatism (in adults
older than 40 years).35,38–40,42,43 This shift in
astigmatic axis in older age appears to be
due to changes in corneal curvature.38–40,42
In a cross-sectional study of corneal and
total astigmatism, Anstice38 found that
internal astigmatism remained relatively
stable over time and that changes in astig-
matism throughout life were due prima-
rily to changes in corneal curvature.
Baldwin and Mills39 investigated longitudi-
nal changes in corneal and total astigma-
tism in patients over a 40-year period and
found a steepening of the cornea and an
increase in ATR astigmatism with aging.
The majority of this change in astigmatism
was due to corneal change, that is, a steep-
ening of the horizontal meridian of the
cornea. As will be discussed later, this
change in corneal curvature may be
related to the reduction in tension of the
eyelids that typically occurs with age.
In summary, young adult subjects typi-
cally display small degrees of WTR astig-
matism and in older adult years a shift in
astigmatism occurs where ATR astigma-
tism becomes more prevalent. Astigma-
tism most commonly occurs due to the
curvature of the cornea and the changes
in astigmatism that occur throughout life
also appear to be due primarily to corneal
change.
ASTIGMATISM IN RIGHT AND
LEFT EYES
There is widespread agreement that some
degree of symmetry exists between the
refractive errors of right and left eyes. Sev-
eral studies have noted mirror symmetry
to occur between the axes of astigmatism
of right and left eyes.16,44,45 McKendrick
and Brennan41 measured corneal and
ocular refraction (with autorefraction and
autokeratometry) for both eyes in a group
of subjects. The mean and spread of astig-
matic errors was similar for right and left
eyes. The axes of corneal and total astig-
matism were found to be similar between
the two eyes.46 Most subjects were found to
display either mirror (for example, right
eye axis 10°, left eye axis 170°) or direct
(for example, right eye axis 10°, left eye
axis 10°) symmetry of their astigmatic
axes. There was no predominance of
either mirror or direct symmetry of astig-
matic axes when analysis was carried out
for the population. Figure 4 illustrates the
corneal topography from a normal subject
who shows mirror symmetry between the
corneal astigmatism of the right and left
eyes.
ASTIGMATISM AND OTHER
REFRACTIVE ERRORS
There is some evidence to suggest that the
presence of astigmatism may be associated
with the presence of spherical refractive
errors. The presence of astigmatism has
been found to be associated with myopic
refractive errors, that is, astigmatism was
associated with higher degrees of myo-
pia.6–10,47,48 Fulton, Hansen and Petersen6
suggested that uncorrected astigmatic
errors influenced the development of
myopia and that the optical blur from
uncorrected astigmatism may be a trigger
for myopic development. The presence
and changes in astigmatism have been
found by some investigators to be associ-
ated with an increased progression of
myopia.6,10,49 In a longitudinal study of
© 2007 The Authors

Figure 4. Axial curvature corneal topographical maps
from the right and left eye of a subject who shows distinct
mirror symmetry between the corneal astigmatism of the
two eyes
refractive error, Gwiazda and colleagues7
found that their subjects exhibiting signif-
icant ATR astigmatism and myopia in
infancy were more likely to develop myo-
pia at school age. In contrast with these
studies, other investigators50,51 have found
little to no association between the pres-
ence of astigmatism and the presence and
progression of myopic refractive errors.
While there is some equivocal evidence,
there does appear to be an association
between astigmatism and the develop-
ment and progression of myopia. The
exact nature of this relationship and the
mechanisms underlying it are not fully
understood.
ASTIGMATISM IN ETHNIC GROUPS
The studies that have been discussed up
to this point have generally been con-
ducted on populations consisting of pre-
dominantly healthy Caucasian subjects.
Studies of populations with different eth-
nic backgrounds (particularly those with
higher incidences of astigmatism) may
provide further insight into the aetiology
of astigmatism. Several different ethnic
groups appear to exhibit an increased
prevalence of astigmatism.
Subjects of Native American ethnic
origin have an increased prevalence of
high levels of astigmatism, particularly
WTR.52–57 The recent study by Harvey,
© 2007 The Authors
Journal compilation © 2007 Optometrists Association Australia
Astigmatism and its genesis Read, Collins and Carney
Dobson and Miller57 on a population of
Native American school children, found
that 42 per cent of subjects exhibited ocu-
lar astigmatism of 1.00 D or greater. This
high degree of astigmatism is corneal in
origin55,56 and it has been postulated that
these high degrees of WTR astigmatism
may relate to heredity or nutritional fac-
tors.52,53,55,58 Lyle, Grosvenor and Kean53
postulated that poor nutrition may lead to
reduced corneal rigidity and result in
increased corneal astigmatism due to pres-
sure from the upper eyelid causing the
cornea to become flatter in the horizontal
meridian and steeper in the vertical.
There is also an increased prevalence of
astigmatism in some populations of East
Asian subjects.10,59–61 Kame, Jue and
Shigekuni60 presented retrospective longi-
tudinal data on changes in corneal astig-
matism in a clinical population of East
Asian subjects. They found that subjects
younger than 30 years generally showed
an increase in WTR astigmatism and sub-
jects older than 30 years showed a
decrease in WTR astigmatism. The rates of
change of astigmatism were found to be
greater for the Asian subjects studied than
for those reported in previous longitudi-
nal studies of Caucasian subjects. The
authors suggested that the greater tight-
ness of the Asian eyelids and narrower
palpebral apertures may have led to the
observed greater rates of change of astig-
Clinical and Experimental Optometry 90.1 January 2007
matism. Fan and associates10 reported a
high prevalence of predominantly WTR
astigmatism (55.8 per cent of children
tested exhibited an astigmatic refractive
error of 0.50 D or greater) in a study of
Chinese schoolchildren aged three to six
years.
In a large study of the refractive error
of American children, Kleinstein and
colleagues62 noted an increased preva-
lence of astigmatism in children of Asian
and Hispanic origin. Asian children dis-
played a prevalence of astigmatism of one
or more dioptres of 33.6 per cent and
Hispanic children a prevalence of 36.9 per
cent.
A recent study63 of the refractive error
of the indigenous people of Brazil
reported a very low prevalence of myopia
(2.7 per cent) and a relatively high preva-
lence of astigmatism (with 16 per cent of
subjects exhibiting greater than 1.00 D of
astigmatism). In this population, the astig-
matism was predominantly ATR. Fuller
and co-workers64 found a high proportion
of WTR astigmatism in a small population
of Bangladeshi children living in East
London.
ASTIGMATISM RESULTING FROM
OCULAR SURGERY
Ocular surgery can lead to significant
changes in astigmatism. The fact that
some surgical procedures can cause highly
significant changes in corneal curvature
and astigmatism provides information
regarding the biomechanical properties
of the cornea and may also give clues to
the aetiology of astigmatism. Meek and
Newton65 suggested that the structural
and mechanical properties of the cornea
(including the arrangement of collagen
fibrils in the cornea and sclera) can
explain the alteration in corneal curvature
and the resulting astigmatic changes fol-
lowing some ocular surgery.
Modern surgical techniques for cataract
involve a small incision in the cornea and
can lead to alterations in astigmatism.
Incisions made in the cornea generally
cause a flattening in the incised corneal
meridian (and a subsequent steepening of
the orthogonal meridian), thus leading to
9
Astigmatism and its genesis Read, Collins and Carney
astigmatic change.66,67 Therefore, the loca-
tion of the corneal incision made during
cataract surgery will influence the induced
astigmatism, whereby a superior incision
typically results in a flattening of the verti-
cal meridian (and an increase in ATR
astigmatism) and temporal incision place-
ment leads to a flattening of the cornea
in the horizontal meridian (that is, an
increase in WTR astigmatism).67,68 The size
of the incision (with larger incisions caus-
ing greater astigmatic change)69–71 and
the location of the incision in relation to
the corneal centre (with incisions closer to
the centre of the cornea being associated
with greater astigmatic change)72 will
influence the induced astigmatism. The
changes in corneal astigmatism following
cataract surgery appear to be related to
the anatomical and biomechanical prop-
erties of the cornea.65,73 By understanding
these corneal changes following incisional
surgery, strategies are now employed
that take advantage of these astigmatic
changes in the cornea to reduce the over-
all level of refractive astigmatism following
cataract surgery.66,67
Retinal detachment surgery involving
scleral buckling causes significant changes
in astigmatism and corneal curvature.
This appears to be due to indentation of
the sclera by the buckle leading to alter-
ations in corneal curvature,74,75 which can
result in either regular or irregular cor-
neal astigmatism.74,75 The specific buckling
procedure influences the changes in cor-
neal curvature.74,76 Local or segmental
buckles lead to a local steepening in
the corneal quadrant adjacent to the
buckle74,76 and encircling buckles lead to
a more generalised peripheral flattening
and central steepening of the cornea.76
Uneven tightening or asymmetric place-
ment of encircling scleral buckles may also
lead to marked asymmetric astigmatic
change.76 Most studies have noted these
corneal changes to be transient74,77,78 but
significant change can persist up to six
months following surgery.75,76
Trabeculectomy for glaucoma can cause
significant corneal change, which is typi-
cally a steepening in the vertical meridian,
leading to an increase in regular WTR79–81
and irregular astigmatism.82 The size of
Clinical and Experimental Optometry 90.1 January 2007
10
the incision appears to be correlated to
the amount of induced astigmatism with
smaller incisions (as used in ‘microtrabe-
culectomy’ procedures) leading to a
smaller astigmatic change.80 The exact
cause of the corneal change following tra-
beculectomy is not known, although it has
been postulated that it relates to tension
from sutures used in the surgery,82 cauter-
isation of the wound80,82 or wound healing
factors79 leading to steepening of the cor-
nea in the superior meridian.
The growth of a pterygium onto the cor-
nea can lead to significant changes in cor-
neal astigmatism.83–85 Typically, the shift in
astigmatism is an increase in (asymmetric)
WTR astigmatism brought about by a flat- Figure 5. Example of a corneal topo-
tening of the cornea that occurs in the graphical map from a patient with an
horizontal meridian between the corneal advanced pterygium. Note the WTR
apex and the head of the pterygium.83–85 astigmatism and flattening of the cornea
The specific cause of this corneal flatten- adjacent to the head of the pterygium.
ing is thought to be a tear pooling effect
near the head of the pterygium,86 mechan-
ical tractional forces on the cornea from
the pterygium85,86 or a combination of
these factors. The size of the pterygium
appears to be related to the magnitude of resulted in less astigmatism following sur-
the induced astigmatism.83 Figure 5 illus- gery. The difference between the graft and
trates the corneal topographical changes recipient corneal size may also influence
typically brought about by a pterygium. the post-surgical corneal curvature.93
Surgery to remove pterygia typically leads Newer surgical techniques, such as non-
to a reduction of the induced WTR astig- mechanical trephination with the Excimer
matism and an increase in the regularity laser, also appear to lead to a reduction
and symmetry of corneal topography.84,85,87 in post-operative astigmatism compared
The amount of astigmatic change brought to traditional mechanical trephination
about by surgery for pterygium appears to techniques.94
be related to the preoperative size of the
pterygium.84
CAUSES OF ASTIGMATISM
Another ocular surgical procedure that
can result in significant amounts of cor- While much research has been carried out
neal astigmatism postoperatively is pene- into the prevalence and changes in astig-
trating keratoplasty.88–90 Troutman and matism throughout life, questions still
Lawless88 reported an average level of remain of the causes of astigmatism. As
corneal astigmatism of 4.3 D (range of 0– astigmatism most commonly has a corneal
10.5 D) in subjects following penetrating origin, the following sections will concen-
keratoplasty. A number of different proce- trate on the research that has been con-
dures has been suggested to reduce the ducted into the possible causes of corneal
level of astigmatism post-keratoplasty. astigmatism.
Selective manipulation of sutures whereby
the sutures along the steepest corneal Genetics and astigmatism
meridian are loosened has been shown One possible explanation of the aetiology
to reduce the astigmatism.90,91 Belmont, of astigmatism is that astigmatic refractive
Troutman and Buzard92 found intra- errors are genetically determined. Numer-
operative monitoring of corneal curvature ous studies have been undertaken to in-
© 2007 The Authors
Journal compilation © 2007 Optometrists Association Australia

vestigate the influence of genetics on
astigmatic development.
In an early study, Wixson95 investigated
the heritability of corneal power by com-
paring corneal power in a group of par-
ents and children with a group of
husbands and wives. He concluded that
both parents seem to participate in deter-
mining the corneal power characteristics
of the child. Wixson95 suggested that the
inheritance of corneal power appeared to
be best approximated by an autosomal
recessive pattern.
Several studies comparing monozygotic
and dizygotic twins have investigated the
genetic influence on astigmatic refractive
errors,96–99 including Teikari and O’Don-
nell,96 Teikari and associates97 and Valluri
and colleagues.98 All of these studies
found significant differences in the intra-
pair correlations for spherical refractive
errors between monozygotic and dizygotic
twins, suggesting that genetic influences
on myopia and hyperopia are strong. The
correlations between monozygotic twins
for astigmatism were not significantly dif-
ferent from the correlations between dizy-
gotic twins in these studies. This suggests
that the genetic contribution to astigma-
tism is low, with environmental factors
being the major contributors. In another
large study, Hammond and co-workers99
investigated the refractive error of 506
female twins (226 monozygotic and 280
dizygotic). In contrast to the previous
studies of twins, Hammond and co-
workers99 found the correlations for
monozygotic twins for astigmatism to be
greater than the correlations for dizygotic
twins. This suggests more significant
genetic effects on astigmatism than previ-
ous studies. The authors concluded that
the heritability of astigmatism was 50 to 65
per cent (that is, 50 to 65 per cent of the
variance in astigmatic refractive error was
attributed to genetic effects) and that the
heritability predominantly involved domi-
nant genetic effects.
Clementi and associates100 analysed data
from 125 Italian families affected by astig-
matism (476 subjects). Refractive error
and corneal astigmatism were measured
using automated techniques. When the
data were analysed for astigmatism as a
© 2007 The Authors
Journal compilation © 2007 Optometrists Association Australia
Astigmatism and its genesis Read, Collins and Carney
qualitative trait (that is, affected/unaf-
fected), no definite model of inheritance
was found to best fit the data. When the
severity of astigmatism was included in the
analysis, an autosomal dominant model of
inheritance provided the best fit to the
data. The authors estimated that the fre-
quency of the putative gene was low and
that it had more effect on the presence of
astigmatism than on its severity. Clementi
and associates100 suggested that bias (in
subject selection and analysis) in previous
studies may have led to inconsistent
results.
Lee and colleagues101 investigated the
refractive errors of a large population of
families in the Beaver Dam eye study (440
family groups). While strong aggregation
of myopia and hyperopia was found
among siblings in this study (suggesting
a potential genetic influence on these
refractive errors), minimal associations
were found between family members
for astigmatism. This suggests minimal
genetic influence on astigmatic refractive
error.
The studies into genetics and astigma-
tism do present some conflicting results.
Certain studies indicate some degree of
heritability of astigmatism and also tend to
favour an autosomal dominant mode of
inheritance.99,100 Other studies favour a
stronger environmental influence.96–98,101
It would appear that both genetic and
environmental factors have roles in the
development of astigmatism. The exact
nature of these mechanisms is still not
fully understood.
Animal studies and astigmatism
Studies using animals have provided
important insights into refractive error
development and have shown that visual
feedback does play a role in the develop-
ment of some refractive errors. These
studies have generally investigated the
effects of altering an animal’s normal
visual experience. Experiments have
shown that form deprivation (through tar-
ssorhaphy, corneal opacification or with
form depriving goggles) causes axial myo-
pia, which recovers on the removal of the
deprivation.102–105 This indicates that the
retinal image occurring provides informa-
Clinical and Experimental Optometry 90.1 January 2007
tion that is used to control eye growth.104
Imposing defocus on experimental ani-
mals using spherical lenses has also pro-
duced changes in ocular growth, where
the eye grows so that it matches both the
direction and magnitude of the imposed
spherical defocus.104–106 Therefore, it
would seem plausible that astigmatism
may develop through a similar visual feed-
back model (that is, the eye grows in an
astigmatic way in response to the visual
environment). Several studies have been
conducted to assess the effect of inducing
astigmatic refractive errors on eye growth
in experimental animals.
Irving, Callender and Sivak107 induced
astigmatic refractive errors in chick eyes
using goggles and found that the chick
eyes grew to partially compensate for the
induced astigmatic errors. Their results
were consistent with the chick compensat-
ing towards the best sphere of the induc-
ing lens, however, there was a high degree
of variation in response between animals.
Schmid and Wildsoet108 also induced astig-
matic refractive errors in chick eyes. While
they found that the induced astigmatic
errors did cause alterations to ocular
growth, the changes were not consistent
with the hypothesis that chick eyes
compensated for the induced astigmatic
errors.
McLean and Wallman109 used crossed
cylindrical lenses (which produce blurred
retinal images but have no spherical
power) to induce astigmatic blur in chicks.
They found no evidence that the chick’s
eyes compensated for the imposed astig-
matic errors. When the crossed cylinders
were used in conjunction with a spherical
lens, the eyes grew to compensate for the
spherical lens only. This indicates that
large amounts of astigmatic blur did not
interfere with the spherical lens compen-
sation in chick eyes and implies that the
amount of blur present is less important
than the sign of the defocus and that
sharp images are not required for lens
compensation.
There have been studies investigating
the effect of inducing astigmatic refrac-
tive errors in monkey eyes. Kee and
associates110 imposed WTR, ATR and
oblique astigmatic refractive errors in
11
Astigmatism and its genesis Read, Collins and Carney
monkeys. These animals developed signif-
icant amounts of astigmatism (corneal in
origin, oblique in axis and bilaterally mir-
ror symmetric), which were reversible on
the removal of the induced refractive
errors. The axes of the astigmatism that
developed were not appropriate to com-
pensate for the induced astigmatic errors.
These animals also showed changes in
spherical refractive errors as a result of the
induced astigmatic errors.111 Both myopic
and hyperopic refractive errors were
found to occur as a result of the astigmatic
defocus, with the monkeys’ eyes found to
grow axially in compensation to one of
the principal meridians of the astigmatic
lenses.
Kee and colleagues112 investigated
changes in astigmatism occurring in
monkeys as a result of experimentally in-
duced myopia and hyperopia. Significant
amounts of astigmatism were found to oc-
cur as a result of inducing both myopia
and hyperopia (with spherical adapting
lenses). These astigmatic errors were
corneal in origin, oblique in axis and
bilaterally mirror symmetric. The authors
suggested a possible growth-related mech-
anism associated with the development of
the spherical refractive errors that leads to
the astigmatism. These astigmatic errors
were found to diminish on reversal of the
myopia or hyperopia.
These studies have presented some
conflicting results on the exact end point
of emmetropisation when astigmatic
refractive errors are induced in experi-
mental animals. There is only limited evi-
dence to suggest that the eye can grow
to compensate for astigmatic refractive
errors. It is clear that inducing astigmatic
errors has the potential to significantly
affect normal eye growth in these animals
(both axial growth and corneal shape can
be altered as a result of induced astig-
matic errors).
Astigmatism and extraocular
muscles
Howland and Sayles24 suggested that cor-
neal astigmatism may develop as a result
of unequal tension exerted on the cornea
by the extraocular muscles (EOMs) (for
example, an increased degree of tension
Clinical and Experimental Optometry 90.1 January 2007
12
in the horizontal recti muscles may lead to
a bending of the cornea in the horizontal
meridian thus leading to ATR corneal
astigmatism). They proposed that changes
in the tension of the EOMs throughout
life might lead to subsequent changes in
corneal astigmatism. The effect of extraoc-
ular muscle (EOM) tension on corneal
shape is a subject that has received limited
coverage in the literature and the exact
influence that contraction and relaxation
of the EOMs has on corneal topography is
still not fully understood.
Early research into this topic investi-
gated the changes occurring in corneal
curvature during convergence. Some stud-
ies have found that a slight flattening of
the cornea (in the horizontal meridian)
accompanies the act of convergence.113,114
Other investigators found that no signifi-
cant changes in corneal curvature (as
measured with a photokeratoscope) occur
with convergence or with changes in fixa-
tion (that is, changes in EOM tension do
not cause a change in corneal shape).115
All of these studies were limited by the
technology of their time and the tech-
niques used may not have provided a
sufficiently accurate assessment of the
periphery of the cornea to describe any
changes occurring during convergence.
More recent reports of the effect of
EOM tension on astigmatism have centred
on changes occurring in corneal topogra-
phy and refraction following EOM sur-
gery. Kwitko and colleagues116 found that
surgery on rabbit EOM’s caused signifi-
cant changes in corneal topography in
some cases. There have also been several
reports of highly significant changes in
astigmatism117–121 and corneal topo-
graphy122,123 following surgery for strabis-
mus in human subjects.
The exact cause of this change in cor-
neal topography following EOM surgery
is still not known. Alteration in muscle
tension (and subsequent alteration in the
force applied by the muscles to the ante-
rior globe) or changes in tractional forces
due to surgery have both been suggested
as possible causes of these topographical
changes.119,121 Factors relating to surgical
recovery (for example, inflammation in
and around the globe) may also influence
Journal compilation © 2007 Optometrists Association Australia
the corneal topography following strabis-
mus surgery.123 It remains to be seen
whether alterations in EOM tension from
everyday tasks such as convergence and
eye movement also cause significant
changes in corneal topography and astig-
matism.
Eyelid pressure and astigmatism
Pressure from the eyelids on the cornea
has been implicated as a possible factor in
the development of corneal astigmatism.
Grosvenor12 proposed a theory for the
aetiology of astigmatism, whereby the
band-like pressure from the upper eyelid
on the cornea causes the eye to exhibit
WTR astigmatism (as occurs in the
majority of young adults) (Figure 6).
Grosvenor12 suggested that the tightness
of the eyelids and the rigidity of the ocular
surface interacted to produce corneal
astigmatism. The typical shift in astigmatic
axis from WTR in young adults to ATR in
older adults was also explained through
a reduction in lid tension with age,
leading to a reduction in WTR corneal
astigmatism.
There has been a number of experi-
ments examining the effect of the eyelids
on corneal astigmatism. Wilson, Bell and
Chotai124 investigated changes in corneal
astigmatism brought about by lifting the
eyelids. Eighteen subjects had their cor-
neal astigmatism measured (by keratome-
try) with lids in normal position and
retracted (with a speculum). Subjects with
more than one dioptre of WTR astigma-
tism showed a systematic change in the
direction of less WTR astigmatism when
the lids were retracted. Those subjects
showing changes exhibited a steepening
of the horizontal meridian of the cornea
but not a flattening of the vertical merid-
ian as may have been expected. The
results of this experiment suggest that the
position of the lids has an influence on
the degree and direction of corneal
astigmatism.
In a cross-sectional study, Vihlen and
Wilson125 investigated the changes in eye-
lid tension and corneal toricity that occur
with age. A definite reduction in lid ten-
sion, and a change in corneal toricity
towards ATR were found with increasing
© 2007 The Authors
 Astigmatism and its genesis Read, Collins and Carney

Figure 6. Illustration of the eyelid pressure theory of corneal
astigmatism development. According to this theory, pressure
from the eyelids alters corneal shape and leads to a steepening
in the cornea’s vertical meridian. This results in WTR astig-
matism, which is typically seen in the majority of young
subjects.
Figure 7. Example of a subject exhibiting a close correlation
between the angle of the palpebral fissure and the axis of the
corneal cylinder. This subject has a slightly up-slanting palpe-
bral fissure (palpebral fissure angle of five degrees) and a
corneal cylinder axis of 173 degrees. Shown here is a digital
image of the palpebral fissure captured in primary gaze, over-
laid with an axial power corneal topographical map.

age. No association was found between
eyelid tension and corneal toricity (that is,
tighter lids did not correlate with more
astigmatism). Longitudinal studies investi-
gating eyelid tension and corneal toricity
may be required to shed more light on
whether eyelid tension does play a role in
the typical changes in corneal astigmatism
found with age.
The influence of lid position on astig-
matism was also studied by Grey and
Yap.126 Ocular astigmatism was measured
on patients who adopted three different
lid positions (that is, deliberately wid-
ened, normal position and deliberately
narrowed lids). A significant increase in
ocular astigmatism was found for the
deliberately narrowed eyelid position with
subjects showing an increase of WTR
astigmatism.
Lieberman and Grierson127 measured
corneal topography in subjects with and
without the lids touching the cornea. They
found changes in corneal shape occurred
when the lids were retracted from the cor-
nea. This further confirms that the posi-
tion of the eyelids can influence the shape
of the cornea.
If pressure from the eyelids leads to
WTR corneal astigmatism, then one may
expect that certain correlations exist
between the axis and magnitude of astig-
matism and the angle and position of the
eyelids. It should be noted that the exist-
ence of correlations between eyelid mor-
phological features and astigmatism does
not prove that eyelid pressure is causing
astigmatism. Garcia and associates45 stud-
ied a population of children with high
astigmatism (greater than 1.5 D). Cyclo-
plegic retinoscopy, corneal topography
and palpebral fissure slant were measured.
Most astigmatism was WTR. The majority
of subjects also displayed an up-slanting of
the palpebral fissure (that is, temporal
canthus higher than the nasal canthus). A
significantly higher proportion of patients
with high corneal and total astigmatism
also displayed abnormally slanted palpe-
bral fissures. The axis of astigmatism was
found to be significantly correlated with
the degree of palpebral fissure slant. The
steeper corneal axis was found to be ori-
ented perpendicular to the horizontal
axis of the palpebral fissure. Garcia and
associates45 suggested two possible mecha-
nisms for the association between palpe-
bral fissure slant and astigmatic axis:
developmental factors may lead to corre-
lated growth between the lids and the cor-
nea or the mechanical effects of the
slanting eyelid caused alterations in the
corneal shape.
Read, Collins and Carney128 recently
carried out an experiment investigating
corneal astigmatism and eyelid morphol-
ogy in a group of 100 young normal adult
subjects. Corneal astigmatism was assessed
through the analysis of corneal topo-
graphical data and eyelid morphological
information was ascertained through anal-
ysis of digital images taken of the anterior
eye and adnexae (in primary gaze, 20
degrees downgaze and 40 degrees down-
gaze). In this group of normal subjects,
significant correlations were found be-
tween the parameters describing the axis
of corneal astigmatism and the angle of
the upper and lower eyelid and palpebral
fissure in primary gaze. Figure 7 illustrates
these correlations.
Astigmatism in diseases and
syndromes
There are several genetic syndromes that
are associated with eyelid abnormalities
and also with an increased prevalence of
astigmatism. Studies into populations of
subjects with these syndromes tend to
support the notion that pressure from

© 2007 The Authors Clinical and Experimental Optometry 90.1 January 2007
Journal compilation © 2007 Optometrists Association Australia 13
Astigmatism and its genesis Read, Collins and Carney
the eyelids may contribute to corneal
astigmatism.
Down syndrome has been associated
with significant ocular abnormalities. Da
Cunha and de Castro Moreira129 noted
that 82 per cent of the Down syndrome
patients exhibited up-slanting palpebral
fissures (that is, temporal canthus is
higher than nasal canthus) and 60 per
cent exhibited astigmatism. Astigmatism
(greater than 0.5 D) was the most com-
mon refractive error found in the popula-
tion and severe astigmatism (greater than
3 D) was found in 20 per cent of the chil-
dren. Haugen, Hovding and Lundstrom130
presented longitudinal data on 60 chil-
dren with Down syndrome. They found 57
per cent of the children have astigmatism
(the majority being WTR). The reduction
in infant astigmatism seen in the first years
of life in a normal population was not
exhibited by the Down syndrome popula-
tion (that is, there was a failure of the
emmetropisation process in this popula-
tion). Eleven children had oblique astig-
matism, which displayed distinct mirror
symmetry of axes between right and left
eyes. The authors suggested that this dra-
matic mirror symmetry for oblique astig-
matism may be caused by mechanical
factors exerted on the cornea by the up-
slanting of the palpebral fissures.131 Cregg
and colleagues132 also found a failure of
emmetropisation in Down syndrome chil-
dren. Of those children with oblique axes,
the majority showed mirror symmetry of
the axes between eyes.
Wang and associates133 reported on
the ocular findings of 14 patients with
Treacher Collins syndrome, a rare congen-
ital disorder. The patients generally exhib-
ited a downward slanting of the palpebral
fissure. Corneal astigmatism (greater than
2 D) was present in five of the 14 patients.
There was an overall correlation between
the degree of facial deformity and the
presence of astigmatism. Generally, the
axis of astigmatism was found to be in
the same quadrant as the horizontal
palpebral fissure axis.
Ocular abnormalities are also found
in spina bifida. Paysse and co-workers134
found exaggerated up-slanting of the
palpebral fissure to be a common finding
Clinical and Experimental Optometry 90.1 January 2007
14
in their 73 subjects with spina bifida. A
high prevalence of oblique astigmatism
was also found. The majority of the
patients with up-slanting palpebral fis-
sures exhibited astigmatism (greater than
0.75 D). Of the patients with astigmatism
and up-slanting palpebral fissures, the axis
of astigmatism tended to be oriented per-
pendicular to the angle of the palpebral
fissure, similar to the trends reported with
Down syndrome.
All of the above populations exhibit a
high prevalence of astigmatism. It appears
that in some cases, the increased preva-
lence of astigmatism and axis of astigma-
tism can be explained by changes in the
mechanical interactions of the eyelids with
the cornea. Asymmetric corneal growth is
also possible.
Nystagmus and astigmatism
Nystagmus is characterised by rapid invol-
untary oscillatory eye movements. These
back and forth eye movements typically
occur horizontally. Nystagmus may occur
as a physiological phenomenon or be a
congenital or acquired defect. Congenital
nystagmus can be associated with many
different ocular and neurological defects.
Subjects with nystagmus have been shown
to display an increased prevalence of high
degrees of astigmatism.135–137 The astigma-
tism in these subjects is generally WTR
and corneal in origin.138,139
It appears that the process of emmetro-
pisation (that is, the normal process of
reduction of neonatal refractive errors
with eye growth) is impaired in subjects
with nystagmus.137 These subjects show a
wide spread of refractive errors, with high
degrees of WTR corneal astigmatism
being particularly common. While the
exact cause of the high degrees of astigma-
tism is not known, mechanical interaction
between the eyelids and the cornea
(which would be increased as a result of
the constant nystagmoid eye movement)
may play a role.136,137,139 Changes in the
influence of the EOMs on corneal shape
or asymmetric visual experience are other
possible explanations for the increased
prevalence of corneal astigmatism in sub-
jects with nystagmus.
Journal compilation © 2007 Optometrists Association Australia
Eyelid pathology and astigmatism
There have been numerous reports of
how certain eyelid pathologies can cause
corneal distortions and changes in cor-
neal astigmatism. These reports highlight
the influence that changes in eyelid pres-
sure can play on corneal topography and
astigmatism.
The presence of a chalazion in the eye-
lid has been shown to cause significant
corneal distortions and resultant changes
in corneal topography and astigmatism in
some patients.140–142 Surgical removal of
the chalazion generally leads to resolution
of the corneal changes.
Records143 presented various causes of
monocular diplopia. He suggested that
external irregularities of the cornea and
eyelids including chalazia and unusually
tight lids may produce corneal distortions
that may lead to monocular diplopia.
Robb144 reported that 16 of 37 infants
with eyelid and orbital haemangiomas
exhibited astigmatic refractive errors. In
almost all cases of astigmatism, the hae-
mangioma appeared to be in a position
where it exerted pressure on the eye in a
direction perpendicular to the axis of
astigmatism. Hence, the astigmatism was
probably related to the pressure exerted
by the lesion on the cornea. Plager and
Snyder145 reported three cases in which
the surgical resection of eyelid and orbital
capillary haemangiomas in infants caused
a resolution of astigmatism. Pressure from
the haemangioma on the globe was sug-
gested as the cause of the astigmatism in
these infants.
Ptosis and the surgical repair of ptosis
have been implicated in the development
of astigmatism. Patients with congenital
ptosis have a higher degree of corneal
topographic assymetry and irregularity, as
well as a higher degree of corneal astigma-
tism.146 In addition, astigmatism appears
to change following surgical repair of con-
genital ptosis,147 possibly due to changes in
the lid/cornea interaction following sur-
gery. Superior corneal steepening was
reported in a 62-year-old man with bilat-
eral blepharoptosis.148 Repair of the ptosis
led to relief of symptoms of monocular
diplopia and amelioration of the corneal
distortion.
© 2007 The Authors
 Astigmatism and its genesis Read, Collins and Carney

changes in central corneal topography im-

mediately following a 60-minute reading
task. The change in corneal shape was
described as a wave-like distortion, which
corresponded closely to the position and
angle of the lids during reading. Signifi-
cant changes were also found in corneal
refractive power and astigmatism. The
change in corneal astigmatism following
reading was towards ATR. Further to this
study, Buehren, Collins and Carney160
showed that the significant corneal topo-
Figure 8. Example of the typical changes that can occur in corneal graphical changes that occur as a result of
topography following downgaze reading tasks. Note the horizontal reading in downgaze also lead to signifi-
band of distortion in the superior cornea in this map of corneal cant changes in the eye’s total higher
tangential power (right), captured after the subject had been reading order aberrations and astigmatism.
in downgaze for one hour. This area of distortion correlates closely to Figure 8 illustrates the typical changes
the position of the eyelids during downgaze reading (left). Figure that can occur in corneal topography fol-
courtesy of Dr Tobias Buehren. lowing downgaze near work. In addition,
a recent study has shown that significant
diurnal variation can occur in corneal
topography and astigmatism, which ap-
pears to be related, in part, to corneal
Blepharoplastic surgery in adult pa- noted to be returning towards pre- distortion due to pressure from the eyelids
tients typically causes an increase in treatment levels. on the cornea.161
WTR astigmatism.149–151 As some of these Lid-loading procedures (with metal lid The effects of different visual tasks on
changes regressed with time after surgery, weights) to treat lagophthalmos have also corneal topography were investigated by
Holck, Dutton and Wearly149 concluded been shown to induce one to two dioptres Collins and colleagues.162 Corneal topog-
that the astigmatic changes may be due to of WTR astigmatism in some patients.153 raphy was measured before and after sub-
post-surgical eyelid swelling. Detorakis, Io- The astigmatism in these cases was attrib- jects performed a 60-minute reading task,
annakis and Kozobolis151 investigated uted to implants that were too heavy or of a microscopy task and a computer task.
changes in corneal topography following incorrect radii that caused increased pres- Eyelid induced corneal topographical
lower eyelid surgery for involutional ectro- sure on the cornea. changes were evident following each of
pian. An increase in the percentage of All of these eyelid pathologies increase the tasks. The reading and microscopy
subjects exhibiting WTR corneal astigma- the influence of the eyelids on the cornea. generally resulted in larger, more centrally
tism was found after blepharoplasty sur- Resolution or removal of these patholo- located corneal topographical changes. A
gery to restore the normal lower eyelid gies generally leads to a reversal of the number of subjects showed significant
position. corneal changes. These results support changes in corneal astigmatism (in the
Moon, Lee and Kim152 investigated the the concept of astigmatic development, form of an increase in ATR astigmatism)
corneal topography of subjects who suf- where eyelid pressure is involved and illus- following reading and microscopy. The
fered from essential blepharospasm or trate how increasing eyelid pressure can pattern of topographical change appeared
hemifacial spasm. These subjects were lead to alterations in corneal curvature. to be related to the position of the eyelids
treated with a botulinum toxin-A injection and the amount of horizontal eye move-
to relax the eyelid muscles and relieve the Visual tasks and corneal ment involved in the task. Tasks involv-
blepharospasm. Corneal topography mea- astigmatism ing more horizontal eye movements (for
surements one month after botulinum Sustained pressure on the cornea from example, reading) and narrower palpe-
injection (a time where the Botulinum normal eyelids may also lead to corneal bral apertures exhibited more localised
Toxin is thought to reach its maximum changes. Several reports have appeared in corneal changes.
effect) revealed a trend for a reduction in the literature relating episodes of monoc- Evidence indicates that sustained pres-
the amount of WTR corneal astigmatism ular diplopia (caused by corneal distor- sure on the cornea from normal eyelids
compared to pre-treatment levels. Six tion) to periods of near work in downward can result in significant corneal change.
months after the injection (where the gaze.154–158 With recent developments in corneal
effects of the toxin are thought to have Buehren, Collins and Carney159 found topography and improved methods of
disappeared), corneal astigmatism was that 12 of 20 subjects showed significant visualising and analysing the shape of the

© 2007 The Authors Clinical and Experimental Optometry 90.1 January 2007
Journal compilation © 2007 Optometrists Association Australia 15
Astigmatism and its genesis Read, Collins and Carney
cornea, corneal astigmatic and more com-
plex corneal shape changes have been
revealed resulting from the pressure of
the eyelids on the cornea in visual tasks
involving downgaze. These studies indi-
cate the potential of certain visual tasks to
cause short-term corneal topographical
and astigmatic changes. Further research
is required to explore the influence that
these short-term changes may have on
longer term refractive change and devel-
opment of astigmatism.
CONCLUSIONS/FUTURE RESEARCH
DIRECTIONS
The exact cause of astigmatism is still not
known. Current research indicates that
genetic influences may play a role in the
development of astigmatism. Other pos-
sible contributing factors include eyelid
pressure, EOM tension and visual feed-
back. Interaction between the cornea and
the eyelids seems to be a likely explana-
tion of increased astigmatism in a number
of ethnic groups and diseases. Pathology
of the eyelids and pressure from the eye-
lids during reading also produce changes
in corneal astigmatism. Recent research
into children with high astigmatism indi-
cates that the eyelids influence the axis
and degree of corneal astigmatism. While
it is clear that the eyelids can influence
corneal shape, there is still no conclusive
evidence that pressure from the eyelids
causes corneal astigmatism.
There are several areas for further
research that may help to shed more light
on the causes of corneal astigmatism. As
interactions between the rigidity of the
cornea and the angle, position and ten-
sion of the eyelids may all contribute to
determining the shape of the cornea, a
study that accurately measures all of these
factors on a large population of subjects
may further our understanding of the
causes of astigmatism. Longitudinal stud-
ies investigating corneal astigmatism, eye-
lid morphology and tension in subjects
whose corneal astigmatism is known to
be changing (for example, populations of
older subjects whose astigmatism typically
changes towards more ATR) should also
Clinical and Experimental Optometry 90.1 January 2007
16
increase our understanding of the causes
of astigmatism. With advances in technol-
ogy, our ability to measure and define ocu-
lar astigmatism and its components has
improved markedly. Therefore, with the
rapid technological advances in the oph-
thalmic field, our understanding of the
aetiology of astigmatism should increase
in years to come.
REFERENCES
1. Porter J, Guirao A, Cox IG, Williams DR.
Monochromatic aberrations of the human
eye in a large population. J Opt Soc Am A
2001; 18: 1793–1803.
2. Levene JR. Sir George Biddell Airy FRS
(1801–1892) and the discovery and cor-
rection of astigmatism. Notes Rec R Soc
1966; 21: 180–199.
3. Brown SA, Weih LM, Fu CL, Dimitrov P,
Taylror HR, McCarty CA. Prevalence of
amblyopia and associated refractive errors
in an adult population in Victoria, Austra-
lia. Ophthalmic Epidemiol 2000; 7: 249–258.
4. Abrahamsson M, Sjostrand J. Astigmatic
axis and amblyopia in childhood. Acta
Ophthalmol 2003; 81: 33–37.
5. Dobson V, Miller JM, Harvey EM, Mohan
KM. Amblyopia in astigmatic preschool
children. Vision Res 2003; 43: 1081–1090.
6. Fulton AB, Hansen RM, Petersen RA. The
relation of myopia and astigmatism in
developing eyes. Ophthalmology 1982; 89:
298–302.
7. Gwiazda J, Grice K, Held R, McLellan J,
Thorn F. Astigmatism and the develop-
ment of myopia in children. Vision Res
2000; 40: 1019–1026.
8. Tong L, Saw S-M, Carkeet A, Chan W-Y,
Wu H-M, Tan D. Prevalence rates and epi-
demiological risk factors for astigmatism
in Singapore school children. Optom Vis Sci
2002; 79: 606–613.
9. Fairbrother JA, Welsby JW, Guggenheim
JA. Astigmatic axis is related to the level of
spherical ametropia. Optom Vis Sci 2004;
81: 18–26.
10. Fan DSP, Rao SK, Cheung EYY, Islam
M, Chew S, Lam DSC. Astigmatism in
Chinese preschool children: prevalence,
change and effect on refractive develop-
ment. Br J Ophthalmol 2004; 88: 938–941.
11. Read SA, Collins MJ, Carney LG, Franklin
RJ. The topography of the central and
peripheral cornea. Invest Ophthalmol Vis Sci
2006; 47: 1404–1415.
12. Grosvenor T. Etiology of astigmatism. Am
J Optom Physiol Opt 1978; 55: 214–218.
13. Grosvenor T, Quintero S, Perrigin DM.
Predicting refractive astigmatism: a sug-
gested simplification of Javal’s rule. Am J
Optom Physiol Opt 1988; 65: 292–297.
Journal compilation © 2007 Optometrists Association Australia
14. Keller PR, Collins MJ, Carney LG, Davis
BA, Van Saarloos PP. The relation be-
tween corneal and total astigmatism.
Optom Vis Sci 1996; 73: 86–91.
15. Kelly JE, Mihashi T, Howland HC. Com-
pensation of corneal horizontal/vertical
astigmatism, lateral coma and spherical
aberration by internal optics of the eye. J
Vision 2004; 4: 262–271.
16. Dunne MCM, Elawad MEA, Barnes DA. A
study of the axis of orientation of residual
astigmatism. Acta Ophthalmol 1994; 72:
483–489.
17. Dunne MCM, Royston JM, Barnes DA.
Posterior corneal surface toricity and total
corneal astigmatism. Optom Vis Sci 1991;
68: 708–710.
18. Oshika T, Tomidokoro A, Tsuji H. Regular
and irregular refractive powers of the
front and back surfaces of the cornea. Exp
Eye Res 1998; 67: 443–447.
19. Prisant O, Hoang-Xuan T, Proano C, Her-
nandez E, Awad S, Azar DT. Vector sum-
mation of anterior and posterior corneal
topographical astigmatism. J Cataract
Refract Surg 2002; 28: 1636–1643.
20. Dubbelman M, Sicam VADP, Van der
Heijde GL. The shape of the anterior and
posterior surface of the aging human cor-
nea. Vision Res 2006; 46: 993–1001.
21. Atkinson J, Braddick O, French J. Infant
astigmatism: Its disappearance with age.
Vision Res 1980; 20: 891–893.
22. Dobson V, Fulton AB, Sebris SL. Cyclople-
gic refractions of infants and young
children: the axis of astigmatism. Invest
Ophthalmol Vis Sci 1984; 25: 83–87.
23. Gwiazda J, Scheiman M, Mohindra I, Held
R. Astigmatism in children: Changes in
axis and amount from birth to six years.
Invest Ophthalmol Vis Sci 1984; 25: 88–91.
24. Howland HC, Sayles N. Photokeratomet-
ric and photorefractive measurements of
astigmatism in infants and young chil-
dren. Vision Res 1985; 25: 73–81.
25. Abrahamsson M, Fabian G, Anderson A-K,
Sjostrand J. A longitudinal study of a
population based sample of astigmatic
children. 1. Refraction and amblyopia.
Acta Ophthalmol 1990; 68: 428–434.
26. Ehrlich DL, Braddick OJ, Atkinson J,
Anker S, Weeks F, Hartley T, Wade J,
Rudenski A. Infant emmetropization:
Longitudinal changes in refraction com-
ponents from nine to twenty months of
age. Optom Vis Sci 1997; 74: 822–843.
27. Friling R, Weinberger D, Kremer I,
Avisar R, Sirota L, Snir M. Keratometry
measurements in preterm and full term
newborn infants. Br J Ophthalmol 2004;
88: 8–10.
28. Mutti DO, Mitchell L, Jones LA, Friedman
NE, Frane SL, Lin WK, Moeschberger ML,
Zadnik K. Refractive astigmatism and the
© 2007 The Authors

toricity of ocular components in human
infants. Optom Vis Sci 2004; 81: 753–761.
29. Isenberg SJ, Del Signore M, Chen A, Wei 46.
J, Christenson PD. Corneal topography of
neonates and infants. Arch Ophthalmol
2004; 122: 1767–1771. 47.
30. Varughese S, Varghese RM, Sreenivas V,
Puliyel JM. Refractive error at birth and its
relation to gestational age. Curr Eye Res
2005; 30: 423–428.
31. Asbell PA, Chiang B, Somers ME, Morgan 48.
KS. Keratometry in children. CLAO J 1990;
16: 99–102.
32. Cowen L, Bobier WR. The pattern of astig-
matism in a Canadian preschool popula-
tion. Invest Ophthalmol Vis Sci 2003; 44: 49.
4593–4600.
33. Shankar S, Bobier WR. Corneal and len-
ticular components of total astigmatism in
a preschool sample. Optom Vis Sci 2004; 81: 50.
536–542.
34. Huynh SC, Kifley A, Rose KA, Morgan I,
Heller GZ, Mitchell P. Astigmatism and its
components in 6-year-old children. Invest 51.
Ophthalmol Vis Sci 2006; 47: 55–64.
35. Saunders H. Age-dependence of human
refractive errors. Ophthalmic Physiol Opt 52.
1981; 1: 159–174.
36. Satterfield DS. Prevalence and variation of
astigmatism in a military population. J Am 53.
Optom Assoc 1989; 60: 14–18.
37. Fledelius HC, Stubgaard M. Changes in
refraction and corneal curvature during
growth and adult life. A cross sectional 54.
study. Acta Ophthalmol 1986; 64: 487–
491.
38. Anstice J. Astigmatism—Its components 55.
and their changes with age. Am J Optom
Arch Am Acad Optom 1971; 48: 1001–1006.
39. Baldwin WR, Mills D. A longitudinal study 56.
of corneal astigmatism and total astigma-
tism. Am J Optom Physiol Opt 1981; 58: 206–
210.
40. Hayashi K, Hayashi H, Hayashi F. Topo-
graphic analysis of the changes in corneal 57.
shape due to ageing. Cornea 1995; 14: 527–
532.
41. McKendrick AM, Brennan NA. Distribu-
tion of astigmatism in the adult popula-
tion. J Opt Soc Am A 1996; 13: 206–213. 58.
42. Goto T, Klyce SD, Zheng X, Maeda N,
Kuroda T, Ide C. Gender and age-related
differences in corneal topography. Cornea 59.
2001; 20: 270–276.
43. Guirao A, Redondo M, Artal P. Optical
aberrations of the human cornea as a
function of age. J Opt Soc Am A 2000; 17:
1697–1702. 60.
44. Dingeldein SA, Klyce SD. The topography
of normal corneas. Arch Ophthalmol 1989;
107: 512–518. 61.
45. Garcia ML, Huang DH, Crowe S, Tra-
boulsi EL. Relationship between the axis
and degree of high astigmatism and obliq-
© 2007 The Authors
Journal compilation © 2007 Optometrists Association Australia
Astigmatism and its genesis Read, Collins and Carney
uity of palpebral fissure. J AAPOS 2003; 7:
14–22.
McKendrick AM, Brennan NA. The axis of
astigmatism in right and left eye pairs.
Optom Vis Sci 1997; 74: 668–675.
Ninn-Pedersen K. Relationship between
preoperative astigmatism and corneal
optical power, axial length, intraocular
pressure, gender and patient age. J Refract
Surg 1996; 12: 472–482.
Heidary G, Ying G-S, Maguire MG, Young
TL. The association of myopia and astig-
matism and spherical refractive error in a
high myopia cohort. Optom Vis Sci 2005;
82: 244–247.
Goss DA, Erickson P. Meridional corneal
components of myopia progression in
young adults and children. Am J Optom
Phys Opt 1987; 64: 475–481.
Goss DA, Shewey WB. Rates of childhood
myopia progression as a function of type
of astigmatism. Clin Exp Optom 1990; 73:
159–163.
Pärssinen TO. Astigmatism and school
myopia. Acta Ophthalmol 1991; 69: 786–
790.
Abraham JE, Volovick JB. Preliminary
Navajo optometric study. J Am Optom Assoc
1972; 43: 1257–1260.
Lyle WM, Grosvenor T, Dean KC. Corneal
astigmatism in Amerind children. Am J
Optom Arch Am Acad Optom 1972; 49: 517–
524.
Mohindra I, Nagaraj S. Astigmatism in
Zuni and Navajo Indians. Am J Optom Phys-
iol Opt 1977; 54: 121–124.
Goss DA. Meridional analysis of with-the-
rule astigmatism in Oklahoma Indians.
Optom Vis Sci 1989; 66: 281–287.
Dobson V, Miller JM, Harvey EM. Corneal
and refractive astigmatism in a sample of
3- to 5-year old children with a high prev-
alence of astigmatism. Optom Vis Sci 1999;
76: 855–860.
Harvey EM, Dobson V, Miller JM. Preva-
lence of high astigmatism, eyeglass wear
and poor visual acuity among Native
American grade school children. Optom
Vis Sci 2006; 83: 206–212.
Heard T, Reber N, Levi D, Allen D. The
refractive status of Zuni Indian children.
Am J Optom Physiol Opt 1976; 53: 120–123.
Lam CSY, Goh WSH. The incidence of
refractive errors among school children in
Hong Kong and its relationship with the
optical components. Clin Exp Optom 1991;
74: 97–103.
Kame RT, Jue TS, Shigekuni DM. A longi-
tudinal study of corneal changes in Asian
eyes. J Am Optom Assoc 1993; 64: 215–219.
Wu H-M, Seet B, Yap EP-H, Saw S-M, Lim
T-H, Chia K-S. Does education explain eth-
nic differences in myopia prevalence? A
population-based study of young adult
Clinical and Experimental Optometry 90.1 January 2007
males in Singapore. Optom Vis Sci 2001; 78:
234–239.
62. Kleinstein RN, Jones LA, Hullett S, Kwon
S, Lee RJ, Friedman NE, Manny RE, Mutti
DO, Yu JA, Zadnik K. Refractive error and
ethnicity in children. Arch Ophthalmol
2003; 121: 1141–1147.
63. Thorn F, Cruz AAV, Machado AJ, Car-
valho RAC. Refractive status of indigenous
people in the northwestern Amazon
region of Brazil. Optom Vis Sci 2005; 82:
267–272.
64. Fuller JR, Baxter LA, Harun S, Levy IS.
Astigmatism in Bangladeshi and white
school entrants in East London: a prospec-
tive comparative study. Eye 1995; 9: 794–
796.
65. Meek KM, Newton RH. Organization of
collagen fibrils in the corneal stroma in
relation to mechanical properties and sur-
gical practice. J Cataract Refract Surg 1999;
15: 695–699.
66. Budak K, Friedman NJ, Koch DD. Limbal
relaxing incisions with cataract surgery. J
Cataract Refract Surg 1998; 24: 503–508.
67. Tejedor J, Murube J. Choosing the loca-
tion of corneal incision based on pre-
existing astigmatism in phacoemulsifica-
tion. Am J Ophthalmol 2005; 139: 767–776.
68. Simsek S, Yasar T, Demirok A, Cinal A,
Yilmaz ÖF. Effect of superior and tempo-
ral clear corneal incisions on astigmatism
after sutureless phacoemulsification. J Cat-
aract Refract Surg 1998; 24: 515–518.
69. Hayashi K, Hayashi H, Nakao F, Hayashi
F. The correlation between incision size
and corneal shape changes in sutureless
cataract surgery. Ophthalmology 1995; 102:
550–556.
70. Kohnen T, Dick B, Jacobi KW. Compari-
son of the induced astigmatism after tem-
poral clear corneal tunnel incisions of
different sizes. J Cataract Refract Surg 1995;
21: 417–423.
71. Oshika T, Nagahara K, Yaguchi S, Emi K,
Takenaka H, Tsuboi S, Yoshitomi F, Naga-
moto T, Kurosaka D. Three year prospec-
tive, randomized evaluation of intraocular
lens implantation through 3.2 and 5.5 mm
incisions. J Cataract Refract Surg 1998; 24:
509–514.
72. Olsen T, Dam-Johansen M, Bek T, Hjort-
dal JØ. Corneal versus scleral tunnel inci-
sion in cataract surgery: A randomized
study. J Cataract Refract Surg 1997; 23: 337–
341.
73. Kohnen S, Neuber R, Kohnen T. Effect of
temporal and nasal unsutured limbal tun-
nel incisions on induced astigmatism after
phacoemulsification. J Cataract Refract Surg
2002; 28: 821–825.
74. Tomidokoro A, Oshika T, Kojima T. Cor-
neal astigmatism after scleral buckling
surgery assessed by Fourier analysis of
17
Astigmatism and its genesis Read, Collins and Carney
videokeratography data. Cornea 1998; 17:
517–521.
75. Örnek K, Yalcindag FN, Kanpolat A,
Günalp I. Corneal topographic changes
after retinal detachment surgery. Cornea
2002; 21: 803–806.
76. Hayashi H, Hayashi K, Nakao F, Hayashi
F. Corneal shape changes after scleral
buckling surgery. Ophthalmology 1997; 104:
831–837.
77. Weinberger D, Lichter H, Loya N, Axer-
Siegel R, Muzmacher L, Gabbay U, Yassur
Y. Corneal topographic changes after ret-
inal and vitreous surgery. Ophthalmology
1999; 106: 1521–1524.
78. Domniz YY, Cahana M, Avni I. Corneal
surface changes after pars plana vitrec-
tomy and scleral buckling surgery. J Cata-
ract Refract Surg 2001; 27: 868–872.
79. Hong YJ, Choe CM, Lee YG, Chung HS,
Kim HK. The effect of mitomycin-c on
postoperative corneal astigmatism in trab-
eculectomy and a triple procedure. Oph-
thalmic Surg Lasers 1998; 29: 484–489.
80. Vernon SA, Zambarakji HJ, Potgieter F,
Evans J, Chell PB. Topographic and
keratometric astigmatism up to 1 year
following small flap trabeculectomy
(microtrabeculectomy). Br J Ophthalmol
1999; 83: 779–782.
81. Egrilmez S, Ates H, Nalcaci S, Andac K,
Yagci A. Surgically induced corneal refrac-
tive change following glaucoma surgery:
non-penetrating trabecular surgeries ver-
sus trabeculectomy. J Cataract Refract Surg
2004; 30: 1232–1239.
82. Hayashi K, Hayashi H, Oshika T, Hayashi
F. Fourier analysis of irregular astigmatism
after trabeculectomy. Ophthalmic Surg
Lasers 2000; 31: 94–99.
83. Lin A, Stern G. Correlation between ptery-
gium size and induced corneal astigma-
tism. Cornea 1998; 17: 28–30.
84. Tomidokoro A, Miyata K, Sakaguchi Y,
Samejima T, Tokunaga T, Oshika T.
Effects of pterygium on corneal spherical
power and astigmatism. Ophthalmology
2000; 107: 1568–1571.
85. Lindsay RG, Sullivan L. Pterygium-
induced corneal astigmatism. Clin Exp
Optom 2001; 84: 200–203.
86. Oldenburg JB, Garbus J, McDonnell JM,
McDonnell PJ. Conjunctival pterygia.
Mechanism of corneal topographic
changes. Cornea 1990; 9: 200–204.
87. Stern GA, Lin A. Effect of pterygium exci-
sion on induced corneal topographic
abnormalities. Cornea 1998; 17: 23–27.
88. Troutman RC, Lawless MA. Penetrating
keratoplasty for keratoconus. Cornea 1987;
6: 298–305.
89. Brierly SC, Izquierdo L, Mannis MJ. Pene-
trating keratoplasty for keratoconus. Cor-
nea 2000; 19: 329–332.
Clinical and Experimental Optometry 90.1 January 2007
18
90. Hayashi K, Hayashi H. Long-term changes
in corneal surface configuration after pen-
etrating keratoplasty. Am J Ophthalmol
2006; 141: 241–247.
91. Hirst LW, McCoombes JA, Reedy M. Post-
operative suture manipulation for control
of corneal graft astigmatism. Aust N Z J
Ophthalmol 1998; 26: 211–214.
92. Belmont SC, Troutman RC, Buzard KA.
Control of astigmatism aided by intraoper-
ative keratometry. Cornea 1993; 12: 397–
400.
93. Javadi MA, Mohammadi MJ, Mirdehghan
SA, Sajjadi SH. A comparison between
donor-recipient corneal size and its effect
on the ultimate refractive error induced
in keratoconus. Cornea 1993; 12: 401–
405.
94. Seitz B, Langenbucher A, Kus MM, Küchle
M, Naumann GOH. Non-mechanical
corneal trephination with the Excimer
laser improves outcome after penetrating
keratoplasty. Ophthalmology 1999; 106:
1156–1165.
95. Wixson RJ. Refraction pedigrees: part two
the cornea. Am J Optom Arch Am Acad
Optom 1965; 42: 10.
96. Teikari JM, O’Donnell JJ. Astigmatism in
72 twin pairs. Cornea 1989; 8: 263–266.
97. Teikari J, O’Donnell JJ, Kaprio J, Kosken-
vuo M. Genetic and environmental effects
on oculometric traits. Optom Vis Sci 1989;
66: 594–599.
98. Valluri S, Minkovitz JB, Budak K, Essary
LR, Walker RS, Chansue E, Cabrera GM,
Douglas DK, Pepose JS. Comparative cor-
neal topography and refractive variables
in monozygotic and dizygotic twins. Am J
Opthalmol 1999; 127: 158–163.
99. Hammond CJ, Sneider H, Gilbert CE,
Spector TD. Genes and environment in
refractive error: the twin eye study. Invest
Ophthalmol Vis Sci 2001; 42: 1232–1236.
100. Clementi M, Angi M, Forabosco P, Di-
Gianantonio E, Tenconi R. Inheritance of
astigmatism: evidence for a major autoso-
mal dominant locus. Am J Hum Genet 1998;
63: 825–830.
101. Lee KE, Klein BEK, Klein R, Fine JP.
Aggregation of refractive error and 5-year
changes in refractive error among families
in the Beaver Dam eye study. Arch Ophthal-
mol 2001; 119: 1679–1685.
102. Phillips CI. Aetiology of myopia. Br J Oph-
thalmol 1990; 74: 47–48.
103. Troilo D. Neonatal eye growth and
emmetropisation—a literature review. Eye
1992; 6: 154–160.
104. Norton T, Siegwart JT. Animal models of
emmetropization: matching axial length
to the focal plane. J Am Optom Assoc 1995;
66: 405–414.
105. Wildsoet CF. Active emmetropization—
evidence for its existence and ramifica-
Journal compilation © 2007 Optometrists Association Australia
tions for clinical practice. Ophthalmic Phys-
iol Opt 1997; 17: 279–290.
106. Smith EL. Spectacle lenses and em-
metropization: the role of optical defocus
in regulating ocular development. Optom
Vis Sci 1998; 75: 388–398.
107. Irving EL, Callender MG, Sivak JG.
Inducing ametropias in hatchling chicks
by defocus—Aperture effects and cylin-
drical lenses. Vision Res 1995; 35: 1165–
1174.
108. Schmid KL, Wildsoet CF. Natural and
imposed astigmatism and their relation to
emmetropization in the chick. Exp Eye Res
1997; 64: 837–847.
109. McLean RC, Wallman J. Severe astigmatic
blur does not interfere with spectacle lens
compensation. Invest Ophthalmol Vis Sci
2003; 44: 449–457.
110. Kee C-S, Hung L-F, Qiau Y, Smith EL.
Astigmatism in infant monkeys reared
with cylindrical lenses. Vision Res 2003; 43:
2721–2739.
111. Kee C-S, Hung L-F, Qiao-Grider Y, Roorda
A, Smith EL. Effects of optically imposed
astigmatism on emmetropisation in infant
monkeys. Invest Ophthalmol Vis Sci 2004; 45:
1647–1659.
112. Kee C-S, Hung L-F, Qiao-Grider Y,
Ramamirtham R, Smith EL. Astigmatism
in monkeys with experimentally induced
myopia or hyperopia. Optom Vis Sci 2005;
82: 248–260.
113. Fairmaid JA. The constancy of corneal
curvature. An examination of corneal
response to changes in accommodation
and convergence. Brit J Physiol Opt 1959;
16: 2–23.
114. Lopping B, Weale RA. Changes in corneal
curvature following ocular convergence.
Vision Res 1965; 5: 207–215.
115. Mandell RB, St Helen R. Stability of the
corneal contour. Am J Optom Arch Am Acad
Optom 1968; 45: 797–806.
116. Kwitko S, Suwasch MR, McDonnell PJ,
Gritz DC, Moreira H, Evensen D. Effect of
extraocular muscle surgery on corneal
topography. Arch Ophthalmol 1991; 109:
873–878.
117. Reynolds RD, Nelson LB, Greenwald M.
Large refractive change after strabismus
surgery. Am J Ophthalmol 1991; 111: 371–
372.
118. Preslan MW, Cioffo G, Min Y-I. Refractive
error changes following strabismus sur-
gery. J Pediatr Ophthalmol Strabismus 1992;
29: 300–304.
119. Denis D, Bardot J, Volot F, Saracco J-B,
Maumenee IH. Effects of strabismus sur-
gery on refraction in children. Ophthalmo-
logica 1995; 209: 136–140.
120. Killer HE, Bahler A. Significant immedi-
ate and long-term reduction of astigma-
tism after lateral rectus recession in
© 2007 The Authors

divergent Duane’s syndrome. Ophthalmo-
logica 1999; 213: 209–210.
121. Bagheri A, Farahi A, Guyton DL. Astigma-
tism induced by simultaneous recession of
both horizontal rectus muscles. J AAPOS
2003; 7: 42–46.
122. Kwitko S, Feldon S, McDonnell PJ. Cor-
neal topographic changes following stra-
bismus surgery in Graves’ disease. Cornea
1992; 11: 36–40.
123. Nardi M, Rizzo S, Pellegrini G, Lepri A.
Effects of strabismus surgery on corneal
topography. J Pediatr Ophthalmol Strabismus
1997; 34: 244–246.
124. Wilson G, Bell C, Chotai S. The effect of
lifting the lids on corneal astigmatism. Am
J Optom Physiol Opt 1982; 59: 670–674.
125. Vihlen FS, Wilson G. The relation
between eyelid tension, corneal toricity
and age. Invest Ophthalmol Vis Sci 1983; 24:
1367–1373.
126. Grey C, Yap M. Influence of lid position
on astigmatism. Am J Optom Physiol Opt
1986; 63: 966–969.
127. Lieberman DM, Grierson JW. The lids
influence on corneal shape. Cornea 2000;
19: 336–342.
128. Read SA, Collins MJ, Carney LG. Eyelid
morphology influences normal corneal
shape. Invest Ophthalmol Vis Sci. In press.
129. Da Cunha PR, de Castro Moreira JB. Ocu-
lar findings in Down’s Syndrome. Am J
Ophthalmol 1996; 122: 236–244.
130. Haugen OH, Hovding G, Lundstrom I.
Refractive development in children with
Down’s syndrome: a population based,
longitudinal study. Br J Ophthalmol 2001;
85: 714–719.
131. Haugen OH, Hovding G, Lundstrom I.
Biometric measurements of the eyes in
teenagers and young adults with Down
Syndrome. Acta Ophthalmol 2001; 79: 616–
625.
132. Cregg M, Woodhouse JM, Stewart RE,
Pakeman VH, Bromham NR, Gunter HL,
Trojanowska L, Parker M, Fraser WI.
Development of refractive error and stra-
bismus in children with Down Syndrome.
Invest Ophthalmol Vis Sci 2003; 44: 1023–
1030.
133. Wang FM, Millman AL, Sidoti PA, Gold-
berg RB. Ocular findings in Treacher Col-
lins syndrome. Am J Ophthalmol 1990; 110:
280–286.
134. Paysse EA, Khokhar A, McCreery KMB,
Morris MC, Coats DK. Up-slanting palpe-
bral fissures and oblique astigmatism
associated with A-Pattern strabismus and
overdepression in adduction in spina
bifida. J AAPOS 2002; 6: 354–359.
135. Nathan J, Kiely PM, Crewther SG,
Crewther DP. Astigmatism occurring in
association with pediatric eye disease. Am
J Optom Physiol Opt 1986; 63: 497–504.
© 2007 The Authors
Journal compilation © 2007 Optometrists Association Australia
Astigmatism and its genesis Read, Collins and Carney
136. Ohmi G, Reinecke RD. Astigmatism of
nystagmus subjects. Invest Ophthalmol Vis
Sci 1993; 34: s1125.
137. Sampath V, Bedell HE. Distribution of
refractive errors in albinos and persons
with idiopathic congenital nystagmus.
Optom Vis Sci 2002; 79: 292–299.
138. Dickinson CM, Abadi RV. Corneal topog-
raphy of humans with congenital nystag-
mus. Ophthalmic Physiol Opt 1984; 4: 3–13.
139. Wildsoet CF, Oswald PJ, Clark S. Albinism:
its implications for refractive develop-
ment. Invest Ophthalmol Vis Sci 2000; 41: 1–
7.
140. Nisted M, Hofstetter HW. Effect of cha-
lazion on astigmatism. Am J Optom Physiol
Opt 1974; 51: 579–582.
141. Rubin ML. The case of the dramatic
impression. Surv Ophthalmol 1975; 20:
133–136.
142. Cosar CB, Rapuano CJ, Cohen EJ, Laibson
PR. Chalazion as a cause of decreased
vision after LASIK. Cornea 2001; 20: 890–
892.
143. Records RE. Monocular diplopia. Surv
Ophthalmol 1980; 24: 303–306.
144. Robb RM. Refractive errors associated
with hemangiomas of the eyelids and
orbits in infancy. Am J Ophthalmol 1977; 83:
52–58.
145. Plager DA, Snyder SK. Resolution of astig-
matism after surgical resection of capillary
hemangiomas in infants. Ophthalmology
1997; 104: 1102–1106.
146. Ugurbas SH, Zilelioglu G. Corneal topog-
raphy in patients with congenital ptosis.
Eye 1999; 13: 550–554.
147. Cadera W, Orton RB, Hakim O. Changes
in astigmatism after surgery for congenital
ptosis. J Ped Ophthalmol Strab 1992; 29: 85–
88.
148. Kim T, Khosla-Gupta B, Debacker C. Ble-
pharoptosis-induced superior keratoco-
nus. Am J Ophthalmol 2000; 130: 234–235.
149. Holck DEE, Dutton JJ, Wehrly SR.
Changes in astigmatism after ptosis sur-
gery measured by corneal topography.
Ophthal Plast Reconstr Surg 1998; 14: 151–
158.
150. Brown MS, Siegel IM, Lisman RD. Pro-
spective analysis of changes in corneal
topography after upper eyelid surgery.
Ophthal Plast Reconstr Surg 1999; 15: 378–
383.
151. Detorakis ET, Ioannakis K, Kozobolis VP.
Corneal topography in involutional ectro-
pian of the lower eyelid. Preoperative and
postoperative evaluation. Cornea 2005; 24:
431–434.
152. Moon NJ, Lee H, Kim JC. The changes in
corneal astigmatism after Botulinum
Toxin-A injection in patients with ble-
pharospasm. J Korean Med Sci 2006; 21:
131–135.
Clinical and Experimental Optometry 90.1 January 2007
153. Goldahn A, Schrom T, Berghaus A,
Krause A, Duncker G. Corneal astigma-
tism as a special complication after lid-
loading in patients with lagophthalmos.
Ophthalmologe 1999; 96: 494–497.
154. Mandell RB. Bilateral monocular diplopia
following near work. Am J Optom Arch Am
Acad Optom 1966; 43: 500–504.
155. Knoll HA. Bilateral monocular diplopia
after nearwork. Am J Optom Physiol Opt
1975; 52: 139–140.
156. Bowman KJ, Smith G, Carney LG. Corneal
topography and monocular diplopia fol-
lowing near work. Am J Optom Physiol Opt
1978; 58: 818–823.
157. Ford JG, Davis RM, Reed JW, Weaver RG,
Craven TE, Tyler ME. Bilateral monocular
diplopia associated with lid position dur-
ing near work. Cornea 1997; 16: 525–530.
158. Golnik KC, Eggenberger E. Symptomatic
corneal topographic change induced by
reading in downgaze. J Neuroophthalmol
2001; 21: 199–204.
159. Buehren T, Collins MJ, Carney LG. Cor-
neal aberrations and reading. Optom Vis Sci
2003; 80: 159–166.
160. Buehren T, Collins MJ, Carney LG. Near
work induced wavefront aberrations in
myopia. Vision Res 2005; 45: 1297–1312.
161. Read SA, Collins MJ, Carney LG. The diur-
nal variation of corneal topography and
aberrations. Cornea 2005; 24: 678–687.
162. Collins MJ, Buehren T, Bece A, Voetz SC.
Corneal optics after reading, microscopy
and computer work. Acta Ophthalmol Scand
2006; 84: 216–224.
Corresponding author:
Dr Scott A Read
Contact Lens and Visual Optics
Laboratory
School of Optometry
Queensland University of Technology
Victoria Park Road
Kelvin Grove QLD 4059
AUSTRALIA
E-mail: sa.read@qut.edu.au
19