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Myopia

Article initiated by:

Gregory I. Ostrow, MD FAAO FAAP, Laura Kirkeby, CO

All authors and contributors:

Francesc March de Ribot, MD, PhD, Gregory I. Ostrow, MD FAAO FAAP, K.
David Epley, M.D., Rafael Iribarren, Sudha Nallasamy, MD

Assigned editor:
Sudha Nallasamy, MD

Review:
Assigned status Update Pending

by Sudha Nallasamy, MD on July 26, 2022.

Myopia
Myopia is a significant, prevalent
disease in children with
DiseasesDB
increasing rates of progression.
8729
With over 80 million reported
myopic children world wide ICD-10
there are considerable H52.1
socioeconomical and public
MedlinePlus
health concerns. More over, High
001023
myopia is associated with
potentially blinding MeSH
complications such as glaucoma, D009216
retinal detachment, and myopic
macular degeneration. A
substantial amount of research has been done to determine the etiology of myopia, the
risk factors associated with myopia, techniques to prevent myopia and ways to treat
myopia.

Disease Entity

MYOPIA

Cornea

Retina

Pupil

Light

OpticNerve

Lens

NORMALEYE

Light

Figure 1: Human myopic eye, showing the cornea and lens bending (refracting) incoming
light rays so they focus in front of the retina [1].

Myopia (nearsightedness) is an ocular disorder in which the optical power of the eye is too
strong for the corresponding axial length. Light rays from an object at infinity entering a
non-accommodating myopic eye are converged too strongly and focus in front of the
retina.[2]The far point of a myope is located in front of the eye, between the cornea and
optical infinity. Visual acuity of an uncorrected myope will continue to decrease as objects
are located further away from the far point and closer to optical infinity. Conversely, visual
acuity is greater for objects located between the far point of the eye and the near point of
accommodation[3].

Classification
Myopia is generally classified into two groups: non-pathologic and pathologic myopia.
Both groups have separate disease processes, clinical features, and prognoses. Non-
pathological myopia is also commonly referred to as physiological, simple or school
myopia. In non-pathologic myopia the refractive structures of the eye develop within
normal limits, however the refractive power of the eye does not correlate with the axial
length. The degree of non-pathologic myopia is usually minimal to moderate (< 6.00
diopters) and onset usually begins during childhood or adolescence[4]. Myopic progression
generally continues throughout the adolescent growth period and slows or becomes
stable early in the second decade. Less commonly, a second myopic shift may occur late
during the second decade or early in the third decade[5].

Pathologic myopia is generally classified as a high myopic refractive error that is

progressive and generally presents very early in childhood. Pathologic myopia is usually
defined as spherical equivalent > 6.00 diopters or axial length >26.5mm[4]. Patients with
high axial myopia are at a greater risk of developing progressive retinal degeneration and
other vision threatening pathology. See pathology section for more detail.

Etiology
Myopia is a complex disease with a multi-factorial etiology. It is well documented that
pathological non-syndromic high myopia and associated syndromic high myopia show
evidence of familial inheritance. Although non-syndromic high myopia is most commonly
inherited in an automosomal dominant pattern, multiple chromosomal loci have been
identified which suggests genetic heterogeneity[6]. High myopia is also a symptom of
several multi-system complex diseases. The genetic mutations for these syndromes have
been identified and the subsequent structural defects of the eye are most commonly
related to connective tissue and retina[6]. This type of myopia is only a small proportion of
the overall myopic population and to date, there is no known isolated gene associated with
physiologic myopia.

Epidemiology
The prevalence of myopia varies greatly between different populations and ethnic groups.
The prevalence rates of myopia in the United States have been reported as 20-50% and as
high as 80-90% in some parts of Asia[6]. The majority of the myopic population consists
primarily of patients with non-pathologic myopia; approximately 66% of patients with
myopia have less than 2 diopters (D) of myopia and 95% of myopic patients have less than
6 diopters[7]. In 2003 a multi-center study the US reported significantly different
prevalence rates among children of four different ethnic groups. The highest rates were
found among Asian children with a prevalence of 18.5% and hispanic children with
13.2%[8]. Lower prevalence rates were found in African American children with 6.6%
followed by Caucasian children with a prevalence rate of 4.4%. A large epidemiological
study in 2000 by Lin et al. showed that myopic prevalence rates for Taiwanese children
were reaching 80%[9]. It is reported that there are over 80 million myopic children world
wide[10].

Associated Disease
In addition to physiologic, pathologic and syndromic myopia, other processes involving the
refractive structures of the eye can also produce myopia. The power of the lens can be
increased by osmotic changes (diabetes, galactosemia, uremia, sulfonamides), nuclear
sclerotic cataracts, anterior lenticonus, and changes in lens position or shape (miotics,
anterior lens dislocation, excessive accommodation). Changes to the cornea secondary to
keratoconus, congenital glaucoma, and contact lens-induced corneal warpage can also
cause myopia. Myopia can also be the result of increased axial length secondary to
retinopathy of prematurity, posterior staphyloma, scleral buckle surgery and congenital
glaucoma[4].

Syndromes with associated myopia are listed

below.
Ocular Disease
Congenital Glaucoma
ROP
RP
Cataract
CSNB
Keratoconus
Aland eye disease
Gyrate Atropy
Pseudomyopia
Albinism

Multi-system disease
Sticklers Syndrome
Diabetes Mellitus (uncontrolled)
Marfan
Weill-Marchesani
Knobloch
Ehlers Danlos

Pathology
There are distinct pathological signs that are associated with high myopia. Dilated fundus
examination may reveal various pathological changes in the posterior pole including:
myopic crescents, Fuch’s spots (pigmented, circular lesions secondary to subretinal
neovascularization and hemorrhage), exudates, posterior staphyloma, retinal breaks,
scarring and retinal detachment. The optic discs may appear flat or tilted. The vitreous
may also be affected with opacification, liquification and detachment. Cataracts and open
angle glaucoma are also risk factors of high myopia[7].

The ocular pathology that is associated with high myopia is not generally observed with
isolated physiologic myopia. In 2003, Luo et al. used optic coherence tomography (OCT) to
study the association of macular volume and thickness with refraction and axial length.
The study included 104 Chinese school children with refractions between +1.00 to -4.5
diopters. After controlling for gender and age, the authors found that increasing axial
myopia was associated with reduced macular volume and parafoveal thickness[11]. The
authors suggested that OCT may be a useful tool for determining early macular changes in
physiologic myopia.

Risk Factors
Genetic Factors
Many studies have investigated the heritability of parental myopia associated with
physiological myopia. Numerous studies have shown a higher rate of myopia in children
with myopic parents and an even higher risk for children with two myopic parents[12], [6].
Many studies are confounded by strong environmental factors and research has shown
that associated parental heritability could be the result of shared environments rather
than shared genes. Moreover, investigators have also shown variation in the prevalence of
myopia for individuals of the same racial or ethnic group in different geographic locations.
In 2008 Rose et al. compared the prevalence and risk factors of myopia in children of
Chinese ethnicity in both Sydney and Singapore with inclusion criteria that required both
parents to have Chinese ethnicity. The prevalence of myopia in children of Chinese
ethnicity was significantly higher in Singapore (29.1%) than in Sydney (3.3%)[13]. There is a
general agreement that physiologic myopia has a multi-factorial etiology with both
genetic and environmental influences.

Environmental Factors
Environmental factors including near work, accommodation, accommodative lag,
spectacle correction, intelligence scores, urbanization and diet have been investigated for
their role in myopia and myopic progression.

Near work and Reading

Many studies have reported a correlation between near work and increased myopia,
however the association is usually weak and the data tends to be confounded by other
genetic and environmental factors. A large study in 2008 by Ip et al. suggested a
correlation between high intensity near work and increased rates of myopia. The authors
showed a minimal correlation between hours spent engaged in continuous reading and
parental reports of close reading distance with increased myopia. Time spent doing
homework or time spent doing near activities did not show a correlation, in fact time
spent playing hand held console games was associated with a more hyperopic refraction in
crude analysis[14]. This data suggests a link between near work and myopia but does not
conclude a causative relationship. A number of studies have looked at computer use and
myopia and found no significant correlation[15].

Accommodation and Accommodative lag

Accommodation is a significant covariant of reading and near work and as a result, several
studies have focused on the association between accommodation, accommodative lag and
myopic progression. A study in 2004 by Gwiazda et al. demonstrated that children with
higher degrees of myopia also had increased accommodative lag[16]. The children enrolled
in the study were already myopic and although a correlation between myopia and
accommodative lag can be assumed, it does not represent a causative relationship. More
recent studies have shown opposite results to those of Gwianda et al. In 2006 Mutti et al.
showed no changes in accommodative lag prior to the onset of myopia, moreover
accommodative lag was only documented in children after the onset of myopia. The
authors speculate that accommodative lag may be a consequence rather than a cause of
myopia and is unlikely a predictive factor[17]. This was further supported in 2008 by
Weizhong et al who showed no significant relationship between accommodative lag and
myopic progression[18].

Higher Intelligence
There are numerous multi-cultural studies that have shown higher intelligence quotient
(IQ) scores in children with myopia. Although the causal relationship has yet to be
determined, it is hypothesized that ocular axial length is directly related to cerebral
development. It has also been speculated that similar genes influence both IQ and myopia.
Seang-Mei et al studied 1204 children in Singapore to determine the association between
intelligence and myopia. After controlling for age, gender, parental myopia and education,
and books read per week they showed that children with higher IQ scores had
significantly more myopia than those with lower IQ scores[19]. The authors suggest that
non-verbal IQ may be an independent and stronger risk factor than increased reading
(books per week). In 2008 a similar study was performed in the UK on 6871 children and
after adjusting for ethnicity and parental myopia a strong correlation was shown between
higher performance on school-based standardized tests, verbal IQ and risk of myopia[20].
Evidence based research has shown a strong correlation between increased intelligence
scores and risk of myopia but the reason for the association has yet to be determined.

Urbanization
There are several studies that have reported urbanization as a potential determinant of
physiologic myopia. Many studies that have shown an association between increased
myopia in urban areas as compared to rural areas are confounded by variables such as
level of education, IQ, socioeconomic status, near related activities and outdoor exposure.
In 2008, a Polish study of 2206 students found that children living in the city had a two-
fold increase in the rate of myopia when compared to children living in rural areas[21].
Although they were able to show a correlation between urbanization and myopia, the
authors did not control for the above mentioned co-variants and a causative relationship
cannot be assumed.

Ambient Lighting
There is controversy in the literature as to whether ambient light while sleeping is a risk
factor for developing myopia in young children. In 1999, a study published in Nature by
Quinn et al. investigated the affects of ambient lighting on refractive development in 479
young children. Parents of children admitted to a pediatric ophthalmology clinic were
given questionnaires on the child’s night time light exposure. The authors found an
association between night-light exposure during the first two years of life and the
development of physiologic and high myopia. They reported a dose-dependant risk
showing an even higher prevalence of myopia in children who slept with room lights on
before the age of two[22]. This article has been the subject of debate and with many
researchers questioning the validity of their findings. A similar study in 2003 was
performed in the UK where parents of 122 university students answered questions on
their child’s artificial light exposure during the first two years of life. The study controlled
for a number of variables including parental myopia and showed no significant association
between nighttime light exposure and myopia. Conversely, they found myopia was more
common in children who slept in darkness during infancy, although the data was not
statistically significant[23]. There is currently no consensus on whether ambient nighttime
lighting during early childhood is a true risk factor for myopic development.

Nutrition
Although several studies have investigated the effect of diet and nutrition as
environmental determinants of myopia and myopic progression, there are significant
inconsistencies in the results. A recent study in 2010 by Lim et al. evaluated the
association between myopia, axial length and dietary factors of 851 Chinese children
using food frequency questionnaires. After the authors controlled for age gender, body
mass index, socioeconomic status, parental education, time spent outdoors and books
read per week they found that higher saturated fat and cholesterol were correlated with
longer axial lengths[24]. They did not find a significant association between myopic
refractive error and any other nutrients analyzed.

Diagnosis
Signs
Children with physiologic myopia commonly present with complaints of blurred distance
vision. Parents may also notice their child squint their eyes while viewing distance objects.
If the degree of myopia is moderate or high then children may be observed sitting closer to
the television and computer or holding reading material closer.

Pathologic changes related to high myopia are discussed in the pathology section.

Symptoms
The most common symptom of myopia is decreased distance vision. Patients with
pathologic myopia may also report visual distortion secondary to retinal pathology.

Diagnostic procedures
Myopia can be detected in children by various vision screening procedures at the
pediatrician’s office or at school. A significant refractive error is suspected when visual
acuity is reduced during a routine eye exam or vision screening. Although vision screening
techniques such as photo-screening and auto-refraction can detect myopia, the
prescription can only be accurately quantified using manifest or cycloplegic refraction.
See clinical diagnosis.

Clinical diagnosis
Myopia is most accurately quantified using manifest or cycloplegic refraction. Cycloplegic
refraction is the gold standard for diagnosing any refractive error in a child. Children
generally over-accommodate during manifest and auto-refractions, causing their
refractive error to appear more myopic. Cycloplegic refraction is therefore necessary to
determine the most accurate prescription and to avoid over-minusing children.
The pathology that can be associated with pathologic high myopia is diagnosed with a
dilated fundus exam.

Figure 2: Retinoscopy. A hand-held instrument (retinoscope) projects a beam of light into

the eye. The ophthalmologist neutralizes the movement of the reflected light with lenses
to determine the patient’s refractive error [25].

Management
General treatment
The standard treatment for myopia in children is glasses. A concave lens is used to diverge
the light rays entering the eye and place the focal point on the retina.

Figure 3: Light rays exiting a concave lens have less positive vergence, placing the focal
point on the retina[26].

Once children have matured enough to handle the responsibility, then contact lenses may
be an option. Most ophthalmologists agree that patients should be in their pre-teen or
early teenage years before considering contact lenses; however the decision is made for
each patient based on their level of maturity. In special circumstances, refractive surgery
may be indicated for children with neurological impairment, neurobehavioural issues,
facial deformities (craniofacial, hemifacial microsomia, ear deformity) or severe
anisometropia that render it impossible for glasses wear. Although contact lenses are
usually the secondary treatment option for children with developmental anomalies, there
are concerns for infection, mishandling, and expense. Refractive surgery for the general
population is usually only indicated once the patient has stopped growing which generally
occurs in the late teens to early twenties.

Surgery
Keratorefractive surgery uses lasers to re-shape the cornea and attempts to produce an
emmetropic eye. If the surgery is successful then the patient will have excellent visual
acuity without glasses or contact lenses. Photorefractive keratectomy (PRK), laser in situ
kertomileusis (LASIK) and laser epithelial keratomileusis are the most commonly
performed refractive surgeries. Intraocular refractive surgeries are becoming more
commonplace.

Primary Prevention
Various therapeutic modalities have been implemented for the treatment of myopic
progression. The efficacy and safety of several of these treatment methods have not yet
been determined. Currently there are no general guidelines for preventing myopia and the
use of non-medically proven treatments remains controversial. Studies have shown that
intensive near work may be a contributing factor for myopia and myopic progression.
Many authors have speculated that accommodating during near work may be contributing
to the progression and development of myopia. Both refractive and pharmocological
methods of eliminating accommodative demands while participating in near work have
been investigated.

Bifocals, Progressive Lenses, and Multifocal

Contact Lenses
Many studies have investigated the effect of decreasing accommodation in myopic
patients using single vision, bifocal and multifocal lenses. In 2003, the Correction of
Myopia Evaluation Trial (COMET) studied the effects of progressive additional lenses
(PVLs) and single vision lenses (SVLs) in 469 myopic children. Their preliminary data
showed a slowing of myopic progression by a statistically small amount during the first
year of PVLs when compared to SVLs[27]. The authors concluded that it did not warrant a
change in clinical practice.

There is significant debate over the efficacy and long term outcome of bifocals for the
prevention of myopic progression. A recent study in 2010 by Cheng et al. studied the
effects of bifocals and prismatic bifocal spectacles on myopic progression in Chinese
Canadian children. The authors showed a greater reduction of myopic progression and
axial elongation at two years for children in bifocals and prismatic bifocals as compared to
the SVLs group[28]. Unfortunately, the study did not provide long-term follow-up data.

In 2019, the FDA approved the first contact lens to slow the progression of myopia,
MiSight. MiSight contact lenses have a central zone with distance correction and
concentric peripheral zones alternating myopic defocus with distance correction, and
have been shown to slow the rate of myopia progression by 59% and axial elongation by
52% over 3 years in a randomized, double-masked trial of 53 test patients versus 56
control patients wearing single vision distance correction contact lenses. [29] Similarly,
high add power (+2.50 D) multifocal contact lenses have been shown to significantly slow
the rate of myopia progression (by 45%) over 3 years. [30] Further research is needed to
understand the clinical importance of these observed differences.

Atropine and Pirenzepine

Accommodation can be inhibited by using an eyedrop that contains a muscarinic receptor
antagonist. Atropine and pirenzepine have been the focus of studies investigating
pharmocologic prevention of myopic progression.

A study in 2016 by Chia et al. compared 0.5%, 0.1%, and 0.01% atropine for prevention of
myopia progression, finding that although at the 2 year mark there was a dose-dependent
reduction in myopia progression (high concentration meant greater reduction in myopia
progression), during a 1 year washout period, there was a larger rebound effect associated
with higher concentrations of atropine. Essentially, over 5 years, the 0.01% atropine group
was found to be most effective in slowing myopia progression and axial elongation with
less visual side effects compared with higher doses of atropine. [31] A report by the
American Academy of Ophthalmology in 2017 concluded that there is level 1 evidence
that supports the use of atropine to prevent myopia progression, and that given the more
sustained effect and fewer adverse effects of 0.01% atropine, it may the most reasonable
approach, though the optimal time to initiate and discontinue therapy is not known.
Ultimately, clinicians, patients, and families must decide whether the effects of atropine
0.01% are clinically significant enough to warrant its use. [32] More recently, a study by
Yam et al. in 2020 compared 0.05%, 0.025%, and 0.01% atropine eye drops, and
demonstrated that 0.05% atropine had double the efficacy of 0.01% atropine over 2 years,
but it is still unknown whether there will be a significant rebound effect during a washout
period. [33]

Pirenzepine is another muscarinic receptor antagonist, and unlike atropine it is relatively

selective for the M1 receptor and less likely to cause cycloplegia and mydriasis. Two
similar studies invested the efficacy of Pirenzepine using multicenter, double-masked,
placebo-controlled treatment trials. A 50% reduction in myopic progression was shown in
patients that used 2% pirenzepine gel in 2005 by Tan et al. and again in 2008 by Siatkowski
et al.[34][10]. Both studies showed an excellent safety profile with significantly less side
effects than seen with atropine. Currently there are no long term follow-up data on
pirenzepine.

Overnight Contact lenses

A highly controversial treatment modality for retarding myopic progression is the use of
overnight rigid contact lenses (orthokeratology). These lenses temporarily change the
refractive state of the eye by applying pressure to the cornea, creating a non-physiological
shape. There are currently no large studies that have shown a benefit to overnight rigid
contact lenses. There are several studies that suggest temporary benefits of
orthokeratology, however due to small sample size and no long term follow up data, these
studies remain inconclusive. In 2003 Katz et al. performed a large randomized trial of 298
Singaporean children that showed that myopic progression was not reduced
with overnight contact lens wear and the authors concluded that there is no
apparent benefit to orthokeratology for the treatment of myopic progression[35]. In 2019,
a report by the American Academy of Ophthalmology reviewed 13 articles on
orthokeratology including only one with level 1 evidence, and concluded that
orthokeratology may be effective in slowing progression of myopia, with potentially
greater effect when initiated younger (6-8 years); however, rebound effect can occur after
discontinuation, and safety remains a concern. [36] There are potential sight-threatening
and devastating risks associated with overnight contact lens wear and numerous reports
of corneal infection and scarring have been published.

Outdoor activity
The positive effect of outdoor activity for reducing myopic progression has been
documented in numerous studies. Physical activity, sports, and low accommodative
demands have been postulated as the cause of this protective effect. The Sydney Myopia
Study in 2008 demonstrated a significant reduction in the prevalence of myopia in
children who spent more time outdoors. After adjusting for time spent on near work,
parental refractive error and ethnicity, they showed that increased time spent outdoors,
rather than physical activity was associated with less myopia[37]. The authors of the article
suggest that light intensity when outdoors may be the contributing factor, by increasing
depth of field and decreasing image blur. They also comment on the possible effects of
light on the release of dopamine from the retina which is an eye growth inhibitor.

In 2015, Read et al. used a wrist worn light sensor to objectively measure mean daily
ambient light exposure and found that children who experienced low average daily
ambient light exposure exhibited significantly greater eye growth than children
experiencing moderate or high levels of exposure. [38]

A study from Taiwan published in 2018, explored the merits of a school-based

intervention aimed at increasing outdoor activities and sunlight exposure, and found that
this sort of intervention can be effective in slowing the progression of myopia. The study
also found that shorter outdoor time with high bright light exposure was roughly
equivalent to longer outdoor time in moderate intensity light in slowing myopia
progression. [39]

Prognosis
Patients with early onset and high myopia have a worse prognosis for long term visual
acuity. These patients tend to have a higher rate of myopic progression with longer axial
lengths. Patients with longer axial lengths are at a greater risk for developing myopic
retinal degeneration and other associated pathology.

Animal and Human Basic Research

During the late 70’s animal models of myopia were developed in monkeys, chicks and tree
shrews[40][41][42]. Form deprivation by frosted occluders was found to produce axial
elongation and myopia in the occluded eye. Ten years later, the model was expanded to
include myopia produced by negative lenses (and hyperopia produced by positive lenses)
applied to the eyes of 7 day-old chicks[43] [44]. The models have been extended to a variety
of mammals (see reference [45] for review). It is generally accepted that the mechanism
leading to changes in ocular elongation involves local retinal image processing which
sends a “stop” or “go” message to the sclera, regulating scleral matrix properties and its
rate of elongation.

Somehow the growth mechanisms are sensitive to where the principal image plane is
falling. If the principal image plane falls behind the retina, the eye tends to grow more, and
vice versa, when the image plane lies in front of the retina, the choroid thickens and the
eye stops growing. Most studies on animals have been carried out during a period that
would be equivalent to the first year or two of life in humans. In that period, non treated
congenital ptosis, corneal scars and non-treated dense congenital cataracts often produce
axial myopia in humans similarly as form deprivation develops in animal models.

The signalling cascade from the retina to the sclera is still under study. Amacrine cells have
been implicated in retinal processing of the signal[46]. The choroid[47] and the sclera
[48]show biochemical changes associated with ocular growth in the animal models. Two

drugs which have potential to prevent myopic progression in children, atropine and
pirenzepine, appear to block axial elongation in some of the animal models by pathways
which do not involve accommodation[49], perhaps by acting directly on the retina [50] or
the sclera[51].

By the 90’s, the link found between education and myopia development in epidemiological
studies, was generally explained by the possible regulation of the rate of axial elongation
by defocus during reading[52]. In other words, the lag of accommodation present in
humans while reading, places the image plane behind the retina and it was suggested that
this hyperopic defocus could induce axial elongation in humans, as it does in animal
models [53] [54]. Bifocals and progressive addition lenses applied to myopic children
showed some ability to slow myopic progression, consistent with this idea, although the
effects were generally not strong, and it was not clear why some subjects developed
myopia while others did not if all children lag to some extent while reading[16]. Evidence
on whether accommodative lag precedes or is a consequence of myopia is conflicting[17].

More recent experimental data showed that children [55] or adults[56] with myopia had
relative peripheral hyperopic defocus (images in the peripheral retina fell behind the
retinal plane in optically corrected myopic subjects) so it was postulated that the
peripheral refractive error could drive the emmetropization mechanisms leading to
changes in ocular growth patterns[56]. More recent evidence suggests that the difference
in eye shape may be a consequence, rather than a cause of myopia.

In 2002 it was shown, in the chick model, that the stop signal produced by positive lenses
was more robust than the grow signal of negative lenses[57]. One hour of clear distance
vision or exposure to positive lenses for short periods (i.e. images in front of the retina),
cancelled the myopia produced in chicks by whole day of frosted ocludders or negative
lens wear. Experiments in monkeys with foveal ablation and lenses or occluders with
central holes that allowed for clear central vision showed that defocus in the peripheral
retina could significantly affect axial growth of the eye[58][59]. This suggests that even if
peripheral hyperopic defocus is not a cause of myopia, if images in the periphery are
placed in front of the retina (myopic defocus), the stop signal could decrease axial
elongation in human eyes. Spectacles and contact lenses with peripheral plus add are
being tested in humans and there has been success in decreasing myopia progression in
selected cases[60][61]. More research is needed in this area before this technology is
available.

Contributing Authors: Rafael Iribarren MD, Ian Morgan PhD.

Pertinent clinical trials

Atropine for the Treatment of Myopia I (ATOM I)
2006
Ophthalmol 2006;113:2285 | Ophthalmol 2009;116:572 | Ophthalmol 2012;119:347.

Objectives
The goal was to determine if atropine can affect the progression of myopia in myopic
Asian children and the effect after the cessation of the treatment.

Design
Double-masked, randomised, placebo-controlled trial, where children received 1%
atropine or placebo to one of their eyes every night for two years, with a followed-up for 1
and 3 years.

Inclusion criteria were 6-12 years, refractive error of spherical equivalent between -1 D
and -6 D, BCVA in both eyes of logMAR 0.2 or better, astigmatism of less than 1.50 D,
anisometropia of less than 1.50 D.

Main outcome measures

Spherical equivalent (by cycloplegic autorefraction) and axial length (by A-scan
ultrasonography).

Results
346 children completed the 2-year study. Myopia progression and axial elongation in
placebo was -1.20+/-0.69 D and in atropine was 0.38+/-0.38 mm. The differences in
myopia progression and axial elongation between the 2 groups were -0.92 D in placebo
and 0.40 mm in atropine. In the atropine group, the myopia progression was only
-0.28+/-0.92 D, and the axial length remained essentially unchanged compared with
baseline (-0.02+/-0.35 mm). No serious adverse events related to atropine were reported.
The differences were statistically significant. The fellow eye of the atropine treated eye
progressed in its myopia that was not statistically different from either of the placebo
eyes.

Despite the success of atropine in reducing myopia progression in the treated eye when
given for two years, there was a rebound phenomenon observed over the following 12
months once atropine was stopped. The spherical equivalent of the atropine treated eye
progressed by -1.14D ± 0.80 over the third year compared to -0.38D ± 0.39 in the placebo
group. However, overall, after the third year, the eyes treated with atropine were less
myopic than the eyes in the placebo group: Mean total spherical equivalent was -4.29 D ±
1.67 in atropine compared to -5.22 D ± 1.38 in placebo.

Limitations
This study was conducted at a single centre in Singapore with a high prevalence of myopia.

The mechanism for atropine is incompletely understood.

Conclusions
Atropine may limit the progression of low/moderate myopia in children. There is a
rebound effect after cessation of treatment. Overall despite the rebound effect, the total
spherical equivalent may be less in eyes treated with atropine.

Pearls for clinical practice

Atropine is a treatment to stop the progression of low/moderate myopia in children.

Atropine for the Treatment of Myopia II (ATOM II)

2014
Ophthalmol 2012;119:347 | Am J Ophthalmol 2014;157:451 | Ophthalmol
2016;123:391.

Objectives
The goal was to determine if atropine can slow the progression of myopia without causing
side effects from cycloplegia and mydriasis in different concentrations and the results
after the cessation of the atropine treatment.

Design
Double-masked, randomized study of children aged 6-12 years with myopia of at least -2.0
diopters (D) and astigmatism of -1.50 D or less, were randomly assigned in a 2:2:1 ratio to
0.5%, 0.1%, and 0.01% atropine to be administered once nightly to both eyes for 2 years.
Cycloplegic refraction, axial length, accommodation amplitude, pupil diameter, and visual
acuity were noted at baseline, 2 weeks, and then every 4 months for 2 years.

Inclusion criteria were 6-12 years, refractive error of spherical equivalent of at least -2 D
in both eyes, astigmatism of less than 1.50 D, progression of at least 0.5 D over the last 12
months.

Main outcome measures

Myopia progression at 2 years. VA while wearing best corrected distance spectacle
correction, the near point of accommodation (by RAF rule), spherical equivalent (by
cycloplegic auto-refraction) and axial length (by coherence interferometry).

Results
400 children were randomised to 2:2:1 ratio to 0.5%, 0.1%, and 0.01% atropine. The mean
myopia progression at 2 years was -0.30±0.60, -0.38±0.60, and -0.49±0.63 D in the
atropine 0.5%, 0.1%, and 0.01% groups, respectively (P=0.02 between the 0.01% and 0.5%
groups; between other concentrations P > 0.05). The mean increase in axial length was
0.27±0.25, 0.28±0.28, and 0.41±0.32 mm in the 0.5%, 0.1%, and 0.01% groups,
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0.5% groups). However, differences in myopia progression (0.19 D) and axial length