Journal of Binocular Vision and Ocular Motility

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Double vision in adults

Travis Peck & David Goldberg

To cite this article: Travis Peck & David Goldberg (2018) Double vision in adults, Journal of
Binocular Vision and Ocular Motility, 68:3, 63-69, DOI: 10.1080/2576117X.2018.1481265

To link to this article: https://doi.org/10.1080/2576117X.2018.1481265

Published online: 21 Jun 2018.

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JOURNAL OF BINOCULAR VISION AND OCULAR MOTILITY
2018, VOL. 68, NO. 3, 63–69
https://doi.org/10.1080/2576117X.2018.1481265

Double vision in adults

a
Travis Peck, MD and David Goldberg, MDa,b
a
Department of Medicine, Tower Health System, Reading, Pennsylvania; bEye Consultants of Pennsylvania, Reading, Pennsylvania

ABSTRACT ARTICLE HISTORY

Purpose: To determine the patient characteristics, patterns in presentation and incidences of the Received 12 March 2018
various etiologies in adult patients with the chief complaint of double vision. Accepted 14 May 2018
Design: Retrospective review. KEYWORDS
Subjects: All persons greater than 18 years of age who presented to a single provider (DG) in a Strabismus; diplopia; XT; ET;
nonacademic private practice over a 2-year period, from 2011 to 2013, with the chief complaint of prisms; strabismus surgery;
double vision. The provider is part of a multispecialty eye care group practice with both ophthal- non-strabismic diplopia
mologists and optometrists. This group practice provides a large adult referral base.
Methods: Examination for each patient included refraction, versions, alignment in different
positions of gaze at distance and at near, binocular sensory testing, neuro-ophthalmologic
examination, and dilated fundus examination if not recently documented. Alignment was mea-
sured with cover–uncover testing and alternate cover testing with prism bars or free prisms, using
Snellen letters for fixation. Appropriate refractive correction was ensured. Alignment was mea-
sured in the primary position at distance and in gaze directed 20 degrees L, R, up, and down. The
near deviation was measured in the reading position with the large letters on a near card for
fixation. Sensory testing was performed with the Worth 4-dot at distance and near and with the
Titmus stereopsis test. Vectograph testing was also performed at distance on many patients,
particularly those with small-angle deviations. The prismatic correction necessary to correct
diplopia subjectively at distance in the primary position and at near in the reading position was
also recorded.
Primary outcome: Ocular alignment and etiology of diplopia. Management, response to treat-
ment, and outcome were also recorded.
Results: A total of 125 patients were included in the analysis. Subjects ranged from 18 to 93 years
of age. Most cases of idiopathic strabismus were in the elderly, but the age range varied with
category of underlying strabismus. Small-angle HT was the most common type of strabismus,
comprising 21% of all subjects. ET, usually of the divergence insufficiency type (20%); XT (14%);
and palsies not including trochlear palsy (12%) and trochlear palsy (8%) were the next most
common etiologies. No strabismus was found in 11% of subjects.
Conclusions: Most cases of diplopia in adults presenting as an outpatient can be classified into a
few categories based on their type of strabismus. These categories of strabismus share typical age
ranges and features. While diplopia in adults is usually idiopathic, diplopia can be the presenting
sign of serious underlying pathology. Thus, a thorough history; examination; and, in some cases,
diagnostic testing is necessary.

Introduction
Double vision in an elderly patient is a relatively common
yet concerning chief complaint. It is most often a result of
ocular misalignment or strabismus. Although strabismus
is primarily thought of as occurring in childhood,
approximately 4% of adults are diagnosed with new
onset strabismus.1 Adults who have had strabismus
since childhood are far more likely to have developed
suppression rather than diplopia and, as such, would
not be included in this study of double vision.
Previous population-based studies that describe dou-
ble vision in adults have specifically focused on the
prevalence and etiologies of adult strabismus.1–3 Our
study analyzed diplopia rather than strabismus and so
included patients with transient diplopia and non-stra-
bismic etiologies for their diplopia. In addition, this
study analyzed the characteristics of the subjects in
more detail. In order to continue to improve outcomes
in these patients, it is critical to further document the
rates and presentations of the various causes of

CONTACT Travis Peck, MD travispeckj@gmail.com Department of Medicine, Reading Health System, S. 6th avenue and Spruce Street, West
Reading, Pennsylvania 19611.
Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/uaoj.
© 2018 American Orthoptic Journal Inc.
64 T. PECK AND D. GOLDBERG
strabismus and diplopia and to report the treatment
and outcomes observed. This will enable clinicians to
more accurately diagnose the underlying etiology in
adults with diplopia, avoid unnecessary testing, and
initiate effective treatment.
Methods
This was a retrospective study approved by the
institutional review board and done in compliance
with HIPPA. All patients over 18 years of age who
presented to a single provider for the first time with
the chief complaint of diplopia were identified.
Exclusion criteria included orbital fractures and
strabismus without diplopia. An examination was
done for each patient that included the following
components: refraction, versions, alignment in dif-
ferent positions of gaze at distance and at near,
binocular sensory testing, neuro-ophthalmologic
examination, and dilated fundus examination if
not recently documented. The primary measures
were ocular alignment and etiology of diplopia.
Management, response to treatment, and outcome
were also recorded for these patients. Demographic
characteristics such as age, gender, and ocular and
medical history were also analyzed. Subjects with
strabismus were classified according to previously
published criteria.4 Those subjects with both verti-
cal and horizontal deviations were classified accord-
ing to the larger deviation in the primary position
at distance.
Results
A total of 125 patients presented for an initial evalua-
tion of diplopia to the senior author during this 2-year
time period. Although not a criterion for exclusion, no
subjects had undergone strabismus surgery prior to
inclusion in the study. The ages of patients included
in the study can be seen in Figure 1. The number of
Age (years)
30
25
20
15
10
5
0
under 20 20-29 30-39 40-49 50-59 60-69 70-79
Figure 1. Number of patients in each age-group seen in this
study.
Type of Strabismus
Number of patients
30
25
20
15
10
5
0
Figure 2. Number of patients with each type of strabismus seen
in this study.
patients with each type of strabismus is displayed in
Figure 2. Data from all of the subsets are described in
the following sections.
Non-paralytic ET
Twenty-five of 125 subjects were found to have ET as
the cause of their diplopia. Twenty of these 25 subjects
were found to have divergence insufficiency. Analyzing
those subjects with divergence insufficiency ET
revealed an age range of 45–93 years. Only two subjects
were under 69 years of age. Of the 20 subjects with
divergence insufficiency ET, 5 had a possible identifi-
able cause of their strabismus, while ET was idiopathic
in the remaining 15 subjects. One subject presented at
60 years of age with diplopia after a hypoxic brain
injury. An additional subject was 45 years of age and
had divergence insufficiency ET and a history of nar-
cotic use. One subject presented with the acute onset of
diplopia with a small-angle intermittent ET. The
patient was treated with oral antibiotics after a positive
Lyme titer was discovered and the diplopia resolved.
One additional subject was found to have an old right-
sided pontine infarct on MRI and one patient devel-
oped a horizontal and vertical deviation after an epi-
sode of herpes zoster ophthalmicus.
Twelve of the 20 subjects with divergence ET were
treated with BO prism glasses, 1 was placed in a Fresnel
prism, and 4 underwent strabismus surgery. Patients
were placed in prism glasses to correct their distance
deviation. Three subjects had diplopia at near while
wearing BO prism glasses. One subject resorted to tap-
ing one bifocal lens and two subjects tolerated a BI
Fresnel prism over one bifocal segment.
Acquired ET without divergence insufficiency was
found in four subjects. One subject developed the
80-89 90 and acute onset of strabismus while withdrawing from nar-
over
cotic use and another acquired ET from Lyme menin-
gitis. An acute ET, which only lasted for 1 day, caused
diplopia in a subject with high myopia after removal of

a scleral buckle. One patient with Parkinson’s disease
had a small-angle incomitant ET.
Non-paralytic HT
Non-paralytic HT as a cause of diplopia was observed
in 26/125 (20.8%) subjects. Subjects with non-paralytic
HT ranged from 35 to 84 years of age. Twenty-five of
the 26 subjects were over 70 years of age, and the one
exception was a 35-year-old with sensory HT. The
angle of deviation in the primary position ranged
from 0 to 9 PD with 13/26 having a deviation less
than 3 PD. Five subjects with non-paralytic HT also
demonstrated horizontal deviations, two showed ET
and three had XT. Seventeen of 26 subjects with non-
paralytic HT had no identifiable etiology for their stra-
bismus. Of these subjects with no identifiable etiology,
three demonstrated hypo-elevation in adduction.
Three patients had poor vision in one eye and had a
presumably sensory cause for their deviation. Other
secondary etiologies included one case each of demen-
tia, scleral buckling surgery, epiretinal membrane, and
an acute hypo-elevation which resolved.
Prism glasses were prescribed in 10 subjects. The
diplopia was well controlled with prism glasses in 7/
10 patients, and the other 3 did not return for follow-
up. Fresnel prisms were prescribed in three subjects.
One subject with sensory HT could not fuse with
prisms and preferred to not use prism so the images
would be widely separated. Two subjects had a signifi-
cantly different deviation at near and required slab-off
in their bifocal to fuse at near. One subject underwent a
mini-tenotomy of the inferior rectus, which successfully
controlled the diplopia.5
Non-paralytic XT
Non-paralytic XT was observed as a cause of diplopia
in 18/125 (14%) of subjects with an age range of
40–85 years. Eight of the subjects with XT had CI,
which was defined as diplopia while reading with a
near X/XT greater than 10 PD and no diplopia at
distance with X less than 10 PD. These patients ranged
in age from 58 to 85 years and all but one was 71 years
or older. The XT was intermittent in three subjects.
Distance deviation in those with XT without CI
ranged from 2 to 45 PD. These subjects could be
divided into four patients with small-angle XT (2–8
PD at distance) and five patients with large-angle XT
(14–45 PD at distance). All but one subject with small-
angle XT had an associated HT, while no subjects with
a large-angle XT had an associated vertical deviation.
Four of the subjects with XT without CI had underlying
JOURNAL OF BINOCULAR VISION AND OCULAR MOTILITY 65
neurologic dysfunction with one patient each having
early onset Alzheimer’s dementia, Parkinson’s disease,
myotonic dystrophy, and narcotic use.
Two subjects with small-angle XT without CI were
successfully treated with prism glasses. Two subjects
with large-angle XT and intermittent deviation under-
went successful strabismus surgery. Two patients with
large-angle XT were treated successfully with Fresnel
prisms. One of these two patients had 18 PD XT at
distance and 45 PD XT at near as well as severe
Parkinson’s disease. This subject was treated with a
Fresnel prism for distance and occlusion of one bifocal
lens.
For those subjects with CI, a Fresnel prism at near
was prescribed in four subjects. One of these subjects
did not tolerate the Fresnel, and two did not return for
follow-up. One subject was treated with a separate pair
of BI reading glasses.
Palsies
Twenty-four of 125 subjects (19%) developed diplopia
due to a palsy of the EOMs. Of these, 5 patients devel-
oped an oculomotor palsy, 9 patients developed an
abducens palsy, and 10 patients were diagnosed with a
trochlear palsy. These subjects ranged from 33 to
83 years of age.
In the five patients with an oculomotor palsy, two
had a neurovascular etiology with one patient having
uncontrolled hypertension and one patient having
long-standing diabetes mellitus type II. One subject
with oculomotor palsy was diagnosed with Lyme dis-
ease and his diplopia resolved with intravenous anti-
biotics. One subject developed an oculomotor palsy
after head trauma and was treated with strabismus
surgery, and one subject with oculomotor palsy had
an idiopathic palsy that did not resolve.
Abducens palsy occurred in nine subjects. Two sub-
jects had a neurovascular etiology with severe systemic
hypertension. One subject was diagnosed with a menin-
gioma and had suffered from diplopia for several
months before presentation. He demonstrated
decreased abduction of the involved eye and an R
optic neuropathy. The remaining six patients had an
idiopathic origin for the abducens palsy. The palsy
resolved spontaneously in 5/6 subjects.
Ten subjects were diagnosed with a trochlear palsy.
Three subjects developed a trochlear palsy after signifi-
cant head trauma. One subject had a neurovascular
etiology with underlying diabetes mellitus type II and
the remainder of the subjects had no obvious etiology
for their strabismus. The diplopia resolved in one sub-
ject and was improving in another two subjects who
66 T. PECK AND D. GOLDBERG
were lost to follow-up. Prism glasses were prescribed in
five subjects. Of those subjects with prism glasses, one
required slab-off lenses for a greater deviation at near
and one only required prism in a separate pair of read-
ing glasses. One subject underwent strabismus surgery
and developed an overcorrection after surgery.
Other neurologic disease
Five of 125 subjects developed diplopia due to cerebro-
vascular disease. One subject developed a vertical skew
deviation associated with labyrinthitis, and another sub-
ject developed a skew deviation with ET and nystagmus
after excision of a midbrain tumor. Of the subjects with
cerebrovascular disease, one developed an acute ET
measuring 7 PD in the primary position both at distance
and near with a mild increase on left gaze. The diplopia
resolved 2 months after onset. Two subjects with multi-
ple cerebrovascular accidents developed a small acute
vertical deviation which resolved. A 91-year-old subject
developed an acute internuclear ophthalmoplegia that
was presumably ischemic in origin. This subject’s moti-
lity improved over several months.
Orbit
Four patients developed diplopia due to orbital dis-
ease. Three of the four subjects with an orbital etiol-
ogy for their diplopia demonstrated significantly
decreased duction of one eye. One subject had prop-
tosis due to an orbital lymphoma, but the other three
subjects did not have proptosis. One subject had
significantly decreased motility in one eye associated
with severe nasal polyps. Another subject was
88 years of age when she developed progressive
Hypotropia and decreased elevation of one eye. She
had undergone scleral buckle surgery 12 years pre-
viously. A CT scan demonstrated EOM enlargement
and she was diagnosed with Graves’ disease. An infer-
ior rectus recession resulted in an undercorrection.
One subject with orbital disease had 6 PD of XT and
12 PD of L HT, which was comitant. Imaging
revealed a right orbital hemangioma.
Myasthenia
Myasthenia was newly diagnosed by the senior author
in four cases. Subjects with myasthenia ranged in age
from 60 to 82 years. The diplopia was intermittent in
two subjects and of acute onset in one subject. Two
subjects demonstrated a mixed horizontal and vertical
deviation. Associated symptoms were present in three
subjects including ptosis in two subjects and neck
weakness in one subject. Anti-acetylcholine antibodies
were elevated in all subjects diagnosed with myasthenia.
Lyme disease
Three subjects in this study were diagnosed with Lyme
disease. One subject presented with acute divergence
insufficiency ET, one with oculomotor palsy, and the
last developed acute Lyme meningitis. The subject
with Lyme meningitis developed a right facial palsy
and right facial numbness. This subject had already
begun treatment with intravenous antibiotics 4 weeks
prior to his ocular examination. At the time of his
examination for our study, this subject had 25 PD of
ET at distance, which was comitant, and 8 PD of
intermittent ET at near. There was no papilledema at
the time of his ocular examination. The etiology for
his strabismus is unclear but may be related to abdu-
cens nerve weakness either from increased intracranial
pressure or direct damage to the nerve in the subar-
achnoid space.
No strabismus
No strabismus was detected in 14/125 (11%) subjects
who presented with diplopia. Five of these subjects had
a history of transient binocular diplopia, which was not
present on the day of the examination. One subject
with transient diplopia was diagnosed with polycythe-
mia vera as a cause of his transient diplopia. Another
subject had a history of Factor V Leiden, a mutation of
one of the clotting factors in the blood, with recurrent
venous thrombosis and presumably had a vascular
etiology for the diplopia. No etiology was discovered
in three subjects with transient diplopia.
Ten subjects had constant diplopia without strabis-
mus. Five subjects experienced monocular diplopia,
which resolved in three subjects with a change in
refraction. Two subjects had diplopia due to poor
fusion secondary to severe bilateral visual field constric-
tion. One patient noted diplopia that was presumably
secondary to age-related macular degeneration. One
elderly subject complained of diplopia while driving.
Vectograph and red-light testing elicited unclear
responses. The remainder of a binocular vision exam-
ination was normal. However, this subject demon-
strated mild optic atrophy, which may have been the
etiology for his complaints.
Discussion
This review of all patients who presented to a general
ophthalmology practice with the chief complaint of

double vision illustrates the relative frequencies of the
etiologies of diplopia in adults. It is not a population-
based study showing incidences among all adults. The
utility is in illustrating the various causes of diplopia,
the proportion of cases they represent, patient out-
comes, and response to treatment. There is a bewilder-
ing array of etiologies and categories of acquired
strabismus in adults. The most common types of stra-
bismus were paralytic (22%), HT (21%), ET greater at
distance (16%), and XT (6%). Diplopia without strabis-
mus on exam was noted in 11% of the patients.
The rates reported here are largely consistent with
prior studies.1,2,4,6,7 In the largest study to date,
Martinez-Thompson et al. report the four most com-
mon subtypes of adult strabismus as paralytic (44.2%),
CI, small-angle HT (13.3%), and divergence insuffi-
ciency (10.6%).1 The study by Martinez-Thompson
included records from ophthalmologists and neurolo-
gists but not optometrists. Therefore, the population
may have been skewed toward those with paralytic
strabismus. In addition, the authors note that a sub-
stantial amount of the paralytic strabismus in the
study was a trochlear palsy. Perhaps some of these
patients that they classified with a trochlear palsy
may have been included as a small-angle HT in the
current study.
Divergence insufficiency ET and non-paralytic HT
were the most common types of strabismus in this
study. These subjects did not demonstrate an extraocu-
lar muscle palsy or skew deviation. Those subjects with
divergence insufficiency ET demonstrated full abduc-
tion and had comitant deviations on side gaze. The
subjects with non-paralytic HT did not show the char-
acteristics of a trochlear palsy or the associated symp-
toms of a skew deviation.
Age-related changes in the EOM pulleys have been
proposed as the mechanism behind the idiopathic cases
of both ET greater at distance and small-angle vertical
deviations. Also known as the sagging eye syndrome,
displacement of the lateral rectus–superior rectus (LR-
SR) band may lead to divergence insufficiency and
small-angle HT. This band supports the vertical posi-
tion of the LR and thins and weakens with age. These
changes result in inferior displacement of the horizon-
tal rectus muscles. It is also associated with changes in
the lids such as superior sulcus atrophy, ptosis, and
lower lid fat prolapse. One study of 56 patients sus-
pected of having age-related degenerative changes as
the cause of their strabismus found that rupture of
the LR-SR band was present in 91% on MRI.8
An observation in this study that supports sagging eye
syndrome is that 8 of the 20 patients with ET greater at
distance also had small-angle HT. Further evidence that it
JOURNAL OF BINOCULAR VISION AND OCULAR MOTILITY 67
is an age-related process is that all cases of idiopathic ET
at distance were seen in patients over 75 years of age.
Another mechanism proposed for this process is micro-
vascular ischemic insults to the area of the brain stem
where divergence is controlled.9 It is also possible that the
age-related changes occur in the muscles, specifically the
medial rectus, rather than the LR-SR band.10
An entity not previously described was a small-angle
HT with hypo-elevation in adduction of one eye. These
subjects demonstrated HT of the contralateral eye. Our
clinical impression is that patients with the hypo-eleva-
tion in adduction tend to be quite elderly, frail, and
enophthalmic. Hypo-elevation in adduction may also
be due to asymmetric atrophy of the EOM pulleys.
Forced duction testing was not performed to differenti-
ate these cases from a Brown syndrome, but there were
no other symptoms or signs of Brown syndrome such
as point tenderness over the trochlea or a click.11
Another entity not well described previously is
small-angle comitant XT with an associated vertical
deviation. This motility pattern was demonstrated in
five patients and is of unknown etiology.
Management of patients is primarily with prisms.
Correction of diplopia in patients with divergence
insufficiency begins with correcting full distance ET.
Most patients with divergence insufficiency ET can
fuse the full distance BO prism at near. However,
some patients cannot tolerate BO prism at near without
developing a near XT. In those patients, the bifocal can
be nasally displaced to induce some BI prism at near,
although this displacement is not possible with progres-
sive lenses. Separate reading glasses with less or no
prism may be helpful in patients using progressive
lenses. A BI Fresnel prism over one bifocal or occlusion
of a bifocal lens may be necessary.
Vertical prism is necessary in those patients with a
small-angle HT. In some patients, correction of a small-
angle deviation can provide significant relief of symp-
toms. In both divergence insufficiency ET and HT, the
prism required is often slightly greater than the objec-
tive deviation seen on alternate cover testing.
In those with vertical deviations, the near deviation
should also be measured. Patients with incomitance at
near may benefit from a slab-off or reverse slab-off to
induce a different prism in the bifocal than at distance.
In addition, anisometropia must be considered when
prescribing prism. Many elderly patients with diplopia
will have other ocular conditions. Consideration should
be given to anisometropia, retinal aniseikonia, epiret-
inal membranes, visual field loss, and ocular surface
disease.
The most common type of paralytic strabismus was
trochlear nerve palsy. Trochlear palsy was diagnosed
68 T. PECK AND D. GOLDBERG
when patients displayed superior oblique under-action
and an increase in HT by at least 2 PD in contralateral
horizontal gaze or ipsilateral head tilt. However, some
of our cases categorized as trochlear palsy may not
actually be due to palsy of the SO. Previous studies
have shown no atrophy of the SO on high resolution
MRI in patients with incomitant HT in a superior
oblique palsy (SOP) pattern.12 There are other mechan-
isms that could masquerade as trochlear palsies includ-
ing heterotopy of rectus pulleys, unstable rectus pulleys,
and degeneration of the LR-SR band.13 In light of this,
it may be more appropriate to classify patients with a
trochlear palsy pattern of strabismus as incomitant HT
unless a clear etiology for SOP is present.
The majority of patients with divergence insufficiency
or small-angle HT were not found to have a serious
underlying etiology. Neuroimaging was performed in six
of the patients with comitant divergence insufficiency ET
and was non-revealing in all of the cases except for one
patient who was found to have an old pontine infarction.
The only patient identified with a central nervous system
neoplasm had clear limitation of ocular motility. Lyme
disease and myasthenia were more rare causes of strabis-
mus noted in this study. In most cases of myasthenia,
there was a clue to the diagnosis such as a variable devia-
tion or ptosis.
Other serious potential etiologies of strabismus not
seen in this study include temporal arteritis, demyeli-
nating disease, increased intracranial pressure, and car-
diovascular insufficiency. A careful history and neuro-
ophthalmologic examination is recommended for all
patients with diplopia. Characteristics that should par-
ticularly warn the clinician to investigate strabismus
further include younger age, history of cerebrovascular
disease, rapid progression, decreased versions, variable
deviations, deviations that do not fit into the character-
istic categories seen in this study, ptosis, or orbital signs
such as proptosis.
Transient diplopia, even of short duration, can be a
sign of underlying cerebrovascular disease. It is critical
to initiate a thorough systemic work-up in patients with
transient diplopia as these authors have seen serious
diseases such as temporal arteritis, new onset atrial
fibrillation, and increased intracranial pressure present
with transient diplopia.
Diagnosis of non-strabismic causes of diplopia often
requires careful refraction and ophthalmologic examina-
tion with attention to macular disease. In some patients,
no etiology for their subjective complaints of diplopia can
be found.
Despite the need to rule out serious underlying
diseases, most cases of diplopia are not a manifesta-
tion of life-threatening pathology and can be corrected
with prisms or strabismus surgery. This study con-
firms previous data that the most common causes of
diplopia in the elderly population are a result of age-
related degenerative changes in the orbit. It also
demonstrates that the majority of strabismus and dou-
ble vision in these patients can be managed. If refrac-
tion is optimized, prisms are used creatively, and
patients are educated on the limitations of treatment,
the prognosis for treatment of double vision in adults
can be quite good.
A limitation to this study is that it does not show true
incidence or prevalence. This would require sampling a
population to determine rates of diplopia and the various
subtypes, such as is done by Martinez-Thompson et al.1
There is also limited follow-up in this study with no
minimum follow-up criteria after time of diagnosis.
Underlying etiologies for the diplopia may have become
apparent over time. Most patients’ response to initial
treatment was documented. This is also a single observer
study and as such is prone to individual biases in diag-
nosis, management, and patient population.
Disclosure statement
No potential conflict of interest was reported by the authors.
Funding
None
ORCID
Travis Peck http://orcid.org/0000-0001-9041-5776
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