Seminars in Ophthalmology

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Evaluation and Management of Acute Acquired

Comitant Esotropia in Children

Aubrey L. Gilbert, Euna B. Koo & Gena Heidary

To cite this article: Aubrey L. Gilbert, Euna B. Koo & Gena Heidary (2016): Evaluation and
Management of Acute Acquired Comitant Esotropia in Children, Seminars in Ophthalmology,
DOI: 10.1080/08820538.2016.1228398

To link to this article: http://dx.doi.org/10.1080/08820538.2016.1228398

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Seminars in Ophthalmology, Early Online, 1–6, 2016
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ISSN: 0882-0538 print / 1744-5205 online
DOI: 10.1080/08820538.2016.1228398

ORIGINAL ARTICLE

Evaluation and Management of Acute Acquired

Comitant Esotropia in Children
Aubrey L. Gilbert, Euna B. Koo, and Gena Heidary

Department of Ophthalmology, Boston Children’s Hospital, Harvard Medical School, and Massachusetts Eye
& Ear Infirmary, Boston, MA, USA

ABSTRACT
Acute acquired comitant esotropia (AACE) is characterized by a sudden-onset eye misalignment with an equal
angle of deviation in all fields of gaze. This form of esotropia is distinct from common forms of childhood
esotropia, such as infantile esotropia and accommodative esotropia, in the rapid tempo and typically later timing
of onset; further, AACE is distinct from restrictive or paretic strabismus, which usually results in an incomitant
angle of deviation that varies with the direction of gaze. The underlying etiologies for AACE are broad but, in
some cases, it may be associated with significant neurologic disease. Therefore, the purpose of this article is to
examine and summarize the current literature on AACE to provide a framework for the evaluation and manage-
ment of this form of acquired strabismus.
Keywords: Chiari malformation, pediatric strabismus

TYPES OF AACE by Bielschowsky (1922), is associated with moderate

Historically, AACE was initially organized into three
subtypes by Burian and Miller (1958).1 The first sub-
type, originally described by Swan (1947), is hypothe-
sized to occur from an acute disruption of fusion.2 This
may result from monocular occlusion, as was the case
for one of Swan’s original reported subjects, a nine-
year-old hyperopic boy who developed AACE after
initiation of patching. In this category, there also
have been case reports of subjects developing an eso-
tropia after acute eye trauma. Whether patients in this
category have a pre-existing esophoria that decompen-
sates after monocular occlusion remains unclear and is
a continued subject of debate. Burian and Miller
described a second subtype, called “Franceschetti”.
Characteristically, this subtype is considered idio-
pathic and patients have a low degree of hyperopia
and a relatively large angle of deviation. In the initial
descriptions, this subtype was thought to possibly be
induced by a preceding debilitating illness or other
physical or psychological stress. The third subtype,
described originally by VonGraefe (1864) and again
myopia, is typically progressive, and may present with
an esotropia that is larger for distance than for near
targets.3,4 While it has been hypothesized that this
might result from excess convergence tone associated
with near work, many authors feel that these patients
are more accurately described as having a divergence
insufficiency. Importantly, recent studies have high-
lighted a subtype of AACE which is associated with
neurologic findings or symptoms, and there have been
many reports of an association of AACE with intracra-
nial pathology.5 Thus, comitance of the strabismus
does not rule out the possibility of a serious, under-
lying neurological condition, and patients who present
with AACE must be evaluated with this consideration
in mind.
INTRACRANIAL PATHOLOGY IN AACE
Liu et al. (1997) performed a retrospective chart review
of 30 children with acquired esodeviation associated
with neurologic pathology and found that 40% of

Correspondence: Aubrey L. Gilbert, MD, Ph.D, Pediatric Ophthalmology and Strabismus Fellow, Department of Ophthalmology, Massachusetts
Eye & Ear Infirmary, 243 Charles Street, 3rd floor, Ophthalmic Education Office, Boston, MA 02114, USA. E-mail: aubrey_gilbert@meei.harvard.edu

1
2 A. L. Gilbert et al.
them demonstrated comitant deviations. Of those with
comitance, half had abnormal abduction but the other
half did not. They conclude that comitant esodeviation
can be common in children with identifiable neurolo-
gic insults.6 Williams and Hoyt (1989) reported on six
children with AACE who had posterior fossa tumors,7
and Vollrath-Junger, and Lang (1987) reported on a
group of patients who manifested esotropia as a sign
of hydrocephalus in the setting of shunt failure.8 There
have also been many reports of patients with Chiari
malformation presenting with AACE, and these are
detailed in the following.
REPORTED CASES OF AACE IN
ASSOCIATION WITH CHIARI I
MALFORMATION
The literature is replete with small case series examin-
ing the possible association between AACE and the
presence of a Chiari I malformation. While the mechan-
ism is clear by which an esotropia may result from
abduction limitation, as in abducens palsy in the setting
of increased intracranial pressure due to obstructive
hydrocephalus, the mechanisms by which a Chiari mal-
formation might result in an esotropia are less certain.
There are a number of recent studies which examine the
role of the cerebellum in divergence that seem to indi-
cate a role for the vermis in this action. In monkeys,
lesions of the dorsal cerebellar vermis result in an
esodeviation.9 Versino et al. (1996) used eye tracking
to compare nine patients with cerebellar dysfunction to
a control group of healthy patients and determined that
patients with certain cerebellar lesions tend to develop
esodeviations.10 Since the esodeviation in the setting of
cerebellar disease is usually greater at distance, it has
been attributed to a divergence paralysis.11 In this sec-
tion, we summarize the case reports associating AACE
with a Chiari I malformation in an effort to provide a
thorough reflection on these cases and to demonstrate
the current absence of a consistent guideline regarding
the management of AACE in the setting of a Chiari I
malformation.
Passo et al. (1984) reported the first case of acquired
esotropia in association with Chiari I malformation.12
Their patient was a 24-year-old woman, first diagnosed
with esotropia at age nine, who had recurrence of eso-
tropia with downbeat/torsional nystagmus one year
after strabismus surgery. Her deviation resolved and
her nystagmus dampened after decompression surgery
was performed following demonstration of a Chiari I
malformation on imaging. Subsequently, many addi-
tional cases have been reported and, while some have
involved neurological signs beyond just esodeviation,
there are also cases of isolated esotropia in the setting of
Chiari I malformation.
Bixenman and Laguna (1987) published the case of
a 13-year-old girl who originally presented with a
divergence palsy and gaze-evoked nystagmus.13 The
esotropia became increasingly comitant over a short
period of time and was successfully treated with stra-
bismus surgery but, three years later, she developed
downbeat nystagmus and a Chiari I malformation was
found on imaging. She subsequently underwent neu-
rosurgical decompression with resolution of the
nystagmus.
Akman et al. (1995) reported two cases of acute
acquired, divergence insufficiency type esotropia with
nystagmus.14 One of their patients was a 14-year-old
girl and the other was a 35-year-old man. Both patients
were ultimately found to have Chiari I malformation.
The younger patient was simply observed with no
change in her exam. The older patient underwent neu-
rosurgical decompression, also with no improvement.
In 1996, Lewis et al. reported on five patients from
ages 17–36.15 All five of their patients had gaze-evoked
nystagmus, two had skew deviations, and one had an
internuclear ophthalmoplegia. Four of the patients
underwent neurosurgical decompression, all with
improvement in their deviations and other symptoms.
The fifth patient refused surgery and no follow-up is
reported. Two of their patients had oculography that
showed normal peak abducting saccade velocity, caus-
ing them to favor a divergence paralysis mechanism
for the esotropia over abducens palsy.
Weeks and Hamed (1999) published a report on two
patients with Chiari I malformation who presented
with AACE, one a 14-year-old boy and one a 35-year-
old woman who had initially been diagnosed with
AACE at age 14.16 Both had divergence insufficiency
pattern esotropia. In addition, questionable temporal
disc pallor was noted in the 14-year-old boy and nys-
tagmus was noted in the older patient. Both patients
underwent strabismus surgery and both experienced
recurrence of their esotropia, one patient at three
months after surgery and the other at 1.5 years. The
deviations resolved for both patients after subsequent
Chiari I decompression surgery, leading the authors to
recommend neurosurgical decompression first in simi-
lar cases.
In 2000, Biousse et al. reported on four patients,
aged 5, 14, 16, and 37, with isolated AACE who were
found to have Chiari I malformations.17 Two of the
four patients underwent neurosurgical decompression
with resolution of their deviations and the other two
underwent strabismus surgery. In one of these latter
patients, there was recurrence of the deviation that
required repetition of the strabismus surgery; in the
other, the follow-up was limited to only two months.
Based on these cases, the authors conclude that man-
agement of patients with Chiari I malformation with
isolated ocular findings should be pursued on a case-
by-case basis.
Imes and Quinn (2001), in response to the pre-
viously summarized paper by Weeks and Hamed
(1999), wrote a letter to report one additional case of
Seminars in Ophthalmology

a patient with Chiari I malformation who presented
with AACE.18 In that case, the deviation was the same
at distance and near, but the patient did demonstrate
nystagmus and impaired smooth pursuit. She under-
went decompression surgery and, as her deviation was
unchanged four months later, she received a botuli-
num A toxin injection to the left medial rectus muscle,
and her diplopia resolved within a few days. Six
months later, her nystagmus was also gone and she
was stable in long-term follow-up for at least 15 years.
It is unclear if the esotropia and nystagmus would
have resolved without the botulinum injection, as
only four months was allowed after decompression
prior to secondary intervention; however, the authors
still support Weeks and Hamed’s recommendation to
pursue neurosurgical treatment for Chiari I malforma-
tion prior to performing any strabismus procedures.
Deefoort-Dhellemmes et al. (2002) reported on the
case of a nine-year-old boy who presented with AACE
and headache as well as both vertical and horizontal
small amplitude nystagmus.19 The patient underwent
Chiari I decompression surgery with resolution of his
diplopia, but not until nine months later, and the
sensorimotor exam did not show orthophoria until
approximately 15 months after surgery. Based on this
and on their review of the literature, the authors advo-
cate primary decompression for AACE in patients
with Chiari I malformation, but they specifically
recommend a follow-up period of at least one year to
assess surgical effects.
In 2004, Pokharel and Siatkowski described the case
of a 13-year-old girl with isolated divergence pattern
AACE whose imaging revealed 1–2 mm of tonsillar
ectopia; not a sufficient amount to qualify as a Chiari
malformation.20 The patient was initially treated with
Fresnel prisms but, due to her dislike of this option,
she eventually underwent strabismus surgery. A few
months later, she had recurrence of her diplopia and
repeat imaging revealed further tonsillar ectopia, mea-
suring 3–4 mm—still not enough to qualify as Chiari
malformation. Based on this progression, though, she
underwent decompression surgery but had no
improvement in her symptoms or sensorimotor exam-
ination, so ultimately had a second strabismus surgery
with good effect. While the paper is titled “Progressive
cerebellar tonsillar herniation with recurrent diver-
gence insufficiency esotropia,” the contribution of the
tonsillar herniation in this case is unclear.
In a paper from the neurosurgical literature,
Liebenberg et al. (2005) performed a retrospective
review of 40 patients with Chiari I malformation who
underwent posterior fossa decompression.21 Of those
cases, 12 manifested oculomotor and vestibulo-ocular
symptoms/signs and, of those, eight patients demon-
strated complete and one patient demonstrated partial
resolution after surgery. One impressive finding of this
paper was the mean time to resolution—15.5 months
(range 3–71 months). The authors conclude that, in
© 2016 Taylor & Francis
Acute Acquired Comitant Esotropia in Children 3
most cases, decompression is highly effective in treat-
ment of oculomotor and vestibulo-ocular symptoms/
signs associated with Chiari I malformation. It should
be noted that the patients included in this report were
mostly adults (age range 16–62) and that many of
them presented with nystagmus and abduction
limitation.
Henschel et al. (2005) described a case of a Chiari I
malformation presenting with AACE in a five-year-old
boy.22 A posterior fossa decompression was performed
with immediate postoperative improvement in the eso-
tropia, and complete resolution by seven months after
surgery. The authors suggest that, for patients with
AACE, even subtle symptoms and signs should prompt
imaging and they favor consideration of posterior fossa
decompression prior to strabismus surgery.
Kowal et al. (2006) published a case series of 12
patients with Chiari I malformations with strabismus,
most frequently comitant esotropia, as part of their
initial presentation.23 The majority of their patients
were treated with just prism glasses; one patient
improved with strabismus surgery alone, and three
patients underwent neurosurgical decompression, all
with minimal improvement of their strabismus; one of
these three then underwent successful strabismus sur-
gery. They conclude that neurosurgical intervention is
not required in most cases and that primary manage-
ment of strabismus—even just with prisms—may be a
viable and effective alternative, especially when stra-
bismus is the only specific finding.
Firth and Burke (2007) published the interesting
case of a 16-year-old girl who initially presented with
an isolated intermittent AACE that progressed to a
larger angle with a divergence insufficiency pattern
and over two weeks.24 Her saccades also became
hypometric and she developed an abducting nystag-
mus. MRI revealed Chiari I malformation with tonsil-
lar descent to about 12 mm below the foramen
magnum, with loss of cerebrospinal fluid spaces.
Neurosurgery was delayed for eight months and,
three months after esotropia onset, the patient received
a botulinum A toxin injection to the right medial rectus
muscle. She initially had a small exotropia result but,
shortly thereafter, she experienced great improvement
in the deviation and only a minimal phoria was pre-
sent at eight months. She still underwent neurosurgi-
cal decompression at that time, but did not have any
improvement in her nystagmus or hypometric sac-
cades by three months later. The authors focus on the
idea of botulinum injection being used as an interim
therapy while awaiting definitive management.
In 2013, Rech et al. reported the case of a patient with
an isolated AACE with Chiari I malformation.25 Their
case was a little different from many of the others noted
earlier as the patient did have a history of anisometro-
pic amblyopia and had been followed from 10 months
of age and treated previously with glasses and patch-
ing. Her occlusion therapy was stopped at age six and
4 A. L. Gilbert et al.
she was noted to have 20/20-2 acuity in her previously
amblyopic eye and 100 seconds of arc at that time.
Seven months later, she presented with sudden-onset
left esotropia without any accompanying neurologic
symptoms. Distance and near deviations were initially
identical, but the near angle had increased slightly by
one month later. MRI was obtained and revealed a
Chiari I malformation. No intervention was pursued
at that time and, by six months after onset, the devia-
tion had increased significantly. She underwent a bone-
only foramen magnum decompression with improve-
ment of the angle of deviation within two weeks. By
three months later, there was a small residual esotropia,
larger at near than distance, and this was addressed
with a left-sided recession/resection procedure along
with left inferior oblique myectomy to address concur-
rent overaction. At follow-up 12 months later, she main-
tained excellent alignment.
As demonstrated by the mixed results in these case
reports with respect to the impact of posterior fossa
decompression for AACE, the contribution of Chiari I
malformation to the strabismus continues to remain
uncertain and this makes management decisions diffi-
cult. In our practice, we have found that there is no
standardized algorithm for management in these cases
and treat on a case-by-case basis. When a patient pre-
sents with AACE and is discovered to have a Chiari I
malformation, we refer these patients to our neurosur-
gical colleagues. At their discretion, some neurosur-
geons opt for decompression surgery, while others
prefer to observe or to evaluate after direct interven-
tion has been made to address the strabismus, either
with prisms, surgery, botulinum toxin injections, or
some combination of these.
EVALUATION OF AACE: INDICATIONS
FOR NEUROIMAGING
When patients present to ophthalmologic practice with
AACE, there is no evidence-based method for deciding
which individuals should undergo neuroimaging to rule
out intracranial pathology. Williams and Hoyt (1989) sug-
gest that, whenever there is associated nystagmus, com-
plete neurological evaluation is warranted.7 In a later
paper, Hoyt and Good (1995) expand upon their previous
recommendations to suggest that AACE, when associated
with a history of previous strabismus, occlusion therapy,
monocular visual loss, or myopia, is likely benign in
origin.26 They still recommend evaluation for possible
underlying pathology for any case without apparent
cause and focus again on the presence of nystagmus, as
well as the inability to restore binocularity, as sufficient to
warrant further investigation. Schreuders at al. (2012)
report a case of AACE in a five-year-old boy with a diffuse
pontine glioma and summarize three prior papers that
make recommendations of when to pursue work-up for
patients with AACE.27 In 1996, Cruysberg et al. wrote that
the same risk factors considered relevant in cases of
paralytic strabismus should be evaluated for in cases of
AACE.28,29 These authors put forth a mnemonic, “DON’T
PANIC,” standing for Diplopia, Ophthalmic symptoms,
Neurological and general symptoms, Trauma, Papille
dema, Anisocoria, Nystagmus, Incomplete visual fields,
and Corneal hypoesthesia, to help guide when further
evaluation should be pursued. Lyons et al. (1999) conclude
that no single clinical sign can reliably indicate which
AACE patients might have intracranial pathology and
that a very high index of suspicion should be maintained
and neuroimaging considered in the absence of hyperme-
tropia or fusion potential, or in the presence of neurologi-
cal signs or any other atypical features.30 The same year,
Brown and Iacuone stated that absence of sensory or
motor fusion may be sensitive but not specific for intracra-
nial disease.31
MOST RECENT WORK ON AACE
In 2015, Buch and Vindig aimed to identify character-
istics of pediatric patients who develop AACE with
and without intracranial disease.32 They published a
retrospective review of 48 children who were consecu-
tively referred with AACE. All individuals with neu-
rological signs, recurrent AACE, or less than three
diopters of hyperopia were imaged. They found that
the mean age of onset for AACE was 4.7 years, but
that this was significantly higher in children found to
have intracranial disease. They identified seven cause-
specific types of AACE in childhood: acute accommo-
dative, decompensated monofixation syndrome or
esophoria, intracranial disease (three patients), idio-
pathic, occlusion related, secondary to different etiolo-
gic disease, and cyclic AACE. Of the three patients
who had intracranial disease, one had hydrocephalus,
one had a pontine glioma, and one had a thalamic
glioma. Two of these three had no obvious neurologi-
cal signs. Importantly, the authors identify four signif-
icant risk factors for intracranial disease: larger
esodeviation at distance, recurrence of AACE, pre-
sence of neurological signs such as papilledema, and
an older age at onset (>6 years).
Another recent, large study focused on a slightly
older cohort of patients. Chen et al. (2015) aimed to
describe the clinical characteristics and discuss the clas-
sification and etiology of AACE in a group of 47
patients referred to their institution.33 Their mean age
of onset was 26.6 ± 12.2 years. Based on their review,
they suggest that AACE be divided into two subgroups
consisting of patients with relatively small versus large
angle deviations. Nearly all of their patients with devia-
tions of less than or equal to 20 prism diopters were
treated successfully with prism glasses, while most of
their patients with larger deviations underwent strabis-
mus surgery. They also found three patients to have
intracranial pathology, two with a cerebellopontine
Seminars in Ophthalmology

angle tumor, and one with spinocerebellar ataxia. They
suggest neurological and/or neuroradiological investi-
gation under conditions where neurological findings
such as headache, papilledema, clumsiness, poor
motor coordination, or nystagmus are present.
MANAGEMENT OF AACE
For children without inciting intracranial pathology,
treatment options include prisms, strabismus surgery,
and botulinum toxin A injections. In 1999, Dawson
et al. reported a retrospective, interventional, noncom-
parative series of 14 pediatric patients with AACE
who were treated with botulinum A toxin injection
into a unilateral medial rectus muscle.34 In total, 11
of their patients gained improved stereopsis and main-
tained satisfactory ocular alignment with that therapy
alone. Two of the remaining three underwent subse-
quent strabismus surgery, and the third patient
refused further intervention. They conclude that there
is a definite role for botulinum toxin therapy in the
treatment of childhood AACE and that, in many
patients, it may obviate the need for traditional stra-
bismus surgery.
More recently, a retrospective, comparative, cohort
study by Wan et al. directly compared botulinum toxin
injection to traditional strabismus surgery for treat-
ment of pediatric AACE.35 They found no significant
differences in median stereoacuity or angle of devia-
tion with 18 months of follow-up. They also highlight
the advantages of botulinum toxin in terms of signifi-
cantly shorter general anesthesia and peri-operative
times and less expensive overall cost. While they did
document a couple of instances of transient exotropia
and ptosis associated with the injections, there was no
increase in serious or lasting complications.
SUMMARY/CONCLUSIONS
A number of case reports and series with varied pre-
sentations, evaluation, management, and outcomes
have been published on children with AACE. Acute
acquired comitant esotropia can be the sole presenting
sign in a child with serious intracranial pathology. It
can also be seen in patients without any other issues
and in patients with intracranial abnormalities of
unclear significance. The decision of when to perform
further neurologic evaluation and/or neuroradio-
graphic imaging on a child presenting with AACE is
controversial, but many authors suggest doing so
when there is no precipitating history of illness or if
there are any other abnormal findings on ocular exam,
especially nystagmus, abduction limitation, or optic
nerve swelling, or any neurologic symptoms such as
headache, vertigo, imbalance, weakness, or nausea. A
more conservative approach practiced by many
© 2016 Taylor & Francis
Acute Acquired Comitant Esotropia in Children 5
pediatric ophthalmologists is to screen any patients
presenting with AACE for the first time with a brain
MRI.
Further study is required to determine the association
of Chiari I malformation with AACE and whether or not
there are any finer nuances to the association. There are
also not sufficient data available to determine the most
efficacious management plan for children with Chiari I
malformation and AACE. Some case reports detail
improvement with strabismus surgery alone, others
with decompression alone, and others describe failure
of one or both of these treatment options. It seems that
improvement of the strabismus may be quite delayed
following decompression and this factor may not have
been a consideration in many of the case reports dis-
cussed earlier.
With respect to treatment, studies suggest that stra-
bismus surgery for AACE is anticipated to successfully
restore good binocular function in patients without an
underlying intracranial process. Treatment with botu-
linum toxin A may be an effective and promising
alternative to surgical treatment in some cases of
AACE.
DECLARATION OF INTEREST
The authors report no conflicts of interest. The authors
alone are responsible for the content and writing of
this article.
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