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246 Theory and Practice of Squint and Orthoptics
prescribed to neutralize the deviation. In
some patients, the esodeviation will increase
as the patient 'eats-up' the prism. Surgery is
planned for the full prism-adapted deviation.
– Enhanced or augmented surgery has been
advocated by some workers as an alternative
to surgery with prism adaptation.
Note. Various formulas are used to augment
standard surgery. A simple and effective
method to determine the target angle is by
averaging the near deviation without correction
(largest deviation) and the distance deviation
with correction (smallest deviation).
INFANTILE ACCOMMODATIVE ESOTROPIA
Infantile accommodative esotropia is the term
used for rare cases of accommodative esotropia
occurring at 3 to 4 months of age.
Differential diagnosis from essential infantile
esotropia can be made by:
• Presence of straight eyes for the first 2 to
3 months,
• Variable angle of deviation at the onset, and
• Presence of hypermetropia >2D.
Treatment consists of:
• Full hypermetropic correction should be done
immediately after cycloplegic refraction.
• Amblyopia should be treated, when present.
• Surgery is indicated when spectacles correction
cannot allign the eyes to within 10 PD (see
partially accommodative esotropia).
ESSENTIAL ACQUIRED ESOTROPIA
OR LATE ONSET ESOTROPIA
In general, all forms of non-accommodative
esodeviations other than essential infantile
esotropia may be labelled as 'acquired nonaccommodative esotropias'. However, in
strabismic practice, the term acquired nonaccommodative esotropia or the late onset nonaccommodative esotropia or essential acquired
esotropia by common use has come to mean a
non-accommodative esotropia that occurs
during the first few years of life and that cannot
be grouped with other forms of esotropia. It
includes following clinical types:
• Basic esotropia
• Non-accommodative convergence excess
esotropia
• Divergence insufficiency esotropia
Basic esotropia
Clinical features
1. Onset is in childhood (early a few years of
life) but decidedly after 6 months of age.
2. Deviation is usually equal at distance and
near. At the onset, the angle of deviation is
smaller than essential infantile esotropia but the
angle may increase to 30 to 70.
3. Accommodative factor is characteristically
absent.
4. Refractive error is insignificant.
5. AC/A ratio is normal.
ACQUIRED NON-ACCOMMODATIVE
ESOTROPIAS
This group includes all the acquired esodeviations in which the amount of deviation is not
affected by the state of accommodation. These
include the following clinical entities:
• Essential acquired or late onset esotropia
• Acute concomitant esotropia
• Microtropia
• Nystagmus blockage syndrome
• Cyclic esotropia
• Divergence paresis
• Stress-induced esotropia
• Esotropia in myopia
• Esotropia due to spasm of near reflex
Etiopathogenesis
In view of the above clinical features,
Costenbader postulated that this deviation is
due to excessive convergence tonus and so
suggested the term 'acquired tonic esotropia' for
basic esotropia.
Clinical work-up
• It should be on the general lines for work up
of any squint patient.
• A special word of caution has been conveyed
by many reports in the literature to rule out
any possibility of an underlying lesion of
malformation in the central nervous system
in all patients with 'acquired non-accommodative esotropia'.
Concomitant Esotropias and Exotropias
247
Treatment
1. Amblyopia, when present, should be treated
first of all (see page 202).
2. Surgery is the ultimate treatment for basic
esotropia. It should be performed as early as
possible after the amblyopia therapy. Results,
in terms of binocular visual potential, are better
than the infantile esotropia.
Non-accommodative convergence
excess esotropia
Clinical features
It is characterized by following features:
1. Onset of deviation is usually between 2 and
5 years of age.
2. Deviation is characteristically large-angle
esotropia for near with a small angle esotropia/
esophoria or orthophoria at distance (similar to
non-refractive accommodative esotropia). Near
distance disparity is 15 PD.
3. AC/A ratio determined by lens gradient
method is normal or even low and the use of
bifocals has no effect on near deviation (unlike
non-refractive accommodative esotropia due to
high AC/A ratio). In view of the above,
determining the AC/A ratio by heterophoria
method (by comparing the near and distance
deviation) is likely to miss such a condition and
patient may be wrongly prescribed bifocals to
which they will not respond.
4. Near point of accommodation is within
normal limits. This observation differentiates the
condition from the hypoaccommodative type of
non-refractive accommodative esotropia.
5. Refractive error. Patients are usually hyper-
metropic or emmetropic.
Treatment
Surgical correction by bilateral medial rectus
recession with Faden operation (suturing the
muscle to the sclera 12 mm behind the muscle
insertion) is the treatment of choice. von
Noorden has reported that conventional
recession procedure of bilateral medial rectus
(4 to 5 mm) with or without Faden operation is
usually ineffective. Therefore, a large recession
between 5 and 8 mm should be planned.
Divergence insufficiency esotropia
Clinical features
• It is characterized by a greater deviation for
distance than near. Near-distance disparity
should be 15 PD.
• It is usually comitant; but the possibility of an
underlying neurological lesion causing mild
sixth nerve palsy should always be ruled out.
Treatment
Base-out prism may be tried to help the patient.
However, often surgical treatment with bilateral
rectus resection is required.
ACUTE CONCOMITANT ESOTROPIA
It refers to sudden onset of large-angle
concomitant esotropia without any paralytic
element. It is typically associated with diplopia.
Voluntary closure of one eye may often be the
only sign in preverbal infants. Following two
forms of acute concomitant esotropia have been
reported.
1. Acute strabismus after artificial
interruption of fusion
• It has been reported to occur in patients with
no previous history of squint, after interruption
of fusion under following conditions:
– Prolonged bandaging of one eye for any
surgery or perforating injuries.
– Occlusion of one eye for treatment of
ambylopia without squint (e.g. anisometropic amblyopia).
– Swelling of the lids following blunt trauma.
• It has been postulated that perhaps these
patients have latent esodeviation and/or
uncorrected hypermetropia which was fully
controlled by the well-functioning fusion
mechanism without any symptoms. However,
the deviation becomes manifest after the
fusion is disrupted and the compensatory
mechanism is thus suspended following
occlusion of one eye.
Treatment
• Spontaneous improvement occurs in some
patients after the occlusion is removed.
• Correction of underlying hypermetropia may
straighten the eyes in other patients.
• Surgery may be required to correct esotropia
in a few patients.
248 Theory and Practice of Squint and Orthoptics
2. Acute concomitant esotropia without
preceding disruption of fusion
Etiopathogenesis
It has been postulated that perhaps such patients
have an asymptomatic esophoria with only a
slim reserve of fusional amplitude that
maintains alignment of the eye over the years
but that may become lost under the influence of
physical or emotional strain.
Clinical features
• Onset is acute with diplopia.
• Deviation is relatively large.
• Refractive error is insignificant.
• Disruption of fusion is not the associated
factor.
• No signs of paralysis of lateral rectus muscle.
• Good potential for binocular co-operation is
there.
Treatment
Excellent functional results are obtained in such
patients with surgical treatment.
MICROTROPIA
Depending upon the degree of deviation, Lange
classified heterotropia as follows:
• Microtropia: 1°–5°
• Small angle esotropia: 5°–12°
• Large angle esotropia: >12°
Monofixation syndrome versus microtropia
The sine quo non of the monofixation syndrome
is the absence of bifoveolar fusion with the
presence of peripheral fusion. There are various
causes of monofixation syndrome. Microtropia
is the most common cause of monofixation
syndrome (Park's syndrome). Thus, microtropia
is a cause and not synonymous with monofixation syndrome as used previously in the
strabismic literature.
An array of other terms have also been used
to describe the microtropia. Some of these are:
Fixation disparity, fusion disparity, monofixational esophoria, retinal slip, retinal flicker
and minisquint.
Diagnostic features
Based on the fixation pattern, Lang has
described three types of microtropia:
• Type-I—central fixation,
• Type-II—eccentric fixation without identity,
and
• Type-III—eccentric fixation, with identity, i.e.
angle of anomaly is same as the eccentricity
of fixation.
Features of microtropia as described by Lange
and also adopted by von Noorden et al. can be
grouped as:
• Consistent findings, and
• Variable findings.
Consistent findings
1. Amblyopia. A microtropia should always be
suspected in unilateral decrease of visual acuity
(usually not worse than 6/18) for which no
organic cause can be found in patients without
apparent strabismus or a history of such and
without significant refractive error or
anisometropia. Amblyopia is not the cause but
a result of microtropia.
2. Abnormal retinal correspondence (ARC) as
deter-mined with: (i) Bagolini's striated glasses
(see page 137) and (ii) Foveo-foveal test of Cupper
(see page 141).
3. Relative scotoma on the fovea or in the case of
parafoveal fixation, the fixation point of the
deviated eye. Tests for identifying a monocular
scotoma in the binocular visual field include:
• Worth four-dot test (see page 140)
• Binocular scotometry (see page 197)
• 4 base-out prism test (see page 183)
• Bagolini striated glasses (see page 137)
• A–O Vectographic Project-O-Chart slide
(see page 185).
4. Normal or near normal peripheral fusion with
amplitudes is present in patients with microtropia
despite the fact that such patients have 3°–5°
central scotoma in one eye during binocular
viewing and retinal image disparity of up to 10.
This is possible because the Panum's fusional
space is wide in the peripheral retina (up to 5°)
as compared to central retina (only 20 minutes
of arc). It has been reported that peripheral
Concomitant Esotropias and Exotropias
249
fusion begins at some point in the retina that is
anywhere from 9° to 12° from the foveola.
5. Defective stereoacuity. Stereoacuity for near
should at least be 3000 seconds of arc. A minimal
requirement for gross stereopsis of distance is
not necessary for diagnosis. However, about
one-third patients with monofixation syndrome
have a distance stereoacuity between 240 and
120 seconds of arc.
Variable findings
1. Size of deviation can measure up to 10
horizontally and up to 3 vertically.
2. Fixation pattern is non-foveal but may be
foveal. Diagnosis of microtropia is difficult in
patients with minute degrees of fixation
anomalies.
3. Anisometropia may or may not be present.
Identification of microtropia is more difficult in
isometropic patients.
4. Cover test may be positive or negative. In
patients with positive cover test, diagnosis is
clearly established by a very small fixation
movement (flick) of the deviated eye upon
covering the fixating eye. When the cover test is
negative (Fig. 10.8), special diagnostic procedures
are required to differentiate a microtropia with
identity from non-strabismic causes of
decreased vision in one eye.
Treatment
1. In young patients who are visually immature
(age 6 or under), full-time occlusion therapy
should be done to treat amblyopia after full
refractive correction. Even microtropia is reported
to disappear following energetic occlusion
therapy. In patients showing recurrence, parttime occlusion should be continued for a long
time.
2. Older children or adults with microtropia
need not be treated, since they have comfortable
and nearly normal binocular vision with good
peripheral fusional amplitude.
Fig. 10.8 Microtropia with identity: (A) Eyes appear straight and both eyes take up fixation; the right esotropic eye has
parafoveal fixation due to central scotoma; (B) on cover test, right eye continues to fixate with the same parafoveal point
and thus there occurs no fixation movement.
250 Theory and Practice of Squint and Orthoptics
NYSTAGMUS BLOCKAGE SYNDROME
Definition and etiology
The term 'nystagmus blockage syndrome' has
been suggested for the occurrence of esotropia
in a child with congenital nystagmus. It has been
reported that in a bid to dampen the nystagmus,
there occurs adduction or excessive convergence
which results in esotropia. Others believe that
nystagmus is not the sole cause of esotropia.
Such patients usually have a static angle
infantile esotropia unrelated to nystagmus on
which is superadded a dynamic angle due to
convergence for dampening nystagmus.
Clinical features
1. Esotropia. Nystagmus blockage syndrome is
characterized in its acute form by an esotropia
of early onset with a variable angle, changing
from orthotropia with manifest nystagmus during
periods of visual inattention to esotropia without
nystagmus during visual attention. Eventually
esotropia may become constant.
2. Nystagmus intensity is inversely proportional
to the angle of deviation. Nystagmus appears
as the fixing eye moves from adduction to
abduction. This is an important distinguishing
feature from infantile esotropia with associated
latent nystagmus which lacks inverse relationship.
3. Pseudoparalysis of both lateral recti results due
to maintaining the eyes in a position of
convergence. It can be differentiated from a true
paresis of lateral recti by means of the Doll's
head manoeuvre (see page 232).
4. Fixation occurs with the adducting eye.
5. Head turn may exist towards the side of
fixating eye. When one eye is covered, a face turn
in the direction of the uncovered eye may be
demonstrated. A periodic shifting of the head
from side to side may be observed in the
presence of alternate fixation.
6. Visual acuity is increased with adduction due
to dampening of nystagmus. Therefore, best
visual acuity is at near fixation.
Treatment
Treatment is surgical but unsatisfactory.
1. In the presence of a face turn, a recession of the
medial rectus combined with Faden operation
and a resection of the lateral rectus of the
adducting eye should be performed. This
procedure will relieve the face turn and also
correct esotropia.
2. In the absence of face turn, a bilateral medial
rectus recession with Faden operation should
be preferred.
CYCLIC ESOTROPIA
It is rare but fascinating form of esotropia
characterized by a strabismic and a nonstrabismic phase of 24 hours each. This 48 hour
cycle is encountered most commonly, but
72 hours and 96 hours cycles have also been
reported in the literature.
Onset. Cyclic esotropia can be acquired at
virtually any age but most frequently occurs
between 2 and 6 years of age.
Cyclic nature of strabismus may last from
4 months to several years, after which the cycle
breaks and esotropia becomes constant.
Clinical features
1. During strabismic phase (24 hours)
• Deviation is usually large, 40 to 70, and is
consistent on subsequent examinations.
• Suppression occurs in deviated eye, so usually
there is no history of amblyopia.
• Fusional amplitudes are defective or absent.
2. During non-strabismic phase (next 24 hours)
• Deviation. There is no manifest deviation,
however, esophoria may be present.
• Fusion and stereopsis are both normal.
Treatment
• Surgery in the form of either bilateral medial
rectus recessions or recession of the medial
rectus and resection of the lateral rectus
constitutes the treatment.
• Amount of muscle surgery is based on the
degree of deviation during strabismic phase.
• No overcorrection is seen on alternate days,
as is expected.
DIVERGENCE PARESIS
It is a poorly understood condition characterized
by comitant esodeviation present at distance
Concomitant Esotropias and Exotropias
251
fixation in patients having normal ductions and
versions.
Etiology
1. Idiopathic. Etiology is not known in many
cases. These cases are usually self-limiting.
2. Neurological disorders may be associated in
some cases, so neurologic consultation is
indicated for all such cases. A few reported
causes include tabes, encephalitis, disseminated
sclerosis, poliomyelitis, influenza, pontine
tumour, increased intracranial pressure, trauma,
and Arnold-Chiari syndrome.
Clinical features
1. Diplopia. There is history of sudden onset of
uncrossed diplopia at distance fixation. When
an object is brought near to the patient, the
images become closer, and patient fuses them
at 25–50 cm.
2. Deviation. Esotropia is usually more for
distance with a near-distance disparity of 15
PD. The angle of esotropia remains unchanged
or may decrease on lateroversion.
3. Abduction and versions are completely
normal bilaterally.
4. Field of fixation is unrestricted.
Differential diagnosis
1. Sixth nerve palsy. The condition is differen-
tiated from either unilateral or bilateral sixth
nerve palsy by the fact that in divergence
paresis, the deviation is equal in both right and
left lateral gaze and that abduction is completely
normal bilaterally.
2. Convergence spasm. Occasionally, divergence
paralysis may be confused with convergence
spasm, since in both the conditions patient
presents with uncrossed diplopia at distance
fixation. However, presence of unimpaired
fusional divergence and decreased visual acuity
for distance are diagnostic features of
convergence spasm. Further, the esotropia will
be more for near (15 PD) than distance.
Treatment
Note. Neuroimaging studies, as well as
neurologic consultation are indicated to rule out
possible neurologic disease.
1. Prismotherapy. Since in most of the cases,
divergence paralysis is self-limiting and
disappears within 5–6 months, so base-out prisms
may provide adequate relief from diplopia. The
minimum power that gives the patient
comfortable single vision at distance fixation
should be used and should be decreased
periodically as the deviation improves.
2. Surgery. If the condition does not disappear
within 6 months, resection of both lateral rectus
muscles should be considered.
SENSORY ESOTROPIA
DEFINITION
It refers to the esotropia which develops due to
poor visual function in one eye in the childhood.
ETIOPATHOGENESIS
Sensory esotropia results from monocular lesions
(from infancy to childhood) which either prevent
the development of normal binocular vision or
interfere with its maintenance. Examples of such
lesions are: Congenital or acquired cataracts,
paediatric aphakia, corneal opacities, anisometropia, optic atrophy, retinoblastoma, macular
lesions, severe congenital ptosis and so on.
It has been reported that if the loss of vision
in one eye occurs in the first few months of life,
there may occur sensory esotropia or exotropia;
and after that till childhood, usually there occurs
sensory esotropia. Occurrence of poor vision in
adulthood due to any reason tends to cause a
sensory exotropia. However, Sidikaro and von
Noorden have reported that up to 5 years of age,
there are almost equal chances of getting sensory
esotropia and sensory exotropia; and after
5 years definitely there are more chances of
developing sensory exotropia.
Mechanism of sensory heterotropia. The exact
mechanism of development of sensory heterotropia is not known; however, following views
have been put forward:
1. Chavasse's theory. He reported that possibly
strong tonic convergence during childhood and
perhaps the diminishing tonic convergence with
age contribute to the direction of sensory
heterotropia.
2. Bielschowsky's theory. He explained the
increased incidence of sensory exotropia with
252 Theory and Practice of Squint and Orthoptics
advancing age as a gradual change of topographic anatomic orbital factors in adolescence,
favouring divergence rather than convergence.
This explanation is difficult to reconcile with the
observation by Mann that the orbital axes
actually converge rather than diverge.
3. Worth's theory. Worth speculated that the
direction of a sensory heterotropia is determined
by the refractive error of the sound eye; that is,
the blind eye will diverge, if the sound eye is
myopic, and will converge, if the sound eye is
hypermetropic. However, this view has not been
supported by other workers. Sidikaro and von
Noorden have reported an equal distribution of
refractive errors in patients with sensory squint.
4. Spielmann's theory. He reported that there is
a frequent association between monocular vision
loss, esotropia and manifest latent nystagmus. He
suggested that these signs together with
optometeric asymmetry are manifestations of
optokinetic immaturity occurring from lack of
normal binocular inputs during early infancy.
From the above discussions, it is quite clear that
still the mechanism of sensory esotropia is illusive.
CLINICAL FEATURES
1. Monocular visual loss due to any cause is
always associated.
2. Deviation. Sensory esotropia is always
comitant. However, limitation of abduction due
to contracture of medial rectus or conjunctiva
or both may occur in long-standing cases.
Vertical deviation due to overaction of inferior
oblique muscle is a frequent association.
3. Amblyopia may be superimposed over the
originally caused organic visual loss.
TREATMENT
• Surgical treatment is usually required to improve
cosmetic appearance, since visual loss is due
to some intractable organic lesion. However,
in all such cases, the refractive error and
accommodational status of the straight eye
needs to be evaluated before contemplating
cosmetic surgery.
• In children with sensory esotropia due to un-
corrected aphakia or traumatic cataract,
functional results may be obtained sometimes.
In these cases, cataract surgery, treatment of
aphakia and occlusion therapy for amblyopia
should be tried first, followed eventually by
squint surgery.
• Medial rectus recession with or without lateral
rectus resection depending upon the size of
deviation. Should always be performed on the
eye with poor vision. Inferior oblique weakening should be performed for associated
overaction of this muscle.
• Patients should always be informed that an
esotropia may recur or a consecutive exotropia
may develop years after.
CONSECUTIVE ESOTROPIA
Consecutive esotropia refers to occurrence of
esotropia in an eye which was previously
exotropic. It has been reported to occur under
following two clinical situations:
1. Surgical overcorrection of exotropia, is the
cause of consecutive esotropia in almost all the
cases. Its management has been discussed in
detail on page 261.
2. Spontaneous consecutive esotropia, i.e.
change of exotropia into esotropia without any
exogenous mechanical factor or an acquired
paralysis of lateral rectus muscle is an extremely
rare condition. Hardly any such case has been
reported in the literature.
CONCOMITANT EXOTROPIAS
Concomitant exotropia is the term used to
describe any manifest divergent deviation of the
visual axes in which the amount of deviation in
the squinting eye remains constant (unaltered)
in all the positions of gaze and there is no
associated limitation of ocular movements.
Concomitant exotropia may be divided into
four types:
• Congenital (infantile) exotropia
• Primary exotropia
• Sensory exotropia
• Consecutive exotropia
CONGENITAL (INFANTILE) EXOTROPIA
Congenital (infantile) exotropia is an extremely
rare condition.
Systemic associations. It is reported to occur in
patient with:
• Craniofacial anomalies,
Concomitant Esotropias and Exotropias
253
• Ocular albinism, and
• Cerebral palsy
• Prematurity
Characteristic features of congenital exotropia
include:
• Onset, usually before 6 months of age
• Large angle constant exodeviation mostly more
than 35 PD. Equal at distance and near
• Fusion, prospectives are poor
• Amblyopia, incidence is much higher than
intermittent exotropia
• Patterns. V-pattern more common than A-
pattern
• Associations include dissociated vertical
deviation (DVD), primary inferior oblique
overaction (IOOA). Rarely superior oblique
overaction (SOOA) is also reported.
Differential diagnosis. Congenital exotropia needs
to be differentiated from variable small-angle
exodeviation seen in 70% of normal newborn
infants, which is a transient exodeviation and
resolves by 2 to 4 months of age.
Treatment consists of:
• Amblyopia therapy to be started at the earliest.
• Surgical treatment in the form of bilateral lateral
rectus recession should be performed after
6 months of age, usually before the age of
24 months.
PRIMARY EXOTROPIA
Primary exodeviation is an idiopathic condition
in which the deviation is the essential feature,
in contrast to other types in which divergence
occurs as a result of certain obstacles in the
development or maintenance of binocular single
vision or due to defective action of the extraocular muscles.
ETIOLOGY
Etiology of primary exotropia is speculative.
Following factors have been implicated:
Predisposing factors
1. Mechanical factors, which have been
implicated to predispose a person for development of exotropia include:
• Shape and axes of the orbit,
• Interpupillary distance,
• Size of the eyeball,
• Mechanical properties of the conjunctiva or
Tenon's capsule and
• Extraocular muscle characteristics.
2. Innervational factors perhaps have been
thought to play more important role than the
mechanical factors in development of primary
exotropia. Duane hypothesized that primary
exotropias are caused by an innervational
imbalance that upsets the reciprocal relationship
between active convergence and divergence
mechanism. He suggested that exodeviation is
caused either by hypertonicity of divergence or
convergence insufficiency or both.
Precipitating factors
Precipitating factors which cause decompensation of exophoria to intermittent exotropia
include bright light, fatigue, ill health and day
dreaming.
Stages of development of exodeviation
In general, development of an exodeviation has
got three stages:
1. Stage of latent exodeviation. In this stage,
exodeviation is kept latent by the control of
fusional convergence reserve. It is also called as
stage of exophoria. It has been described in detail
on page 220.
2. Stage of intermittent exotropia. In this stage,
the fusional convergence reserves which usually
keep the deviation latent, become inadequate
intermittently resulting in intermittent manifest
exodeviation (intermittent exotropia).
3. Stage of constant exodeviation. When the
fusional convergence amplitude becomes
inadequate to maintain the latency of deviation,
a permanent manifest exodeviation, i.e. constant
exotropia occurs. Constant exotropia may be
unilateral or alternating.
CLASSIFICATION
I. In terms of the state of fusion, the exodeviations can be classified into:
• Exophoria (see page 221),
• Intermittent exotropia, and
• Constant exotropia (unilateral or alternating)
II. Duane's classification. It is based on the
assumption that divergence is an active process
254 Theory and Practice of Squint and Orthoptics
rather than relaxation of the convergence with
a return of the eyes to parallelism or a
divergence position by mechanical or elastic
forces. In Duane's classification, the primary
comitant exodeviations (which include
exophoria, intermittent exotropia and constant
exotropia) are further subdivided as follows:
1. Basic exodeviation. Exodeviation is equal at
distance and at near, i.e. within 10PO of each
other. It is thought to be associated with both
divergence excess and convergence insufficiency.
Therefore, it is also called mixed type exodeviation.
2. Divergence excess type. The exodeviation is
at least 10 greater at distance than at near even
after performing the patch test.
Note: Most of the patients with true divergence
excess type exotropia have high AC/A ratio, and
such patients are prone to postoperative
overcorrection, if the distance measurement is
used as the target angle.
3. Pseudodivergence excess type. Apparently,
the exodeviation appears to be greater at
distance than at near (e.g. XT 25D at distance
and 10D at near). However, with special tests
such as the patch for 30 minutes, the pattern is
shown to be basic type. (e.g. 25D at distance,
25D at near).
This occurs because patients with pseudodivergence excess have increased tonic fusional
convergence, which acts more at near. The
prolonged monocular patching dissipates tonic
Table 10.2 Phases of exodeviations and clinical
presentations
Clinical presentation
Phase Deviation Deviation Other features
at distance at near
I Exophoria Orthophoria Asymptomatic
goes undetected
II Intermittent Orthophoria Symptomatic
exotropia or exophoria for distance (no
suppression
scotoma)
III Exotropia Exophoria or Binocular vision
intermittent for near, suppressexotropia ion, scotoma for
distance
IV Exotropia Exotropia No binocular
single vision
fusional convergence, thereby disclosing the full
latent deviation. Short period of monocular
occlusion that occur with alternate cover test is not
enough to break the tonic fusional convergence.
4. Convergence insufficiency type. The exo-
deviation is at least 15 greater at near than at
distance.
These four varieties of primary exodeviation
must not be considered as being in 'water-tight'
compartments.
III. Phases of divergence excess type of
exodeviation: Calhounz et al. have described
four phases of divergence excess type of
exodeviation (Table 10.2).
IV. Kushner’s classification of intermittent
exotropia is depicited in Table 10.3.
Table 10.3 Kushner's classification of intermittent exotropia
Type Definition
Basic Distance and near measurements are equal
Tenacious proximal fusion Distance measurement initially exceeds near, but the near
measurement increases after 30–60 minutes of monocular occlusion
High AC/A ratio Distance measurement exceeds near measurement, even after 60
minutes of monocular occlusion and a high AC/A ratio is present
Proximal convergence Distance measurement exceeds near measurement, even after 60
minutes of monocular occlusion. AC/A ratio is normal
Low AC/A ration Near measurement exceeds distance measurement. A low AC/A
ratio is demonstrated
Fusional convergence insufficency Near measurement exceeds distance measurement. Patient has
poor fusional convergence amplitudes
Pseudoconvergence insufficiency Near measurement exceeds distance measurement, but distance
measurement increases with 60 minutes of monocular occlusion.
AC/A = Accommodative convergence/accommodation
Concomitant Esotropias and Exotropias
255
INTERMITTENT EXOTROPIA
Intermittent exotropia occurs much more
frequently than constant exotropia. It comprises
between 70% and 90% of all exotropias.
As discussed earlier, intermittent exotropia is
usually preceded by a stage of exophoria. In
intermittent exotropia, the deviation becomes
manifest intermittentely when the fusional
convergence fails to control the deviation.
Clinical features
1. Time of onset. The onset of intermittent
exotropia is usually in early childhood. About
50% of the children develop intermittent
exodeviation before 6 months of age and nearly
70% develop within first two years of life. Some
begin at birth or shortly thereafter. Only a few
develop the exotropia after 5 years of age.
2. Sex distribution. Exodeviations are more
common in females (70.0%) than males (30.0%).
The exact reason for female preponderance is
not known, possibly there might be some genetic
factor.
3. Refractive errors. Earlier reports suggested
that myopia was more common in exotropia.
However, recent view is that distribution of
refractive errors in exotropes resembles that in
the orthotropes and that there is no role of
underlying refractive errors in the etiology of
primary exotropia.
4. Precipitating factors. The heterotropic phase
of intermittent exotropia most commonly occurs
under conditions of fatigue, ill-health, bright
light, day dreaming, drowsiness or visual
inattention.
5. Symptoms are as follows:
i. Transient diplopia may be experienced in the
beginning. However, suppression and later
anomalous retinal correspondence (ARC) develop
quickly to protect the patient from diplopia.
ii. Closing of one eye in bright light, conventionally
referred to as photophobia is a conspicuous
symptom of intermittent exotropia. The usual
history is that child closes one eye in bright light.
No convincing explanation is available in the
literature for this phenomenon. Recent view is
that, perhaps, the bright light adversely affects
the amplitude of fusional convergence in
patients who maintain a delicate balance
between exophoria and intermittent exotropia,
causing them to close one eye.
iii. Asthenopic symptoms may occur in the initial
phases, when fusion begins to succumb and the
eyes deviate momentarily from the orthoposition. Patient may experience eye strain,
blurring, headache, difficulty with prolonged
periods of reading and other asthenopic
symptoms. However, soon the children become
asymptomatic due to development of sensory
adaptation. While adult patients with intermittent exotropia commonly have symptoms of
decompensated exophoria.
iv. Micropsia is a comparatively less known
symptom of intermittent exodeviation. It is
explained to occur owing to use of accommodative convergence to control the exodeviation.
6. Deviation. At first, the deviation is typically
manifest only at distance. With increasing age,
the deviation progresses and there occurs an
increase in the duration and frequency of the
tropia phase. Ultimately, a manifest deviation
appears at near also (Tables 10.2 and 10.3).
Factors that may influence progression are:
• Decline in tonic convergence with increasing
age,
• Gradual lessening of accommodative power,
• Development of suppression, and
• An increase in the divergence of the orbits
with advancing age.
Associations
Intermittent exotropia may be associated with:
• A–V-pattern (common)
• Comitant vertical deviation
• Dissociated vertical deviation
• Incomitant vertical deviation
Sensory adaptations
• Suppression and anomalous retinal corres-
pondence develop quickly to protect the
patient from diplopia during exotropic phase.
• During non-strabismic phase, normal retinal
correspondence is present.
• Deep amblyopia with eccentric fixation is a
rare finding in exotropia.
Clinical evaluation
Detailed clinical evaluation should be carried
out on the general lines (see page 108). However,