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216 Theory and Practice of Squint and Orthoptics
correction of deviation. Though, in clinical
practice, paradoxical diplopia is a fleeting
phenomenon limited to the immediate
postoperative period, which usually disappears
after a few days or weeks of surgery. However,
rarely it can persist long and may make the
patient's life miserable.
Monocular diplopia
Monocular diplopia is a condition which
sometimes occurs in patients with ARC, when
an object stimulating a retinal area is projected
in two different visual directions, i.e. the normal
one and the abnormal one. Under binocular
viewing, the patient may have binocular
triplopia. In rare cases, binocular triplopia
occurs spontaneously, but just like paradoxical
diplopia, binocular triplopia can frequently be
provoked instrumentally, e.g. by appropriate
stimulation with synoptophore.
Postoperative changes in correspondence
Now most of the workers believe that in ARC
there occurs point-to-area correspondence, i.e.
numerous retinal elements in the deviating eye
can apparently be coupled with a single retinal
element in the deviating eye. Thus, with the
change in the angle of deviating eye, the retinal
point of the non-deviating eye starts corresponding with some other retinal point of the
deviating eye. Thus, the angle of anomaly may
adapt to considerable variations in the angle
of strabismus. Disappearance of ARC after
surgical correction of strabismus has been
explained on the same basis. Following three
stages have been postulated for the occurrence
of changes in ARC after surgical correction of
strabismus:
1. Stage of ARC (continues for some time).
2. Stage of rivalry between normal and anomalous
correspondence (sometimes patient may
complain of monocular diplopia during this
stage).
3. Stage of normal correspondence (develops in
favourable cases). It has also been reported
that all patients may not develop NRC after
surgical correction of strabismus.
Factors which influence the postoperative changes
in correspondence are as follows:
• Age of the patient at the time of operation.
• Depth of ARC.
• Use of the eyes made by the patient.
• Individual adaptability.
TESTS FOR ARC
See page 137.
MANAGEMENT OF ARC
The important points to be noted are:
• Great emphasis used to be laid on the treatment of
ARC in the past before the surgical treatment of
strabismus. However, according to the current
views, orthoptic treatment for ARC in patients
with strabismus is not required.
• Treatment modalities used for ARC in the past
(now of historical interest only) included:
Occlusion therapy, prismatic overcorrection
of the ocular deviation and use of major
amblyoscope for retinal stimulation (retinal
massage).
• Presently, it is believed that the most effective
treatment for terminating ARC, is surgical
realignment of the eyes.
• A small-angle, cosmetically inconspicuous
residual strabismus with ARC is now
considered an acceptable or even desirable end
stage of therapy in infantile esotropia.
MOTOR ADAPTATIONS
As discussed above, suppression and ARC are
the sensory adaptations which help the
strabismus patients to deal with annoying
diplopia and/or confusion. These mechanisms
are available only to the visually immature
children who acquire strabismus after developing singular binocular vision. The older,
visually mature patients, have no capacity to
develop sensory adaptations. However, these
patients may deal with the confusion and/or
diplopia by developing motor adaptations,
which include:
• Control of ocular deviation by an alteration
in tone of extraocular muscle,
• Compensatory head posture,
217Adaptations to Strabismus and Amblyopia
• Blind spot syndrome, and
• Blind spot mechanism.
CONTROL OF OCULAR DEVIATION BY
AN ALTERATION OF TONE OF
THE EXTRAOCULAR MUSCLES
Occasionally, a small degree of ocular deviation
may be controlled by an alteration of tone of
extraocular muscles, which may be of the nature
of an active contraction or an active relaxation.
The alterations in the extraocular muscles are
induced by the compelling influence of the fusion
reflexes so that there is a disappearance of the
squint and a consequent absence of any diplopia
or confusion. In this way, a manifest deviation is
converted into a latent one. The success of such
an adaptation, however, may be frustrated to
some extent by an inadequacy of the fusional
reserves, so that the deviation is controlled only
at the expense of significant discomfort.
However, sometimes this adaptation permits a
satisfactory degree of functional control.
COMPENSATORY HEAD POSTURE
Compensatory head posture is a common motor
adaptation used by visually mature patients to
deal with the diplopia and/or confusion. It
occurs under following circumstances:
1. Paralytic strabismus is a particularly
common situation in which compensatory head
posture is used to achieve fusion of the images
seen by the two eyes. For details see page 303.
2. A- and V-pattern strabismus may also be
associated with an abnormal head posture.
• Chin is depressed in A-pattern exotropia and
V-pattern esotropia.
• Chin is elevated in A-pattern esotropia and V-
pattern exotropia.
3. Nystagmus patients may place their head in
such a way that the eyes are positioned in the
null zone, thereby improving binocular visual
acuity.
divergence to regain foveal fixation. In this
condition, a motor response tends to move the
eye further to the esotropic side, projecting the
image seen by the deviating eye on to the blind
spot (optic disc) (Fig. 8.17).
Characteristics of blind spot syndrome
• Esotropia of 12° to 18° (25 to 35).
• Good visual acuity in each eye.
• Normal retinal correspondence (NRC).
• No suppression other than the fovea of the
deviated eye.
• Normal fusional vergences.
• Diplopia is elicited, when the deviation is
prismatically reduced.
• Occasional diplopia and/or confusion in
casual seeing. Transitory diplopia is most
commonly noted, when approaching car
lights are seen at night.
• Good fusion potentialities demonstrated on
haploscopic devices.
BLIND SPOT MECHANISM
The blind spot mechanism is a coincidental type
of esotropia in which the image of the fixated
object falls on the blind spot (optic disc) of the
deviated eye (Fig. 8.17).
BLIND SPOT SYNDROME
The blind spot syndrome is a motor adaptation
to cope up with the diplopia and/or confusion
in patients with esotropia. It occurs, when the
esotropia is of small to moderate degree with
annoying diplopia and without sufficient
Fig. 8.17 Blind spot syndrome or mechanism. Note, image
in the right esotropic eye is formed on the optic disc.
218 Theory and Practice of Squint and Orthoptics
Characteristics of blind spot mechanism
• Amblyopia of the non-dominant eye
• Abnormal retinal correspondence
• Deep suppression
• ARC and suppression may coexist
Presence of the above abnormal sensory
findings makes the differential diagnosis
between the blind spot syndrome and blind spot
mechanism.
PSYCHOLOGICAL ADAPTATION
IGNORING
Ignoring is a psychological adaptation which is
learnt by some visually mature patients to deal
with the annoying diplopia. It probably falls
somewhere between conscious and unconscious
thought. All patients cannot learn to ignore
diplopia. Further, it has also been reported that
the patients with excellent acuity in each eye
may be able to ignore the weaker image while
the patients with poor vision cannot. How this
occurs is not known exactly. Perhaps the
individual's psychologic factors play an
important role in the development of rare
phenomenon of ignoring.
BIBLIOGRAPHY
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amblyopia Invest Ophthalmol Vis. Sci. 26:88,
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3. Bagolini B. Presentazione di una sbarra di filtri
a densita scalare assorbenti i raggi luminosi
Boll Ocul 36:638, 1957.
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23:346, 1967.
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7. Baker, FH, Grigg, P and Noorden, GK von:
Effects of visual deprivation and strabismus on
the response of neurons in the visual cortex of
the monkey, including studies on the striate
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Res. 66: 185, 1974.
8. Bielschowsky A: Lectures on motor anomalies,
V Development and causes of strabismus. Am
J Ophthalmol. 22:38, 1939.
9. Boeder, P: Anomalous retinal correspondence
refuted. Am J Ophthalmol 58:366, 1964.
10. Bradley, A, and Freeman, RD: Is reduced vernier
acuity in amblyopia due to position, contrast,
or fixation deficits. Vision Res. 25:55, 1985.
11. Burian, HM: Sensorial retinal relationship in
concomitant strabismus. Trans Am Ophthalmol
Soc. 81: 373, 1945.
12. Burian, HM: Normal and anomalous correspondence. In Allen, JH, editor: Strabismus
ophthalmic symposium I, St. Louis, 1950,
Mosby-Year Book, Inc., p130.
13. Burian, HM: Anomalous retinal correspondence:
Its essence and its significance in diagnosis and
treatment. Am J Ophthalmol 34:237, 1951.
14. Burian, HM: Adaptive mechanisms. Trans Am
Acad Ophthalmol Otolaryngol 57:131, 1953.
15. Burian, HM: Thoughts on the nature of
amblyopia exanopsia. Am Orthopt J 6:5, 1956.
16. Burian, HM: The behavior of the amblyopic eye
under reduced illumination and the theory of
functional amblyopia. Doc Ophthalmol 23: 189,
1967.
17. Burian, HM, and Cortimiglia, RA: Visual acuity
and fixation pattern in patients with strabismic
amblyopia. Am Orthopt J 12:169, 1962.
18. Cantolino SJ: and Noorden. GK von: Heredity
in microtropia. Arch Ophthalmol 81:753, 1969.
19. Capobianco, NM: The subjective measurement
of the near point of convergence and its significance in the diagnosis of convergence insufficiency. Am Orthopt J 2:40, 1952.
20. Chavasse, BF: Worth's squint or the binocular
reflexes and the treatment of strabismus,
Philadelphia, 1939 P Blakiston's Son & Co. Inc.
21. Crawford MLJ, visual deprivation syndrome.
Ophthalmology (Rochestter 85: 465, 1978.
22. Firth, AY: Pupillary responses in amblyopia. Br
J Ophthalmol 74:676, 1990.
23. Garey L, Blakemore C: Monocular deprivation:
Morphological effects on different classes of
neurons in the lateral geniculate nucleus. Science
195:414, 1977.
24. Grunwald MJ, Parks MM: Amblyopia. In
Tasman W, Jaeger EA (eds): Duane's clinical
Ophthalmology, Philadephia, JB Lippincott
1990, VPI Ch. 101 pp 1-22.
219Adaptations to Strabismus and Amblyopia
25. Hielschowsky, A: Application of the afterimage
test in the investigation of squint. Am J
Ophthalmol 20:408, 1937.
26. Hubel, DN, and Wiesel, TN: Receptive fields,
binocular interaction and functional architecture
in the cat's visual cortex. J Physiol (Lond.)
160:106, 1962
27. Hubel, DH, and Wiesel,TN: Receptive fields of
single neurons in the cat's striate cortex. J
Physiol 148:574, 1959
28. Hubel, DH, and Wiesel, TN: Stereoscopic vision
in macaque monkey, cells sensitive to binocular
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Nature 225:41, 1970
29. Jampolsky, A: Characteristics of suppression in
strabismus. Arch Ophthalmol 54:683. 1955.
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screening. J Pediatr Ophthalmol 1:30, 1964.
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fixation. Doc Ophthalmol. 23:263, 1967.
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Trans. Am. Ophthalmol. Soc. 67:698, 1969.
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2020 Nov;68(11):2462–2465.
220 Theory and Practice of Squint and Orthoptics
9
Heterophoria
HETEROPHORIA
Definition
Etiology
Types
Esophoria
•
Exophoria
•
Hyperphoria
•
Cyclophoria
•
HETEROPHORIA
DEFINITION
Heterophoria, also known as 'latent strabismus',
is a condition wherein the tendency of the eyes
to deviate is kept latent by the fusion reflex.
However, when the fusion is interrupted, for
example, by occluding one eye, the visual axis
of the occluded eye deviates from its position
and if the occluder is removed, the fusion reflex
will turn the eye back into the orthoposition.
While, orthophoria is a condition of perfect
alignment of the two eyes which is maintained
even after the removal of influence of fusion.
However, orthophoria is just a theoretical ideal.
Practically, a small amount of heterophoria is
of universal occurrence and is known as
'physiological heterophoria'. The incidence of
distance heterophoria in primary position has
been reported to be as high as 80% and that for
near phorias close to 100%. When tested in
different directions of gaze, almost everyone is
found to have small degree of heterophoria.
ETIOLOGY
In general, the factors which play role in the
etiology of heterophoria are the same as for
heterotropia. For details see page 104.
Symptoms
Compensated heterophoria
•
Decompensated heterophoria
•
Evaluation
Treatment
Indications of treatment
•
Choice of treatment
•
Treatment modalities
•
TYPES OF HETEROPHORIA
Depending upon the direction of deviation,
heterophoria may be:
• Esophoria
• Exophoria
• Hyperphoria, and
• Cyclophoria.
ESOPHORIA
In this condition, when fusion is interrupted,
the non-fixating eye becomes convergent,
i.e. deviates nasally. Esophoria is less frequent
than exophoria. Only about 33% of all patients
with a distance phoria are esophoric. Near
esophorias occur even less frequently.
Clinical types
Esophoria may be:
1. Convergence excess type. Esophoria is greater
on near fixation than on distant fixation.
2. Divergence weakness type. Esophoria is greater
on distant fixation than on near fixation.
3. Non-specific type. Esophoria which does
not vary significantly in degree for any
distance.
Heterophoria
221
Etiology (Causes)
Esophoria can have various underlying causes,
including:
• Refractive errors: Uncorrected or improperly
corrected nearsightedness (myopia) or
farsightedness (hyperopia) can contribute to
esophoria.
• Muscle imbalance: Imbalances in the muscles
that control eye movement can lead to the
inward deviation of the eyes.
• Accommodative excess: Overuse of the focusing
mechanism of the eyes (accommodation) can
lead to eye strain and esophoria.
• Fatigue and stress: Prolonged visual tasks, such
as reading or using digital devices, can cause
eye muscles to fatigue, leading to temporary
esophoria.
• Medical conditions: Certain medical conditions
like convergence insufficiency, convergence
excess, or neurological disorders can
contribute to esophoria.
Types
Common etiological types of esophoria are as
follows:
1. Accommodative esophoria. It may be
associated with:
a. Uncorrected high hypermetropia. In this condition, excessive use of accommodation in a bid to
clear the blurred retinal image is associated with
increased accommodative convergence. It may
result in esophoria for distance and near in
proportion to the accommodation used and the
patient's fusional divergence.
b. High AC/A ratio may be associated with
esophoria. Effect of AC/A ratio on basic
esophoria is depicted in Table 9.1.
2. Tonic esophoria. Most of the non-accomm-
odative esophorias are due to increased tonic
convergence which may be due to either overactivity or insufficient inhibition of the involved
centres of the central nervous system.
Table 9.1 Effect of AC/A ratio on basic esophoria
AC/A ratio Esophoria
Normal E
High E
Low E
1
slightly smaller than E
1
almost equal or greater
than E
1
smaller than E
3. Esophoria due to other causes includes those
due to anatomical and innervational factors.
EXOPHORIA
In this condition, the non-fixating eye becomes
divergent on dissociation, i.e. when fusion is
interrupted. However, under condition of
bifoveal single vision, the deviation is corrected
by the fusional convergence. Exophoria is the
commonest variety of heterophoria. It constitutes about 60% of all cases of heterophoria for
distance and about 80% of all cases of
heterophoria for near.
Etiology (Causes)
Exophoria can have various underlying causes,
including:
• Refractive errors: Uncorrected or improperly
corrected myopia (nearsightedness) or
hyperopia (farsightedness) can contribute to
exophoria.
• Muscle imbalance: Imbalances in the muscles
that control eye movement can lead to the
outward deviation of the eyes.
• Accommodative insufficiency: Weak or inefficient
focusing ability of the eyes (accommodation)
can contribute to exophoria.
• Fatigue and stress: Prolonged visual tasks, such
as reading or using digital devices, can cause
eye muscles to fatigue, leading to temporary
exophoria.
• Convergence insufficiency: Difficulty in bringing
the eyes together to focus on near objects can
result in exophoria.
• Medical conditions: Certain medical conditions
or neurological disorders can also be
associated with exophoria.
Types
Exophoria may be of following types:
1. Convergence weakness type. Exophoria is
greater on near fixation than on distant fixation.
In this condition, symptoms primarily occur
during close work. Such patients frequently
complain that during reading letters run
together. The blurring is due to accommodation
and occurs when fusional convergence becomes
insufficient to cope up with the deviation, e.g.
during prolonged close work.
222 Theory and Practice of Squint and Orthoptics
2. Divergence excess type. Exophoria is greater
on distant fixation than on near fixation. In such
patients, asthenopic symptoms occur during
activities connected with distant vision.
3. Non-specific type. This type of exophoria does
not vary significantly in degree for any distance.
Relation of near exophoria to
distance exophoria
The basic deviation in exophoria is measured
while the patient fixates a distant target using
his/her full optical correction and near exophoria
is measured, when patient fixates a target at
33 cm. The patient's AC/A ratio influences the
magnitude of near phoria (X') in relation to
distance phoria (X) as depicted in Table 9.2.
HYPERPHORIA
It is a vertical deviation occurring on dissociation in which one eye rotates upwards or the
other downwards depending upon the fixation.
In orthoptic practice, the term hypophoria is
avoided and it has become customary to use the
term right or left hyperphoria depending upon
the eye which remains up as compared to the
other. For example, in a right hyperphoria, the
right eye rotates upwards, when it is not fixating
and when the right eye is fixating, the left eye
rotates downwards, and reverse to it occurs in
left hyperphoria.
The incidence of hyperphoria has been
reported to be about 30%. Frequently, hyperphoria is combined with horizontal phorias.
Since vertical fusional vergences are of small
amplitude, asthenopic symptoms are more
marked in hyperphorias than the horizontal
phorias. For the same reason, even the minor
prismatic action of glasses (due to vertical
decentring) may be difficult to compensate.
A hyperphoria may be comitant or
incomitant. Paresis of an extraocular muscle and
anatomic anomalies of muscles and tendons
Table 9.2 Effect of AC/A ratio on near vs distance
exophoria
AC/A ratio Exophoria
Normal X
High X1 almost same or smaller
Low X
1
slightly greater than X
than X
1
greater than X
and/or their insertions constitute the major
causes of hyperphoria. Since, more frequently,
hyperphoria is incomitant, measurements
should be taken: (a) with either eye being the
fixating eye, (b) in the cardinal positions, and
(c) in the reading position. The latter is obviously
more important since a special therapeutic
solution has to be found, if the patient's
deviation in the reading position differs from
that in the primary position.
CYCLOPHORIA
It is the tendency of the either eye to wheel
rotate around the anteroposterior axis on
dissociation. When the 12 O'clock meridian of
cornea rotates nasally, it is called incyclophoria
and when it rotates temporally, it is called
excyclophoria. Excyclophoria is of more frequent
occurrence than the incyclophoria. In general,
cyclophorias of clinical significance are of rare
occurrence and are frequently associated with
vertical deviation. Asthenopic symptoms are
most marked with cyclophorias.
Etiology
Cyclophoria can have various underlying
causes, including:
• Muscle imbalance: Imbalances in the extraocular
muscles that control eye movements can lead
to the rotational misalignment.
• Neurological factors: Neurological conditions
affecting the control of eye movements can
contribute to cyclophoria.
• Trauma: Head injuries or trauma to the eye
area can affect the orientation of the eye and
lead to cyclophoria.
• Anatomical abnormalities: Structural differences
in the eye or orbit can result in cyclophoria.
SYMPTOMS OF HETEROPHORIA
Symptoms that may be caused by phorias are
of a very non-specific nature and they may also
occur for other reasons. In general, the term
asthenopia is used to denote the symptom
complex produced by heterophoria. As already
mentioned, asthenopia is most marked with
cyclophoria followed by hyperphoria. Small
degrees of esophoria and exophoria produce
little or no symptoms.
Heterophoria
223
Depending upon the symptoms, heterophoria
can be divided into compensated and decompensated.
Compensated heterophoria. It is associated with
no subjective symptoms. Compensation of the
phoria depends upon the reserve neuromuscular power to overcome the muscular
imbalance and individual's desire for maintenance
of binocular vision.
Decompensated heterophoria. It is associated
with multiple symptoms which may be grouped
as under:
1. Symptoms of muscular fatigue. These result
due to continuous use of the reserve neuromuscular power and are usually more marked
after the day's work. These include:
• Headache and eye ache after prolonged use of
eyes, which is relieved when the eyes are
closed for a while.
• Difficulty in changing the focus from near to
distant objects of fixation or vice versa.
• Photophobia, itching and burning may also be
experienced by some patients. Photophobia
due to muscular fatigue is not relieved by
using dark goggles, but is relieved by closing
one eye.
2. Symptoms due to failure to maintain
binocular vision. These include:
• Blurring or crowding of words while reading.
• Intermittent diplopia due to temporary manifest
deviation under conditions of fatigue.
• Intermittent squint (without diplopia) may
occur in patients who involuntarily learn to
suppress. It is usually noticed by the patient's
close relations or friends.
3. Symptoms of defective postural sensations
cause problems in judging distances and positions, especially of the moving objects. This
difficulty may be experienced particularly by
cricketers, tennis players and pilots during
landing.
EXAMINATION (EVALUATION) OF
A CASE OF HETEROPHORIA
It should include the following tests:
1. Testing of visual acuity and refraction. It is
of prime importance in management of
heterophoria.
2. Testing for ocular movements. Uniocular as
well as binocular movements should be tested
meticulously (see page 120).
3. Cover-uncover test. It is quite useful in
detecting the presence of a heterophoria. When
using an occluder to dissociate the eyes, the
fusion reflex innervation does not immediately
close completely covering one eye, although all
fusional stimuli are excluded by the cover.
Therefore, the cover should be kept in front of
the eye for a few moments before proceeding
with the test.
4. Measurement of heterophoria. A heterophoria should be measured for both distance
and near. To obtain the basic measurement of a
heterophoria, the patient should fixate a distant
target and should not accommodate. It is
necessary, therefore, that he/she wears full
optical distance correction. It should also be kept
in mind that lenses that are decentred before the
eye have a prismatic effect and that this may
obscure the true situation because the patient
has to overcome such an effect during binocular
vision through fusional vergence. Thus a phoria
may be simulated or depending on the direction
of prismatic displacement, an existing phoria
may be exaggerated or minimized, if lenses of
sufficient power are decentred to a significant
degree during the phoria test.
The near phoria should be measured at a
fixation distance of about 33 cm using a target
which requires accommodation rather than a
flashlight. In presbyopes, the near phoria should
be determined while they fixate through their
reading glasses.
Commonly employed tests to measure the heterophoria
are as follows:
Objective tests: Prism and cover test (see page 112)
Subjective tests include:
• Maddox rod test (see page 116)
• Maddox wing test (see page 118)
• Double prism test (see page 120)
5. Measurement of convergence, accommodation
and AC/A ratio. A knowledge about these para-
meters is quite useful in the management of
heterophoria.
6. Measurement of fusional reserve. It is
essential to examine the patient's fusional
224 Theory and Practice of Squint and Orthoptics
vergence amplitude to form a meaningful
opinion of the significance of his/her phoria.
During this examination, an excessive demand
is placed on the vergence mechanism. This may
induce a transient phoria in some patients.
Therefore, in clinical practice, the phoria should be
measured first and the vergence amplitude
determined afterward.
The power of the fusional vergence that
opposes and overcomes the phoria during
bifoveal vision is very important in planning the
treatment of phoria. The fusional vergence
available in excess of the amount necessary to
overcome the phoria and to bring the eyes into
orthoposition is called the fusional reserve or the
relative vergence. Though there does not exist
any relationship between the amount of fusional
reserve and degree of phoria producing
symptoms, but, in general, bifoveal vision is
comfortable, when the fusional reserve is twice
as large as the phoria.
7. Assessment of state of binocular vision. It is
also helpful in planning the management of a
heterophoria. For details of the various tests, see
page 89.
Neurological examination
If necessary, a neurological assessment may be
conducted to rule out any underlying
neurological conditions.
TREATMENT OF HETEROPHORIA
choice of a particular modality in a given patient
depends upon different factors, some of which
are as follows:
1. Age and cooperation of the patient, e.g. in a
small child, miotics may be used to facilitate
accommodation.
2. Etiology of heterophoria
• If a phoria is entirely or partly caused by a
refractive error, glasses will eliminate or
improve the condition.
• When a phoria is due to abnormal AC/A ratio,
orthoptic exercises to increase the fusional
amplitudes are the method of choice.
• Surgery is indicated in phorias of anatomic
or paretic origin for which other treatment
methods cannot be successful.
3. Size and type of heterophoria
• When the heterophoria is too large to be
controlled easily with other methods, surgery
will be necessary.
• When vertical phorias are associated with
horizontal phorias, an attempt should be
made to eliminate the vertical deviation first,
since in a number of instances, this will enable
the patient to control the horizontal phorias
with much less effort.
4. The speed of recovery to binocular single vision
on cover test. Symptomatic phorias with very
slow recovery require surgical treatment more
often than those with a quick recovery.
INDICATIONS OF TREATMENT
• In adults, treatment is indicated only if the
patient is suffering from symptoms. Sometimes it is difficult to decide whether or not
the asthenopic symptoms are due to the
phoria. In such cases, occlusion may be used
to diagnose. If this relieves the symptoms, it
is very likely that the phoria is the cause.
• In children, however, treatment is indicated, if
the phoria is showing a tendency to decompensate into a manifest deviation, whether
symptoms are present or not.
CHOICE OF TREATMENT
The treatment modalities employed in heterophoria includes, glasses, miotics, orthoptic
exercises, prismotherapy and surgery. The
TREATMENT MODALITIES
1. Optical correction
In all cases, a meticulous refraction should be
performed and correct glasses prescribed.
Optical correction may eliminate the underlying
cause of the phoria in some patients. General
guidelines for prescribing glasses are as
follows:
• Astigmatic errors and spherical differences
between the two eyes should be eliminated
completely.
• In exophoria, both eyes may be undercorrected
by an equal amount of spherical plus power.
This forces the patient to accommodate
constantly and accordingly induces accommodative convergence. However, it should be
Heterophoria
225
kept in mind that constant accommodation
itself may lead to eye strain.
• In esophoria, the patient should receive as
much spherical plus correction as is
compatible with his/her best visual acuity.
Bifocal glasses decrease or eliminate the need
for accommodation during near vision and
thus may be useful in patients having
esophoria of convergence excess type. Bifocals
should be used as a temporary aid to orthoptic
treatment aiming to reduce the bifocal
segment as soon as possible.
• In hyperphoria, if feasible, the lenses of the
patient's optical correction may be decentred
to achieve a prismatic effect thus relieving the
stress on patient's vertical vergence control.
• In cyclophoria, the best efforts should be made
to correct the astigmatic refractive error, when
associated.
2. Orthoptic treatment
Aim of orthoptic treatment of heterophoria is
to improve fusional reserves so that the bifoveal
single vision can be maintained without efforts.
Orthoptic treatment also known as ‘vision
therapy’ includes:
A. Conventional or non-computerised excercise for:
• In-office vision therapy, and
• Home vision therapy
B. Computerised orthoptic excercises for:
• In-office vision therapy, and
• Home vision therapy
Note: Conventional, i.e. non-computerised
excercises are described here. For computerised
exercises see page 153.
Orthoptic exercises for esophoria
In general, the orthoptic treatment of esophoria
is aimed at improving the amplitude of fusional
divergence (relative negative convergence). This
can be accomplished by the following exercises:
a. Divergence exercises with prisms. Prisms of
increasing strength are placed base-in before one
eye while he/she is fixating an object at any
distance (preferably at a distance where the
esophoria is maximum). Patient is trained to
maintain a single vision by relaxing the convergence.
Loose prisms, a prism bar or rotatory (Risley)
prisms may be used for this purpose. A prism
bar should be preferred. Prism exercises are
performed for a few minutes at each weekly
visit.
b. Divergence exercises on synoptophore. These
exercises are performed on synoptophore using
stereopsis slides, because they provide the
strongest stimulus to fusion. After fusing the two
pictures, patient is trained to maintain a single
vision (by relaxing convergence) while the
instrument tubes are diverged. These exercises
should be performed for about 5 minutes at each
weekly visit.
c. Physiologic diplopia exercises using
stereograms in the crossed position. To perform
this exercise, patient is first trained to appreciate
crossed physiological diplopia with a flash light
or pencil. Once the patient is trained, the exercise
is performed as below:
While the patient is fixating a distant object,
the stereogram card (Fig. 9.1) is held about 25 cm
in front of his/her eyes. Patient will perceive
four pictures (because of crossed physiological
diplopia). He/she is trained to adjust its position
until the two central pictures are fused
and patient perceives three pictures (Fig. 9.2).
Patient is trained to maintain the joined pictures
and to see it clearly. While doing so, patient is
converging for the distant target but
accommodating for near (distance of the card)
and thus relatively relaxing his/her
convergence.
Once the patient is trained to perform this
exercise, he/she can practice at home for a few
minutes several times a day.
d. Exercises using diploscope. For details see
page 149.
Fig. 9.1 Cat card stereogram.