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- •Preface to the Fourth Edition
- •Preface to the First Edition
- •Contents
- •Extraocular Muscles and Orbital Fascia
- •Anatomy of Third, Fourth and Sixth Cranial Nerves
- •Basic Kinematics
- •Mechanics of Actions of Extraocular Muscles
- •Ocular Movements
- •Agonist, Synergists, Antagonists and Yoke Muscles
- •Fundamental Laws Governing Ocular Motility
- •Components of Visual Acuity
- •Measurement of Visual Acuity
- •Contrast Sensitivity
- •4. Binocular Vision
- •Binocular Vision: Definition and Grades
- •Psychophysics and Sensory Aspects of Binocular Vision
- •Development of Binocular Vision
- •Binocular Vision Tests
- •Definition and Classification
- •Etiology of Strabismus: An Overview
- •Evaluation of a Case of Strabismus
- •Orthoptic Instruments
- •Computer-based Orthoptic Vision Therapy Programs and Instruments
- •Convergence
- •Divergence
- •Accommodation
- •Sensory Adaptations
- •Amblyopia
- •Motor Adaptations
- •9. Heterophoria
- •Concomitant Esotropias
- •Concomitant Exotropias
- •Vertical Strabismus
- •Cyclodeviations
- •12. Incomitant Strabismus
- •Paralytic Squint
- •Restrictive Ocular Motility Defects
- •Supranuclear Control of Eye Movements
- •Supranuclear Disorders of Eye Movements
- •14. Nystagmus and Related Oscillations
- •Nystagmus
- •Non-surgical Management
- •Surgical Management
- •Outlines of Strabismus Management
- •Index

176 Theory and Practice of Squint and Orthoptics
Fig. 7.7 Far point in emmetropic eye (A); hypermetropic
eye (B) and myopic eye (C).
see clearly at near point) – I/a (dioptric power
needed to see clearly at far point); i.e. A (at age
10) = 14 dioptres. Similarly, A at age 40 years =
(100/25 – I/a) = 4 dioptres; at age 45 years, A =
3 dioptres and at 50 years = 2 dioptres. Since,
we usually keep the book at about 25 cm, so we
can read comfortably up to the age of 40 years
and after that the near point recedes beyond the
normal reading or working range. This
condition of failing near vision due to related
decrease in the amplitude of accommodation or
increase in the near point (punctum proximum)
is called presbyopia.
ANOMALIES OF ACCOMMODATION
Anomalies of accommodation are not uncommon.
These include:
I. Deficient or decreased accommodation
1. Presbyopia (physiological deficiency of
accommodation).
2. Insufficiency of accommodation (pathological deficiency of accommodation).
3. Paralysis of accommodation
II. Excessive accommodation or spasm of accommo-
dation
Fig. 7.8 Decrease in the amplitude of accommodation
with age in human (from Duane A: Arch Ophthalmol 54:
566–587, 1925).
and about 50 cm at the age of 50 years. Therefore,
at the age of 10 years, amplitude of accommodation (A) = 100/7 (dioptric power needed to
INSUFFICIENCY OF ACCOMMODATION
The term insufficiency of accommodation is
used, when the accommodative power is
significantly less than the normal physiological
limits for the patient's age. Therefore, it should
not be confused with presbyopia in which the
physiological insufficieny of accommodation is
normal for the patient's age.
Causes
1. Premature sclerosis of lens.
2. Weakness of ciliary muscle due to systemic
causes of muscle fatigue such as debilitating
illness, anaemia, toxaemia, malnutrition,
diabetes mellitus, pregnancy stress and so on.
3. Weakness of ciliary muscle associated with
primary open angle glaucoma.
Clinical features
All the symptoms of presbyopia are present, but
those of asthenopia are more prominent than
those of blurring of vision.

177Anomalies of Convergence, Divergence and Accommodation
Treatment
1.The treatment is essentially that of the
systemic causes.
2.Near vision spectacles in the form of weakest
convex lens which allows adequate vision
should be given till the power of accommodation improves.
3.Accommodation exercises help in recovery, if the
underlying debility has passed.
PARALYSIS OF ACCOMMODATION
Paralysis of accommodation, also known as
cycloplegia, refers to complete absence of
accommodation.
Causes
1.Drug-induced cycloplegia results due to the
effect of atropine, homatropine or other
parasympatholytic drugs.
2.Internal ophthalmoplegia (paralysis of ciliary
muscle and sphincter pupillae) may result
from neuritis associated with diphtheria,
syphilis, diabetes, alcoholism, cerebral or
meningeal diseases.
3.Paralysis of accommodation as a component of
complete third nerve paralysis may occur due to
intracranial or orbital causes. The lesions may
be traumatic, inflammatory or neoplastic in
nature.
Clinical features
1.Blurring of near vision. It is the main complaint
in previously emmetropic or hypermetropic
patients. Blurring of near vision may not be
marked in myopic patients.
2.Photophobia (glare) due to accompanying
dilatation of pupil (mydriasis) is usually
associated with blurring of near vision.
3.Examination reveals, abnormal receding of
near point and markedly decreased range of
accommodation.
Treatment
1.Self-recovery occurs in drug-induced
paralysis and in diphtheric cases (once the
systemic disease is treated).
2. Dark glasses are effective in reducing the glare.
3.Convex lenses for near vision may be
prescribed, if the paralysis is permanent.
SPASM OF ACCOMMODATION
Spasm of accommodation refers to exertion of
abnormally excessive accommodation.
Causes
1.Drug-induced spasm of accommodation is
known to occur after the use of strong miotics
such as echothiophate and DEP.
2.Spontaneous spasm of accommodation is
occasionally found in children who attempt
to compensate for a refractive anomaly that
impairs their vision. It usually occurs, when
the eyes are used for excessive near work in
unfavourable circumstances such as bad
illumination, bad reading position, lowered
vitality, state of neurosis, mental stress or
anxiety.
Clinical features
1. Defective vision due to induced myopia.
2. Asthenopic symptoms are more marked than
the visual symptoms.
Diagnosis
Diagnosis is made with refraction under atropine.
Treatment
1. Relaxation of ciliary muscle by atropine for a
few weeks and prohibition of near work allow
prompt recovery from spasm of accommodation.
2.Correction of associated causative factors,
prevent recurrence.
BIBLIOGRAPHY
1. Convergence Insufficiency Treatment Trial
(CITT) Study, Group. “The convergence
insufficiency treatment trial: design, methods,
and baseline data.”. Ophthalmic epidemiology.
2008;15 (1): 24–36.
2. Cooper J, Duckman R. Convergence insufficiency:
incidence, diagnosis, and treatment. J Am Optom
Assoc 1978; 49:673-80.
3. Cooper J. Accommodative dysfunction. In: Amos
JF, ed. Diagnosis and management in vision
care. Boston: Butterworths, 1987:431–59.
4. Daum KM. Divergence excess: characteristics and
results of treatment with orthoptics. Ophthalmic
Physiol Opt 1984; 4:15–24.

178 Theory and Practice of Squint and Orthoptics
5. Duane A. Studies in monocular and binocolar
accommodation with their clinical applications.
Am J Ophthalmol 1922;5:865.
6. GK. Van Norden, “Anomalies of convergence
and divergence,” in Binocular Vision and Ocular
Motility, GK. Von Norden, Ed., Mosby, 4th
edition, 1990.
7. Goss, DA. Ocular accommodation, convergence,
and fixation disparity: a manual of clinical
analysis, 2nd ed. Newton, MA: ButterworthHeinemann, 1995:14.
8. MattiWestman; M. Johanna Liinamaa. “Relief of
asthenopic symptoms with orthoptic exercises
in convergence insufficiency is achieved in both
adults and children”. Journal of Optometry. 2012;5
(2). pp. 62–67.
9. Morgan MW Jr. Relationship between accommodation and convergence. AMA Arch Ophthalmol
1952;47:745–759.
10. Rutstein RP, Daum KM, Amos JF. Accommodative spasm: a review of 17 cases. J Am
OptomAssoc 1988; 59:527–38.
11. Scheiman M, Mitchell GL, Cotter S, Cooper J,
Kulp M, Rouse M, Borsting E, London R,
Wensveen J, Convergence Insufficiency
Treatment Trial Study Group (Jan 2005). “A
randomized clinical trial of treatments for
convergence insufficiency in children”. Arch
Ophthalmol. 123 (1): 14–24.
12. Scheiman M, Mitchell GL, Cotter S, Kulp MT,
Cooper J, Rouse M, Borsting E, London R,
Wensveen J. “A randomized clinical trial of
vision therapy/orthoptics versus pencil
pushups for the treatment of convergence
insufficiency in young adults”. Optom Vis Sci.
2005; 82 (7): 583–95.
13. Wilson ME, Saunders RA, Berland JE. Dissociated
horizontal deviation and accommodative
esotropia: treatment options when an eso- and
an exodeviation co-exist. Journal of Pediatric
Ophthalmology and Strabismus. 1995;32(4):228–
230.

Adaptations to
Strabismus and Amblyopia
8
INTRODUCTION
SENSORY ADAPTATIONS
Suppression
Physiological suppression
•
Pathological suppression
•
Mechanism and seat of suppression
•
Retinal areas of suppression
•
Tests for detection of suppression
•
Measurement of depth
•
Treatment
•
Monofixation syndrome
Definition and causes
•
Characteristic features
•
Amblyopia
Classification and terminology
•
Pathogenesis and pathophysiology
•
Clinical characteristics and
•
laboratory findings
Clinical evaluation and diagnosis
•
INTRODUCTION
When the visual functions are normally developed, the individual possesses a binocular
single vision, which implies a point-to-point
normal correspondence of two retinae with
foveas being the principal corresponding point.
With the occurrence of strabismus, the
alignment of the corresponding retinal points
is disturbed. Consequently, the fixation point is
imaged in the centre of the fovea of the nondeviating eye and some extrafoveal (peripheral
retinal) point in the deviated eye. This results
in diplopia and confusion.
• Diplopia occurs due to formation of image on
dissimilar points of the two retinae (Fig. 8.1) and
Prevention of amblyopia
•
Treatment of amblyopia
•
Abnormal retinal correspondence
General considerations
•
Harmonious versus unharmonious ARC
•
Development of ARC
•
ARC and suppression
•
• Quality of binocular vision of ARC
Clinical phenomena associated with ARC
•
Tests for ARC
•
Management of ARC
•
MOTOR ADAPTATIONS
Control of ocular deviation by an alteration of
•
the tone of extraocular muscles
Compensatory head posture
•
Blind spot syndrome
•
Blind spot mechanism
•
PSYCHOLOGIC ADAPTATION
Ignoring
•
• Confusion occurs due to formation of image of
two different objects on the corresponding
points of the two retinae (Fig. 8.2).
• To escape the disabling and troublesome situation
created by diplopia and confusion, the
strabismic patients (below the age of 7–9 years;
with immature visual system) develop certain
adaptations which allow them to have a
comfortable single vision. Older patients who
develop strabismus for the first time suffer
from diplopia and confusion for a long time
till they learn to ignore (psychological
adaptation).
Adaptations to strabismus. To avoid repetition,
adaptations to strabismus are being discussed

180 Theory and Practice of Squint and Orthoptics
• Suppression
• Anomalous retinal correspondence (ARC)
Note. Amblyopia, not actually a sensory
adaptation, may occur as a consequence of
suppression, and so is described in this chapter.
The term strabismic amblyopia is used for the
amblyopia seen in patients with unilateral
constant squint.
Motor adaptations
• Compensatory head posture
• Blind spot syndrome and mechanism
Psychological adaptations
• Ignoring
SENSORY ADAPTATIONS
Fig. 8.1 Diplopia due to formation of image on dissimilar
points of the two retinae.
Fig. 8.2 Confusion due to formation of image of two different
objects on the corresponding points of two retinae.
A sensory adaptation may be defined as the
manner in which a patient makes sensory
adjustments to an interruption in the normal
binocular single vision caused by the occurrence
of squint. In other words, sensory adaptations
are nature's way out of trouble but at the cost of
binocular single vision. Sensory adaptations are
more frequent in patients with strabismus of
childhood onset as compared to the patients
with strabismus of adult onset.
Sensory adaptations include the following:
• Suppression
• Monofixation syndrome
• Amblyopia (not actually an adaptation but a
consequence of suppression)
• Anomalous retinal correspondence (ARC)
SUPPRESSION
Suppression may be defined as a temporary
active cortical inhibition of the image of an object
formed on the retina of the squinting eye. This
phenomenon occurs (to avoid diplopia and/or
confusion) only during binocular vision (i.e.
with both eyes open). However, when the
fixating eye is covered, the squinting eye fixates,
i.e. suppression disappears (Fig. 8.3).
before the clinical description of different
varieties of strabismus. Adaptations to
strabismus include the following:
Sensory adaptations
• Monofixation syndrome
TYPES OF SUPPRESSION
Suppression has been variously classified:
I. Depending upon the etiopathogenesis
1. Physiological suppression

181Adaptations to Strabismus and Amblyopia
Fig. 8.3 Suppression in esotropia: (A) Central suppression in left esotropic eye obviates confusion; (B) Nasal retinal
suppression scotoma obviates diplopia. Suppression in exotropia: (C) suppression scotoma in left fovea obviates
confusion; and (D) Temporal retinal scotoma obviates diplope; Suppression in left esotropic eye during binocular vision.
2. Pathological (abnormal) suppression. It is
further of two types:
a. Facultative suppression
b. Obligatory suppression
1. Foveal suppression
2. Macular suppression
3. Peripheral suppression
4. Large regional suppression
III. Depending upon the constancy
II. Depending upon the retinal area where image is
suppressed
1. Intermittent suppression
2. Constant suppression

182 Theory and Practice of Squint and Orthoptics
IV. Depending upon the eye involved
1. Monocular suppression
2. Alternating suppression
Physiological suppression
Physiological suppression refers to the suppression present in everyday life of every
individual having normal binocular single
vision. It occurs due to retinal rivalry and to
avoid physiological diplopia. As a matter of fact,
the physiological suppression is very helpful in
everyday life, since it allows greater concentration on the object of interest. The specific
examples of physiological suppression in
everyday life while using one eye with both eyes
open are as follows:
• While using monocular microscope, the image
of the other is suppressed.
• A watchmaker keeps both eyes open but
normally suppresses one eye while viewing
the delicate parts of a watch through a
monocular magnifying instrument with the
other eye.
• While looking down the barrel of a rifle with
the dominant eye, the person may suppress
his nondominant eye.
Pathological suppression
It refers to the suppression of the image of one
eye that occurs to avoid diplopia and/or
confusion. It occurs in patients with strabismus
and anisometropia. It can be described as:
• Facultative versus obligatory suppression,
and
• Central versus peripheral suppression
Facultative versus obligatory suppression
Facultative suppression. It occurs to avoid
diplopia and/or confusion under conditions of
binocular vision but ceases, when the fixating
or the dominant eye is covered. It may occur
under following situations:
• Latent squint
• Intermittent squint
• Alternating squint (there is alternate sup-
pression)
• Manifest deviations of recent onset with
normal retinal correspondence.
Obligatory suppression. It refers to constant
suppression of the image from one eye which
occurs under all conditions and remains even
when the fixating or dominant eye is covered.
Obligatory suppression in the long run leads to
amblyopia and decreased visual acuity in the
affected eye.
Central versus peripheral suppression
Central suppression occurs to suppress the
image formed at the fovea of the deviating eye
to avoid confusion (Fig. 8.3A and C).
Peripheral suppression, i.e. suppression of the
image formed at some peripheral area of the
retina of the deviating eye that corresponds to
the image falling on the fovea of the fixating
occurs to prevent diplopia (Fig. 8.3B and D).
Size and shape of suppression scotoma
Size and shape of suppression scotoma are
different in esotropia as compared with an
exotropia.
• In esotropia, a small round scotoma involving
nasal retinal area corresponding to the fovea
of fixating eye is produced (Fig. 8.3B). Rarely
this scotoma can be bit larger.
• In exotropia, a comparatively much larger
scotoma occurs on temporal retina of the
deviated eye (Fig. 8.3D). This is explained by
the fact that intermittent exotropia, slowly
increases in size and so is the area of
suppression scotoma.
PATHOGENESIS
Mechanism of suppression
Retinal rivalry, i.e. struggle for dominance of each
eye is considered a prerequisite to suppression.
Retinal rivalry is a situation that occurs when
dissimilar objects are presented to the two eyes.
That is, two complete images of the dissimilar
objects are not seen. In an area of the field, part
of one image predominates while the corresponding part of the second image is suppressed
as shown in Fig. 8.4. This condition is constantly
changing and the different parts of the image
are suppressed in turn.
Burian popularized the concept that suppression is merely an exaggeration of the same
process which is involved in blocking out certain

183Adaptations to Strabismus and Amblyopia
ABCD
Fig. 8.4 Retinal rivalry occurring due to dissimilar objects being present to the left (A) and the right (B) eyes. Patient will
not see the picture as shown in (C) but will see as shown in (D) due to suppression.
parts of the image seen by each eye in binocular
rivalry. However, Smith and coworkers concluded that though the retinal rivalry may be an
important phase in the development of the
strabismic suppression, but the suppression and
the retinal rivalry are mediated by different
mechanisms.
Present knowledge is far from complete to
authentically designate the primary seat of the
suppressive mechanism. However, most studies
implicate the cortex as being the probable seat
of suppression, since normal ERG with
reduction in the amplitude of the VER has been
reported in patients with suppression. Results
of some of the electrophysiological and
psychophysiological studies are mentioned in
the discussion of amblyopia.
Selective suppression. Burian believes that
suppression may be selective even with regard
to a specific retinal function; that is, the ability
to resolve only contours may be defective
momentarily.
Suppression pattern usually corresponds with
the deviation pattern, i.e. suppression is
intermittent in patients with intermittent squint,
monocular and constant in patients with
uniocular constant deviation and it is alternating
in patients with alternating squint.
TESTS FOR SUPPRESSION
Tests for detection of suppression
1. Worth's four-dot test. This test can be
employed to diagnose the suppression involving
the peripheral retina. As described in detail on
page 140, the patients having left suppression
will see only two red lights and that having right
suppression will see only three green lights
(Fig. 6.32). In the presence of alternate suppression, patients will see alternately two red lights
and three green lights.
Disadvantages. Worth's four-dot test is not a
very useful test for suppression because of the
following reasons:
• It does not detect foveal suppression.
• Since the eyes are easily dissociated with red-
green glasses, a patient with unstable but
functionally useful binocular vision may
exhibit a suppression response with this test.
• In a patient having ARC, a normal fusion
response (the patient sees all four dots in a
rectangular arrangement) occurs even in the
presence of suppression.
2. The 4D base-out prism test (Fig. 8.5). This
test popularized by Jampolsky is performed for
detection of small angle heterotropias and the
presence of central suppression scotoma.
Technique. To perform this test, patient fixates
a penlight (Fig. 8.5A). Then a 4D prism is placed
with base-out in front of the right eye and the
examiner observes the presence of a biphasic
corrective movement of the left eye (Fig. 8.5B
and C). This is absent in the presence of a central
suppression scotoma (Fig. 8.5D).
Mechanism of biphasic corrective movements
can be explained as below:
• The prism displaces the image towards its
base, in other words, from the fovea of the
right eye towards a point on the temporal half
of the retina (4D or 2° away from the fovea).
The relaxation movement of the right eye will
elicit conjugate movements of both eyes to the
left (levoversion), if the right eye has no foveal
suppression (Fig. 8.5B).
• This displaces the image in the left eye from
the fovea to the temporal retina and thus the

184 Theory and Practice of Squint and Orthoptics
Fig. 8.5 The 4 D base-out prism test with its optical principle (for explanation, see text).
left eye now makes a fusional movement in
the opposite direction, if no foveal suppression
is present (Fig. 8.5C). In the presence of central
suppression scotomal this will be absent
(Fig. 8.5D)
• The test should be repeated with prism over
the left eye (Fig. 8.5E) and observation for a
biphasic corrective movement in the right eye
should be made.
3. Diplopia test or red glass test. See page 139.
4. Bagolini’s striated glass test. A foveal
(central) suppression scotoma in orthotropic
patient or a fixation point scotoma in the
presence of microtropia can be detected with
Bagolini’s striated glass test. As described on
page 137 and shown in Fig. 6.31, a patient with
fixation point suppression will see a central
interruption of the light streak.

185Adaptations to Strabismus and Amblyopia
5. Visual acuity test with Project-O-Chart slide
of American optical. It is a very effective test to
detect foveal suppression in patients with
microtropia or in patients with subnormal
binocular vision after surgical correction of
essential infantile esotropia. In this test, visual
acuity of each eye is measured under binocular
conditions with the Project-O-Chart slide of
American optical. Presence of decreased visual
acuity in one eye that is not present, when the
eye is tested under monocular conditions
indicates the foveal suppression.
6. Synoptophore test. Suppression can be
diagnosed with the use of simultaneous
perception slides (e.g. a cage and a lion) as well
as fusion slides (e.g. identical pictures of a rabbit,
one having a candle and the other having
flower). When simultaneous perception slides
are used, normally patient should see the lion
in the cage. In the presence of suppression,
patient sees either lion or cage.
To begin with, simultaneous foveal perception
(SFP) slides are used. When foveal suppression
is present, the simultaneous macular perception
(SMP) slides are used. In the presence of macular
suppression, simultaneous paramacular perception (SPP) slides are used and observations
are made. While using fusion slides, if the
patient sees a rabbit with both the candle and
flower, it indicates normal binocular single
vision. In the presence of suppression, either the
candle or the flower is absent. The fusion
pictures are graded according to the size in the
same way as the simultaneous perception
pictures.
Suppression scotoma can be mapped out, at
least in the horizontal meridian with synoptophore. One arm of the instrument is rotated, and
the points are noted at which the target carried
by the moving arm disappears and reappears.
Test for measurement of
depth of suppression
Depth of suppression is not equal in all the
patients. The degree to which facultative
suppression can produce obligatory suppression
probably depends upon the age of the child,
when facultative suppression begins. The
deeper the suppression, more difficult it is to
overcome.
Depth of suppression can be measured with
the help of red filter ladder (Fig. 8.6) which
contains a series of red filters of increasing
density. The red filter ladder usually consists of
gelatine fibres, beginning with one layer and
increasing to six or eight layers. The more the
layers, the darker the filter.
To measure the depth of suppression, the
patient is asked to fixate a small light, and the
filters in increasing density are placed in front
of the fixating eye till the patient sees double
lights. Some patients see double with a filter
made of single layer; while the others require
filters of three or more layers depending upon
the depth of suppression. The greater the
number of layers needed, the deeper is the
suppression.
TREATMENT OF SUPPRESSION
Indications
The role of antisuppression orthoptic therapy is
controversial, since it is not clear whether
patients treated by antisuppression orthoptic
therapy gain better functional results than others
who receive passive treatment such as alternating occlusion or no treatment at all. Further,
in some cases, antisuppression therapy may
cause either intractable diplopia or confusion as
suppression disappears.
In general, suppression should be treated only
when one expects to achieve bifoveal single
vision. The suitable cases for suppression
therapy are:
1. Patients with intermittent tropias in whom
fusion is present, when the deviation is
controlled, are the most suitable cases. In
intermittent tropias, the suppression is more
superficial than in constant deviation and is,
therefore, less difficult to disrupt.
Fig. 8.6 Red filter ladder used for measuring depth of suppression.
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