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186 Theory and Practice of Squint and Orthoptics
2. Patients with convergence insufficiency and
suppression are also suitable candidates for
therapy. They should perform antisuppression
exercises in conjunction with convergence
exercises.
3. Patients with constant tropias in whom
fusion ability can be demonstrated during
examination, usually are those in whom the
deviation occurred after about 2½ years of age.
4. Patients with fully corrected accommodative esotropia who continue to have an
intermittent deviation with suppression, should
receive suppression therapy. In such cases, antisuppression exercises should be combined with
divergence exercises to increase fusional
divergence amplitude.
5. Postsurgical patients with slight under
correction who are suppressing and thereby
inhibiting the potential for fusion also need
antisuppression exercises.
Methods of treatment
In fact, therapy for suppression involves the
treatment of the strabismus as a whole which
includes:
• Proper refractive correction wherever
indicated to render both eyes emmetropic.
• Occlusion therapy to permit equal and
alternate use of each eye and to overcome any
amblyopia which may be present.
• Alignment of the visual axes to permit simul-
taneous stimulation of corresponding retinal
elements by the same object.
• Antisuppression orthoptic exercises may be
needed before and/or after the surgical
therapy of strabismus.
Antisuppression orthoptic exercises
Antisuppression orthoptic exercises are undertaken stepwise to overcome the tendency of the
image from one eye to suppress the images from
other eye, when both eyes are open. Ideally, the
steps involved in antisuppression orthoptic
exercises are as follows:
• First step is to make the patient aware of diplopia.
• Second step is to make the patient learn to hold
fixation with either eye, always seeing the
blurred image from the deviated eye off to the
side (simultaneous perception). However, if the
deviation is sufficiently large, surgical
alignment should be considered first.
• Third step is to make the patient learn fusion
on both an instrument and in free space.
• Fourth step is to improve the fusional amplitude.
(A)
Diplopia exercises
The aim is to make the patient aware of
physiological diplopia in heterophoria and
intermittent tropia and of diplopia in
heterotropia.
1. Awareness of physiological diplopia.
Awareness of physiological diplopia is an
effective means of treating suppression in
patients with phorias, intermittent tropias and
phorias recently converted from tropias by
surgery and/or orthoptics. Patients should be
taught to experience both homonymous and
heteronymous physiological diplopia (as
described below). This will stimulate both the
nasal and temporal elements of the retina and
thus will help the patient to overcome
suppression over the entire retina.
I. Awareness of homonymous (uncrossed)
diplopia. Patient is asked to make note of light
situated about 6 metres from him/her while
fixating a light held 33 cm directly in front of
his/her nose. While doing so, by practice, patient
will learn to see one light at near (33 cm) and
two lights at distance (6 metres) simultaneously.
Now, if the orthoptist slowly covers and
uncovers his/her right eye several times with an
occluder, the patient should recognize that the
right light at distance intermittently disappears.
Similarly, if the left eye is covered, the left light
at distance disappears. Thus, patient experiences
homonymous (uncrossed) diplopia, due to
bilateral nasal retinal stimulation by the distant
light while patient is fixating on near light
(Fig. 8.7).
II. Awareness of heteronymous (crossed)
diplopia. Patient is asked to make a note of light
held 33 cm in front of his/her nose while fixating
a light situated 6 metres away. While doing so,
by practice, patient will learn to see one light at
distance and two lights at near simultaneously.
Now, if the orthoptist slowly covers and
uncovers patient's right eye several times with
Fig. 8.7 Homonymous (uncrossed) diplopia.
an occluder, the patient should recognize that
the left light situated at near intermittently
disappears. Similarly, if the left eye is covered,
the right light at near disappears. Thus the
patient experiences heteronymous (crossed)
diplopia due to bilateral temporal retinal
stimulation by the near light while patient is
fixating at distant light (Fig. 8.8).
III. Exercises utilizing physiological diplopia
i. Framing. Framing is a good home exercise
based on physiological diplopia. Patient is asked
Fig. 8.8 Heteronymous (crossed) diplopia.
187Adaptations to Strabismus and Amblyopia
to make note of a pencil held at 15 cm in front of
his/her nose while fixating at a distant object in
the room (Fig. 8.9A). Patient should see two
pencils and one distant object (awareness of
heteronymous diplopia) (Fig. 8.9B). Now the
patient is asked to move the pencil away from
his/her nose. During this procedure, patient will
note that two pencils are moving closer to each
other. Similarly, when the pencil is moved
towards the nose, its two images will be seen
moving farther apart from each other. Once the
patient learns this, he/she is asked to fix at
different distant objects in the room and move
the pencil backward or forward so that the
distant object is framed between the two pencils,
i.e. the object is centred with pencils touching
its each side (Fig. 8.9C).
ii. Bar reading. Bar reading exercise is also based
on the principle of awareness of crossed
physiological diplopia. Patient is asked to hold
bar (thumb, finger, pencil or any other bar) about
5–6 cm from his/her nose and asked to read a
print kept at about 33 cm from his/her eyes
(Fig. 6.43). As the patient reads the print
binocularly, he/she perceives the bar in crossed
diplopia, each image of the bar hiding a portion
of the print from one eye, but not the other, so
that patient can read the print normally. Such a
practice of maintaining the correct position of
his/her eyes despite the obstacle will strengthen
the binocular vision of the patient. However, till
suppression is present, he/she will see only one
bar, which will hide some of the print and thus
continuous reading will be impossible. So, the
patient will either shift his/her head or move the
bar to see the print.
The better way to eradicate suppression with
this exercise is to start the patient with a few large
letters on a card. Slowly the amount of letters on
a line may be increased and the size of the letters
decreased as the suppression disappears until he/
she can easily read a page of small print.
2. Diplopia exercises with coloured filters. These
exercises are based on the fact that a patient with
strabismus suppresses similar images in contrast
to normal person who tends to suppress
dissimilar images. In this exercise, patient is
asked to fixate a white light and a red filter is
placed in front of one eye and a green filter in
188 Theory and Practice of Squint and Orthoptics
A
Fig. 8.9 Framing — a home exercise for suppression (for explanation, see text).
front of the other eye. The dissimilar images
produced by the filters are sufficient to
overcome suppression in most instances and
produce diplopia. After the diplopia is evoked,
patient is asked to look alternately from one
image to the other. During this process, first one
filter and then the other is removed in an
attempt to have the patient notice diplopia
without the help of filters. When patient is able
to do so, the fixation light is exchanged for
another fixation object which is a less intense
stimulus. In this way, patient should be taught
diplopia during both near and distance
fixations.
3. Diplopia exercise with prisms. In this
orthoptic exercise, a vertical prism (base up or
down) sufficient enough to displace the image
outside the suppression scotoma is placed in
front of one eye. Consequently, the patient will
have diplopia. Gradually, the prism power is
reduced until finally the patient has diplopia
without any vertical displacement of one image.
Once the patient learns to perceive diplopia
without prism, the fixation light is then replaced
by a less intense stimulus. In this way, patient
should be taught diplopia during both near and
distance fixations.
(B) Exercises with use of red filter
1. To treat suppression at near, a red filter is
placed over the dominant eye and patient
(depending upon his/her age and interest) is
asked to do any of the following exercises:
• Colour, trace or draw with a red pencil
matching the red filter.
• Little girls may follow red design drawn on a
white cloth with a needle and a light red or
pink thread.
• Children can draw lines with a red pencil
using the number-to-number games in their
colouring books.
• Children can also select red beads for a
necklace
• The boys can play ping-pong with a red ball.
2. To treat suppression at distance, patient may
be asked to watch colour television with the red
filter over the dominant eye.
(C) Exercises with major amblyoscope
(synoptophore)
1. Macular massage. This exercise stimulates
the retina of deviated eye. It is accomplished by
moving the visual target on the major amblyoscope back and forth across the suppression
scotoma (macular massage) as below:
189Adaptations to Strabismus and Amblyopia
The major amblyoscope tubes having slides
of paramacular simultaneous perception are
locked at the patient's objective angle. While he/
she looks constantly straight ahead, the tubes
are moved rapidly from side to side over a large
arc. Since they are at the objective angle, the
images moving over the retina will always
stimulate normally corresponding areas. In the
periphery, they will be superimposed. When
approaching the suppression area, however, one
picture will disappear or the two will separate.
The excursion of the tubes is gradually reduced
until eventually the patient can maintain
superim-position while looking at the pictures,
when tubes are held still.
2. Crossing technique. A pair of paramacular
simultaneous perception slides is put in the
tubes of major amblyoscope. Patient is asked to
fixate the target viewed by the dominant eye,
while the target in front of the suppressed eye
is moved in from the periphery of the field
towards the suppression scotoma. It will
disappear, when it reaches the suppressed area
and reappear on the other side after the entire
scotoma has been crossed. This back and forth
movement of the target across the suppression
area is continued until this area has decreased
to such an extent that the patient can
simultaneously perceive both targets and can
superimpose the two images. In normal
correspondence, peripheral size targets may be
used first followed by macular and foveal size
targets.
3. Chasing technique. It is a technique of
subjective exercise using the smallest
simultaneous perception slides that the patient
can superimpose. The two arms of the major
amblyoscope are loosened and the patient is
asked to hold the handle of the tube in front of
the suppressed eye. The examiner moves the
picture tube that is in front of the fixating eye in
a random position. The patient is asked to chase
it and superimpose the two pictures by moving
the other tube. This chasing technique
is exercised repeatedly. As the patient's
performance improves, increasingly smaller
pictures are used until he/she can superimpose
the foveal slides.
(D) Exercises with cheiroscope
The cheiroscope is a very good instrument for
antisuppression training. For details see page
152.
(E) Exercises with Tibb's binocular trainer
Tibb's binocular trainer is an excellent instrument for antisuppression exercise, especially for
home. For details see page 152.
(F) Computerised anti- suppression vision therapy
See page 154.
MONOFIXATION SYNDROME
Definition and causes
Monofixation syndrome, also known as Park’s
syndrome, is the term coined by Marshal Park
for the sensory adaptation occurring in patients
with microtropia (angle of strabismus <10 PD).
Other clinical situations associated with
monofixation syndrome are:
• Anisometropic amblyopia, unilateral astig-
matism and
• Unilateral partial cataract.
Characteristic features
It is characterized by absence of bifoveal fusion
(unilateral central suppression) with the presence
of peripheral fusion.
• Central suppression in the microtropic eye
occurs because the central retina has small
receptive field and high spatial resolution
potential, so relatively small difference in
image clarity or retinal image position are
recognized. Patients with monofixation
syndrome usually have stereo acuity in the
range of 30 to 70 seconds of arc and the central
scotoma measures between 2° and 5°.
• Peripheral fusion is maintained because in the
peripheral field slight interocular image
differences are not detected since the
peripheral retina has large receptive field
and relatively low spatial resolution. Small
retinal image discrepancies between fellow
eyes are, therefore, not disruptive in the
peripheral fields and so peripheral fusion
is maintained.
190 Theory and Practice of Squint and Orthoptics
AMBLYOPIA
Amblyopia, by definition, refers to a partial loss
of sight in one or both eyes, caused by abnormal
visual development secondary to abnormal
visual stimulation in the absence of ophthalmoscopic or other marked objective signs.
Literally speaking, amblyopia is a spectrum of
visual loss, ranging from missing a few letters
on the 20/20 lines to hand motion vision.
However, for practical purposes, amblyopia is
labelled, when there is at least two Snellen lines
difference in the visual acuity between the eyes.
Amblyopia occurring in a patient with
strabismus is not a sensory adaptation per se,
but the consequence of suppression which is a
sensory adaptation.
CLASSIFICATION AND TERMINOLOGY
The self-explanatory terms used for amblyopia
in present day orthoptic practice are as follows:
1. Strabismic amblyopia. The term strabismic
amblyopia is used for the amblyopia seen in
those patients with unilateral constant squint
who strongly favour one eye for fixation from
birth to 6 years of age. Peak age for development
of fixation preference in strabismic children is
about 1 year (range 9 months to 24 years).
Strabismic amblyopia is a common form of
amblyopia and typically shows following features
that are uncommon in other forms of amblyopia:
• Grating acuity is often considerably less
reduced than the Snellen's acuity. This is
because forms seen by the affected eye are in
a twisted or distorted manner that interfere
more with letter recognition than with the
simpler task of determining whether a grating
is present or not.
• Neutral density filter effect, i.e. when illumi-
nation is decreased, the acuity of an eye with
strabismic amblyopia does not decline further
while it does so in organic amblyopia.
• Laterality, strabismic amblyopia is always
unilateral and is caused by an active inhibition
within the retinocortical pathways of visual
input originating in the fovea of the deviating
eye. Strabismic amblyopia follows through a
stage of suppression, giving rise to the term
suppression amblyopia.
• Type of strabismus. Strabismic amblyopia is
seen far more often in esotropes than the
exotropes. This might be related to the fact that
in esotropia, the fovea of the deviating eye has
to compete with the strong temporal hemifield
of the fellow eye; while in exotropia, the fovea
of the deviating eye has to compete with the
weaker contralateral nasal hemifield.
• Strabismic amblyopia occurs very rarely in patients
with hypertropia, as they usually manage to
maintain fusion in some positions of gaze with
an anomalous head posture.
• Patients with alternate strabismus do not have
amblyopia but they do have abnormal
binocular function.
2. Stimulus (visual) deprivation amblyopia. It
is caused by those conditions wherein one eye
is prevented from seeing early in life. Such
conditions would include:
• Monocular congenital or traumatic cataract
• Complete ptosis
• Corneal opacity and
• Prolonged patching of the normal eye for
treatment of amblyopia (occlusion amblyopia).
Constant monocular occlusion of the visual
axis for more than a weak per year of life places
a child at significant risk for the development
of stimulus deprivation amblyopia until about
5–6 years of age.
Deprivation amblyopia is characterized by
following features:
• It is the least common but most damaging and
difficult to treat form of amblyopia.
• Amblyopic visual loss resulting from
unilateral deprivation is worse than that
produced by bilateral deprivation of similar
degree. This is because of the fact that in the
unilateral deprivation, interocular effects add
to the direct developmental impact of severe
image degradation.
Bilateral deprivational amblyopia may develop
in small children with bilateral media opacities,
e.g.:
• Bilateral congenital cataract
• Bilateral corneal opacities (Peter's anomaly)
• Bilateral vitreous haemorrhage
3. Refractive amblyopia occurs due to consistent
defocus of the retinal image in one or both eyes
191Adaptations to Strabismus and Amblyopia
due to presence of refractive error. It can be of
following subtypes:
• Anisometropic amblyopia. The term anisome-
tropic amblyopia refers to the amblyopia
occurring in an eye having higher degree of
refractive error than the fellow eye.
• Anisohypermetropic versus anisomyopic
amblyopia. It has been reported that amblyopia
is more common and is of a higher degree in
patients with anisohypermetropia than in those
with anisomyopia. Even 1.5 to 2 dioptre
hyperopic anisometropia may cause amblyopia
while up to 3 dioptre myopic anisometropia
usually does not cause amblyopia. However,
unilateral high myopia (–6D or more) often
results in severe amblyopia. It has been presumed
that both the forms, vision deprivation as well
as the abnormal binocular interaction that is
caused by unequal foveal images in the two
eyes, might be playing role in the development
of anisometropic amblyopia.
Strabismus is frequently associated with
anisometropia. In such cases whether amblyopia
occurs due to anisometropia or strabismus or
both is very difficult to determine.
• Meridional amblyopia. This refers to amblyopia
occurring in patients with uncorrected astigmatic
refractive error due to selective visual deprivation
for visual stimuli of a certain spatial orientation.
Thus, meridional amblyopia is a selective
amblyopia for a specific visual meridian. 1.25D of
arriso astigmatism may cause amblyopia.
• Isoametropic amblyopia. Isoametropic
amblyopia is bilateral amblyopia occurring in
children with bilateral uncorrected high
refractive error. Hyperopia of more than +5.0D
and myopia in excess of –10.0D have a risk of
inducing bilateral amblyopia. Such amblyopia
is usually of milder form. It is supposed to result
from the effect of blurred retinal images alone
(pattern vision deprivation). Bilateral
meridional amblyopia is caused by bilateral
astigmatism. Significant meridional amblyopia
occurs with astigmatism greater than –2.5D.
PATHOGENESIS AND PATHOPHYSIOLOGY OF
AMBLYOPIA
Despite an enormous research in this field,
pathogenesis and pathophysiology of amblyopia
is still not elucidated fully. However, the clinical
features and laboratory findings in eyes with
amblyopia permit certain conclusions for
understanding the nature of the processes
underlying amblyopia and its treatment.
Psychophysical studies in human strabismic,
anisometropic and visual deprivation amblyopia
show differences between the function of the
fovea versus the retinal periphery. Further, there
are also differences in the severity and
reversibility of the various types of amblyopia.
However, the most pertinent factual knowledge
about the changes occurring in amblyopia which
has been obtained through experimental studies
(electrophysiologic and histopathologic) in
kittens suggests that the structural and
functional involvement of the afferent visual
pathway in different forms of amblyopia is the
same as is the sensitive period during which
amblyopia occurs, regardless of the etiology.
Therefore, on the basis of this recent
neurophysiologic research, largely done in
experimental animals, it has been postulated that
the basic amblyogenic mechanisms are—light
deprivation, foveal form vision deprivation,
abnormal binocular interaction and active
cortical inhibition.
The initial development of amblyopia from
any cause rarely occurs in children older than
about 5–6 years. However, once amblyopia has
developed and has been treated with therapy,
it may recur until about 9–11 years of age.
AMBLYOGENIC FACTOR AND PATHOPHYSIOLOGICAL MECHANISM INVOLVED
A. AMBLYOGENIC FACTORS
The basic mechanisms responsible for amblyopia,
which have been recognized on the basis of
neurophysiologic research, largely done in
experimental animals, are as follows:
• Deprivation of form vision
• Light deprivation
• Abnormal binocular interaction
1. Deprivation of form vision
• Monocular deprivation of form vision during
the critical period of visual development results
in amblyopia of the deprived eye. Since the
deprived eye becomes dominated by the normal
192 Theory and Practice of Squint and Orthoptics
eye so a competitive amblyopia of profound
intensity develops. Monocular visual deprivation
works as an amblyogenic factor in strabismic,
anisometropic, stimulus deprivation amblyopia.
• Binocular deprivation of form vision during
the critical period of visual development results
in bilateral deprivational amblyopia. Since in
binocular deprivation, the binocular interaction
is not disrupted so a competitive amblyopia is
not superimposed; so the resultant amblyopia
not so severe as in unilateral deprivation.
Binocular deprivation plays the role of
amblyogenic factor in children with bilateral
cataract, ametropia and bilateral high refractive
errors.
2. Light deprivation
Light deprivation works as an amblyogenic
factor in children with unilateral as well as
bilateral complete cataracts.
3. Abnormal binocular interaction
Abnormal binocular interaction is highly
amblyogenic. It produces a profound amblyopia
due to a competition amblyopia. Abnormal
binocular interaction plays the role of amblyogenic factor in children with strabismic,
anisometropic and unilateral stimulus deprivation amblyopia.
Summary of causes of amblyopia
Thus, the amblyogenic factors for different types
of amblyopia are same. However, their
contribution to each may vary and so is the
severity of amblyopia (Table 8.1).
Based on the amblyogenic factors, causes of
unilateral and bilateral amblyopia are
summarized as below:
Causes of unilateral amblyopia
1. Refractive error: Anisometropia
• Myopia (2–2.5 D difference)
• Hypermetropia (1.5–2.5 D difference)
• Astigmatism (2–2.5 D difference)
2. Strabismus
3. Unilateral visual deprivation
• Unilateral cataract
• Unilateral ptosis
• Unilateral corneal opacity
• Unilateral vitreous haemorrhage due to
trauma
Causes of bilateral amblyopia
1. Refractive errors in both eyes: Ametropia
• High myopia >6.0 D
• High hypermetropia >3.5 D
• High astigmatism >1.5 D
2. Bilateral visual deprivation
1. Bilateral cataract
2. Bilateral ptosis
3.Bilateral corneal opacity
4.Bilateral vitreous haemorrhage due to trauma
NEUROPHYSIOLOGICAL BASIS OF
ROLE OF AMBLYOGENIC FACTORS
The above conclusions about the role of various
amblyogenic mechanisms have been drawn
from the various experimental studies done in
cat, kitten and monkey. A few key studies to
Table 8.1 Role of amblyogenic factors in different types of amblyopia
Types
of Light Deprivation of Abnormal Severity of
amblyopia deprivation form vision binocular amblyopia
• Stimulus deprivation amblyopia
– Unilateral (e.g. cataract) + + + + + +
– Bilateral (e.g. cataract) + + – + +
• Strabismic amblyopia – + + + +
• Anisometropic amblyopia – + + + +
• Ametropic amblyopia – + – +
Amblyogenic factors
interaction
understand the neurophysiologic basis of
normal binocular vision and amblyopia are
described briefly here.
Neurophysiologic basis of
normal binocular vision
Hubel and Wiesel are pioneers in the neurophysiologic studies of binocular vision. They
have concluded that in normal cat or kitten:
• Approximately 80% neurons of striate cortex
are derived from each eye, 10% from the
contralateral eye and 10% from the ipsilateral
eye only. The two receptive fields of binocularly
driven cortical cells are found to have
corresponding location in the two retinae.
• Of the binocularly driven cortical neurons,
only 25% are stimulated equally well from
each eye, while the remaining 75% show
graded degree of influence from the right or
left eye (disparity sensitive binocular cells).
Stereopsis has been linked with horizontal
disparity sensitive binocularly driven cortical
neurons.
• It has been reported that at birth (i.e. without
previous visual experience or training) the
visual system of kittens gives responses which
are in no way different from those obtained
in adult cats. From this, the conclusion was
drawn that the basis for visual recognition and
binocular interaction is already fully
developed at birth. The immaturity of visually
dependent behaviour in young animals, such
as the lack of pursuit movements, therefore,
cannot be explained by incomplete development but must be due to other factors,
possibly lack of interpretation/visuomotor
cooperation.
• To understand the pathophysiologic mecha-
nisms concerned with binocular vision and
development of amblyopia, the visual
pathway carrying visual sensations from the
retina to visual cortex have been classified in
X, Y and W-system (Fig. 8.10) as follows:
X-system. The fibres from the retinal ganglion
cells carrying the sustained response to visual
stimuli are found in the X-cell system—the
medium velocity system. The X-system is
associated with central form vision and,
therefore, central visual acuity. Cells of this
193Adaptations to Strabismus and Amblyopia
Fig. 8.10 X, Y and W-system of cells in the visual cortex.
system project only to the lateral geniculate
nucleus.
Y-system. The fibres from the retinal ganglion
cells carrying a transient response are in the
Y-cell, or fast system. The Y-system is associated
with the peripheral retina and is concerned with
the location of objects in space, which enables
fixation movements to be made. This system
projects to both the lateral geniculate nuclei and
superior colliculus.
W-cell system (slow system). It is believed to
be the pursuit system. It projects only to superior
colliculus.
Neurophysiologic studies in
experimental and clinical amblyopia
Neurophysiology of amblyopia is a complex
mechanism and its understanding is far from
194 Theory and Practice of Squint and Orthoptics
complete. Some of the observations made from
the study of experimental modification of visual
experience in animals and laboratory testing of
amblyopic human beings are given below.
Monocular deprivation studies
Methods. Monocular deprivation was produced
in experimental animals (kitten and monkey) by
suturing the eyelids of one eye during the critical
period of development.
Observations are as below:
• Deprived eye developed amblyopia, probably
because this eye was dominated by the normal
eye due to the interruption in binocular cooperation.
• Changes observed in visual system neuron
functions were as follows:
– In the lateral geniculate body, cells in those
layers receiving input from the deprived eye
showed a profound shrinkage. Larger cells
shrank more than the smaller ones.
– Cells of primary visual cortex either lost
their innate ability to respond to stimulation
or showed significant functional deficiency.
It has been reported that there occurs a
selective reduction in the number of cortical cells
driven by Y-input from retina, suggesting that
perhaps visual deprivation selectively involves
the Y-system.
Note. Similar experiments in adult animals did
not reveal such changes.
Conclusions. These studies indicate that uniocular
visual deprivation produces amblyopia by
changes in the visual system neurons. It has also
been concluded that deprivation during the
early part of critical period of development is
more deleterious than at a later stage. This
experimental work of uniocular deprivation
closely resembles the clinical situation of
unilateral cataract, severe congenital ptosis or
corneal opacity producing profound amblyopia.
Binocular deprivation studies
Technique. Binocular visual deprivation was
made by bilateral tarsorrhaphy in kittens and
monkeys during sensitive period of development
and also in visually mature animals and
following observations made were as follows:
• A mild bilateral amblyopia occurred in infant
animals due to visual deprivation. Perhaps
amblyopia was mild due to the fact that the
competition amblyopia was not superimposed
since the binocular interaction was not
abnormal in binocular equal deprivation.
• Changes observed in visual system neuron
functions were as follows:
– Cell shrinkage produced in lateral geni-
culate body was less than that produced in
uniocular deprivation.
– There occurred a decrease in the specific
responsiveness of cells and an increase in
number of cells that respond sluggishly or
abnormally. In addition, there were many
cells that did not respond at all.
– The number of Y-cells was reduced by 307%.
– It was postulated that in binocular
deprivation, there may be a competition for
synaptic space in the cortex between the
X-cells and the more disadvantaged Y-cells.
Conclusions. The amblyopia produced by
binocular deprivation was less severe than that
produced by uniocular deprivation, owing to
the fact that binocular interaction was not
abnormal. This work closely resembles the
clinical situations of bilateral amblyopia seen in
children with bilateral cataract and also to some
extent the ametropic amblyopia.
Experimental strabismic amblyopia
In monkeys made artificially strabismic, by
disinserting lateral or medial rectus, only the
binocular portion of the lateral geniculate body
showed cell shrinkage, while in visually
deprived monkeys, both the monocular and
binocular portions of the lateral geniculate
nucleus showed shrinkage. Thus, two different
neural mechanisms appear to underlie the
deprivational and strabismic amblyopia.
However, it has been postulated that visual
deprivation (since central fixation is not used in
strabismus), abnormal binocular interaction and
active cortical inhibition similar to that occurs,
in suppression, all play a role in the amblyopia
associated with strabismus. While this seems
reasonable intuitively and laboratory findings
suggest this, but definitive proof is still lacking.
195Adaptations to Strabismus and Amblyopia
Experimental anisometropic amblyopia
Experimental anisometropic amblyopia was
produced in primates by putting high plus
convex lens in one eye and/or atropine.
Observations made were as below:
• Visual cortex cells of striate cortex layer IV and
outside layer IV (driven by the involved eye
and a fraction of binocular driven cells) had
reduced contrast sensitivity.
• Lateral geniculate body showed anatomical
changes in the form of diminution of cell size
limited only to the parvocellular layers that
subserve high spatial frequency.
(B) PATHOPHYSIOLOGICAL MECHANISMS
OF AMBLYOPIA
Pathophysiology of amblyopia involves several
interconnected mechanisms:
1. Neural plasticity
The brain is highly plastic during early
childhood, and it adapts to visual experiences.
If one eye provides a consistently blurry or
conflicting image, the brain's visual cortex can
undergo changes that favor the stronger eye's
input, causing the weaker eye's connections to
weaken and leading to amblyopia.
2. Active cortical inhibition
The brain relies on binocular (two-eyed) vision
to create a single, three-dimensional image.
When there is a significant difference in visual
acuity between the two eyes, the brain might
suppress input from the weaker eye to avoid
confusion and double vision.
The neurophysiologic research points out that
visual deprivation and active cortical inhibition
are the two fundamental mechanisms for the
development of amblyopia. The role of active
cortical inhibition is evidenced by following
studies.
i. Physiologic evidence. In one study, in experi-
mental animals, deprivation amblyopia was
produced in one eye. After 5 months of
deprivation, these animals, were divided into two
groups. In group-I animals the normal eye was
enucleated, while in group-II, the normal was
retained and following observations were made:
In group-I animals (with normal eye enucleated), the amblyopic eye was found to drive 31%
of the visual cortex cells. While in group-II
animals, in which normal eye was retained, only
6% of the visual cortex cells were driven by the
amblyopic eye. In other words, after removal of
the normal eye, the deprived eye showed
marked capacity for recovery indicating thereby
that perhaps the normal eye may be responsible
for an active cortical inhibition in unilateral
amblyopia.
ii. Pharmacologic evidence. It has been ascert-
ained that under normal circumstances, most of
the excitatory synapses in the visual cortex are
cholinergic. Further, it has also been reported
that the visual cortex is inhibited by the gamma
aminobutyric acid (GABA)—an inhibitory
neurotransmitter. The assumption that perhaps
in amblyopia, active cortical inhibition might be
mediated by GABA led the researchers to
perform certain experiments.
Duffy et al. produced deprivation amblyopia
in kittens and studied the effects of some antiGABA agents. Following observations were
made by them:
– Intravenous injection of bicuculline (an anti-
GABA agent) led to stimulation of 60% visual
cortex cells which were otherwise
unresponsive due to deprivation amblyopia.
However, convulsions were noted as a
complication of this drug.
– Intravenous injection of naloxone, another anti-
GABA agent, also restored binocular inputs
in the visual cortex cells which were otherwise
unresponsive due to deprivation amblyopia.
Kasamatsu and Pettigrew produced depletion
of brain catecholamines by using 6-hydroxydopamine and norepinephrine and observed a
failure of ocular dominance shift after
monocular occlusion in kittens.
The above studies provide a pharmacologic
evidence of the role of active cortical inhibition
in the amblyopia.
iii. Critical period: Visual development is most
rapid during a critical period. The critical period
corresponds to the time phase when the neural
wiring in brain is still malleable. It has been
observed to differ for different types of
amblyopia. The upper limit is 6 years for visual