Amblyopia

AMBLYOPIA
derived from Greek language
amblys – dull ops – eye ‘‘dullness of vision’’
• U/L or ( less commonly) B/L reduction of BCVA
• Cannot be attributed directly to any structural abnormality of eye or visual pathways
• A spectrum of visual loss, ranging from missing a few letters on 6/6 line to HM
• At least 2 Snellen lines difference in BCVA b/w 2 eyes
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Definition
Amblyopia is defined as decrease of BCVA in
 1 eye due to abnormal binocular interaction or
1 or both eyes due to pattern vision deprivation during visual immaturity
For which
no cause can be detected during physical examination
reversible by therapeutic measures in appropriate cases
Albrecht von Graefe defined amblyopia as the condition where
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Observer sees nothing and patient very little

• MCC of decreased vision in childhood
• Children susceptible b/w birth and 7 years of age
• Earlier the onset of abnormal stimulation, greater the visual deficit
• Signifies a failure of normal neural development in the immature visual system
Abnormal visual stimulation
Abnormal visual development
Poor vision (amblyopia )

Caused by abnormal visual experience early in life resulting from
1. Strabismus
2. Ref error: anisometropia or high B/l ref errors (isoametropia)
3. Visual deprivation
• Not applied to a decrease in vision caused by
uncorrected ref error
opacification of media
chorioretinal damage

• Time period during which children likely to develop amblyopia is the same, regardless of the
underlying cause.
• Age at which children most sensitive to amblyopia  first 2 to 3 yrs of life
• This sensitivity gradually decreases until child reaches 6 or 7 yrs of age
 visual maturation is complete
 retinocortical pathways and visual centers become resistant to abnormal visual input
• Age limit of 6 years recently confirmed by Keech and Kutschke, using statistical analysis.
• Milder forms of amblyopia may occur even after this period from visual deprivation (traumatic
cataract) and are usually rapidly reversible by occlusion therapy.

Epidemiology
• Responsible for more cases of childhood-onset U/L decreased vision than all other causes
combined
• MCC of U/L visual impairment in adults < 60 years
• Prevalence increased in children with
 Family h/o amblyopia
 Premature babies
Developmental delay

• Difficult to assess freq of amblyopia in general
population.
• Large-scale studies done refer to selected populations
only (eg military draftees, soldiers, schoolchildren,
ametropes)
• Figures vary w/ the populations andVA criterion adopted.
• Thus , 2.0% to 2.5% of gen population have amblyopia.
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Causes of Amblyopia
B/l cases are caused by b/l image blur (anterior visual pathway)
Causes of U/l amblyopia
• MCC- strabismus and anisometropia,
or a combination of the two
• U/l media opacities-
 corneal opacities
 infantile or childhood cataracts
 vitreous hemorrhages
• Spectacles (anisometropia or high myopic or hyperopic refractive error)
• Occlusion (media opacities, retinal disease, optic nerve pathology, corneal ds)
• Strabismus
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O
S
Causes of B/l amblyopia
B/l media opacities
corneal opacities
infantile or childhood cataracts
vitreous hemorrhages
Ametropia
b/l high astigmatism
 high hypermetropia

Pathophysiology and Classification of Amblyopia
In early postnatal development, during Critical periods of cortical development
During these periods,
Visual system’s plasticity allows greatest opportunity for reversal of amblyopia
Neural circuits display sensitivity to environmental stimuli
Developing visual system depends on natural sensory experience for proper formation
Vulnerable to abnormal input due to visual deprivation, strabismus or significant
uncorrected RE
brain damage
abnormalities in visual centers of the brain.
AMBLYOPIA

• Cells of primary visual cortex can lose innate ability to respond to stimulation of 1 or both eyes
• Cells that remain responsive can show significant functional deficiencies.
• Structural and functional damage occurs in lateral geniculate nucleus and striate cortex of
visual center in occipital lobe in form of
 atrophy of connections
 loss of cross-linking b/w connections
loss of laterality of connections

• Primarily a defect of central vision ; Peripheral visual field usually normal
• Receptive fields of neurons in the amblyopic visual system are abnormally large.
• This account for the crowding phenomenon (aka contour interaction ,)

Crowding phenomenon (separation difficulties)
• Inability to discriminate optotypes that are crowded together closely.
• Thus most amblyopic have 2 acuities
line acuity, or ‘‘Snellen’’ acuity
single E acuity
• In amblyopic patients, Compare vision obtained w/VA symbols presented in a row to that
obtained w/ isolated symbols on a uniform background.
• BetterVA reading (1 or 2 Snellen lines better) while single optotype (presented singly against
uniform background), than multiple optotypes in a row (linear optotypes).
• Symbols must be larger for them to be able to see w/ amblyopic eye.

• Linear acuity is more desirable than single optotype as single optotype underestimates
degree of amblyopia.
• In children who get confused w/ multiple optotypes in linear acuity testing Surround bars
used to create crowding around a single optotype
• Diff b/w line acuity and single E acuity varies greatly w/ diff amblyopic eyes.
• This difference is generally greater when line acuity is lower.

OLDER CONCEPTS
Chavasse coined the term amblyopia of arrest
• Consequent disuse of 1 eye  arrest visual development
• VA remains at level of development present at the time strabismus occurred.
• If amblyopia of arrest is allowed to persist, then suppression amblyopia, which he termed
amblyopia of extinction, would become superimposed on it.
• Only that part of amblyopia attributable to inhibition could be reversed by therapy.
Linksz expressed a similar thought and stated that an eye did not become amblyopic but
stayed amblyopic.
This theory is no longer supported in light of current knowledge that vision actually can be
restored to a much higher level than was present at onset of a constant U/l ocular deviation.

• Another view is that amblyopia is a result of disuse, as expressed by term amblyopia of disuse
(amblyopia ex anopsia, i.e., amblyopia from nonseeing).
• This term has been discarded as amblyopic eye of a strabismic patient is not prevented from
being used.
• Light enters it, and images are formed on the retina.
• If amblyopic eye of a strabismic patient is occluded, patient will notice a loss in field of vision
and in many cases, one can detect some cooperation b/w amblyopic eye and its fellow eye.
• Central fixation is the only function for which some amblyopic eyes are not used habitually.

• Amblyopia due to visual deprivation
develops more rapidly
 Deeper with an earlier Critical period for development
than that due to strabismus or anisometropia
2 basic forms of abnormal stimulation:
1. pattern distortion (i.e., blurred retinal image)
2. cortical suppression (i.e., constant suppression of one eye)
• These can occur independently or together to cause amblyopia
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CLASSIFICATION OF AMBLYOPIA
STRABISMIC• Cong Esotropia
• Cong Exotropia
• Acquired constant tropia in childhood
• Accommodative esotropia
• Small angle tropia
• Intermittent exotropia
MONOCULAR PATTERN DISTORTION
• Anisometropia
 Hyperopia >+1.5 D
 Myopia >-3 D
 Meridional >+1.5D
• Media Opacities
• U/L cataract
• U/L corneal opacity
• U/L vit h’ge or vit opacity
B/L PATTERN DISTORTION
• Ametropia
• B/L high Hyperopia >+5 D
• B/L Astigmatism >+2.5D
• Media opacity
• B/L cong cataract
• B/l corneal opacity
• B/L vit h’ge
SUPPRESSION
SUPPRESSION
&
PATTERN DISTORTION
PATTERN DISTORTION

In spite of the similarities of the basic amblyopiogenic mechanisms,
certain clinical differences exist between strabismic, anisometropic, and visual deprivation
amblyopia in terms of following characteristics
Severity
Reversibility
psychophysical

AMBLYOPIA
Strabismic
Monocular
pattern
distortion
Bilateral pattern
distortion
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SUPPRESSION
&
PATTERN DISTORTION
SUPPRESSION PATTERN DISTORTION

Strabismic Amblyopia
• Always Unilateral
• Can be Mod to Severe
• Amblyopia occurs despite both eyes having clearly focused retinal images
• Patients w/ strabismus most likely to acquire amblyopia are those who
Strong fixation preference for 1 eye
Have U/l rather than an alternating fixation pattern
Constantly suppress cortical activity from deviated eye
• Those w/ alternate fixation and alternate suppression do not have amblyopia, but have
abnormal binocular function

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• Occurs in approx 50% of patients w/ cong esotropia (a constant nonalternating heterotropias)
• Amblyopia far more often seen in ESOTROPES than in exotropes as
1. Exotropia is often intermittent at its onset.
2. Nasotemporal asymmetry of the retinocortical projections.
In esotropia  fovea of deviating eye compete w/ strong temporal hemifield of fellow eye
In exotropia  fovea competes w/ the weaker C/l nasal hemifield
• very uncommon in patients w/
intermittent strabismus (e.g., intermittent exotropia)
 incomitant strabismus
heterotropes
as they adopt a compensatory face turn maintain central fusion

Mechanism :
Constant cortical suppression  degrades neuronal connections to deviated eye
Competitive or inhibitory interaction b/w neurons carrying nonfusible input from 2 eyes
Domination of cortical vision centers by input from fixating eye
Reduced responsiveness to input from nonfixating eye
• In young children w/ strabismus, suppression develops rapidly.

Overlap of diff foveal images from retinas of fixating eye
and deviating eye
transmitted to visual centers
Inhibition of visual input from fovea of deviating eye
(visual adaptation to avoid diplopia and visual confusion )
• However ,amblyopia does not always prevent diplopia
• For eg, older patients w/ longstanding strabismus despite presence of significant amblyopia have a
small risk of developing diplopia after strabismus surgery

• Etiology of strabismic amblyopia is similar to that of suppression.
• However,
Suppression restricted to binocular vision ; MonocularVA- normal
Amblyopia exists under binocular and monocular conditions.
• Thus amblyopia may be considered a carryover of suppression into monocular vision, giving
rise to a term, suppression amblyopia
• However, amblyopia may also occur occasionally in strabismus w/out suppression of fovea of
deviated eye.
• Thus, suppression alone cannot always be the cause of amblyopia and other, still unknown
factors may contribute to it.

Features typical of strabismic amblyopia
1. Relatively mild vision loss
2.Grating acuity
Ability to detect patterns composed of uniformly spaced stripes
• often reduced considerably less than recognition acuity measured w/ optotype charts
• Tests based on grating detection eg ,Teller Acuity Cards II and the LEA Grating AcuityTest

2. Neutral density filter effect
• Neutral density filters reduce overall luminance w/out inducing a color change.
• Decreased luminance of visual target  diminished central acuity in normal eyes.
• Decreased illumination of visual targets has less effect on amblyopic eyes as they are not
using central acuity.

• Intraocular differences inVision b/w amblyopic eye and sound eye diminish when patient
looks through a ND filter
eg, a patient with a left amblyopia
in photopic conditions , Vision RE 6/6 LE 6/18 (4 lines difference)
In scotopic conditions, Vision RE 6/12 LE 6/18 (1 line difference)

3. Minor degrees of eccentric fixation
• All amblyopes have some degree of extrafoveal fixation.
• As Fovea is not fixating ,Consistent use of a nonfoveal region for monocular viewing
• Clinically evident eccentric fixation detected by observing a decentered position of corneal
light reflex from fixating amblyopic eye while dominant eye is covered.
• It impliesVA of 6/60 or worse and a poorer prognosis for visual recovery w/ treatment.

Bangerter’s classification of fixation pattern in amblyopia is as follows:
I. Central fixation
II. Eccentric fixation (nonfoveolar)
depending on the retinal area with which the eye appears to fixate
 parafoveolar (adjacent to the foveolar reflex)
 parafoveal (outside but close to the foveal wall)
peripherally eccentric (somewhere b/w edge of the fovea and the disk and occasionally
even beyond the disk).
III. No fixation

• Patients w/ eccentric fixation appear to be looking to the side, not directly at fixation target.
• They have poor smooth pursuits, so they do not accurately follow a moving target.
• Mild amblyopes (6/12– 6/36)  fixate so close to fovea that they appear to fixate centrally
• Severe amblyopes ( 6/60 –CF) use a large parafoveal area for viewing which is not a
pinpoint location but a general area of viewing.
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• Nonfoveolar fixation occurs not only with horizontal but also with vertical eccentricity
• Nonfoveolar fixation always covers an area that is larger the farther it is from the fovea.

• Central as well as nonfoveolar fixation may be steady or wandering.
• Wandering fixation, which occurs only upon covering sound eye, must be distinguished from
the monocular, spontaneous, pendular and vertical oscillations occasionally found in deeply
amblyopic eyes.
• This condition has been designated as the Heimann- Bielschowsky phenomenon.
Normally
• In esotropia  nasal eccentricity of fixation
• In exotropia  temporal eccentricity of fixation.
However ,there are esotropic patients w/ temporal eccentric fixation and exotropic patients w/
nasal eccentric fixation (paradoxical fixation behavior)
• This occurs most frequently in patients w/ consecutive deviations fol Sx
eg, a formerly esotropic patient w/ long-standing amblyopia becomes exotropic, or vice versa.
• This may appear as a primary anomaly.

ARC is quite different from eccentric fixation.
Anomalous retinal correspondence (ARC) –
• Binocular sensory adaptation to strabismus that allows acceptance of images on
noncorresponding retinal points.
• Only active during binocular viewing
• When 1 eye is covered, fixation reverts back to true fovea.
Eccentric fixation
• Dense amblyopia w/out foveal fixation
• Present under monocular or binocular conditions.
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AMBLYOPIA
Strabismic
Monocular
pattern
distortion
Bilateral pattern
distortion
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SUPPRESSION
&
PATTERN DISTORTION

Unilateral or Monocular Pattern Distortion Amblyopia
• Amblyopia ass w/ monocular image blur- “pattern deprivation amblyopia”
• This term is misleading, because
U/L or asymmetrical image blur
pattern distortion and cortical suppression
amblyopia & loss of binocularity depending on the severity of the condition
• A significant blurred image during infancy  severe amblyopia.
• Vision can be as poor as CF w/ total loss of binocular function manifested by development of
sensory strabismus.
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Causes of U/L Blurred image
• Anisometropia
Hyperopia >+1.5 D
Myopia >-3 D
Meridional >+1.5D
• Media Opacities
U/L cataract
U/L corneal opacity
U/L vit h’ge
U/l vit opacity
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• Diff in Ref Error  Image on 1 retina chronically defocused  U/L or asymmetrical image blur
• Foveal pattern vision deprivation plays a further role in anisometropic amblyopia.
• However, since degree of amblyopia cannot be consistently correlated w/ degree of
anisometropia, it follows that pattern vision deprivation cannot be the only factor and that
abnormal binocular interaction caused by unequal foveal images in 2 eyes also must play a
role in production of anisometropic amblyopia.

Anisometropic amblyopia
• One of the most comm types of amblyopia
• This results
 partly from direct effect of image blur
partly from interocular competition or inhibition similar (but not identical) to strabismic amblyopia
• Most patients have straight eyes and appear normal, so only way to identify  vision
screening
• Most patients have relatively good stereopsis ( 70 - 3000s arc), thus Stereo acuity testing
limited value in screening
• Patients usually have peripheral fusion, and most have monofixation syndrome
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• There is active inhibition of fovea in anisometropic amblyopia
• Purpose of inhibition  to eliminate sensory interference caused by superimposition of a
focused and a defocused image originating from the fixation point (abnormal binocular
interaction)
• Due to binocularly elicited foveal inhibition, VA of anisometropic eye is lower under binocular
conditions than when tested monocularly.

• Along w/ reduction of centralVA, there is an overall reduction of contrast sensitivity, which
unlike in strabismic amblyopia involves retinal periphery as well.
• As little as 1 D hypermetropic anisometropia and 2 D myopic anisometropia can be ass w/
amblyopia.
• Astigmatic anisometropic amblyopia does not occur unless there is U/L astigmatism > 1.50D
• In many anisometropic amblyopes w/ no apparent strabismus more detailed examination
 reveal microstrabismus
• If anisometropia is optically corrected, Resulting aniseikonia may be another
amblyopiogenic factor, since retinal images of diff sizes may present an obstacle to fusion

MYOPIC ANISOMETROPIC AMBLYOPIA HYPERMETROPIC AMBLYOPIA
Significant in > - 3.00 D Significant in > + 1.50 D
Less amblyogenic More amblyogenic
often amenable to treatment even in late childhood often difficult to treat past 4 or 5 years of age

High myopia
• usually acquired after critical period of visual development
• In unequal myopia,
More myopic eye  used for near work
Less myopic eye  for distance
• The more myopic eye is in focus for near objects and a baby’s world is up close
• Therefore, unless myopia is of a high degree, both retinas receive adequate stimulation and
amblyopia does not develop.
High hypermetropia
• Patients always use the less hypermetropic eye as it requires less accommodative effort
• constant suppression of the more hypermetropic eye.
• Since details clearly focused on fovea of better eye,no stimulus is provided for further
accommodative effort required to produce a clear image in fovea of more hypermetropic eye.
• Retina of more hypermetropic eye never receives a clearly defined image

AMBLYOPIA
Strabismic
Monocular
pattern
distortion
Bilateral pattern
distortion
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SUPPRESSION
&
PATTERN DISTORTION

Bilateral Pattern Distortion Amblyopia
Pattern distortion in its pure form w/out suppression occurs when there is B/L symmetrical
image blur and no strabismus.
Causes of pure image blur
1. B/l high hypermetropia
2. B/l symmetrical astigmatism
3. B/l ocular opacities such as b/l cong cataracts
4. B/l Peter’s anomaly
• B/l pattern distortion  b/l poor vision.
• Depending on the extent of the distortion, some binocular fusion can develop, usually ass w/
gross stereopsis
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Mechanism:
• Deleterious effect of blurred retinal images on immature visual system.
• Hyperopia > 4.00–5.00 D and myopia > 5.00–6.00 D  risk of inducing isoametropic amblyopia.
• Severe image blur occur during neonatal period  no pattern stimulation extremely poor
vision and sensory nystagmus
• Presence of sensory nystagmus indicate severe amblyopia
• Acquired opacities > 6 months of age usually do not cause sensory nystagmus as motor
component of fixation is already established.
• Uncorrected b/l astigmatism in early childhood  loss of resolving ability limited to the
chronically blurred meridians (meridional amblyopia).
• Degree of cylindrical isoametropia that produces meridional amblyopia is not known, but most
ophthalmologists recommend correction for > 2.00–3.00 D of cylinder.

Ametropic amblyopia (B/l hypermetropic amblyopia)
• usually occurs w/ hypermetropia > 5.00D w/out significant anisometropia
• VA is decreased in each eye
• Eyes usually straight
• Patients usually have gross stereopsis
• When these patients are 1st given their optical correction VA does not significantly
improve examiner seeks an organic cause for decreased vision.
Rx
• prescribe full hypermetropic correction.
• In most cases,VA will slowly improve if the glasses are worn full-time, with finalVA usually
in the range of 20/30 to 20/25 achieved over a period of 6 months to a year.
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Bilateral meridional amblyopia
• caused by B/L astigmatism
• secondary to pattern distortion
• occurs with astigmatism >2.50D.
• To avoid meridional amblyopia, astigmatisms of
2.50D or more should be treated in preschool children
 >3.00D - 4.00D should be treated in infants
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Visual Deprivation Amblyopia (Amblyopia Ex Anopsia)
stimulus deprivation amblyopia, deprivation amblyopia, visual stimulus deprivation
amblyopia, form vision deprivation amblyopia
• Least common
• Most severe and difficult to treat of the forms of amblyopia
• Due to an eye abnormality that obstructs visual axis or interferes with central vision.
Causes
 congenital or early-acquired cataract(MCC)
U/l Blepharoptosis
periocular lesions that obstruct the visual axis
corneal opacities
vit hemorrhage
Blepharospasm
surgical lid closure
Iatrogenically- prolonged and indiscriminate patching (occlusion amblyopia)
prolonged u/l atropinization

• U/l visual deprivation amblyopia tends to be worse than b/l deprivation of similar degree as
interocular competition adds to direct developmental impact of severe image degradation
• However ,even in b/l cases,VA can be 6/60 or worse.
• Thus, the term amblyopia ex anopsia should be reserved for a condition in which disuse or
understimulation of the retina is primary cause of poor vision.
• Reverse amblyopia- a visual deprivation amblyopia that develops in the fellow eye as a result
of patching (occlusion amblyopia) or penalization.

• As amblyopia responsible for permanent vision loss in many ocular abnormalities of early
childhood - greater urgency in management in children.
• In children < 6 years, dense cataracts occupying > central 3 mm of lens capable of causing
severe visual deprivation amblyopia.
• In children > 6 years ,Similar acquired lens opacities - generally less harmful
• Small ant polar cataracts, around which retinoscopy can be readily performed, and lamellar
cataracts, through which a reasonably good view of the fundus obtained  mild to mod
amblyopia or may have no effect on visual development.
• U/l ant polar cataracts ass w/ anisometropia and subtle optical distortion of surrounding
clear portion of the lens  anisometropic and/or mild visual deprivation amblyopia

• Visual deprivation amblyopia may be U/l or B/l
• U/l form - more severe and often accompanied by secondary (sensory) esotropia or
exotropia.

• Decreased optical quality of image received by fovea of
deprived eye
• Competition exists b/w this blurred image and focused
image received by fovea of healthy eye.
In B/l equal density cataracts , b/l uncorrected high
hypermetropia or astigmatism (ametropic amblyopia) ,
• Optical quality of images decreased equally in BEno
such competitive situation  pattern vision deprivation
is the only amblyopiogenic factor
• In meridional amblyopia,
Accurate cylindrical lenses dont correct vision in certain
astigmatic patients as Selective visual deprivation of visual
stimuli of a certain spatial orientation is caused by
uncorrected astigmatism

Pathophysiology of eccentric fixation
• Eccentric fixation may develop in occluded eye, apparently on a uniocular basis, in patients
who do not have strabismus.
• In patients affected unilaterally because of a cataract or surgical lid closure, both pattern
vision deprivation and abnormal binocular interaction are active amblyopiogenic factors

Idiopathic Amblyopia
• Infrequently occurring
• Absence of usual amblyopiogenic conditions
• In apparently normal patients w/ No h/o strabismus, uncorrected ref errors or visual
deprivation.
• Foveal suppression of amblyopic eye
• It is postulated that binocularly provoked inhibition has been conditioned during infancy by an
amblyopiogenic factor ( such as transient anisometropia ) that persists even though this
original obstacle to bifoveal fusion is no longer evident.
• In support of this are observations that clinically significant astigmatism or anisometropia in
infancy may disappear w/ advancing age.
• As in other forms of amblyopia ,VA improves after patching of sound eye, but amblyopia
recurs when treatment is suspended.

• Functional amblyopia (reversible) should be distinguished from organic amblyopia
(irreversible)
Functional amblyopia
• reversible when treated with appropriate visual stimulation during early childhood
• Recovery depends on
Stage of maturity of visual connections at which abnormal visual experience began
 Duration of deprivation
Age at which therapy was instituted
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Organic Amblyopia
• Poor vision caused by structural abnormalities of eye or brain that are independent of sensory
input, such as optic atrophy, macular scar or anoxic occipital brain damage.
• Includes Loss of vision in 1 eye caused by retinal damage not detectable w/ ophthalmoscope
• Absence of gross, readily detectable anomalies in an eye with reducedVA does not exclude
the possibility of subtle, subophthalmoscopic morphologic changes.
• Clinically, one may assume presence of such changes if adequate amblyopia treatment
improves vision in a patient only to a certain level but is unable to restore standard acuity to
the eye indicating that a reversible amblyopia is superimposed on an irreversible one (so-
called relative amblyopia of Bangerter).
• Kushner showed that relative amblyopia may also coexist in patients w/ organic vision loss
from recognizable structural anomalies of ocular media, retina or optic nerve and responds to
occlusion treatment.
• Does not improve by treatment with visual stimulation

• B/l congenital amblyopia has always been regarded as being organic, w/ patients having
 low vision
 nystagmus
poor color vision (achromatopsia)
defective photopic elements in ERG
• Various studies point to an irreversible, generally defective cone function
• These investigators thus suggested that the older term cong amblyopia be abandoned in
favor of the term cone deficiency syndrome

Amblyopia Secondary to Nystagmus
• Nystagmus may account for reducedVA in its latent and manifest form
• However its not easily determined whether nystagmus is the cause or effect of reducedVA
• Nystagmus cannot always be detected on gross clinical examination because of its small
amplitude and high frequency.
In B/l amblyopia,
• observe fixation behavior in each eye with visuscope or direct ophthalmoscope
• When micronystagmus is present  horizontal to-and-fro oscillations of the eye observed.
• These movements consist of a quick and a slow phase, may exist only in certain gaze positions
• Quite diff from irregular jerky fixation pattern in strabismic amblyope or
pendular slow-frequency nystagmus in blind patients or
in those w/ defects of color vision or ocular pigmentation

Detection and Screening
• Amblyopic vision loss is preventable or reversible w/ timely detection and intervention.
• If children w/ or at risk for amblyopia is identified at young age, prognosis for successful
treatment is best.
• Cong cataracts, RB and cong glaucoma require early treatment during infancy.
• Delay in diagnosis  irreversible vision loss and in RB, even death.
• Patients w/ cong cataracts treated during 1st weeks of life  relatively good prognosis, Sx
performed after 2 to 3 months of age  ass w/ a poor visual outcome.
• Perform effective vision screening for all children from newborn infants to older children.

• Amblyopia is diagnosed when a patient
has a condition known to cause amblyopia
has decreasedVA that cannot be fully explained by physical abnormalities of eye.
• Amblyopia sometimes coexists w/ vision loss directly caused by an uncorrectable structural
abnormality of the eye such as optic nerve hypoplasia or coloboma
• Multiple assessments ofVA are sometimes required in order to determine presence and
severity of amblyopia.

Screening for amblyopia
• Regular screening (based on age) throughout childhood allows for timely detection of vision problems,
including amblyopia.
• performed in primary care offices or as part of community-based programs
1.Testing for risk factors-Strabismus, ocular media opacities, Anisometropia, isoametropia
• corneal light reflex tests
• cover testing
• Brückner test
2. Measurement ofVA
• Snellen s chart in older children
• Instrument-based pediatric vision screening in preschool-aged and younger children.
• portable autorefraction devices  refractive errors
• photoscreening devices, which use optical images of the eye  strabismus, refractive errors, and abnormalities of the red reflex.

1.Red reflex test
• single best vision screening exam for infants and young children
• take less than a minute
• Brückner modification simultaneous b/l red reflex.
• Use direct ophthalmoscope and view the patient’s eyes at a distance of approx 2 feet away
• Use broad beam so both eyes are illuminated at same time.
• Dim room lights and have child look directly into ophthalmoscope light.
• Start w/ low illumination then slowly increase illumination until red reflex is seen.
• You will observe a red reflex that fills the pupil and a small (approx 1 mm) white light reflex that
appears to reflect off the cornea
• White light reflex is actually a reflex coming from just behind the pupil and is the “corneal light
reflex” or the “Hirschberg reflex.”
• Thus, the Brückner test gives both a red reflex and the corneal light reflex simultaneously.
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• The key sign of a normal exam is symmetry.
• detect the vast majority of eye pathology
• Abnormal red reflex  an immediate referral to an ophthalmologist
• Blockage of retinal image or large retinal pathology  abnormal red reflex
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CATARACT either block red reflex (Dark or dull reflex) or reflect light to give white reflex (Leukocoria)
VITREOUS H’GE Blocks red reflex (Dark or dull reflex)
RETINOBLASTOMA yellowish-white color and will produce a yellow reflex (LEUKOCORIA)
ANISOMETROPIA unequal red reflex
STRABISMUS a brighter red reflex in the deviated eye, and the corneal light reflex will be decentered

2.Visual AcuityTesting
• Vision screening examinations should start at birth and continue as part of routine checkups for
primary care physicians.
• Acronym I-ARM (inspection—acuity, red reflex, and motility) can be a helpful reminder of the
essential parts of a pediatric screening examination.
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• VA in preschool children (2-3 years ) by
• Allen picture figures
• LEA figures
• HOTV
• lliterate E game
• Wright figures (composed of black and white bars with a constant gap throughout the
figure )
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3.ColorVisionTest
• Color sense in severely amblyopic eyes often abnormal
• Color vision defect resembles one detected in normal eyes when eccentric retinal areas are
tested.
• Thus an erratic response in deep amblyopia could simply be a function of the eccentricity of
fixation
• Color vision is normal in patients w/ functional (reversible) amblyopic and central fixation.
• Thus presence of changes in color sense in patients w/ questionable amblyopia could be used
to diff b/w functional amblyopia and any superimposed organic factors.
• Subtle afferent pupillary defects occur rarely and only in severe cases of amblyopia.
4. Grating Acuity - Teller Acuity Cards II and the LEA Grating AcuityTest
often reduced considerably less
5. Neutral Density Filter- less effect onAmblyogenic eyes as the sound eye

6.Fixation preferenceTesting for Amblyopia
• Widely used in presumptive diagnosis of amblyopia
• often serves as the only guide to monitor effect of occlusion therapy in preverbal children
In a young patient, clinician should keep certain considerations in mind.
1. False-positive results can occur.
• For eg, a child w/ small-angle strabismus may show a strong fixation preference despiteVA
in 2 eyes being equal or nearly so.
2. The young child’s brief attention span frequently results in measurements that fall short
of true limits of acuity; these measurements can mimic those of B/l amblyopia or obscure or
falsely suggest a significant interocular difference.
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Preverbal children can be tested for amblyopia by examining the quality of monocular fixation or
binocular fixation preference to identify amblyopia that might be missed by monocular fixation testing.
MONOCULAR FIXATION TESTING
• Normally developed children at 2 to 3 months of age  central fixation w/ accurate smooth pursuit
and saccadic refixation eye movements.
ToTest for central fixation
1. Cover one of the patient’s eyes
2. Then move a target slowly back and forth to observe accuracy of fixation.
A child w/ central fixation looks directly at the target, visually locks on the target, and accurately
follows moving target.
• Infants often find the human face a much more compelling target than toys or pictures, so try
moving examiner’s head side to side to evaluate the quality of fixation.
• Central fixation indicates foveal vision usually in the range of 6/36 or better.
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• Based on the premise that strong fixation preference
indicates amblyopia.
• If a patient with strabismus spontaneously alternates
fixation, using 1 eye, then the other, this indicates equal
fixation preference and no amblyopia .
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• If child repeatedly and strongly objects to fixating eye being
covered but doesnt mind cover placed over deviated eyeVA in
deviated eye is severely reduced
• This conclusion is reinforced when the child performs searching,
nystagmoid movements w/ deviated eye when fixating eye is
covered.
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• Patients w/ a fixation preference may have amblyopia.
• Strength of fixation preference indicates if amblyopia is present, w/ the weaker preference for 1 eye
being the amblyopic eye.
• Fixation preference can be quantified by briefly covering preferred eye to force fixation to
nonpreferred eye.
• Remove cover from preferred eye, then observe how well and how long the patient will maintain
fixation w/ the nonpreferred eye before refixating back to preferred eye.
• If fixation immediately goes back to preferred eye after the cover is removed, then this indicates
strong fixation preference for the preferred eye and amblyopia of the deviated eye .
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• However, if patient maintains fixation with the nonpreferred eye through smooth pursuit, through a
blink, or for at least 5 s mild fixation preference and no significant amblyopia (vision within 2
Snellen lines difference)
• Ability to maintain fixation w/ nonpreferred eye while following a moving target is a very reliable
indicator of equal vision and detects no significant amblyopia.
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With free alternation one may safely
assume that amblyopia is absent.
If a patient habitually prefers
one eye for fixation, the degree
of this preference may provide
insight into the functional state
of the habitually deviated eye

• Observe length of time required for fixating eye to resume fixation once cover is removed
• If this occurs after a few seconds and before the next blink a strong fixation preference
exists and deviated eye is probably amblyopic.
• However, when formerly deviated eye holds fixation beyond next blink, amblyopia is
probably absent.
• In microtropic or orthotropic children, fixation preference is more difficult to establish.

• However strong fixation preference may occur in absence of amblyopia, esp in small angle
esotropias.
• Also, fixation preference valid as an indirect test of amblyopia only for patients < 5 years
since it is generally impossible to achieve free alternation of fixation in patients who have
reached full vision in the formerly amblyopic eye after 5th year of age
• Specific attention to be paid to the point at which fixation switch occurs as eye follows a
fixation target from adduction to abduction.
 If there is equalVA in both eyes this switch will occur close to primary position
If amblyopia is present ,sound eye will continue to follow fixation target beyond the
primary position into abduction before the amblyopic eye will take up fixation

• Reliability of fixation preference testing for diagnosing amblyopia quite good in large-angle
strabismus > 10 to 15 PD.
• Patients w/ small-angle strabismus, however, will show strong fixation preference in 50% to
70% of cases, even if the vision is equal to within a 2 Snellen lines difference.
• This high overdiagnosis rate in children w/ small-angle strabismus occurs because they have
monofixation syndrome.
• These patients have peripheral fusion but suppress one fovea, so they show strong fixation
preference even if vision is equal.
• This can be rectified by using the vertical prism test, which disrupts peripheral fusion and
temporarily breaks down the monofixation syndrome.
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7.VERTICAL PRISMTEST
(Induced tropia test, 10 diopter fixation test)
• In preverbal children w/ straight eyes or small-angle strabismus.
• Place 10 to 15 D prism base-up or base-down in front of 1 eyeinduces a vertical tropia
• With the induced vertical strabismus, fixation preference can be determined
• If the patient can hold fixation with either eye through a blink or through smooth pursuit eye
movements, no significant amblyopia is present.
• A strong fixation preference indicates amblyopia.
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• In Figure 1, the prism is placed over the left eye, but
the patient still fixates with the right eye, evidenced
by the fact that both eyes are in primary position,
ignoring the prism in front of the left eye
• In Figure2, a base-down prism is placed over the
right eye.The right eye is fixing because both eyes
move up as the right eye fixates through the prism.
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8. Determining Eccentric Fixation
• Grossly eccentric fixation established by
1. holding a small light source in front of the patient’s eyes in the midline of his head
2. the fixating eye is covered
3. the patient is asked to fixate the light with the amblyopic eye.
• If the eye has grossly eccentric fixation, it will make no movement of redress, or perhaps only a
small one, but the reflection of the light will not be centered in the pupil
For routine use, the ophthalmoscope is the most convenient method to determine fixation behavior.

• To detect the more subtle forms of eccentric fixation, it is necessary to resort to entoptic
phenomena marking the fovea as Haidinger’s brushes or Maxwell’s spot
• Both phenomena were originally employed to assess the anatomical integrity of the fovea.
Haidinger’s brushes
• yellowish, brushlike shapes that seem to radiate from the point of fixation when
polarized, preferably blue light is viewed.
• With central fixation center of brushes is superimposed on the fixation point; with eccentric fixation
the brushes appear peripheral to fixation point.
Maxwell’s spot
• another entoptic phenomenon whereby macular region is represented by a dark spot appearing in
blue region of the visible spectrum.
• Its position, relative to that of a fixation mark, should be a sensitive index of the retinal area used for
fixation.

Visuscope
• To identify eccentric fixation point in older cooperative children
• A type of direct ophthalmoscope that projects a focused image onto the retina so examiner
can see image on the retina.
• First, Image is projected onto parafoveal retina, then patient is asked to look at the image.
• If the patient has central fixation, patient refixates to place image precisely on the fovea.
• However, w/ eccentric fixation,patient will view w/ parafoveal retinal area and show a
wandering, unsteady fixation.
• The more peripheral the eccentric fixation, the denser the amblyopia.
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BILATERAL ECCENTRIC FIXATION
• May occur in patients w/out strabismus and w/ b/l central scotomas caused by macular
disease.

In patients w/ latent nystagmus
• Patients w/ strabismus often have latent nystagmus
• horizontal jerk nystagmus that occurs or gets worse in both eyes if one eye is occluded.
• Thus, covering one eye in a patient will increase nystagmus and diminishVA
• To evaluate monocular visual function, blur one eye w/ a plus lens rather than occluding
• Blurring one eye induces less nystagmus than occlusion.
• Use the min amount of plus necessary to force fixation to the fellow eye.
• Usually, a 5.00D lens is sufficient to blur distance vision enough to force fixation to the
fellow eye.
• Linear presentation of optotypes is difficult for patients w/ nystagmus as the optotypes tend
to run together, so try a single optotype presentation.
• Also, take a binocularVA measurement in addition to a monocular acuity in patients w/
nystagmus because binocular vision is usually better than monocular vision.
• To assess the best functionalVA potential in a patient with nystagmus, test binocular vision
while allowing the patient to adopt their preferred face turn or head tilt.
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CROSS-FIXATION
• Patients w/ a large-angle esotropia and tight medial rectus muscles will have difficulty
bringing eyes to primary position, so eyes stay adducted.
• These patients “cross-fixate.”
• Right adducted eye fixes on objects in left gaze, and left adducted eye fixates on objects in
right gaze.
• Cross-fixation has been said to be a sign of equal vision
• Cross-fixation does not guarantee that a patient sees equally with each eye.
• Ability to hold fixation past midline or to hold fixation through smooth pursuit with either eye
is a better criterion for equal vision.
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EFFECT OF EYE POSITION AND OPERATIONS.
• Fixation area of an amblyopic eye may change w/ changes in direction of gaze
• A patient with LR Palsy who is unable to abduct his or her eye to the midline may have very
poor vision in that eye with the head straight but may reach normal or about normal vision
with the head turned so that the image of the test object falls on the foveola.
• Improvement inVA sometimes observed after operative straightening of amblyopic eye
• Eyes capable of spontaneous visual improvement will improve if an operation places them
mechanically in such a position that stimulation of the foveola by the object of attention is
facilitated.

CLINICAL SIGNIFICANCE.
• Steady and peripheral eccentric fixation is an unfavorable sign
• unsteady and wandering fixation are more favorable prognostic signs.
• It does not follow that standard vision can be more readily and permanently restored to an
eye that already has central fixation.
• On the other hand, as it is often difficult to be sure of the presence of central or eccentric
fixation at an early age,it is always appropriate to start treatment with direct occlusion.
• Inverse occlusion is sometimes indicated at beginning of therapy in cases of steady eccentric
fixation.
• Monitoring the fixation behavior in addition to checkingVA may be helpful during Rx for
amblyopia.
• Determination of the fixation behavior is indispensable to the diagnosis of microstrabismus

The Sensitive Period(critical, or susceptible period)
• Capacity of visual system to develop amblyopia is limited by its state of maturity.
• During immaturity of visual system , retinocortical connections are not firmly established
and may be modified by the quantity or quality of the visual input.
• Once visual system reaches maturity, functional modifications by abnormal visual
experience no longer occur.
Identify
Sensitive period during which amblyopia may develop
Sensitive period during which amblyopia, once treated and even cured, may recur
Sensitive period during which amblyopia is reversible.
• These different sensitive periods are not identical

• Capacity to develop strabismic amblyopia extends up to the 7th year of life.
• After that age it would be most unusual for strabismic amblyopia to develop, although milder
and reversible forms of visual deprivation amblyopia may occasionally still be observed.
• Sensitive period during which strabismic amblyopia, once improved or even cured by
treatment, may relapse extends beyond 7TH year of life
• Milder degrees of recurrence can occur as late as early teens.
• The sensitive period during which recovery is possible is less well defined although there
seems to be general agreement that it ends with the 8th year of life.
• On the other hand, Partial or even full recovery ofVA may take place in adults w/ strabismic
amblyopia after loss of vision in the normal eye.
• Individual variability is the hallmark of all sensitive periods; exceptions do occur and may be
related to interindividual differences in the rate of maturation of the visual system.

• When the clinician encounters a doubtful or borderline case and the patient is a young child,
it is appropriate to undertake a trial of amblyopia treatment.
• Improvement in vision confirms that amblyopia was indeed present.
• In some circumstances, it is appropriate to assume that amblyopia is present and to begin
treatment even before decreased vision has been conclusively determined.
• Examples include initiating occlusion therapy with the presence of a high degree of
anisometropia or shortly after surgery for a unilateral cataract.

AMBLYOPIATREATMENT
• Early treatment of amblyopia  bestVA results.
• Basic strategy during the period of visual plasticity (birth to 8 years) is to
1. provide a clear retinal image
2. correct ocular dominance if dominance is present, as early as possible
Correction of ocular dominance  by forcing fixation to amblyopic eye through patching or
blurring vision of sound eye.
Treatment of amblyopia involves the following steps:
1. Eliminate any obstruction of visual axis, such as a cataract.
2. Correct any significant refractive error.
3. Force use of amblyopic eye by limiting use of better eye.
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Clear retinal image
Cataract Removal
• Cataracts capable of producing amblyopia require timely surgery.
• Removal of u/l visually significant cong lens opacities during 1st 4–6 weeks of life necessary for
optimal recovery of vision.
• Significant cataracts w/ uncertain time of onset also deserve prompt and aggressive Rx if
recent development is at least a possibility.

Refractive Correction
• Optical prescription based on the refractive error determined w/ cycloplegia.
• As an amblyopic eye’s ability to control accommodation tends to be impaired, this eye
cannot be relied on to compensate for uncorrected hyperopia as would a normal child’s eye.
• However symmetric reductions in plus power may be required to foster acceptance of
spectacle wear.
• Refractive correction for aphakia fol cat surgery in childhood must be provided promptly to
avoid prolonging visual deprivation that occurs due to a severe uncorrected refractive error.
• Anisometropic, isoametropic, and even strabismic amblyopia may improve or resolve w/ only
refractive correction.
• Many ophthalmologists initiate Rx w/ refractive correction alone, adding occlusion or
penalization later if needed.
• Role of refractive surgery in patients who fail conventional treatment with spectacles and/or
contact lenses is under investigation.

In b/l hypermetropia (5.00D),
• Give full hypermetropic correction, as amblyopic eyes do not fully accommodate.
• Patients given partial correction  very slow or no improvement in their amblyopia.
In large astigmatism (2.50D) (amblyopia secondary to astigmatism or meridional amblyopia)
• Prescribe the full astigmatic correction to provide a clear retinal image.
• Consider correcting astigmatisms of 2.50 to 3.00 or more in small children, even if
astigmatism is b/l.
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• Most anisometropic amblyopes will respond to glasses alone with no or minimal part-time
occlusion of the good eye.
• Children with media opacities, such as a visually significant cataract, should have immediate
surgery with visual rehabilitation using a contact lens or intraocular lens.
• Early treatment is critical; infants w/ a congenital cataract should undergo surgery within 1st
month of life, even as early as 1st week.
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Correct Ocular Dominance
OCCLUSIONTHERAPY (PATCHING )
• Sound eye is covered, obligating child to use amblyopic eye.
• Strabismic patients w/out binocular fusion can be treated w/ full-time occlusion;
• However, full-time occlusion may cause reverse amblyopia in children < 4 to 5 years.
• Adhesive patches are usually used
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• In case of skin irritation or inadequate adhesion - Spectacle-mounted occluders or opaque
contact lenses
• With spectacle-mounted occluders, close supervision to ensure that patient does not peek
around the occluder.
• To prevent reverse amblyopia, do not use full-time occlusion for > 1 week per the child’s age
in years without reexamining vision of the good eye.
• For eg, a 2-year-old child receiving full-time occlusion should be examined every 2 weeks.

Part-time occlusion
• defined as occlusion for 2–6 hours per day
• Shown to achieve results similar to those of prescribed full-time occlusion.
• Relative duration of patch-on and patch-off intervals should reflect degree of amblyopia.
• For severe deficits (VA of 6/36– 3/60), 6 hours per day is preferred.
• Maintenance patching of 1–2 hours per day often prescribed to prevent recurrence of
amblyopia after successful patching.
• Reduces likelihood of occlusion amblyopia or induced strabismus
Full-time occlusion
• Occlusion of the sound eye during all waking hours.
• In rare cases, w/ aggressive patching, strabismus occur due to lack of binocular viewing and
tenuous fusion.
• Therefore, the child whose eyes are consistently or intermittently straight may benefit from
being given some opportunity to see binocularly.

• Amblyopic patients w/ essentially straight eyes (tropias< 8 PD) and peripheral fusion (e.g.,
anisometropic amblyopia and microtropia monofixators) best treated w/ part-time
patching (3 to 4 h/day) or no occlusion.
For anisometropic amblyopia,
• Initially prescribe spectacle correction
• Follow patient each month forVA improvement.
• If vision does not improve on monthly follow-ups, then start part-time patching
• Part-time occlusion or penalization therapy preferred as these methods preserve fusion.
• If vision does not improve with part-time occlusion, then full-time occlusion should be tried.
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• Timing of follow-up should be related to intensity of treatment and age of the child.
• An examination typically scheduled w/in 2–3 months after initiation of Rx
• Subsequent visits can be scheduled at longer intervals based on early response.
• Desired endpoint of therapy for u/l amblyopia is
free alternation of fixation
linear recognition acuity that differs by no more than 1 line b/w 2 eyes
 or both
• Time required for completion of Rx depends on
 severity of amblyopia
choice and intensity of therapeutic approach
 adherence to treatment
age of the patient
• More severe amblyopia and older age - more intensive or longer Rx

• Consistent occlusion during infancy may reverse substantial strabismic amblyopia in < 1
month
• In contrast, an older child who wears a patch only after school and on weekends may require
several months to overcome a moderate deficit.
• Adherence to occlusion therapy declines with increasing age.
• However, studies in older children and teenagers with strabismic or anisometropic
amblyopia have shown that Rx can still be beneficial beyond 1st decade of life.
• This is especially true in children who have not previously undergone treatment.

PENALIZATION
• A method for blurring sound eye to force fixation to amblyopic eye.
• As effective as patching for mild to mod amblyopia (visual acuity of 20/100 or better).
• A cycloplegic agent (usually atropine 1% solution) administered to better-seeing eye so that
it is unable to accommodate.
• As a result, better eye experiences blur w/ near viewing and also, if hyperopia is
undercorrected, w/ distance viewing.
• Penalization actually switches ocular suppression, which can be demonstrated by
a Polaroid vectographic chart or by theWorth 4-dot test.
• Penalization only works if fixation is switched from the sound eye to the amblyopic eye.
• Blurring of the sound eye can be achieved by various methods.
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Optical penalization
• based on over-plussing (prescribing more plus sphere than needed) sound eye to force
fixation to the amblyopic eye for distance targets
• Patient will usually use sound eye for near targets.
• works well for mild amblyopia
• however, some children will look over the tops of their glasses to use their sound eye.

• Optical penalization involves the prescription of excessive plus lenses (fogging) or diffusing
filters for the sound eye.
• This form of treatment avoids potential pharmacologic adverse effects and may be capable
of inducing greater blur.
• If the child wears glasses, application of a translucent filter, such as Scotch MagicTape or a
Bangerter foil to the spectacle lens can be tried.
• Optical penalization may be more acceptable than occlusion therapy to many children and
their parents, but patients must be closely monitored to ensure proper utilization (no
peeking) of spectacle-borne devices.

Atropine penalization
• stronger form of penalization
• useful even in dense amblyopia so long as patient has significant hypermetropia of good
eye.
• Atropine at 0.5% or 1% is placed in the sound eye each day
• optical correction is removed from sound eye, amblyopic eye is given full optical
correction.
• If the patient switches fixation to amblyopic eye under these conditions of penalization,
then penalization will improve vision.

• Cyclopentolate can be used as an in-office test to predict if penalization will work.
• The in-office test consists of providing amblyopic eye w/ full optical correction while
deadening sound eye w/ cyclopentolate and removing optical correction from sound eye
• If fixation switches to amblyopic eye under these conditions patient will improve w/
atropine penalization.
• Atropine penalization usually requires 3.00 or more hypermetropia in sound eye to obtain
significant blur to switch fixation.
• Blurring sound eye to aVA lower than amblyopic eye does not guarantee a switch in fixation
to amblyopic eye.
• Penalization in young children may result in reverse amblyopia (decrease vision in the
previously good eye), so patients 4 years of age or younger should be followed closely when
undergoing atropine penalization therapy.
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• This form of treatment has been demonstrated to be as Atropine may be administered daily,
but weekend administration is as effective for milder amblyopia.
• Depending on depth of amblyopia and response to prior treatment, hyperopic correction of
the dominant eye can be reduced to enhance the effect.
• Regular follow-up of patients whose amblyopia is being treated w/ cycloplegia is important in
order to monitor for reverse amblyopia .
• Pharmacologic penalization offers advantage of being difficult for the child to thwart.
• It does not work well for myopic patients, however, because clear near vision persists in the
penalized eye despite cycloplegia.

OCCLUSIVE CONTACT LENS
• Occlusive contact lens can be used in treating amblyopia.
• should only be considered as a last resort and that these patients require close follow-up.
• complications limited the usefulness
• High recurrence to pretreatmentVA, included conjunctival irritation and poor contact lens fit
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LEVODOPA/CARBIDOPA INTHETREATMENT OF AMBLYOPIA
• Traditionally used to treat Parkinson’s disease.
• Levodopa is a precursor for the catecholamine dopamine, a neurotransmitter/
neuromodulator known to influence receptive fields.
• Levodopa/carbidopa has been studied as an adjunct to patching for the treatment of
amblyopia.
• Treatment remains controversial, as VA improvement has been relatively small, not clearly
better than with patching alone, and there are questions regarding long-term stability of
vision.
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PLEOPTICS
• Pleoptics is a method of treating eccentric fixation associated with dense amblyopia.
• A bright ring of light is flashed around the fovea to temporarily “blind” or saturate the
photoreceptors surrounding the fovea, which eliminates vision from the eccentric fixation
point and forces fixation to the fovea.
• Pleoptic treatments are given several times a week to enhance occlusion therapy.
• Most practitioners found pleoptics to be no better than standard occlusion therapy.
ACTIVE STIMULATION
• Some investigators have suggested active stimulation of the amblyopic eye as a way to
improve vision in the amblyopic eye.
• A high-contrast spinning disc with square-wave grading was one method that has been tried
(CAM).
• CAM treatment has been found to be no better than standard occlusion therapy.
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Complications ofTherapy
• In Occlusion therapy and penalization,risk of overtreatment reverse amblyopia in sound eye
• Development of strabismus is also a risk.
• Full-time occlusion greatest risk of reverse amblyopia and of strabismus
• Consequently, most ophthalmologists do not use full-time occlusion in younger children.
• Parents of a strabismic child should be instructed to watch for a switch in fixation preference
and to report its occurrence promptly.
• Iatrogenic reverse amblyopia can usually be treated successfully w/ judicious patching of the
formerly better-seeing eye or by alternating occlusion.
• Sometimes, simply stopping treatment leads to equalization of vision.

Adherence issues
• Lack of adherence to the therapeutic regimen can prolong Rx period or cause outright failure.
• If difficulties derive from a particular Rx method, clinician should seek a suitable alternative.
• Families who appear to lack sufficient motivation should be counseled
• In infants and toddlers, physical methods such as wearing arm splints or mittens or making
the patch more adhesive with tincture of benzoin may be useful.
• For children > 3 years, creating goals and offering rewards tend to work well, as does linking
patching to play activities
• eg, decorating the patch or patching while the child plays a video game.
• In some patients, skin irritation due to the adhesive may develop.
• Switching to a different brand of patch or preparing the skin with tincture of benzoin can
eliminate most skin related problems.

Unresponsiveness
• Complete or partial unresponsiveness to Rx occasionally affects younger children but more
often occurs in patients > 5 years.
• A repeat comprehensive eye examination to look for potential subtle optic nerve or retinal
anomalies is indicated when there is a significant deviation from expected response to
amblyopia Rx in the face of good adherence to the program.
• Neuroimaging might be considered in cases that inexplicably fail to respond to treatment.
• The decision whether to initiate or continue treatment in a prognostically unfavorable
situation should take into account the wishes of the patient and family.
• Primary therapy should generally be terminated if there is a lack of demonstrable progress
over 3–6 months despite good treatment adherence.
• Amblyopia is not always fully correctable, even at younger ages of treatment.

Recurrence
• When amblyopia treatment is discontinued after complete or partial improvement of vision,
approximately 1/3 rd of patients show some degree of recurrence.
• Reducing the occlusion regimen to 1–2 hours per day or the frequency of pharmacologic
penalization for a few months before cessation decreases the incidence of recurrence.
• If recurrence occurs,VA can usually be improved again with resumption of therapy.
• If the need for maintenance therapy is established, treatment must be continued until
stability of vision is demonstrated with no treatment other than regular spectacles.
• This may require periodic monitoring until age 8–10 years.
• As long as vision remains stable, intervals of up to 12 months between follow-up visits are
acceptable.
• Improvement in vision that is obtained in most children treated between 7 and 12 years of
age is sustained following cessation of treatment.

PROGNOSIS OF AMBLYOPIA
• Depends upon the age of the patient, severity and type of amblyopia
• The earlier the amblyopia occurs and longer it remains untreated, the worse the prognosis.
• In general, b/l amblyopia responds better than u/l amblyopia, and myopic anisometropic
amblyopia responds better than hypermetropic anisometropic amblyopia.
• VA improvement has been documented when children are treated in late childhood after 8
years of age.
• Even adults with dense amblyopia can showVA improvement and prolonged plasticity.
• SignificantVA improvement of the amblyopic eye has been reported in adults who have lost
vision in their good eye and relied on the amblyopic eye for their vision.
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ClinicalTrials in Amblyopia
• Much of the information gained in the past few years has been from studies conducted
by the Pediatric Eye Disease Investigator Group (PEDIG)
• PEDIG studies use a standardVA testing protocol.
• For children< age 7, HOTV letters are presented individually with surround bars to
account for the crowding phenomenon in amblyopia (single-surround HOTV optotypes)
• older children use the electronic ETDRS vision test.

AmblyopiaTreatment Study (ATS) – 1
Purpose
1.To compare patching and atropine as treatments for moderate amblyopia (6/12 to 6/36) in
the amblyopic eye) in children 3 to 7 years old
2.To develop estimates of the success rates of treatment.
3.To identify factors that may be associated with successful treatment
A patient was considered to be successfully treated w/ regard to protocol when amblyopic
eye’sVA was 20/30 or better or had improved 3 or more lines from baseline.
Conclusion :
• Atropine or patching for 6 months followed by best clinical care until 2 years produced
similar improvement of moderate amblyopia in children between 3 and 7 years of age at
enrolment.
• However, on average the amblyopic eye acuity was still approximately 2 lines worse than the
sound eye.
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ATS – 2A
• Purpose
To compare full-time patching (all hours or all but 1 hour per day) to 6 hours of patching per day, as
prescribed treatments for severe amblyopia (20/100 to 20/400) in children < 7 years.
Conclusion
• 6 hours of prescribed daily patching produces an improvement inVA that is of similar rate and
magnitude to the improvement produced by prescribed full-time patching in treating severe
amblyopia in children 3 to less than 7 years of age.
• Prescribing fewer hours of daily patching may ease the implementation of patching therapy and
monitoring of compliance for some parents.

ATS – 2B
Purpose
• To compare 2 hours vs 6 hours of daily patching as treatments for moderate amblyopia
(20/40 to 20/80) in children younger than 7 years.
Conclusion
• When combined with prescribing 1 hour of near visual activities, 2 hours of daily patching
produces an improvement in visual acuity that is of similar magnitude to the improvement
produced by 6 hours of daily patching in treating moderate amblyopia in children aged 3–7
years.
• A shorter duration of patching may ease the implementation of patching therapy and
monitoring compliance for some parents

ATS – 2C
Purpose
• To conduct a prospective study of children who had been successfully treated for amblyopia
and for whom treatment was to be stopped to estimate the risk of amblyopia recurrence
during the following year.
Conclusion
• Approximately one fourth of successfully treated amblyopic children experience a recurrence
within the first year off treatment
• Follow-up through at least 1 year is needed, but follow-up visits during the first 3 months after
stopping treatment might allow detection and retreatment of the majority of recurrences that
occur during the first year
• For patients treated w/ 6 or more hours of daily patching,risk of recurrence is greater when
patching is stopped abruptly rather than when it’s reduced to 2 hours/day prior to cessation.
• A randomized clinical trial of no weaning versus weaning in successfully-treated amblyopia is
warranted to confirm these observational findings.

Purpose
1.To evaluate effectiveness of treatment of amblyopia in children aged 7 to 17 years.
2.To determine frequency of recurrence of successfully-treated amblyopia in children 7–17 years
Conclusion
• Amblyopia improves with optical correction alone in about one fourth of patients aged 7–17
years, although most patients who are initially treated with optical correction alone will require
additional treatment for amblyopia.
• For patients aged 7–12 years, prescribing 2–6 hours per day of patching with near visual
activities and atropine can improve visual acuity even if amblyopia has been previously treated.
• For patients 13–17 years, prescribing patching 2–6 hours per day with near visual activities may
improve visual acuity when amblyopia has not been previously treated but appears to be of
little benefit if amblyopia was previously treated with patching
• It is not yet known whether visual acuity improvement will be sustained once treatment is
discontinued; therefore, conclusions regarding the long-term benefit of treatment and the
development of treatment recommendations for amblyopia in children 7 years and older await
the results of a follow-up study.

Purpose
1.To compare daily versus weekend atropine (two-days) as prescribed treatments for
moderate amblyopia (20/40 to 20/80) in children 3 to <7 years old.
2.To determine the maximum amount of improvement that could be achieved with these
atropine schedules.
Conclusion
• Weekend atropine provides an improvement inVA of a magnitude similar to that of the
improvement provided by daily atropine in treating moderate amblyopia in children 3–7
years old.

REFERENCES
• AAO Series Paediatric ophthalmology
• BinocularVision and Ocular Motility by Von Noorden
• Pediatric Ophthalmology and Strabismus by Kenneth Wright
• Neuro-Ophthalmology by A K Khurana
• Recent advances in Ophthalmology by HV Nema

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