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Strabismus

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INTRODUCTION
In normal binocular single vision (BSV) the two visualaxes intersect at the point of
fixation, with the imagesfrom the two eyes being aligned by the fusion reflex and
combined by binocular responsive cells in the visualcortex to give BSV.

Definitions
Orthophoriaimplies perfect ocular alignment in the absenceof any
stimulus for fusion; this is uncommon.

Heterophoria (‘phoria’) implies a tendency of the eyes todeviate when

fusion is blocked (latent squint).

Heterotropia (‘tropia’)implies a manifest deviation in

which the visual axes do not intersect at the point offixation.

Esophoria→ latent squint inwards turning of the eyes.

Esotropia→ manifest squint inwards turning of the eyes.

Exophoria→latent squint outwards turning of the eyes.

Exotropia→manifest squint outwards turning of the eyes.

Hyperphoria/Hypertropia→latent/manifest upwards turning of the

eyes.

Hypophoria/Hypotropia→latent/manifest downwards turning of the

eyes.

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Axes of the eye

 Visual axis
passes from the fovea, through the nodal point of the eye
to the point of fixation (object of regard).
The fovea is usually slightly temporal to the geometrical
center of the posterior pole so that visual axis cuts cornea
slightly nasally.
 ANATOMICAL AXIS ( pupillary axis) Is a line passing from
the posterior pole through the center of the cornea.
Because the fovea is usually slightly temporal to the
anatomical center of the posterior pole of
the eye , the visual axis does not usually correspond to the
anatomical axis of the eye.
 Optic axis:line passing through the center of the cornea
(P), center of the lens(N), and meets the retina on the nasal
side of the fovea.
 Fixation axis: line joining the fixation point(O), and the
center of rotation(C).

ANGLE KAPPA Is the angle subtended by the visual and theanatomical

(pupillary axis) axes and is usuallyabout 5 degrees .

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The angle is 'positive' when the fovea is temporalto the center of the
posterior pole resulting ina nasal displacement of the corneal reflexand
'negative' when the converse applies .

ANGLE KAPPA

A large angle kappa may give the appearance ofa squint when none is
present ( pseudosquint ) and is seen most commonly asa pseudo-
exotropia following displacement ofthe macula in ROP where the angle
maysignificantly exceed + 5 degrees.

Orbital bones
Angle of the medial and lateral walls of the orbit is 45°, so the orbital
axis forms approximately 23°with both medial and lateral walls.
The orbits are parallel to each The medial walls of 2 other.

Principle of the ocular movement:

1. Because of pear shape of medial and lateral wall of an orbit are at
the angle of 45° of each other.
2. Orbital axis therefore forms 23° with both medial and lateral wall.
3. When the eye is in primary position the visual axis forms 23° of
angle with the orbital axis.
4. Action of the muscle depend on muscle plane in relation to optical
axis.

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Basic knowledge of ocular motility
Extraocular muscles
• Not playing role in vision procedure directly,
but critically important for eyeball motility and
binocular vision function.

Action of extraocular muscles

i. Rotation around center ofrotation
ii. Centre of rotation lies 12/13 mm behindcornea.
iii. 3 types of rotation:
- Rotation around Fick vertical axis Z—side to side
- Fick horizontal axis X– up and down
- Fick anteroposterior axis Y –torsion

The Listing plane and axes of Fick

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Anatomy of extraocular muscles
There are six extraocular muscles for the human
eye.
Namely:
– Medial rectus m.
– Lateral rectus m.
– Superior rectus m.
– Inferior rectus m.
– Superior oblique m.
– Inferior oblique m.

Extraocular Muscles
 4 rectus muscles - origin is in the common
tendous ring (annulus of Zinn)
– Oval ring of connective tissue
– Continuous with periorbita
– Anterior to optic foramen
 Medial and lateral rectus attached to both the
upper and lower tendon limbs.
 The muscles traveling from the this tendon
ring to the insertions create muscle cone.

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 Medial Rectus:
• Originates on both the upper and lower limbof the common tendous
ring and the opticnerve sheath.
• Length 40 mm , thicker than other EOM
• Inserts along a vertical line 5.5 mm from thecornea.
• Fascial expansion from muscle sheath formsthe medial check ligament
and attach tomedial wall of orbit.

• Innervation is via cranial nerve III,( theoculomotor nerve), inferior

division and runsalong the inside of the muscle cone, on the
lateral surface.
• Blood supple. Medial muscular branch ofophthalmic artery
• action: only adduction.

Lateral rectus
• Originates on both the upper and lower limb of the common tendous
ring. And a process of the greater wing of thesphenoid bone.
• parallels the lateral orbital wall until it passes through a connective
tissue pulleyjust posterior to the equator of the globe; at this point it
follows the curve of theglobe to its insertion.
• Inserts parallel to medial rectus 6.9 mm from the cornea.(Tendon 9.2
mm wide, 8.8 long).
• Fascial expansion from muscle sheath forms the lateralcheck ligament
and attach to lateral wall of orbit atWhitnalls tubercle.

• Innervated by the abducens nerve, Cranial nerve VI which enters the

muscle on the medialsurface.
• The abducens nerve., ophthalmic artery and ciliaryganglion lie medial
to the lateral rectus andbetween it and the optic nerve.
• Blood supple. lateral muscular branch ofophthalmic artery
• Action: only abduction.

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 Superior Rectus
• Originate on superior limb of the tendonousring, and optic nerve
sheath.
• Muscle passes forward underneath thelevator, but the two sheaths are
connectedresulting in coordinated movements.
• Insertion 7.4 mm from limbus, and obliquely.
• The angle from the origin to the insertion is23° beyond the sagital axis.
• Frontal nerve runs above the SRand levator.
• The nasociliary nerve and ophthalmic arteryrun below.
• The tendon for insertion of the superioroblique muscle runs below the
anterior partof the superior rectus.
• Innervation is via superior division of CN III,from the inferior surface;
additional branchesmake their way to the levator.

 Action of Superior Rectus:

- Primary action is elevation . But since the insertion on the globe
is lateral as well as superior, contraction will produce rotation
about the vertical axis toward midline
- Thus secondary action is adduction
- Finally, because the insertion is oblique, contraction produces
torsion nasally Intorsion.

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  When the globe is abducted to 23°, the visual and orbital
axiscoincide. In this position superior rectus acts as a pureelevator.
 If the globe were adducted to 67° the angle between thevisual and
orbital axis would be 90° In this position SRwould act as intortor.

Inferior rectus
• Originates on lower limb of commontendonous ring.
• Inserts 6.7 mm from limbus, insertion is an arc
• It is parallel to superior rectus, making a 23°angle beyond the sagittal
axis.
• Innervated by inferior division of CN III whichruns above it (within the
muscle cone).
• Below is the floor of the orbit and inf. oblique
• Fascial attachments below attached to inferior lid coordinate
depression and lid opening.
• Fascia below Inf. Rectus and Inf. Oblique contribute to the suspensory
ligament oflockwood.
• Primary Action downward gaze depression
• Secondary action: Adduction, as is the casefor SR.
• Also extorsion due to oblique arc of insertion.

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Spiral of Tillaux
• The rectus muscle pass through tenon’scapsule and insert into the
sclera.
• The muscles insert at different distances fromthe cornea.
• The insertion pattern is a spiral with themedial rectus closest to the
cornea (5.5 mm)and the superior rectus the furthest away
from the cornea (7.4 mm).

Superior Oblique
• Anatomical origin is on the lesserwing of the
sphenoid bone. Thephysiological origin is the
trochlea, a cartilagenous “U” on the
superiormedial wall of the orbit.
• Longest thinnest EOM, the muscleends before
the trochlea, tendon is2.5 cm, smooth
movementthroughtrochlea.
• Innervation by CN IV,

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  Action of SO:
• Primary action is intorsion _ rotation of 12o’clock position
toward midline.
• Because the insertion of the oblique muscle isin the lateral,
posterior quadrant thesecondary actions are
– Rotating the back half of the globe from lateral tomedial (the
anterior pole will move away)abduction.
– Also depression (posterior superior quadrant ofthe globe being
pulled upward).

○ When the globe is adducted 51°, the visual axis coincideswith the line
of pull of the muscle. In this position it can act only as a depressor.

○ When the eye is abducted 39°, the visual axis and thesuperior oblique
make an angle of 90° with each other. In this position the superior
oblique can cause onlyintorsion.

Inferior Oblique
• Originates on the maxillary bone inferior to the nasolacrimal fossa. The
ONLY EOM originating in the anterior orbit.
• Inserts on the posterior lateral aspect of globe mostly inferior, below
the ant.-post. Horizontal plane.
• Innervation from inferior division of CN III inserts on the upper surface
(within muscle cone.)
•Action of Inf. Oblique:
- Primary is extorsion

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- Secondary action is due to posterior, lateral,inferior insertion being
pulled around,underneath globe and toward the anterior
inferior insertion medially.
- Rotation about the Z axis will be nasal totemporal (abduction).
- Rotation about the X axis will be elevation.

Basic motility function of the eye ball:

Elevation and depression (A, B)
Adduction and abduction (C, D)
Intorsion and extorsion (E, F)

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MUSCLE PULLEYS
The four rectus muscles pass throughcondensations of connective tissue
and smoothmuscle just posterior to the equator. These condensations
act as pulleys and minimizeupward and downward movements of the of
thebellies of the medial and lateral rectus muscles during up-gaze and
down-gaze, andhorizontal movements of the superior rectus and
inferior rectus bellies in Left and right gaze .

Pulleys are the effective origins Of the rectus muscles and play an
important role in thecoordination of eye movements by reducingthe
effect of horizontal movements on vertical muscle actions and vice
versa.

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Displacement of the pulleys can be one cause ofabnormalities of eye
movements such as V and A patterns.

OCULAR MOVEMENTS
DUCTIONS:
Ductions are monocular movements around the axes ofFick . They
consist of adduction , abduction ,elevation , depression , intorsion and
extorsion .They are tested by occluding the fellow eye and askingthe
patient to follow a target in each direction ofgaze .Torsional ductions are
mainly observed in associationwith other abnormal eye movements.

VERSIONS:
Versions are binocular, simultaneous, conjugatemovements ( in the
same direction ) .
Dextroversion and laevoversion ( gaze right, gaze left ), elevation ( up-
gaze ) anddepression( down-gaze ).
These four movements bring the globe into thesecondary positions of
gaze by rotationaround either a vertical Z or a horizontal X axis
of Fick .
Dextroelevation and dextrodepression ( gaze upand right , gaze down
and right ) andlaevoelevation and laevodepression ( gaze up
and left and gaze down and left ).
These four oblique movements bring the eyesinto the tertiary positions
of gaze by rotationaround oblique axes lying in Listing plane,equivalent
to simultaneous movement aboutboth horizontal and vertical axes .
Torsional movements to maintain uprightimages occur on tilting of the-
head . These are known as the righting reflexes. On head tilt tothe right
the superior limbi of the two eyes rotate to the left, causing intorsion of
theright globe and extorsion of the left.

VERGENCES
Vergences are binocular , simultaneous ,disjugate or disjunctive
movements ( in opposite directions).
Convergence is simultaneous adduction ( inward turning ),divergence is

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outwards movement from a convergent position.
Convergence may be voluntary or reflex. Reflex convergence has four
components:

 Tonic convergence : which implies inherent innervational tone to

the medial recti , when the patient is awake .

 Proximal convergence : is induced by psychological awareness of

a near object.

 Fusional convergence : is an optomotor reflex , which maintains

BSV by insuring that similar images are projected onto
corresponding retinal areas of each eye .

Involves disjugate eye movements to overcome retinal image disparity .

Fusional vergence amplitudes can be measured with prisms or in the
synoptophore .
Normal values are :
Convergence : about 15-20 ∆ for distance and 25 ∆ for near .
Divergence : about 6-10 ∆ for distance and 12- 14 ∆ for near .
Vertical : 2-3 ∆
Cyclovergence : about 2-3 °
Fusional convergence helps to control an exophoria whereas fusional
divergence helps to control an esophoria . The fusional vergence
mechanism may be decreased by fatigue or illness, converting a phoria
to a tropia . The amplitude of fusional vergence mechanisms can be
improved by orthoptic exercises, particularly in the case of near fusional
convergence for the relief of convergence insufficiency.

 Accommodative convergence : is induced by the act of

accommodation as part of the synkinetic - near reflex .
Each diopter of accommodation is accompanied by a constant
increment in accommodative convergence , giving the-
accommodative convergence by accommodation ( AC/A ) ratio.

This is the amount of convergence in prism diopters per diopter change

in accommodation .
The normal value is 3-5 prism diopter, this means that one diopter of

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accommodation is associated with 3-5 prism diopters of accommodative
convergence .

These changes in accommodation , convergence and pupil size, which

occur in response to a change in the distance of viewing are known as
the near triad and occur in response to both image blur and temporal
image disparity.

THE AC/A RATIO:

 Definition: The measurement of theconvergence induced by
accommodation perdiopter of accommodation.
 Purpose: To determine the change inaccommodative
convergence that occurswhen the patient accommodates or
relaxesaccommodates a given amount.
 Importance:
– Significant in:
• Diagnosis.
• Treatment.
 NOTE:
o Distance phoria dependent on Tonic vergence.
o Near phoria dependent on AC/A ratio.

Two ways to determine AC/A ratio:

-Calculation/Heterophoric method.
-Gradient method.

Calculated/Heterophoric method:
• AC/A = IPD (cm) + N (m) (D’-D)
IPD = interpupillary distance in centimeters
N = near fixation distance in meters
D’ = near phoria (eso is plus and exo is minus)
D = distance phoria (eso is plus and exo is minus)

NOTE:
-Be sure to use the correct signs for Eso and Exo.
-Be sure to use correct unit.
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– Example: IPD = 60 mm, the patient is 2Δ exophoric
at distance and 10Δ exophoric at near (40 cm)
AC/A = 6 + 0.4(-10 - (-2))
= 6 + 0.4(-10 + 2)
= 6 + 0.4(-8) = 6 + (-3.2)
= 2.8

-Example: IPD = 56 mm, the patient is 3Δ

exophoric at distance and 7Δ esophoric at
near (40 cm)
AC/A = 5.6 + 0.4(7 -(-3))
= 5.6 + 0.4(10)
= 5.6 + 4
= 9.6

CONVERGENCE EXCESS:
n>d esotropia
high AC/A ratio
EX: 3EP(D)-16EP’(N)
Treatment
Near add (overcorrection of plus poweror under correction of minus
powermost effective
Base-out prism (alternative method )
Base-in training(not so effective)

 DIVERGENCE INSUFFICIENCY
n <d esotropia
 low AC/A ratio
EX: 8EP-3EP’
 Treatment
Base-out prism.

 CONVERGENCE INSUFFICIENCY
n>d exotropia
 Low AC/A ratio
EX:3XP(D)-15XP’(N)
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 Treatment:
Base-out training (most effective)
“ Pencil push-up” training.

 DIVERGENCE EXCESS
n<d exotropia
high AC/A ratio
EX:15XP(D)-5XP’(N)
Treatment:
overcorrection of minus power orundercorrection of plus power
 in mild case base-in prism for full time wear.

Gradient method:
– Phoria is measured a second time using a -1.00/+1.00 lens.
– The change in phoria with the additional minus or
plus is the AC/A ratio.

AC/A=(a-a')/F

a= phoria at near.

a'=phoria at the same distance but through a lens power(F).

– Example: If the near phoria is 2Δ eso through the

subjective finding and with -1.00 it is 7Δ eso
– AC/A ratio is 5/1

– Example: If the near phoria is 4Δ exo through thesubjective finding and

with +1.00 it is 10Δ exo.
- AC/A ratio is 6/1.

• Clinically both methods are used

– Calculation
• Only requires a cover test and simple math
– Gradient
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• Quick and easy.
• Gives Dr immediate feedback.

• Differences between the two methods

– Proximal vergence
– Lag of accommodation

– Calculated AC/A includes the effect of proximalvergence

– Gradient AC/A measures the near phoria twice ata fixed distance,
proximal vergence is heldconstant and thus does not alter the final
result.

Response vs Stimulus
• Alpern et.al (1959) found that the accommodativeresponse will be
about 10% less than the stimulus. Thuswhen we measure
accommodative response directlywe find for a +2.50 D (40 cm) stimulus
there will be alag of accommodation of about +0.25 to +0.75D
– Clinically we measure the stimulus AC/A.

Expected AC/A Ratio values

– 4/1with a standard deviation of +/- 1
– Between 3-5 normal
Morgan (1944)
• High > 6/1
• Low < 3/1

• Clinical Examples:
Case1:
• AC a 7 year old girl presents with complains of
headaches and eye strain with near work
• Unaided VA’s
OD 20/20
OS 20/20

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• Cover test at distance ortho and 5EP' at near
• IPD=53mm

• AC/A=? , High or low?

AC/A- calculation
AC/A = 5.3 + 0.4(5 - 0)
= 5.3 + 0.4(5)
= 5.3 + 2
= 7.3/1

-High AC/A
-Convergence excess

•Gradient:
Trial frame + 1.00 DS
Remeasure CT at near find?

• Through +1.00 DS AC’s near phoria measures

2XP’

AC/A=(5-(-2))/1

=7/1
• Treatment
– Rx +1.00 DS OU for near only
– RTC 1 month.

CASE 2:
• TA a 8 year old boy presents with complaints of
headaches and eye strain with near work
• Unaided VA’s at distance
OD 20/50
OS 20/50
At near 20/20 OD,OS,OU
• Cover Test: 2XP @distance/10XP’ @near
• IPD=54mm

• AC/A=? , High or low?

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• AC/A- calculation
AC/A = 5.4 + 0.4(-10 - (-2))
= 5.4 + 0.4(-8)
= 5.4 + (-3.2)
= 2.2/1

• To accurately determine the AC/A we need to

have the best refraction in place.
• Do we have that?

• Unaided VA’s at distance

OD 20/50
OS 20/50

• Examination findings:
• Refraction:
– OD: -1.50 DS 20/20
– OS: -1.50 DS 20/20

• Management
– Rx -1.50 DS OU
– RCT 1 month
– What do we expect?

• F/U visit one month after Rx wear

• Aided VA’s at distance
OD 20/20
OS 20/20
At near 20/20 OD,OS,OU
• Cover Test: 2XP/8XP’
• Pt. still symptomatic c/o HA’s and asthenopia.

• Treatment;
– Vision Therapy.
• Treat the compensating vergence.

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Eye position for examination
• Primary position:
– With condition in which head being put vertically and straightforward
and two eyes looking straightforward.
• Secondary position:
– The two eyes being in adduction or abduction or elevation or
depression position.
• Tertiary position:
– Two eyes gazing in oblique directions (up or downward).

POSITIONS OF GAZE:
SIX CARDINAL: positions of gaze are those in which one muscle in each
eye has moved the eye into that position as follows :
- Dextroversion ( right lateral rectus and left medial rectus ).
- Laevoversion ( left lateral rectus and right medial rectus ).
- Dextroelevation ( right superior rectus and left inferior oblique ).
- Laevoelevation ( left superior rectus and right inferior oblique ).
- Dextrodepression ( right inferior rectus and left superior oblique).
- Laevodepression ( left inferior rectus and right superior oblique).

NINE DIAGNOSTIC: positions of gaze are those in which deviations are

measured .
They consist of the six cardinal positions, the primary position, elevation
and depression ).

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Terminology of extra-ocular muscle regarding their
physiological functions

• Antagonist m:
– the muscle that counteracts the agonist (or the prime mover);
– lengthening when the agonist muscle contracts.
– e.g., medial rectus and lateral rectus muscles.

• Yoke m:
– The contra-laterally paired extra-ocular muscles of two fellow eyes
thatwork synergistically to direct the gaze in a given direction.
– Example: in directing the gaze to the right, the right lateral rectus and
left medial rectus operate together as yoke muscles.
• Synergist m:
– The muscles moving one single eye ball in the same direction as the
prime moving muscle.
– e.g., inferior oblique m. is the synergist of
superior rectus m. when the
eye turns upward.

Laws of ocular motility

Sherrington law:
• A muscle will relax when its antagonist muscle (e.g., lateral and medial
muscles) is activated.

Hering law:
• The yoke muscles are innervated equally by nervous
system in eye movement.

 Muscle sequelae
Are the effect of interactions described by these laws.they are of
prime importance in diagnosing ocular motility disorders and in

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 particular in distinguishing a recent acquired palsy from long
standing one
For example
In left superior oblique palsy( left 4th nerve palsy)
 Primary underaction left SO
 Secondary contracture of unopposed direct antagonist (left I O)
 Secondary contracture of contralateral synergist yoke muscle(right
IR)
 Secondary inhibitional palsy( right SR)

BINOCULAR VISION
Vision is based on the retinal imageformed in each eye, and monocular
visionalone provides us with much significantdata.

BSVState of simultaneous vision with twoseeing eyes (neither of

which needsnecessarily be normal) when an individualfixes his visual
attention on an object ofregard.

IMPORTANCE OF BINOCULAR VISION:

The clinical applications of our study of thisbasic science include:
 Managing patients with complaints of eye strain, headaches, difficulty
with reading, etc.
 Pediatric ophthalmology
 Scientific basis for vision therapy
 Monovision and contact lenses

Advantages of binocular vision:

 Major Advantages:
 Larger visual field. Without eye movements, the monocular field
is about 145° wide. With both eyes, it’s about 190° wide. In
addition, there is considerable overlap between both monocular

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 visual fields, and it is in this overlap area that we have stereopsis
(depth perception).
 Stereopsis. Stereopsis is the highly accurate senseof depth
perception that is unique to binocularvision, and is considered the
most significantadvantage gained by binocular vision.

 Minor Advantages:
 Spare eye:
◦ If one eye is lost to injury or disease, we will still beable to see
well with the other.

 Binocular summation:
◦ Certain aspects of vision are improved because of theadditional
input provided by the second eye. Theimprovement may be small,
but it definitely improvesthe quality of vision.
◦ Suprathreshold binocular summation
1. Visual acuity
2. Contrast sensitivity
3. Brightness perception
4. Detection of dim light

DISADVANTAGES OF BINOCULAR VISION:

 Many of these problems would not exist ifwe had only one eye:
◦ Incorrect refractive balance.
◦ Dissimilar retinal image sizes (aniseikonia)between the two eyes
due to anisometropiaor retinal disease.
◦ Convergence problems.
◦ Conflicts between the accommodation andconvergence.

SOME MISCONCEPTIONS ABOUT BINOCULAR VISION:

 Some people incorrectly assume that theonly advantage to
binocular vision isstereopsis or that, without binocular vision,one

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 has no depth perception. Actually, thereare many important
monocular cues thatallow a person to judge depth in the absence
of binocular vision.
 In fact, beyond a few meters from the eye ofan observer,
monocular cues are moreimportant (and stereopsis contributes
little)to depth perception.
 Conditions necessary for normal BSV :
1- normal routing of visual pathways with overlapping visual field.
2- binocularly driven neurons in the visualcortex .
3- normal retinal ( retino - cortical (correspondence ( NRC )
resulting incyclopean viewing .
4- accurate neuromuscular development andcoordination , sothat
the visual axesdirected at , and maintain fixation on , theobject of
regard .
5- approximately equal image clarity and
size for both eyes.
 BSV is based on NRC , which requires firstan understanding of
uniocular visualdirection and projection .

Visual Direction
 When a person with normal binocular vision looks at anobject, both
visual axes converge such that they intersect atthe object of regard.
 When this object is at optical infinity (6 meters or greater),and the
patient is emmetropic or myopic, one or two typesof vergence are
responsible for the position of each eye.
 If the person is orthophoric (i.e. has no phoria), then onlyTonic
vergence is responsible for turning each eye to pointat the target.
 Where a heterophoria is present, tonic vergence andfusional vergence
are responsible for turning each eye topoint at the target.

 It is important to note that when fixating an object closer than

6meters (20 feet):
 tonic vergence;
 fusional vergence (if there is a phoria);
 accommodative vergence (whenever we haveaccommodation, we
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have accommodative vergence).
 and proximal vergence (which is an increase inconvergence which
occurs because a person knows thatthe object he/she is looking at is
close to him/her).
 all combine to determine the direction in which each
eye will
point.

Is the projection of a given retinal element in aspecific direction in the

subjective space .
PRINCIPAL visual direction is the direction inexternal space
interpreted as the line of sight.This is normally the visual direction of
fovea andis associated with a sense of direct viewing .
SECONDARY visual directions are the projectingdirections of extra-
foveal points with respect tothe principal direction of the fovea ,
associated with indirect ( eccentric ) viewing .

PROJECTION
is the subjective interpretation of theposition of an object in space on
thebasis of stimulated retinal elements.If a red object stimulates the
right fovea( F ) , and black object which lies in thenasal field stimulates a
temporal retinalelement (T) , the red object will beinterpreted by the
brain as havingoriginated from the straight aheadposition and the black
object .

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RETINO – MOTOR VALUES
The image of an object in the peripheral visualfield falls on an
extrafoveal element. To establishfixation on this object a saccadic
version ofaccurate amplitude is required . Each extrafovealretinal
element therefore has a retino – motorvalue proportional to its distance
from the fovea, which guides the amplitude of saccadicmovements
required to ( look at it ) .
Retino – motor value, zero at the fovea,increases progressively towards
the retinal periphery.

Retinal Correspondence
 When a person with normal binocular
vision looks atan object, the image of that
object falls on bothfoveas. In this case both
foveas receive informationfrom the same
object. The foveas are then said to
berelated (conjugate or corresponding).
This is NormalRetinal Correspondence
(NRC).
 Abnormal retinal correspondence occurs
when theimages from the object above fall on
the fovea of oneeye, and on an extra-foveal
point of the other eye. Inthis case, the fovea of
one eye is conjugate with theextra-foveal point

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of the other eye.

 The term Horopter:

describes an arc,which contains all the objects thatstimulate exactly
corresponding areas on the left and right retina.

Object on the horopter project images to the corresponding retinal

points and seen as a single image.

 PANUM FUSIONAL SPACE:

-Is a zone in front of and behind the horopter in which objects
stimulate slightly non corresponding retinal points ( retinal

31
 disparity ).
-Objects are seen singly and the disparity information is used to
produce a perception of binocular depth ( stereopsis ) .
-Objects in front of and behind Panum space appear double .
-This is the basis of physiological diplopia .

Panum space is shallow at fixation( 6 sec. of arc )and deeper towards the
periphery( 30 – 40seconds of arc at 15 deg. From the fovea ),Therefore
objects on the horopter are seensingly and in one plane . -Objects in
Panumfusional area are seen singly andstereoscopically .-Objects
outside Panumfusional area appear double .
-Physiological diplopia is usually accompaniedby physiological
suppression and manysubjects remain unaware of thisphenomenon .

Binocular vision as defined by Worth can be classified

into three grades:
◦ Simultaneous Perception.
◦ Fusion.
◦ Stereoscopic Vision.

Fusion Development in the Infant:

 Birth: fixation reflex poor with random eye movements
 2-3 weeks: follows light monocularly
 6 weeks to 6 months: follows light binocularly
 4 weeks to 6 months: convergence developing
 By 6 months: accommodation developing – lags behind convergence.

Simult
aneou
s
Perce
ption;
 This
occurs

32
in both binocular singlevisible (BSV) and binocular vision (BV)where the
images of the object of regardfrom both eyes are
simultaneouslyperceived in the brain.

Fusion:
Is characterized by the ability to fuse theimages from the two eyes and
to perceivebinocular depth .
- SENSORY FUSION :involves theintegration by the visual areas of
thecerebral cortex of two similar images, one from each eye, into one
image. It may be central , which integrate the image falling on the fovea,
or peripheral, whichintegrates parts of the image falling outsidethe
fovea.
It is possible to maintain fusion with acentral visual deficit in one eye,
butperipheral fusion is essential to BSVand may be affected in patients
withfield loss as in advanced glaucoma .

- MOTOR FUSION : involves themaintenance of motor alignment

ofthe eyes to sustain bifoveal fixation . It is driven by retinal image
disparity,which stimulates fusional vergences .

Stereopsis:
 Fusion of these slightly different retinal
images is theprecursor to Stereopsis.
Stereopsis enables the perception of depth (3-
D vision) and helps in the accurate judgment
of relative distance between two objects, and
relative speed (or change of speed) of
oneobject with relation to another.
 There are many cues to the perception of
depth, butstereoscopic depth is the most
important.
Stereoscopic cues are caused almost
exclusively by retinaldisparities.
 Retinal disparities are small positional displacementsbetween
otherwise well-matched images.
 In the visual system, because of thehorizontal separation of the eyes,

33
onlyhorizontal disparities convey depthinformation.
 The horizontal shift in the objects’positions is what happens in
normalvision, and is the result of the difference in horizontal positions of
both eyes.
 Fusion and stereopsis only occur in binocular single vision.
 The ability for the brain to fuse both retinal images isdependent on
where the images of an object of regard fall onboth retinas.
 We have already discussed the fact that, in normal
retinalcorrespondence, when both eyes look at an object, bothvisual
axes intersect at the object of regard so the eachimage falls exactly on
the fovea of each eye.
 Subsequently the brain is able to fuse these two images into one visual
perception.

- The question is: Can the brain fusethe images of both eyes if one
imagefalls on the fovea, for example, theleft eye, and the other image
falls onan extrafoveal point of the right eye?

→The answer to the question above isYES, but only if the image on the
righteye falls within a circumscribed areaknown as Panum’s Fusional
Area. Ifthe image falls outside of this area,then fusion is not possible.
The firstconsequence of this is diplopia which may or may not progress
to corticalsuppression.

 To conclude: In abnormal retinalcorrespondence where the image of

anobject falls on the fovea on one retinaand on an extrafoveal point of
theopposite eye, fusion and stereopsis willoccur only if the extrafoveal
point lieswith Panum’s area. If not, there will beno fusion, no stereopsis
and thereforethere will be diplopia.

34
Sensory adaptation to strabismus
NOTE:
- It should now be apparent that binocular vision is not inborn.
-A series of conditioned reflexes develop in the first three years of life to
produce binocular input to the cortical cells -leading to the development
of binocularly driven cells in the cortex.
-These reflexes become firmly established by about 5to6 years (the
plastic period) and hence become unconditioned reflexes.

However
• If strabismus develops before three years:
 adaptation to normal development occurs to prevent symptoms,
leads to abnormal unconditioned reflexes developing by age
6years.
•Usually no symptoms if strabismus acquired from 6years to adult:
-binocular vision is well established (symptoms very likely to occur).
•if strabismus is acquired at 3-6years:
 symptoms will occur .
 but the system is unstable and readily breaks down .
 adaptations will develop (plastic period) .
 and again symptoms are unlikely to occur .

Binocular Vision is embarrassed in two ways :

 Diplopia .
 Confusion .

DIPLOPIA:
Object of interest seen by fovea of one eye and peripheral retina of the
other eye.

35
Visual confusion:
Fovea of both eye (or corresponding retinal point ) are seen 2 object s of
interested interpreted as coming from the same point in space.
CONFUSION:
Is the simultaneous appreciation of two superimposed
but dissimilar images caused by stimulation of
corresponding retinal points ( usually the foveae ) by
images of different objects .

PATHOLOGICAL DIPLOPIA:
Is the simultaneous appreciation of two images of the same
object in different positions and results from images of the
same object falling on non- corresponding retinal points .
-In esotropia the diplopia is homonymous ( uncrossed ).
-In exotropia the diplopia is heteronymous ( crossed ).

Monocular diplopia:
More than one image of the object of regard is formed in the retina of
one eye or both eyes, like in :
- Irregular astigmatism (corneal scars, haze, corneal distortion).
- Subluxated clear lenses .
- Poorly fitting contact lenses .
- Early cataract .
- Macular disorder (edema, CNVM etc.) .

In young patients sensory adaptations overcome diplopia and confusion.

- These sensory adaptations are:
o Suppression .
o abnormal (anomalous) retinal correspondence (ARC) .

36
 - Suppression and ARC are interrelated adaptations to strabismus
occurring before 6 years.
- Is a binocular sensory adaptation that occurs when the patient is
using both eyes in the presence of a strabismus to avoid confusion
and diplopia.
- Is a cortical adaptive phenomena which prevents images in the
strabismic eye from reaching a conscious level.
- Also represents an obstacle in trying to restore normal
sensorimotor function.
- In small strabismus < 25Δ: both suppression and ARC usually occur
In larger strabismus > 25Δ: suppression dominates .
- Suppression is an extension of normal visual processing .

SUPPRESSION:
- involves active inhibition , in the visual cortex , of an image from
one eye when both eyes are open .
- Stimuli for suppression include diplopia , confusion and a blurred
image from one eye resulting from astigmatism / anisometropia .
Clinically , suppression may be :

 CENTRAL OR PERIPHERAL:
in central suppression the image from the fovea of the deviating eye
is inhibited to avoid confusion. Diplopia on the other hand , is
eradicated by the process of peripheral suppression , in which the
image from the peripheral retina of the deviating eye is inhibited .
 -MONOCULAR OR ALTERNATING:
- suppression is monocular when the image from the dominant eye
always predominate over the image from the deviating eye ( or more
ametropic ) eye , so that the image from the latter is constantly
suppressed . This type of suppression leads to amblyopia .
- When suppression alternates ( switches from one eye to the other )
amblyopia does not develop .

37
  FACULTATIVE OR OBLIGATORY:
- facultative suppression occurs only when the eyes are misaligned .
Obligatory suppression is present at all times , irrespective of whether
the eyes are deviated or straight .
- Examples are seen in intermittent exotropia and Duane syndrome .

Abnormal retinal correspondence:

• When the fovea of one eye has a common visual direction with an
extrafoveal area in the other eye .
• Angle of squint is small and the extrafoveal point is close to the fovea
to regain the binocular advantage, although anomalous .
•This results in the eyes seeing binocularly single inspite of a manifest
squint.
• Under binocular conditions the fovea and the extrafoveal point share
the common subjective visual direction .
• When the normal eye is closed the extrafoveal element loses any
advantage over the fovea of that eye, which retains its primary visual
direction.
•Abnormal retinal correspondence is a physiological part of normal
binocular vision in many persons and is a natural accompaniment of the
binocular adjustment when the visual axes are not parallel in all
positions.
•It is a binocular condition and not a uniocular adaptation of projection.
•Anomalous retinal correspondence (ARC) is a neural adaptation to eye
misalignment in which non- corresponding retinal points are linked in
the visual cortex to provide binocular fusion.

Conditions for development of ARC:

 Strabismus before 4 years old (especially before 30 months) .

38
  Delay in treatment.
 Small constant strabismus angle.
 Esotropia>exotropia.
 Unilateral > alternating.
Classification
1. Harmonious ARC(HARC) :
 angle of anomaly is equal to the objective angle of deviation )
subjective angle = o).
 This indicates that the ARC fully corresponds to the strabismus.
 Provides a compensation for the angle of squint.
 Eliminate the awareness of diplopia and confusion.

2-Unharmonious ARC (UN-HARC):

 angle of anomaly is less than the objective angle of deviation.

3-Paradoxical(PARC):
 when the angle of anomaly is greater than the objective angle of
deviation.

ARC can be detected on the synoptophore as follows :

The subjective angle of deviation is that at which the simultaneous
perception slides are superimposed . The examiner determines the
objective angle of the deviation by presenting each fovea alternately
with a target by extinguishing one or other light and moving the slide in
front of the deviating eye until no movement of the eyes is seen . If the
subjective and objective angles coincide then retinal correspondence is
normal .
If the objective and subjective angles are different , ARC is present . The
difference in degrees between the subjective and objective angles is the
angle of anomaly . ARC is said to be harmonious when the objective
angle equals the angle of anomaly and unharmonious when it exceeds
the angle of anomaly . It is only in harmonious ARC that free space

39
binocular responses can be demonstrated , the unharmonious form may
be a lesser adaptation or an artifact of testing .

Advantages:
- Avoids the necessity for dense amblyopia (HARC).
- Permits anomalous fusion range and some degree of stereopsis.
- Prevents consecutive divergence.
- Allows a form of binocular convergence to take place.
Disadvantages
- Prevents the development of normal retinal correspondence, true
fusion and normal stereopsis.
- Represents an abnormal reflex development.
Treatment
- Occlusion Preventive as well as curative measure.
- Prolonged alternating occlusion is not recommended.
- Prevent further development of ARC as well as normal
correspondence.
- Exercises with major amblyoscope.

Eccentric fixation
 A uniocular condition in which some part of retina other than
fovea is used for fixation, but in which the fovea retains its normal
straight ahead projection.
 It may be associated with a defect of central vision caused by a
structural lesion of fovea.
 Eccentric fixation can be present during both monocular and
binocular viewing conditions, but it is best diagnosed under
monocular viewing conditions.
 This is important to keep in mind to avoid confusion with
anomalous correspondence.
 Anomalous correspondence is relevant only during binocular
fusion.

40
Monofixation Syndrome
The term monofixation syndrome is used to describe a particular
presentation of a sensory state in strabismus.
The essential feature of this syndrome is the presence ofperipheral
fusion with the absence of bi -macular fusion due to a macular scotoma.
A patient with monofixation syndrome may have no manifest deviation
but usually has a small heterotropia,most commonly esotropia.
Stereoacuity is present but reduced. And amblyopia is a common
finding.
Monofixation may be a primary condition. It is a favorable outcome of
infantile strabismus surgery.
This syndrome can also result from anisometropia or macular lesions.
It can be the cause of unilaterally reduced vision when no obvious
strabismus is present.

Amblyopia
Amblyopia is a unilateral or, less commonly, bilateral reduction of best
corrected VA that cannot be attributed directly to the effect of any
structural abnormality of the eye or the posterior visual pathways.
Amblyopia is caused by abnormal visual experience early in life resulting
from one of the following:
• strabismus.
• anisometropia or high bilateral refractive errors (isometropia).
• stimulus deprivation.
With a prevalence of 2%- 4%in the North American population.
This fact is particularly distressing because, in principle, most amblyopic
vision loss is preventable or reversible with timely detection and
appropriate intervention.
Screening plays an important role in detecting amblyopia and other
vision problems at an early age and can be performed in the primary
care practitioner's office, Amblyopia is primarily a defect of central
vision, the peripheral visual field is usually normal.

41
In general, the critical period for stimulus deprivation amblyopia occurs
earlier than that for ocular misalignment or anisometropia.
Furthermore, the time necessary for amblyopia to occur during the
critical period is shorter for stimulus deprivation than for strabismus or
anisometropia.
Amblyopia has traditionally been subdivided in terms of the major
disorders that may be responsible for its occurrence.

1-Strabismic Amblyopia:
The most common form of amblyopia develops in the consistently
deviating eye of a child with strabismus.
Constant, non-alternating heterotropias (typically esodeviations) are
most likely to cause significant amblyopia. Strabismic amblyopia is
thought to result from competitive or inhibitory interaction between
neurons carrying the non-fusible inputs from the two eyes, which leads
to domination of cortical vision centers by the fixating eye and
chronically reduced responsiveness to input by the non-fixating eye.
Amblyopia itself does not as a rule prevent diplopia.
Older patients with long-standing deviations might develop double
vision after strabismus surgery despite the presence of substantially
reduced visual acuity from amblyopia.
When visual acuity is checked with the use of a neutral-density filter, the
acuity of an eye with amblyopia tends to decline less sharply than that of
a normal eye. This phenomenon is called the neutral-density filter effect.

Eccentric fixation:
Eccentric fixation refers to the consistent use of a non-foveal region of
the retina for monocular viewing by an amblyopic eye, Minor degrees of
eccentric fixation, detectable only with special tests such as visuscopy,
are seen in many patients with strabismic amblyopia and relatively mild
acuity loss. A visuscope projects a target with an open center
surrounded by two concentric circlesonto the retina, and the patient is

42
asked to fixate on the target. If the target is not directed at the fovea,the
degree of eccentric fixation can be measured using the concentric circles
as a guide,Many ophthalmoscopes are equipped with a visuscope.
Clinically evident eccentric fixation, detectable by observing the non -
central position of the corneal reflection from the amblyopic eye while it
fixates a light with the dominant eye covered, generally implies visual
acuity of 20/200 or worse.
Use of the non-foveal retina for fixation cannot, in general, be regarded
as the primary cause of reduced acuity in affected eyes.

2-Anisometropic Amblyopia:
Second in frequency to strabismic amblyopia, anisometropic amblyopia
develops when unequal refractive errors in the twoeyes causes the
image on 1 retina to be chronically defocused.
This condition is thought to result partly from the direct effect of image
blur on visual acuity development in the involved eye and partly from
interocular competition or inhibition similar (but not necessarily
identical) to that responsible for strabismic amblyopia.
Relatively mild degrees of hyperopic or astigmatic anisometropia(1.00-
2.00 D) can induce mild amblyopia.
Mild myopic anisometropia (less than -3.00 D) usually does not cause
amblyopia, but unilateral high myopia (-6.00 D or greater) often results
in severe amblyopic vision loss, Unless strabismus ispresent, the eyes of
a child with anisometropic amblyopia look normal to the family and
primary care physician, typically causing a delay in detection and
treatment.

3-Ametropic Amblyopia:
Ametropic amblyopia, a bilateral reduction in acuity that is usually
relatively mild, results from large, approximately equal, uncorrected
refractive errors inboth eyes of a young child.
It's mechanism involves the effect of blurred retinal images alone.
Hyperopia exceeding about 5.00 D and myopia in excess of 6.00 D carry
a risk of inducing bilateral amblyopia.

43
Uncorrected bilateral astigmatism in early childhood may result in loss
ofresolving ability limited to the chronically blurred meridians
(meridional amblyopia).
The degree of cylindrical ametropia necessary to produce
meridional amblyopia is not known, but most ophthalmologists
recommend correction of greater than 2.00 D of cylinder.

4-Stimulus Deprivation Amblyopia:

 Deprivation amblyopia may occur when the visual axis is
obstructed.
 The most common cause is a congenital or early acquired cataract,
but corneal opacities and vitreous hemorrhage may also be
implicated.
 Deprivation amblyopia is the least common but most damaging
and difficult to treat of the various forms of amblyopia.
 Amblyopic vision loss resulting from a unilateral occlusion of the
visual axis tends to be worse than that produced by bilateral
deprivation of similar degree because interocular effects add to
the direct developmental impact of severe image degradation.
 Even in bilateral cases, however, acuity can be 20/200 or worse.
 In children younger than 6 years, dense congenital cataracts that
occupy the central 3 mm or more of the lens must be considered
capable of causing severe amblyopia. Similar lens opacities
acquired after age 6 years are generally less harmful. Small polar
cataracts, around which retinoscopy can be readily performed,
and lamellar cataracts, through which a reasonably good view of
the fundus can be obtained, may cause mild to moderate
amblyopia or may have no effect on visual development.
 Occlusion amblyopia is a form of deprivation amblyopia that may
be seen after therapeutic patching.

44
Diagnosis
 Amblyopia is diagnosed when a patient is found to have a
condition known to increase the risk of amblyopia and when
reduced visual acuity cannot be explained entirely on the basis of
physical abnormalities of the eye.
 Characteristics of vision alone cannot be used to reliably
differentiate amblyopia from other forms of vision loss.
 The crowding phenomenon‘ for example, is typical of amblyopia
but is not pathognomonic or uniformly demonstrable.
 Afferent pupillary defects rarely occur in amblyopia, and then,
only in severe cases.
 Amblyopia sometimes coexists with vision loss directly caused by
an uncorrectable structural abnormality of the eye such as optic
nerve hypoplasia or coloboma.
 When the clinician encounters doubtful or borderline cases of this
type ("organic amblyopia") in a young child, it is appropriate to
undertake a trial of occlusion therapy.
 Improvement in vision confirms that amblyopia was indeed
present.
 Multiple assessments using a variety of tests orperformed on
different occasions are sometimesrequired to make a final
judgment concerningthe presence and severity of amblyopia.
 Trying to determine the degree of amblyopic vision loss in a young
patient should keep certain special considerations in mind.
 The fixation pattern, which indicates the strength ofpreference for
1 eye or the other under binocularviewing conditions, is a test for
estimating the relativelevel of vision in the 2 eyes for preverbal
children with strabismus.
 This test is quite sensitive for detecting amblyopia, but results can
be falsely positive, showinga strong preference when vision is
equal or nearlyequal in the 2 eyes, particularly with small-
anglestrabismus.
 A variety of optotypes can be used to directly measure acuity in
children 3-6years old. When possible, it is best to use linear
symbols to measure visual acuity. Often, however, only isolated
45
 symbols can be used, which may lead to underestimated
amblyopic vision loss due to the crowding phenomenon.
 Crowding bars help alleviate this problem. In addition, the young
child's brief attention span frequently results in measurements
that fall short of the true limits of acuity; these results can mimic
bilateral amblyopia or obscure or falsely suggest a significant
interocular difference.

Treatment
Treatment of amblyopia involves the following steps:

1. Eliminate (if needed) any obstacle to vision, such as a cataract.

2. Correct any significant refractive error.
3. Force use of the poorer eye by limiting use of the better eye.

 Cataract Removal:
Cataracts capable of producing amblyopia require surgery without
unnecessary delay. In young children, amblyopia may develop as quickly
as 1 week per age of life. Removal of visually significant congenital lens
opacities during the first 4-6 weeks of life is necessary for optimal
recovery of vision. In symmetric bilateral cases, the interval between
operations on the first and second eyes should be no more than 1-2
weeks.
Acutely developing severe traumatic cataracts in children younger than 6
years should be removed within a few weeks of injury, if possible.

 Refractive Correction:
In general, optical prescription for amblyopic eyes should be based on
the refractive error as determined with cycloplegia. Because 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. Sometimes, however, symmetric decreases
in plus lens power may be required to foster acceptance of spectacle
wear by a child.

46
-Refractive correction for aphakia following cataract surgery in childhood
must be provided promptly to avoid compounding the visual deprivation
effect of the lens opacity with that of a severe optical deficit.
-Both anisometropic and ametropic amblyopia may improve or resolve
with refractive correction alone over several months. Given this, many
ophthalmologists wait to initiate patching or penalization. in order to see
whether the vision improves with spectacle correction alone. The role of
refractive surgery in those patients who fail conventional treatment with
spectacles and/ or contact lenses is under investigation.

 Occlusion and Optical Degradation:

Full-time occlusion of the sound eye is defined as occlusion during all
waking hours. This treatment is usually performed using commercially
available adhesive patches. Spectacle mounted occluders or special
opaque contact lenses can be used as an alternative to fulltime patching
if skin irritation or inadequate adhesion is a significant problem,
provided that close supervision ensures that the spectacles remain in
place consistently.
Rarely, strabismus may result during full-time patching; it is not known
whether strabismus would have occurred with other forms of amblyopia
treatment. Therefore, the child whose eyes are consistently or
intermittently straight may benefit by being given some opportunity to
see binocularly.
Modest reductions in patching are employed by many ophthalmologists
(removing the patch for an hour or two a day) to reduce the likelihood of
occlusion amblyopia or of inducing strabismus.
Part-time occlusion, defined as occlusion for 1-6 hours per day, has been
shown to achieve the same results as the prescription of full-time
occlusion.
The relative duration of patch-on and patch-off intervals should reflect
the degree of amblyopia; for moderate to severe deficits, at least 6
hours per day is preferred.
Compliance with occlusion therapy for amblyopia declines with
increasingage.

47
The effectiveness of more acceptable part-time patching regimens in
older children is being actively investigated. Furthermore, studies in
older children with amblyopia have shown that treatment can still be
beneficial beyond the first decade of life. This is especially true in
children who have not previously undergone treatment.

 Other methods of amblyopia treatment:

Involve optical degradation of the better eye's image to the point that it
becomes inferior to the amblyopic eye's, an approach often called
penalization. Use of the amblyopic eye is thus promoted within the
context of binocular seeing. Studies have demonstrated that
pharmacologic penalization can be used to successfully treat moderate
levels of amblyopia.
The improvement in vision has been shown to be similar to that
obtained with the prescription of patching.
A cycloplegic agent (usually atropine 1% drops or homatropine 5%
drops) is administered to the better-seeing eye so that it is unable to
accommodate.
As a result, the better eye experiences blur with near viewing and, if
uncorrected hyperopia is present, with distance viewing. This form of
treatment has been demonstrated to be as effective as patching for mild
to moderate amblyopia (visual acuity of 20/100 or better in the
amblyopic eye).
Depending on the depth of amblyopia and the response to prior
treatment, the hyperopic correction of the dominant eye can be reduced
to enhance the effect. Regular follow-up of patients whose amblyopia is
being treated with cycloplegia is important to avoid reverse amblyopia in
the previously preferred eye.
Pharmacologic penalization offers the particular advantage of being
difficult to thwart even if the child objects. Alternative methods of
treatment based on the same principle involve prescribing excessive
plus-power lenses (fogging) or diffusing filters. These methods avoid
potential pharmacologic side effects and may be capable of inducing
greater blur. If the child iswearing glasses, application of translucent

48
tape or a Bangerter foil (a neutral-density filter) to the spectacle lens can
be tried. Proper utilization (no peeking!) of spectacle-borne devices
must be closely monitored.
Another benefit of pharmacologic penalization and other non-occluding
methods in patients with straight eyes is that the eyes can work
together, a great practical advantage in children with latent nystagmus.

 Complications of Therapy
Any form of amblyopia therapy introduces the possibility of
overtreatment leading to amblyopia in the originally better eye.
Full-time occlusion carries the greatest risk of this complication and
requires close monitoring, especially in the younger child.
The first follow-up visit after initiation of treatment should occur within
1 week for an infant and after an interval corresponding to 1 week per
year of age for the older child (e.g., 4 weeks for a 4year-old). Subsequent
visits can be scheduled at longer intervals based on early response.
Part-time occlusion and optical degradation methods allow for less
frequent observation, but regular follow-up is still critical.
The parents of a strabismic child should be instructed to watch for a
switch in fixation preference and to report its occurrence promptly.
Iatrogenic amblyopia can usually be treated successfully with judicious
patching of the better-seeing eye or by alternating occlusion.
Sometimes, simply stopping treatment altogether for a few weeks leads
to equalization of vision.
The desired endpoint of therapy for unilateral amblyopia is free
alternation of fixation (although 1 eye may still be used somewhat more
frequently than the other), linear Snellen acuity that differs by no more
than 1 line between the 2 eyes, or both.
The time required for completion of treatment depends on the
following:
• degree of amblyopia
• choice of therapeutic approach
• compliance with the prescribed regimen
• age of the patient

49
More severe amblyopia, less complete obstruction of the dominant
eye's vision, and older age are all associated with a need for more
prolonged treatment.
Full-time occlusion during infancy may reverse substantial strabismic
amblyopia in 1 week or less.
In contrast, an older child who wears a patch only after school and on
weekends may require a year or more of treatment to overcome a
moderate deficit.

 Unresponsiveness
In some cases, even conscientious application of an appropriate
therapeutic program fails to improve vision at all or beyond a certain
level. Complete or partial unresponsiveness to treatment occasionally
affects younger children but most often occurs in patients older than 5
years. The decision of 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 with good compliance.
Before it is concluded that intractable amblyopia is present,
refraction should be rechecked, the pupils carefully reevaluated,
and the macula and optic nerve critically inspected for subtle evidence
of hypoplasia or other malformation that might have been previously
overlooked. Neuroimaging might be considered in cases that inexplicably
fail to respond to treatment. Amblyopia associated with unilateral high
myopia and extensive myelination of retinal nerve fibers is a specific
syndrome in which treatment failure is particularly common.

 Recurrence
When amblyopia treatment is discontinued after fully or partially
successful completion, approximately 25% of patients show some
degree of recurrence, which can usually be reversed with renewed
therapeutic effort.

50
Institution of a maintenance regimen such as patchingfor 1-3 hours per
day, optical penalization with spectacles, or pharmacologic penalization
with atropine 1 or 2 days per week can prevent backsliding.
If the need for maintenance treatment is established, treatment must be
continued until stability of visual acuity 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 6 months between follow-up
visits are acceptable. The improvement in visual acuity that is obtained
in most children treated between 7 and 12 years of age is sustained
following cessation of treatment.

Motor adaptation to strabismus

This involves the adoption of an abnormal head posture and

occurs in adults who cannot suppress or in children with
good binocular vision potential. Under strabismic conditions,
patients will adopt an abnormal head posture to maintain
BSV and eliminate diplopia. The patient, will turn the head
into the direction of the field of action of the weak muscle, so
that the eyes are then automatically turned in the opposite
direction and as far as possible away from its field of action
(i.e. the head will turn where the eye cannot).

1. Horizontal deviation will result in a face turn. For

example, if one of the muscles that turn the eyes to the left
is paralysed, the face will also be turned to the left so that
the eyes no longer need to look towards the left.

2. Vertical deviation will result in elevation or depression of

the chin. If one of the elevators is weak, the chin will be
elevated so that the eyes become depressed (Fig. 16.15).

3. Torsional deviation will result in a head tilt to one or the

other shoulder. For example, if an intortor such as the left

51
superior oblique is paralysed, the left eye will become
extorted. In order to compensate for this, the head will tilt
to the right, shoulder, effectively 'intorting' the left eye

NB: As a rule of thumb, a head tilt often accompanies \

vertical misalignments.The tilt is usually towards the lower
eye, but not due to the vertical misalignment, but to the
accompanying (and less apparent) torsional deviation.

Heterophoria and Vergence abnormalities:

 Most binocular anomalies result in the misalignment of the visual

axes.
 The fusion reflex maintains correct alignment of the two eyes.
 If this fusion reflex is suspended the eyes will adopt the fusion
free’ position and a measurable deviation of the visual axes will
occur in.
 The error of alignment that takes place when fusion is suspended
is called heterophoria or phoria.

52
 In distance fixation (assuming emmetropia) the phoria will
represent the error between the position of the eyes produced by
tonic convergence, and parallelism (fusional divergence).
 In near fixation the phoria represents the error between the
position of the eyes produced by tonic, accommodative and
proximal convergence and the vergence required for the fixation
distance.
 In heterophoria the eyes are kept aligned by motor fusion and
hence sensory fusion should develop normally .
 In cases of large heterophoria sensory problems may occur e.g.
suppression or reduced stereopsis.
 Small heterophorias are usually asymptomatic indeed most
people have some degree of heterophoria that can be considered
as physiological, or normal.
 The likelihood of symptoms increases with the size of the
deviation and may include: asthenopia, headaches and diplopia.
Increased severity and/or frequency of symptoms imply poor
compensation.

53
  Classification of Heterophoria:

Compensated vs Decompensated Heterophoria

 Heterophoria in many cases is a physiological normal and is

asymptomatic and gives the individual no trouble i.e.
(compensated)
 Sometimes however the phoria may lead to the patient
complaining of symptoms
 When the binocular system is under stress due to the presence of
phoria then it is said to be decompensated.
 Decompensated phorias may require clinical treatment.

Classification in terms of Fixation distance

 Heterophoria may also be classified on the basis of the distance of

fixation

54
 - This is usually taken either at : 6m (optical infinity) or near (30 - 40
cm)
- The measurements taken are known as distance phoria and near
phoria respectively, and they may differ in degree and direction
from one another.

Esophoria
a) Divergence Weakness Esophoria
Distance esophoria > Near esophoria
b) Convergence Excess Esophoria
- Near esophoria > Distance Esophoria
- high AC/A ratio is a common cause
c) Basic Esophoria
Does not significantly alter between distance and near fixation.

Exophoria
a) Convergence Weakness Exophoria
Near Exophoria > Distance Exophoria
b) Divergence Excess Exophoria
Distance Exophoria > Near Exophoria
c) Basic Exophoria
Does not significantly alter between distance and near fixation.

MIXED PHORIA
Incidence of Heterophoria:
Most investigators have found some heterophoria in 70 - 80% of the
population.
- Abraham (1931) found esophoria in 38%, exophoria in 30% and
hyperphoria > 0.5Δ in 16%

55
Partially accommodative strabismus30%
Non-accommodative strabismus 20%
Fully accommodative strabismus17%
Hypertropia and decompensated hyperphoria 6%
Exotropia and decompensated exophoria 27%

Treatment:

 Orthoptic treatment is of most value in convergence weakness

exophoria .
 Any significant refractive error should be appropriately corrected .
 Symptom relief may otherwise be obtained using temporary stick-
on Fresnel prisms and may be subsequently incorporated into
spectacles ( maximum usually 10-12 Δ split between the two
eyes).
 Surgery may occasionally be required for larger deviations .

Vergence abnormalities:

CONVERGENCE INSUFICIENCY:

Convergence
 Disjugate simultaneous and synchronous inward rotation of both
eye which results from co- contraction of the two medial rectus
muscles.
 Allows bifoveal single vision maintained at near fixation distance.
 Does not deteriorate with age.
 Can be improved by exercises
 One-third of convergence relates to tonic, fusional and proximal
convergence.
 Two-thirds is accommodative .
 NPC value is greater than 10 cm .

56
CONVERGENCE INSUFICIENCY:

 Inability of eyes to obtain or maintain adequate binocular

convergence.
 Most common cause of ocular asthenopic symptoms.

 First described by von Graefe in 1855 and later elaborated by

Duane.
 One of the most common causes of ocular discomfort.
 Most common cause of muscular asthenopia.

Clinical signs of CI:

The physical diagnosis of convergence insufficiency is based on the
findings of a reduced convergence near-point along with decreased
positive fusional convergence amplitudes at near.

Symptoms due to muscular fatigue:

 Eye strain and sensation of tension around globe.

 Headache and eye ache after intense near work and relieved
when eyes are closed.
 Difficulty in changing focus from distance to near objects .
 Itching, burning and soreness of eyes and even hyperemia of nasal
half of the conjunctiva.

Less common complaints:

 Nausea
 motion sickness
 Dizziness
 panoramic headaches
 gritty sensation in the eyes
 general fatigue

57
Aetiology of CI :
 Primary or idiopathic:
 In many cases, exact etiology is not known.
 May be associate with:
o Wide IPD
o Delayed or inadequate functional development
o General debility
o Psychological instability
o Over work or worry

 Refractive:

 Associated with uncorrected high hyperopia and myopia.

 High hyperopes (>5D) usually make no effort to accommodate
and there is deficient accommodative convergence.
 Myopes may not need accommodation and thus lack
accommodative convergence.

 General physical causes:

 diseases of endocrine gland (e.g. Mobius’ sign in thyroid
ophthalmopathy).
 Psychological causes.
o include anxiety and neurosis.

Clinical features:

 Clinical problem in patient who does intense near work.

o Children with increased school work.
o Desk workers
o Computer users
 Discomfort usually occurs at the end of the day.

58
Treatment:

Optical:
 Proper refractive correction for any presence of ametropia.
 Myopes given full correction and hyperopes under corrected to
stimulate accommodation.

Training of voluntary convergence:
 Prism therapy:
o Base –in prism reading glasses or bifocals with prism in the
lower segment are useful as relieving prism.
o Relieving prisms and bifocals should be prescribed
cautiously in young age.

ACCOMMODATIVE INSUFFICIENCY :

 Is occasionally also present . It may be idiopathic ( primary ) or

post-viral and typically affects school age children .
 The minimum reading correction is prescribed to give clear vision
but is often difficult to discard .

Near reflex insufficiency :

1- paresis of the nearreflex:
presents as an exaggerated of convergence and accommodation
insufficiency . Mydriasis may be seen on attempted near fixation . In
the absence of neurological signs treatment involves reading glasses ,
base-in prisms and possibly Botulinum toxin ( orthoptic exercises
have no effect ) but it is difficult to eradicate .

59
2- complete paralysis
in which no convergence or accommodation can be initiated may be
of functional origin or caused by midbrain disease or follow head
trauma ( recovery possible ) .

Near reflex spasm:

Spasm of the near reflex is a functional condition affecting patients of
all ages ( mainly females ).
1- signs :
Diplopia , blurred vision and headaches are accompanied by
esotropia , pseudomyopia and miosis . The spasm may be triggered
when testing ocular movements . Observing miosis is the key to the
diagnosis . Refraction with and without cycloplegia confirms the
pseudomyopia , which must not be corrected optically.

2- treatment:
Involves reassurance and advising the patient to look away and cease
the activity that triggers the response . If persistent , atropine and a
full reading correction are prescribed but it is difficult later to
abandon treatment without recurrence . Patients usually seem to live
a fairly normal life despite the signs and symptoms .

Divergence insufficiency:

Divergence paresis or paralysis is a rare condition associated with

underlying neurological disease , such as intracranial space-occupying
lesions, CVA and head trauma .
Presentation may be at any age and may be difficult to differentiate
from sixth nerve palsy , but is primarily a concomitant esodeviation
with reduced or absent divergence fusional amplitudes . It is difficult
to treat; prisms are the best option .

60
STRABISMUS

 why squint is important

 A squint may show that the acuity of the eye is impaired.
 A squint may itself cause amblyopia in a child .
 A squint may be a sign of a life threatening condition like
retinoblastoma.

CLASSIFICATION OF STRABISMUS:
1-True:
 1. Fusional status
 Phoria
 Intermettent tropia
 Tropia
 2.DIRECTION OF DEVIATION
 HYPERTROPIA
 HYPOTROPIA
 EXOTROPIA
 ESOTROPIA
 3. COMITANCY
 concomitant / non-paralytic
 incomitant / paralytic
 4. TYPE OF FIXATION
 Alternating
 Monocular
 5. Age of onset
 congenital
 acquired
2- Apparent (pseudo squint)
 1- epicanthic folds
 2- abnormal inter-pupillary distance
 3- angle kappa

61
TRUE STRABISMUS:
Heterophoria:
Heterophoria is a latent tendency for misalignment of the two eyes that
becomes a manifest only if binocular vision is interrupted such as by
covering one eye.
A minor degree of Heterophoria is normal for most individuals.

CONCOMITANT(NON-PARALYTIC):
•The movement of both eyes are full (there is no paresis) but only one
eye is directed towards the fixated target.
•The angle of deviation is constant and unrelated to the direction of
gaze.
•It is the common squint that is seen in childhood.
•Under age of 6, it is rarely caused by serious neurological disease. It’s
usually primary in this age group.
•Strabismus arising later in life may have a specific and serious
neurological basis.

Incomitant (paralytic):
•The degree of misalignment varies with direction of the gaze.
•One or more of the extraocular muscles or nerves may not be
functioning properly, or normal movement may be restricted
mechanically.
•This type of strabismus may indicate either a nerve palsy or extraocular
muscle disease.

Causes of isolated nerve palsies:

•Vascular disease, Ex; DM, hypertension

•Orbital disease, Ex; neoplasia

62
•Trauma, most common cause of palsy of 4th,6th
•Neoplasia, glioma
•Raised intracranial pressure may cause a 3rd or 6th nerve palsy
•Inflammation, sarcoidosis

Extraocular muscle disease:

•Dysthyroid eye disease

•Myasthenia gravis
•Ocular myositis
•Ocular myopathy
•Browns syndrome

Clinical evaluation
History
AGE OF ONSETcan give an indication as to the etiology of a squint.
The earlier the onset , the more likely the need for surgical correction .
The later the onset , the greater the likelihood of an accommodative
component ( mostly arising between 18 – 36 months.)
The longer the duration of squint in early childhood the greater the risk
of amblyopia , unless fixation is freely alternating.
Inspection of the previous photographs may be useful for the
documentation of strabismus or AHP
2- SYMPTOMS may indicate decompensation of preexistent
heterophoria or more significantly a recently acquired , usually paretic
,condition. In the former the patient usually complains of discomfort ,
blurring and possibly diplopia of indeterminate onset and duration
compared to the acquired condition with sudden onset of diplopia. The
type of diplopia ( horizontal , cyclovertical ) should be established , the
direction of gaze in which it predominates and whether any BSV is
retained .
In adults it is very important to determine exactly what problems the
squint is causing as a basis for decisions about treatment . It is not
63
unusual for patients to present with spurious symptoms which mask
embarrassment over a cosmetically noticeable squint.
3-VARIABILITY is significant because intermittent strabismus
indicates some degree of binocularity . An alternating deviation suggests
symmetrical VA in BE.
4- GENERAL HEALTH or developmental problems are significant ( e.g.
children with cerebral palsy have an increased incidence of strabismus ) .
In older patients poor health and stress may cause decompensation and
in acquired paresis patients may report associations or causal factors (
trauma , neurological disease , diabetes etc. ).
5- BIRTH HISTORY including period of gestation , birth weight and any
problems in utero , with delivery or in the neonatal period .
6- FAMILY HISTORY is important because strabismus is frequently
familial , although there is no definitive inheritance pattern .
It is also important to know what therapy was necessary in other family
members.
7- PREVIOUS OCULAR HISTORY including prescription and
compliance with spectacles or occlusion , previous surgery or prism is
important to future treatment options and prognosis .

Assessment of visual acuity

The visual perception of an object is resolved according to

• Light sense

• Form sense ( central & peripheral ) it inclusive for visual acuity &
contrast sensitivity

• Color sense

Visual acuity is a function of the diptoric apparatus of the visual system.

• Central V.A is dependent on the following :

 The minimum visible (recognition )

64
  The minimum separable (resolution )

The minimum visible (recognition )

• This is based on the target subtending the smallest angle which

elicits a positive visual response .

• The minimum visible angle is produced at the nodal point >>

diameter of a cone = .004 mm.

The minimum separable (resolution )

• This requires the identification of two sharp, black edges

separated by a white interval of known dimension .

• Two separated points form two images upon cones separated by

unstimulated cone.

Snellen fraction VA =Test distance .

Distance at which letter subtends 5 min of arc

Why 6 M or 20 Ft distance ?

 Considered to be optical infinity.

 Definition of refractive error when accommodation relaxed.
 Shorter distance –role of accommodation .
 Longer distance - poor legibility..

Visual angle

65
Baby's Vision Development:

What to Expect the First Year

• Birth: adjusting to light and beginning to focus.

• Two to four months old: focusing and tracking moving objects.

• Five to eight months old: reaching, recognition and recall.

• Nine to twelve months: Gripping, grasping and on the go.

Birth: adjusting to light and beginning to focus.

• At birth, an infant is very sensitive to bright Light

• Small pupil

• Peripheral vision is developed before central vision .

• Within a couple of weeks, as their retinas develop, a baby’s pupils

widen

• At about a month – attraction to Large shapes and bright colors

Two to four months old: focusing and tracking moving objects.

• For their first two months, babies’ eyes often do not work
together very well

• At around three months old, your baby may have enough eye and
arm coordination to bat at a nearby moving object

Five to eight months old: reaching, recognition and recall.

• At around five months old, a baby’s ability to see how far an

object is from them (called depth perception) has developed more
fully.

66
 • Good color vision .

• Recognize their parent across a room and smile at them

Nine to twelve months: Gripping, grasping and on the go.

• At about nine months old, babies can generally judge distance

pretty well.

• Baby's eyes are probably their final color.

 Visual acuity tests for infants

Tests for indirect assessment of vision

 Historical and observational tests

 Ability to follow target
 Binocular fixation pattern
 CSM method

Tests for resolution acuity

 Optokinetic nystagmus test OKN

 Preferential looking test PLT
 Visually evoked response VER
 Catford drum test
 Cardiff acuity card test .

Historical and observational tests

 The blink to a bright light .

 Eye popping.

67
 Binocular fixation pattern

CSM Method ( Central Steady Method )

 Done with one eye fixating on an accommodative target held at
40cm
 ' C ' refers to the location of corneal light reflex fixates the
examiner light at monocular conditions .
 Normally reflected light from cornea in near the centre of cornea
and it should be positioned symmetrically in both eyes.
 If fixation target is viewed eccentrically , fixation is termed
uncentral.
 ' S ' refers to the steadiness of fixation at examiners light and also
as it slowly moved about .
 ' M ' refers to the ability of the patient to maintain alignment first
with one eye then the other opposite eye is uncover .

Evaluation
 CSM 6/9 – 6/6
 CSNM 6/36 – 6/60
 Unsteady Central Fixation < 6/60

68
 Fixation of small targets .

• Hundreds and thousands , the infant is presented with one cake

decoration in the palm of the examiner's hand , the examiner
observes the child to see whether the child picks up the object
with a pincer grip with the finger and thumb ,which indicates good
vision & good hand-eye coordination.
 Raking movement indicates poor vision .

Poor vision testing

- Optokinetic Nystagmus Drum
- Vestibular-ocular reflex test

Optokinetic Nystagmus Drum .

- Need cooperative& a awake baby with BE open
- White and black stripes to make contrast .
- The drum is moved RT to LT or UP& Down , slow & fast
- Notice the saccadic and pursuit movements
- Looking for any abnormal symmetrical eye movement .

 Optokinetic Nystagmus

 It's a gross test and is based on preferential looking principle.

 It consists of a drum which has alternate black and white strips.
 The drum is passed through patient field of vision by rotating the
drum and the eye movement of the patient is seen .

69
 Vestibular-ocular reflex test

- The examiner rotates with the child held at arm's length and
facing the examiner which induced horizontal nystagmus .
- If the nystagmus is prolonged , it suggested that the baby is
blind or has severe cerebellar disease.

 Forced choice preferential looking

 First described by Fantz

 He found infants refer to fixate high contrast , bold stripes ,
rather than homogenous fields of light .
 Monocularly done
 Teller cards used
 Evaluation Range approximately
 6/240 in newborns.
 6/60 at 3months.
 6/6/ at 36 months.

70
 Lea paddle

 It is based on the preferential looking and snellen principle.

 The chart is placed at a distance of 1 m from the patient.
 It is usually used for the age group of 3 to 9 months
 There are cards available of various thickness of lines .
 At a time two cards are held infront of the patient , the blank
infront and one with lines held behind it.
 The immediately the second card is flipped out and we keep on
changing the positions.
 The patient should appreciate the card with lines.
 The test is done at same eye level and the eye movement of
patient is seen.

 Visually evoked potentials

 Refers to electroencephalographic EEG recording made from the

occipital lobe in response to visual stimuli.

71
  Objective technique to assess functional state of visual system
beyond the retinal ganglion cells.

Types :

1. Flash VEPs
2. Pattern reversal VEPs
3. Sweep VEPs

Tests for Recognition acuity

 Visual acuity chart for preschool children.

 Landolt C
 Tumbling E
 Sheridan gardiner
 Lea symbol
 Kay picture test
 Cardiff chart
 Allen cards

Visual acuity chart for school going children/ adult.

 Snellen chart
 logMAR chart

72
Sheridan gardiner chart

 It is used for the age group of 2 – 5 yrs

 It is done at 6 meter and if child can't read 6/60 we can do it at 3
meter.
 The chart is available in the form of spiral booklet
 The main chart consists of letters HOTV of different size which are
arranged in circular form.
 The child is given akey card and asked to match with the letter in
the main card.

Lea symbol chart

 It is done at a distance of 3 meter .

 It is a spiral booklet form.
 It consists of 5 symbols in a circular form to develop the crowding
phenomenon .

73
  The examiner shows normally center symbol but at the same time
he can ask for other symbols too
 The patient is given a key card .

Kay picture test

 It is done at a distance of 6 meter .

 It is used for children 2 – 3 yr
 It is based on snellen principle.
 It is in the form of spiral booklets
 Each page has a single picture.
 The patient is given a key card

 Cardiff test chart

 It is done at a distance of 1 meter and if patient can't appreciate

that the chart work up can be done at 1/2 meter also.
 The chart consists of a single picture object.
 The patient is shown the first object and then the second card
having the same object but at different position is shown or the
same first card is rotated and shown to the patient .
 It's based on preferential looking

74
  It's used for screening and V A for pediatric patient.
 The charts are changed fast so that patients eye movement can
be seen .
 The chart has conversions in feet , meter , decimal and logMAR.

Visual acuity chart for school going children/ adult.

 Snellen chart

 It was introduce in 1862 by snellen.

 The chart consists of seven row and sometimes more 6/5 , 6/4 .
 It is most common use
 It is done monocular .
 It has 100 % contrast level same all over the chart
 It can't be used for low vision patients .
 It can't measure the in between visual acuity .

 LogMAR Chart

 It was given b Bailey and lovie in 1916 .

 The measurements are based on logarithm principle.
 Baily and lovie gave another logMAR chart for measurement of
contrast level .

75
76
Stereopsis:
-Implies the ability to obtain an impression of depth by super imposition
of two picture of the same object which have been taken from different
angle.
-Depth perception means the perception of distance of objects from
each other it' s a visual appreciation of three dimensions during
binocular vision.

TESTS FOR STEREOPSIS:

• Stereopsis is measured in seconds of arc ( 1° = 60 minutes of arc ;
1minute = 60 seconds of arc ).
•It is useful to remember that normal spatial VA is 1 minute and normal
stereo-acuity is 60 seconds ( which equals 1 minute ). The lower the
value the better the acuity .
•Various tests are employed using different test principles:
1) The TNO stereo test
2) Lang Stereotest II(random dot)
3) Frisby Stereo Test
4) Titmus Fly Test(Polaroid vectograph)

1) The TNO stereo test

• It graded to provide retinal disparities ranging from 15 to 480 sec
of arc.
• it consist of a booklet containing seven plates
• Each test plate consists of a stereogram in which various shapes have
been created by random dots in complementary colour
• The plates contain two types of figures the one which can be perceived
when viewed binocularly with red green spectacles by normal subject
having stereopsis.
• The second set of figures can be seen with andwithout spectacles even
in the absence of stereopsis.

PROCEDURE:

1. Explain the test to the patient: I am now going to test your 3D vision.
Ask the patients to wear the red/green goggles.
2. Ask the patient to hold the booklet at about 40cm.
3. Keep the room lights on.
77
4. For general screening test, the first four plates are useful as the
disparity is large & provides a qualitative assessment of stereopsis.
(a) Plate I: two butterflies; one is easily seen monocularly, the other is
only seen in stereopsis.
(b) Plate II: four discs; Two are seen without stereopsis. Ask the
patient: how many circles? Which is the biggest?
(c) Plate III : four “hidden” shapes( circle/square/triangle/diamond) are
arrange around a centrally easily visible cross.
(d) Plate IV : Three disc. One seen with right eye, one seen by left &
one seen binocularly.

5. Plate V to VII: grade stereoacuities from 480-15 seconds of arc.

6. If patients are hesitant about an answer, allow
them plenty of time to view the test plate.
7. Record the patient’s stereoacuity in seconds
of arc.
Recording:
• If the stereo shapes are identified in plates I-III
but not V-VII, record “gross stereopsis”.
• If plate IV is incorrect, record which is the
suppressing eye.
• For plates V-VII,record the stereoacuity as at least the highest level
where both responses were correct,e.g. “TNO stereoacuity <_ 15”

2) Lang test
- This test( Lang,i983) was designed to simplify stereopsis screening in
children.
- Itis based on two principles; random dots & cylindrical gratings.
- The test is a single card that can be held easily by yourself or the Pt.
- It has three levels of stereopsis, all of which are at a
low level.
• The test presented at 40cm the pt. has to locate the arc of the
moon(2oseconds),a star(2oo seconds),a car(4oo seconds) & an
elephant(600 seconds).

78
3) Frisbytest

• In this test consist of three plastic cards each containing for squares of
small random shape one of this squares in each plate contains a hidden
circle which is seen disparity.
• The disparity is created by displacement of random
shapes by the thickness of the plate so this test also does
not require use of glasses.
•The disparities measured range from 600 – 15 seconds
of arc . It is important not to allow the subject to tilt the
plate or move their head during testing as this gives
monocular clues .

4) TITMUS

•The Titmus test cosists of a three-dimensional Polaroid vectograph

consisting of two plates in the form of booklet viewed through Polaroid
spectacles . On the right is a large fly , and on the left is a series of circles
and animals . The test is performed at a distance of 40cm .
• The fly is a test of gross stereopsis (3000 seconds), and is
especially useful for young children. It should
appear to stand out from the page and the
child is encouraged to pick up the tip of one
of its wings between finger and thumb.
• The animals component consists of
three rows of stylized animals (400–100
seconds), one of which will appear forward of
the plane of reference.
• The circles comprise a graded series measuring 800–40 seconds;
one of a set of four circles should appear to stand out from the plate
surface.

79
TESTS FORSENSORY ANOMALIES:
SUBJECTIVE MEASUREMENT TESTS
 Subjective dissimilar image tests are of limited value in the
assessment of strabismus . They require simultaneous perception
( cannot be used in manifest strabismus with suppression ) and do
not reveal the full deviation .

1- Maddox wing : dissociates the eyes for near fixation ( 1/3

meter ) and measures heterophoria .

the instrument is constructed in such a way that the right eye sees only
a white vertical arrow and a red horizontal arrow , whereas the left eye
sees only horizontal and vertical rows of numbers

Measurements are made as follows :

- The horizontal deviation is measured by asking the patient to

which number the white arrow points .

- The vertical deviation is measured by asking the patient which

number the red arrow intersects .

- The amount of cyclophoria is determined by asking the patient to

move the red arrow so that it is parallel with the horizontal row of
numbers .

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2-MADDOX ROD TEST:
 Maddox rod test uses a device consisting of series of parallel
cylinders that converts apoint source of light in to line image.
 The Maddox rod can be used to test for horizontal and vertical
deviation and when used in conjunction with another Maddox rod
,for cyclodevation.

Method for measuring horizontal deviations:

 When performing the clinical test, the room lights should be
dimmed and only one light source should be visible.
 When testing at near, the patient is to fixate on light source at 33
cm, which is held at eye level. When testing at distance, the
patient is to fixate on a light source at 6m.
 Patient is instructed to fixate on the light source with both eyes
opened.
 The Maddox rod is then placed over the fixating eye.
 To measure the horizontal deviation, the Maddox rod is placed in
front of the right eye (it is done on both eyes) with the cylinder
horizontal, making the red line will be vertical.
 The patient is then asked whether the white light is superimposed
on the red line, or if it is to the left or right of the red line.

Method for measuring vertical deviations:

 The patient is held for granted to hold the Maddox Rod in front of
their right with the cylinders vertical, making the red line
horizontal.
 The patient is then asked whether the white light is superimposed
on the red line or if it appears above or below the red line.

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The Maddox rod Test Results:
A- Esodeviation(uncrossed images).
B- Exodeviation(crossed images).
C- Hypodeviation(Redline from right eye over the dot from left eye).
D- Hyperdeviation(Redline from right eye under the dot from left
eye).
E- 1→without having deviation " NRC".
2→with deviation " ARC".
** If he saw one of them then its suppression.
** If he saw the line and dot alternating then its alternating suppression.

DOUBLE MADDOX ROD TEST:

The double Maddox rod test can also be used to assess torsion and
measure cyclotropias.
1-The room lights should be dimmed and only one
light source should be visible.
2-Maddox rods are placed into the trial frames, one
before each eye.
3-Cylinders are placed into trial frame vertically,
making the two red lines horizontal.
4-Vertical prism can also be added into the trial
frames to separate the two red lines.
5-The degree of deviation and the direction (incyclo or excyclo) can be
determined by the angle of rotation that causes the line images
toappear horizontal and parallel.

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6-The amount of cyclodeviation is measured in degrees.
7-Patient is instructed to fixate on the light source with both eyes
opened.
8-Patient is asked to rotate OR the examiner rotates the cylinders with
the axis knob on the trial frame until the 2 red lines are parallel.
9-This test can be repeated for the secondary and tertiary positions of
gaze.
-The test is repeated using increasing prism powers until the deviated
eye no longer shift
-Simultaneous prism and cover test provide the best indication of size of
deviation .

WORTH FOUR DOT TES:

 Definition:
 Is often considered atest of sensory fusion.
 it Best use to test suppression scotoma.
 This is a dissociation test that can be used with both
distance and near fixation and differentiates between BSV,
ARC and suppression.
 Results can only be interpreted if the presence or absence
of a manifest squints known at time of testing.
 Procedure:
 The patient wears a red lens in front of the right eye ،which
filters out all colors except red and a green lens In front of
the left eye which will filter out all colors except green.,
 so red and green dot are each seen by only one eye while
the white dot seen by both eye.
 The patient then views target consisting of 4 dot.
 the stimulus dots can be presented in awall –mounted
display or by handheld flashlight.
 The test should administered in good light so peripheral
feature in the room can stimulate motor fusion .

RESULTS FOR ( WITH FOR DOTS TEST):

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 • If there is scotoma , the perception of 4 dot indicates the scotoma
must be smaller than the test target.
• Seeing 5 dot is diplopia response, the patient has manifest
strabismus without suppression or ARC.
• In monofixation syndrome worth 4 dot test can be used to
demonstrate both presence of peripheral fusion and absence of
bifixation.

BAGOLINI STRIATED GLASSES:

 Definition: This is a test for detecting BSV, ARC or
suppression. Each lens has many narrow striations running parallel
in one meridian like maddox and case fixation light to appear
elongated streak.
 Procedure: the lens are usually placed in 135in front of right eye
and at 45 in left eye.

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4 Δ PRISM TEST:
 This test distinguish bifoveal fixation (normal BSV) from foveal
suppression (also known as a central suppression scotoma – CSS)
in microtropia .
 Document the presences of small facultative scotoma in patient
with monofixation syndrome and no manifest deviation.

RESULTS FOR 4 PRISM TEST :

 If foveal fixation exist:

1- The prism is placed base out (microtropia is commonly Esotropic not

exotropic) in front of the right eye with deviation of the image away
from the fovea temporally, Followed by corrective movement of both
eyes to the left.
2- The left eye then converges to fuse the images.
3-Patient with bifixation usually show bilateral
movement away from the eye covered by brism
followed by unilateral fusional convergence
movement of the eye not behind prism .

 Procedure:

1- The patient fixates a distance target with both

eyes open And a 4 Δ prism is placed baseout in front of the eye With
suspected CSS .

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2- The image is moved temporally in the left eye but falls within the CSS
and no movement of either eye is observed.
3- The prism is then moved to the right eye which adducts to maintain
fixation; the left eye similarly moves to the left consistent with the
Hering law of equal innervation, but the second image falls within
the CSS of the left eye and so no subsequent refixation movement is
seen .

• 4 prism base out is the least reliable method of documenting the

presence of macular scotoma.

Measurement of the deviation:

 Objective methods.
 Subjective methods

1-Objective methods:

- Hirschberg corneal reflex test

- Krimsky’s test
- Bruckner test
- Cover uncover test
- Alternate cover test

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- Prism bar cover test
- Synoptophore

2.Subjective methods:

- Maddox rod test

- Maddox wing test
- Double maddox rod
- Maddox double prism
- Red green glass test
- Diplopia field

 Hirschberg corneal light reflex :

•Objective assessment of ocular alignment.

•In newborn and often in young children it may be the only feasible
method.
•Normally the light is reflected on each cornea symmetrically and in the
same position relative to the pupil and visual axis on each side.
•In deviating eye the light reflection will be not centrally positioned and
in direction opposite to that of the deviation
•Example: pupil margin 15:,limbus 45:,iris 30:.
- Used as initial screening test for strabismus.
- Amount of deviation: note location of corneal light reflex 1mm = 7: or
15Δ.

Corneal reflex at border of pupil = 15°.Corneal reflex at limbus= 45°.

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PSEUDO SQUINT:

1- epicanthic folds:
may simulate an Esotropia .
2- abnormal inter-pupillary
distance:
if short may simulate an ET and if wide an XT .

3- Angle kappa :

- is the angle between the visual and

anatomical ( pupillary ) axes .
- Normally the fovea is situated temporal
to the anatomical center of the posterior
pole . The eyes are therefore slightly
abducted to achieve bifoveal fixation . A light shown onto the cornea will
therefore cause a reflex just nasal to the center of the cornea in both
eyes . This is termed a positive angle kappa .
-A large positive angle kappa may simulate an exotropia . -A negative
angle kappa occurs when the fovea is situated nasal to the posterior
pole ( high myopia and ectopic fovea ). In this situation , the corneal
reflex is situated temporal to the center of the cornea and it may
simulate an esotropia .

 Krimsky test:

This test is used to centralize the corneal reflection in squinting eye as

compared to the reflex in fixing eye.
o Results are expressed in prism diopter (PD).

88
 o Convenient test for quick evaluation of the angle of strabismus,
especially in the abnormal fixation of the squint eye.

 KRIMSKY AND PRISM REFLECTION TESTS

Corneal reflexes are used for the same indications as the Hirschberg test
, but combined with prisms to give a more accurate
approximation of the angle in a manifest deviation.

1- Krimsky test : involves placement of prisms in front

of the fixating eye until the corneal light reflections are
symmetrical . This test reduces the problem of parallax
and is more commonly used than the prism reflection
test .
3- prism reflection test : involves the placement of prisms in front of
the deviating eye until the corneal light reflections are
symmetrical .

 Brukner test:

- Performed by using direct ophthalmoscope to obtain a red reflex

simultaneously in both eyes.
- Deviated eye will have a lighter and brighter reflex than the fixing
eye.
- Bruckner test positive for left eye esotropia.

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  cover-uncover test:

The cover–uncover test consists of two parts:

• Cover test to detect a heterotropia. It is helpful to begin the
near test using a light to observe the corneal reflections and
to assess fixation in the deviating eye. It should then be
repeated for near using an accommodative target and for
distance as follows:
○ The patient fixates on a straight-ahead target.
○ If a right deviation is suspected, the examiner covers the
fixing left eye and notes any movement of the right eye to
take up fixation.
○ No movement indicates orthotropia or left
heterotropia.
○ Adduction of the right eye to take up fixation indicates
right exotropia and abduction, right esotropia
○ Downward movement indicates right hypertropia and
upward movement right hypotropia.
○ The test is repeated on the opposite eye.
• The uncover test detects heterophoria. It should be
performed both for near (using an accommodative target)
and for distance as follows:
○ The patient fixates a straight-ahead distant target.
○ The examiner covers the right eye and, after 2–3 seconds,
removes the cover.
○ No movement indicates orthophoria a keen
observer will frequently detect a very slight latent
deviation in most normal individuals, as few individuals
are truly orthophoric, particularly on near fixation.
○ If the right eye had deviated while under cover, a
re-fixation movement (recovery to BSV) is observed on
being uncovered.
○ Adduction (nasal recovery) of the right eye indicates
exophoria and abduction Esophoria.
○ Upward or downward movement indicates a vertical
phoria.
○ After the cover is removed, the examiner notes the speed
and smoothness of recovery as evidence of the strength of
motor fusion.

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 ○ The test is repeated for the opposite eye.
○ Most examiners perform the cover test and the uncover
test sequentially, hence the term cover–uncover test.

Possible results of the cover testPossible results of the uncover test

 Alternate cover test:

The alternate cover test induces dissociation to reveal the total

deviation when fusion is disrupted. It should be performed only
after the cover–uncover test.
• The right eye is covered for several seconds.
• The occluder is quickly shifted to the opposite eye for 2
seconds, then back and forth several times. After the cover
is removed, the examiner notes the speed and smoothness
of recovery as the eyes return to their pre-dissociated
state.
• A patient with a well-compensated heterophoria will have
straight eyes before and after the test has been performed
whereas a patient with poor control may decompensate to a
manifest deviation.

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  Prism cover test:
The prism cover test measures the angle of deviation, It combines
alternate cover test with prisms .

Procedure: -
 The alternate cover test is performed first .
 Prism of increasing strength placed in front of one eye with base
opposite the direction of deviation.
 Alternate cover test is performed continously as stronger prisms
are used.
 Amplitude of refixation gradually decreases.
 End point reached when no movement is seen.
 To ensure maximum angle is found , prism strength is increased
until movement is observed in opposite direction.
 Then reduced again to find neutral value Angle of
deviation equals the strength of the prism.
Synaptophore(amblyoscope):

o It is an basic orthoptic instrument used for diagnostic

as well as therapeutic purpose.
o The word synaptophore derived from Greek word.
- Synaptophore where sin mean with, ops mean eye, and phore mea
bearing.
History:
- The oldest model is developed by Claud worth .
- Mc. Maddox first develop slides used in early device.
Principle
 Haploscopic principle
It is based on the principle of division of physical
space in to two separate area of visual space each of
which is visible to one eye only.
 Parts
- Two tubes for viewing picture.
- Lenses with in the eyes piece are +6.5 DS.
- Pairs of slides.

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- Controls allow vertical separation of the target as well cyclotorsional
adjustment.
- Mirror in each tube to reflect the image of target through
the eye piece into corresponding eye.
- Scales to measure the amount of deviation.
- Illumination system to increase or decrease the stimulus luminance.

SLIDES:
 Simultaneous perception slides
o Foveal
o Macular
o Para macular
o Peripheral
 Fusion slides
 Stereopsis slides
 Special purpose slides
o After image slides
o Haidinger brushes
o Slide with number or letters

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94
Uses of synaptophore
- The uses of synaptophore divided into two
- Diagnostic uses
- Therapeutic uses
Diagnostic uses
- Estimation of grade of binocular single vision
- Measurement of objective and subjective angle of deviation
- Measurement of deviation in all cardinal direction of gaze
- Measurement of inter pupillary distance
- To investigate the state of retinal correspondence
- Measurement of primary and secondary deviation
- To estimate presence and type of suppression
- Measurement of fusional vergance
- measurement of angle kappa
- Measurement of AC/A ratio

Therapeutic uses:
- It is used in treatment off
- Suppression
- ARC
- Amblyopia with Eccentric fixation
- Accommodative esotropia
- Heterophorias and intermittent heterophorias
Preliminary setting:
1. The patient’s chair and the table should be adjusted so that he is able
to look through the
centre of the eye-pieces comfortably with his head erect.
2. The chin and forehead rest should be adjusted to suit the patient.
3. The patient’s interpupillary distance (I.P.D.) must be measured and
the instrument adjusted
so that the distance between eye-pieces is equal to the interpupillary
distance.
Diagnosis uses:

Estimation of grade of binocular single vision

Simultaneous perception
 First grade of BSV

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  Tested using two dissimilar picture such as an object and a
surround e.g. cage and lion
 Patient is asked to put the lion in cage by moving the arm of
synaptophore
 Ideally the foveal picture must be used. But the target size should
be appropriate to the patient visual acuity.

Recording
 If the patient is able to see both the pictures at a time then S.M.P.
is present and recorded as S.M.P. at zero degree or at a particular
angle.

Fusion
Tested using similar but incomplete picture eg: tworabbit one lacking tail
and one lacking bunch offlowers. If fusion is present one rabbit complete
withtail and flower will be seen.

Sensory fusion:
 One tube is locked and patient is asked to create a composite
image and the position of sensory fusion was achieved is read off
the scale.

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Motor fusion:
 Lock the Colum at their real corrected angle then to measure
negative fusion adduction knob adjusted and for positive fusion
abduction knob is adjusted. Then note the value when the image
split into two.
Recording
 Sensory fusion: present …………degree………
 Motor fusion:
Adduction BP:………………..RP:……………
Abduction BP:………………..RP:……………
Stereopsis
 Tested using two pictures of same object which have been taken
from slightly different angle.
 If the images are fused and is seen three diamensioly stereopsis
present.

Measurement of IPD:
The patient should be seated at the Synoptophore, Then inter-pupillary
distance (IPD) should be
adjusted so the lines on the eyepiece line-up with the corneal
reflections.

Measurement of objective angle of deviation:

Patient seated in front of synaptophore and IPD should be adjusted.
Smaller picture should be placed in front of RE and larger picture placed
in front of LE. An alternate cover test is performed by
alternatively switching off the light illuminating the slides.

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Then according to the directions of eye movement the tube before the
non-fixing eye is adjust until no movement is seen. Then the
measurement is recorded from scale. If the eyes moves out to take
fixation left arm moved in and vice versa. This can be repeated for
vertical deviations.

Measurement of subjective angle of deviation:

- Patient seated in front of synaptophore and IPD should be adjusted
Smaller picture should be placed in front of RE and larger picture placed
in front of LE.
- Ask the patient to pull or push the handle controlling the non-fixing
eye’s tube until the two images are super imposed.
- In the presence of suppression patient fail to superimpose two images.
In this case a larger target should be introduce. If the patient fail to
superimpose in peripheral slide the patient has no BSV.
Measurement of The Angle of Deviation For Near by The Synoptophore:
- Minus 3.00D spheres can be inserted in the lens holders situated in
front of the eyepiece lenses. The patient has to exert 3.00D of
accommodation in order to get a clear image of
the slides.
- In doing so , each eye exerts 3Δ of convergence for each diopter of
accommodation-in other words, 9Δ of convergence in one eye or 18Δ of
convergence.
- recording the angle of deviation, we must keep this in mind and either
subtract 18Δ from or add 18Δ to the major amblyoscope readings.
E.g.:20 prism base out the deviation will be 20-18 = 2 prism base out 20
prism base in the deviation will be 20+18=38 base in.
Recording
SMP using macular slide
Angle of deviation for distance
 Fixing RE
 Objective deviation: 0 degree
 Subjective deviation: 0 degree
Angle of deviation for near
 Fixing RE
 Objective deviation: 0 degree
 Subjective deviation: 0 degree

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Measurement of cyclodeviation with Maddox slide

- Maddox slides (white binding) can aid the assessment of 9 positions of

gaze. Horizontal and vertical deviations are assessed
in the normal way.
- However, with the cross before the fixing eye the
examiner may rotate the torsion control until the
patient is satisfied that it superimposes in the center
of the green surround and all lines.

Measurement of cyclodeviation with SP slides:

- Use SP slides and put lion in front of RE and cage in front of LE

- The patient is asked to look at each one in turn and asked whether
cage appear level.
 If the cage left hand side lower than right hand side incyclophoria
or tropia
 If the cage right hand side lower than left hand side excyclophoria
or tropia
- Incyclophoria corrected by rotating torsional screws towards the
patient
- excyclophoria corrected by rotating torsional screws away from the
patient

Retinal correspondence using SP slides:

- Measure objective and subjective angle using synaptophore

- Find out angle of anomaly:
Objective angle – subjective angle= angle of anomaly

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Recording
Fixing RE
 Objective angle: 0 degree
 Subjective angle: 0 degree
 Angle of anomaly: zero
- Retinal correspondence: normal.
Measuring AC/A ratio
Gradient method is often used:
Measure the deviation with accommodation and without
accommodation divided by change in accommodation gives AC/A ratio
AC/A =ΔL - ΔO /D where ΔL – deviation with add lens, ΔO –
originaldeviation D – dioptric power of lens

E.g.: ΔL - 6 Δ eso, Δ o - 2 Δ exo, D – 2 D concave sphere

AC/A =6-(-2)/2
8/2 = 4 Δ/D
Determination of angle kappa:

- A special slide consist of row of number or letters used for this

- Ask the patient to look at zero. If the corneal reflex is on nasal side the
angle is positive, And if the reflex is on temporal side the angle is
negative.
- The patient is asked to turn the letter or number until the reflex is
centered. The deviation correspond to letter or number is recorded.

To estimate type and presence of suppression:

- The area of suppression initially mapped out by recording the

angle at which the image is suppressed.
- By lowering the angle the illumination of fixating eye until the
SMP is achieved give a rough estimation of type of suppression.
Position of gaze

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 - In complex ocular motility cases, all 9 cardinal positions of gaze
can be subjectively measured along with unilateral ductions with
repeatable, standardized conditions.
- The subjective measurement can be performed
fixing either eye in the primary position, when the
central lock is released on lateral versions and using
the elevation and depression controls up to +/- 30°
vertically.

After image test

- There are two slides available one with vertical slit and other with
horizontal slit.
- Then right fovea is stimulated by vertical sit for 20 sec then left
fovea is stimulated by horizontal slit for 20 sec.
- Ask the patient to draw position of after image.

Haidinger’s Brushes
Haidinger brushes correspond to macula.

- To determine whether amblyopic patient fixate with fovea or not.

- Training technique in amblyopia to improve fixation.

Therapeutic uses:
Anti suppression exercises
• chasing
• flashing
• Macular massage
• Crossing technique

Flashing:
This can be done with an automatic flashing device
or by manual control of the switches. The
tubes are set at the objective angle of deviation.
First one light and then the other is extinguished at
interval of a few seconds. This induces alteration. The speed of
altera
tion
shoul

101
d be slow at first but gradually increased.
CHASING TECHNIQUE
- It is a subjective exercise using the smallest SMP slide that the
patient can superimpose
- The two arms of the synaptophore are loosened and the patient is
asked to hold the tube in front of the suppressed eye
- Examiner moves the other tube in front the fixating eye in a
random position
- patient is asked to chase it and superimpose the two pictures by
moving the other tube
- As the pt.’s performance improves , smaller pictures are used
MACULAR MASSAGE
 This exercise stimulates retina of deviated eye
 It is done by moving the visual target across the suppression
scotoma
CROSSING TECHNIQUE
 Target is moved in front of suppressed eye from
periphery of field towards suppression scotoma
 Target will disappear in suppression area & reappear on the other
side of scotoma
 The movement is continued until this area has decreased to such
an extent that patient can perceive both target and can
superimpose the two object

Fusion exercises
Fusion exercises were given on major amblyoscope with the fusion
slides. Fusion range could be
increased by gradually converging both the tubes of major amblyoscope
till the fusion breaks.
Exercises were given daily or on alternate days for 10 to 15 minutes
depending on the tolerance and
convenience of the patients.

Advantages
 Accurate measurement is possible
 Tube can be move separately
 Large selection of suitable slides are available

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  The patient’s eye can be seen by the orthoptist and the corneal
reflections can be observed.
 There can be rapid interchange from objective to subjective
conditions.

Disadvantages
 Poor fixation
 Not useful in non-cooperative child
 Only corneal reflex is noted
 Bulky instrument, difficult to transfer from one place to other.
 Though the slides are kept in optical infinity distance but still it
stimulates proximal accommodation of the patient.
 Needs expert orthoptist to handle the instrument accurately.

MOTILITY TESTS:
Ocular movements:
1- versions:towards the eight eccentric positions of gaze are tested by
asking the patient to follow a target , usually a pen or a pen-torch (which
offers the advantage of corneal light reflections to aid assessment ).
A quick cover test is performed in each position of gaze to confirm
whether a phoria has become a tropia or the angle has increased and
the patient is questioned regarding diplopia .
They may also be elicited voluntarily , in response to a noise or by the
doll’s head maneuver in uncooperative patients .

2- ductions: are assessed if reduced ocular motility is noted in either or

both eyes . A pen-torch should be used with careful attention to the
position of the corneal reflexes . The fellow eye is occluded and the
patient asked to follow the torch into various positions of gaze .
A simple numeric system may be employed using 0 to denote full
movement, and -1 to -4 to denote increasing degrees of underaction .

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 Force duction test:
• Also known as traction test.
• Described by wolf ,Gifford and jaensch (19001929).
• It is performed to differentiate between the incomitant squint due to
paralysis of EOM and that due to mechanical restriction of the ocular
movement.

A. No restriction is encountered when rotating the adducted eye into

abduction .
B. Contracture of MR muscle prevents examiner from the abducting the
eye .

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Procedures:

• Apply several drops of local anesthesia to limbal area of near the

insertion of possibly mechanically restricted muscle ,which will be on the
opposite side of the possibly paretic muscle. If the lateral rectus muscle
,the anesthesia would be applied near the insertion of medial rectus.
• The patient is then directed to look at a target that is held in the
direction of action of the possible paretic muscle ,which is in the
opposite direction of action of the possible mechanically restricted
muscle .
• If a RLR was the possible paretic muscle ,the patient would be directed
to look at a target to the right .
• The eye is then grasped with toothless forceps near the limbus where
the anesthesia was applied .the eye is grasped close to the limbus to get
as little conjunctiva as possible in the forceps
• An effort is then made to rotate the eye with the forceps in the
direction of action of the possible paretic muscle .if the lateral rectus
was the possible paretic muscle ,the eye would be grasped at the medial
limbus and the rotation attempted would be an abduction movement .
• If the eye can be rotated with the forceps past the voluntary moved
limit -presence of paretic muscle .
• FDT is positive in cases of incomitant squint due to mechanical
restriction and negative in cases of EOM PALSY.

Near point of convergence

-The near point of convergence ( NPC ) is the nearest point on which the
eyes can maintain binocular fixation .
-It can be measured with the RAF rule which rests on the patient’s
cheek. A target is slowly moved along the rule towards the patient’s eyes
until one eye loses fixation and drifts laterally ( objective NPC ) .
-The subjective NPC is the point at which the patient reports diplopia .
-Normal NPC should be nearer than 10 cm without
effort .

105
 Near point of accommodation
-The near point of accommodation ( NPA ) is the nearest point on which
the eyes can maintain clear focus . It can also be measured with the RAF
rule . The patient fixates a line of the print , which is then slowly moved
towards the patient until it becomes blurred . The distance at which this
is first reported is read off the rule and denotes the NPA .
-The NPA recedes with age ; when sufficiently far away to render reading
difficult without optical correction , presbyopia is present .
-At the age of 20 years the NPA is 8 cm and by the age of 50 years it has
receded to 46 cm .

The amplitude of accommodation:

-There are many methods but the most common is pen - push up
method.
-It is used for convergence insufficiency .

Hofstadter's Formula:

Minimum expected amplitude.15 - 0.25 (age)

Average expected amplitude 18.5 - 0.3 (age )
Maximum expected amplitude 25 - 0.4 (age )

Fusional amplitudes:
-Fusional amplitudes measure the efficacy of vergence movements.they
may be tested with prism bars or the synoptophore .
-Increasingly strong prisms are placed in front of one eye , which will
then abduct or adduct ( depending on whether the prism is base-in or
base-out ), in order to maintain bifoveal fixation .
-When a prism greater than the fusional amplitude is reached , diplopia
is reported or one eye drifts the other way. This is the limit of vergence
ability .
-The prism fusion range must be assessed in any binocular patient
before strabismus surgery .

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Postoperative diplopia test
This simple test is mandatory prior to strabismus surgery in all non-
binocular patients over 7-8 years of age to assess the risk of diplopia
after surgery .
Corrective prisms are placed in front of one eye ( usually the deviating
eye ) and the patient asked to fixate a straight ahead target with both
eyes open .The prisms are slowly increased until the angle is significantly
overcorrected .
The patient reports if diplopia occurs . If suppression persists throughout
, there is little risk of diplopia following surgery ; in a consecutive
exotropia of 35∆ diplopia may be reported from 30∆ and persist as the
prism correction mimics an esotropia .
Diplopia may be intermittent or constant but in either case this would be
an indication to perform a diagnostic botulinum toxin test .
Diplopia is not restricted to patients with good VA in the deviating eye ;
intractable diplopia is a difficult condition to treat and is best avoided .

INVESTIGATION OF DIPLOPIA

The Hess test and the Lees screen are two similar tests that plot the
dissociated ocular position as a function of the extraocular muscles .
They enable differentiation of paretic strabismus caused by neurological
pathology from restrictive myopathy ( such as in thyroid eye disease or a
blow-out fracture of the orbit ) , and recent onset paresis from long-
standing

ELECTRONIC HESS CHART

The screen contains a tangent pattern ( 2D projection of a spherical
surface ) printed onto a dark grey background .
- Red lights that can be individually illuminated by a control panel
indicate the cardinal positions of gaze within a central field ( 15°

107
 from primary position ) and a peripheral field ( 30° ); each square
represents 5° of ocular rotation .

- The patient is seated 50cm from the screen and wears red-green
goggles , red lens in front of the right eye , and holds a green
pointer.

- The examiner illuminates each point in turn which is used as the

point of fixation . This can now be seen only with the right eye ,
which therefore becomes the fixating eye .
- The patient is asked to superimpose their green light onto the red
light , so plotting the relative position of the left eye . All the points
are plotted in turn .
- In orthophoria the two lights should be more or less
superimposed in all nine positions of gaze .
- The goggles are then reversed ( red filter in front of the left eye )
and the procedure is repeated .
- The relative positions are marked by
the examiner on a chart and connected
with straight lines .

LEES SCREEN
- The apparatus consists of two opalescent glass screens at right-
angles to each other, bisected by a two-sided plane mirror which
dissociates the two eyes .

- Each screen has a tangent pattern marked onto the back surface
which is revealed only when the screen is illuminated .

1- procedure : the test is performed with each eye fixating in turn .

- The patient faces the non-illuminated screen with the chin

stabilized on a chin rest attached to the mirror support and fixates
the dots in the mirror .

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- The examiner indicates the dot required for the patient to plot .

- The patient positions the pointer on the non-illuminated screen

perceived to be on top of the dot indicated by the examiner .

- When all of the dots have been plotted the patient is repositioned
to face the other screen and the procedure is repeated . The
results are charted as before .

- interpretation :
- The two charts are compared .

Hess chart of a recent right lateral rectus palsy:

- The smaller chart indicates the eye with the paretic muscle .

- The larger chart indicates the eye with the overacting yoke muscle
.

- The smaller chart will show its greatest restriction in the main
direction of action of the paretic muscle ( right lateral rectus ).

- The larger chart will show its greatest expansion in the main
direction of action of the yoke muscle ( left medial rectus ).

- The degree of disparity between the plotted point and the

template in any position of gaze gives an estimate of the angle of
deviation ( each square = 5° )

- Changes with time

109
- Changes with time are very useful as a prognostic guide . For
example , in right superior rectus palsy , the Hess chart will show
underaction of the affected muscle with an over action of its yoke
muscle ( left inferior oblique ) .

- Because of the great incomitance of the two charts , the diagnosis

is straightforward . If the paretic muscle recovers its function , both
charts will revert to normal .

- However if the paresis persists , the shapes of both charts will

change as follows :

- - Secondary contracture of the ipsilateral antagonist ( right inferior

rectus ) will show up on the chart as an overaction which will lead
to a secondary ( inhibitional ) palsy of the antagonist of the yoke
muscle ( left superior oblique ) , which will show up on the chart as
an underaction .

- This could lead to the incorrect impression that the left superior
oblique was the primary muscle at fault .

110
 - With further passage of time , the two charts become more and
more concomitant until it may be impossible to determine which
was the primary paretic muscle .

REFRACTION AND FUNDUSCOPY

It should be emphasized that dilated funduscopy is mandatory in
the context of strabismus , to exclude any underlying ocular
pathology such as macular scarring , optic disc hypoplasia or
retinoblastoma .
Strabismus is often secondary to refractive error .
Hypermetropia , astigmatism , anisometropia and myopia may
all be associated with strabismus .

CYCLOPLEGIA
The commonest refractive error causing strabismus is
hypermetropia . Accurate measurements of hypermetropia
necessitate effective paralysis of the ciliary muscle , in order to
neutralize the effect of accommodation , which masks the true
degree of this refractive error .
1- cyclopentolate : affords adequate cycloplegia in most children
. The concentration employed is 0.5 % under the age of 6
months and 1% thereafter .

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One drop , repeated after 5 minutes , usually results in maximal
cycloplegia within 30 minutes , with recovery of
accommodation within 2-3 hours and of mydriasis within 24
hours .
The adequacy of cycloplegia can be determined by comparing
retinoscopy readings with the patient fixating for distance and
then for near . If cycloplegia is adequate , there will be little or
no difference . If cycloplegia is incomplete there will be a
difference between the two readings and it may be necessary to
wait another 15 min or to instil another drop .
Topical anaesthesia with an agent such as topical
proximethocaine , prior to instillation of cyclopentolate , is
useful in preventing ocular irritation and reflex tearing , thus
affording better retention of the cyclopentolate in the
conjunctival sac and effective cycloplegia .
2- Atropine may be necessary in some children with either high
hypermetropia or heavily pigmented irides , in which
cyclopentolate may be inadequate . Atropine may be used as
drops or ointment . Drops are easier for an untrained person to
instil , but there is less risk of overdose with ointment . The
concentration is 0.5% under the age of 12 months and 1%
thereafter . Maximal cycloplegia occurs at 3 hours ; recovery of
accommodation starts after about 3 days and is usually complete
by 10 days . Atropine is instilled ( by the parents ) b.d. for 3
days before retinoscopy , but not on the day of examination.
The parents should be warned to discontinue medication if there
are signs of systemic toxicity such as flushing , fever or
restlessness, and seek immediate medical attention .

112
Change of refraction:
Because refraction changes with age , it is important to check at
least every year and more frequently in smaller children and if
acuity is reduced . At birth most babies are hypermetropic .
After the age of 2 years there may be an increase in
hypermetropia and a decrease in astigmatism .
Hypermetropia may continue to increase until the age of about 6
years , and then between the ages of 6 and 8 years levels off ,
subsequently decreasing until the early teenage years .
When to prescribe
1- hypermetropia : in general up to 4D of hypermetropia should
not be corrected in a child without a squint unless they are
having problems with near vision . With degrees of
hypermetropia greater than this a two-thirds correction is usually
given . However , in the presence of esotropia the full
cycloplegic correction should be prescribed , even under the age
of two years .
2- astigmatism : a cylinder of 1.50D or more should be
prescribed , especially in cases of anisometropia after the age of
18 months .
2- myopia : the necessity for correction depends on the age of
the child . Under the age of two years -5.00 or more of myopia
should be corrected ;between the ages of 2 and 4 the amount is -
3.00 D . Older children should have correction of even milder
degrees of myopia to allow clear distance vision .
4- anisometropia : after the age of 3 the full difference in
refraction between the eyes should be prescribed if it is more
than 1 D. if there is no squint then any associated hypermetropic
correction may be equally reduced for each eye .
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ESOTROPIA

Concomitant esotropia:

Accommodative:
o A.Refractive
 Fully accommodative
 Partially accommodative
o B. Non-refractive
 With convergence excess
 With accommodation weakness
o c.Mixed
2.Non-accommodative
 Essential infantile
 Microtropia
 Basic
 Convergence excess
 Convergence spasm
 Divergence insufficiency
 Divergence paralysis
 Sensory
 Consecutive
 Acute onset
 Cyclic

 Tropia:
 Primary

 Secondary

 Consecutive

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 Constant
 With Accommodative Element.
 without Accommodative Element.
Intermittent
 Accommodative
 Distance - near eso-distance eso
 Time - cyclic/alternate day squint
 Non-specific

 PHPRIA:
 1-Conv. Excess
 2-Div. Weakness
 3-Non-specific

Accommodative:
A. Refractive Accommodative Esotropia:-

Fully Accommodative Esotropia

 Aetiology:
- Low uncorrected hypermetropia >3 DS
-Squint not develop if patient has sufficient fusional divergences.
- Moderate degrees hypermetropia (3-5DS) – amount of PFR not enough
to overcome esotropia.
- High degree hypermetropia> 5 DS , insuperable hypermetropia patient
remain straight or occasionally diverge.

 Clinical features
•Esotropia which becomes apparent when accommodation is exerted
(usually intermittent at first) .
•Age of onset 1-4 years .
•Hypermetropia of any amount .
•Similar amount of esodeviation at distance and near (normal AC/A
ratio).

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•No residual esotropia for near or distance when wearing full
hypermetropic spectacles correction.
•Normal binocular function when squint not .
•Amblyopia rare (may occur due to anisometropia or if the squint
becomes constant .
•Family tendency .

 Management
-Prescribe fully hypermetropic lenses .
-Glasses worn full time .
-Occlusion – if amblyopia present .
-Orthoptic exercises – to strengthen BSV .

Partially accommodative esotropia:

The squint is reduced, but not eliminated by full correction of
hypermetropia. Amblyopia is frequent as well as bilateral congenital
superior oblique weakness. Most cases show suppression of the
squinting eye although ARC may occur, but of lower grade than in
microtropia.

B-Non-refractive accommodative esotropia

This is associated with a high AC/A ratio in which a unit increase of
accommodation is accompanied by a disproportionately large increase
of convergence . This occurs independently of refractive error , although
hypermetropia frequently coexists. It can be subdivided into :

 1- convergence excess :
-High AC/A ratio due to increased accommodative convergence
(accommodation is normal , convergence is increased ) .
-Normal near point of accommodation .
-Straight eyes with BSV for distance .
-Esotropia for near, usually with suppression .
-Straight eyes through bifocals .

 2- hypoaccommodative convergence excess:

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-High AC/A ratio due to decreased accommodation ( accommodation is
weak, necessitating increased effort , which produces overconvergence).
-Remote near point of accommodation .
-Straight eyes with BSV for distance .
-Esotropia for near , usually with suppression .

Medical treatment:

Refractive error should be corrected , as previously described . In

children under the age of 6 years , the full cycloplegic refraction revealed
on retinoscopy should be prescribed ( with a deduction only for the
working distance ) . In the fully accommodative refractive esotropia this
will control the deviation for both near and distance .
After the age of 8 years , refraction should be performed without
cycloplegia and the maximal amount of ‘ plus ‘ that can be tolerated (
manifest hypermetropia ) prescribed .

For convergence excess esotropia bifocals may be prescribed to relieve

accommodation ( and thereby accommodative convergence ) , thus
allowing the child to maintain bi-foveal fixation and ocular alignment at
near .
The minimum add required to achieve this is prescribed .
The most satisfactory form of bifocals is the executive type in which the
intersection crosses the lower border of the pupil .

The strength of the lower segment should be gradually reduced and

eliminated by the early teenage years .
Bifocals are best suited to hypoaccommodative esotropia and where the
AC/A ratio is not overly excessive , when there is a reasonable chance of
discarding bifocal correction with time .
At higher levels surgery is the better long-term option .
The ultimate prognosis for complete withdrawal of spectacles is related
to the magnitude of the AC/A ratio and also the degree of
hypermetropia and associated astigmatism . Spectacles may be needed
only for close work .

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Surgery:

The aim of surgery is to restore or enhance BSV or to improve the

appearance of the squint .
Surgery should only be considered if spectacles do not fully correct the
deviation and every attempt has been made to treat amblyopia .
-Bilateral medial rectus recessions are performed in patients in whom
the deviation for near is greater than that for distance .
-If there is no significant difference between distance and near
measurements, and equal vision in both eyes , some perform unilateral
medial rectus recession combined with lateral rectus resection , whereas
others prefer bilateral medial rectus recessions.
-In patients with residual amblyopia surgery is usually performed on the
amblyopic eye .
-In constant accommodative esotropia surgery to improve appearance is
best delayed until requested by the child to avoid early consecutive
exotropia and should only aim to correct the residual squint present
with glasses on .

 Treatment of amblyopia is very important before contemplating

surgery .

Non-Accommodative Esotropia
Definition:

Non-Accommodative convergent Squint refers to the ESO-DEVIATIONS

which are not primarily elicited by the direct influence
ofaccommodation. Characterized by
-Comitant Esotropia
-Acquired
-Onset after 6 months to 5 years
-Small to large angle deviation
-little or no hyperopia
-Normal AC/A ratio
-No neurologic or systemic sign or symptoms

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119
 A. ESSENTIAL ESOTROPIA:

1. ESSENTIAL INFANTILE ESOTROPIA

-Esotropia unilateral or bilateral .
-occurs after birth within 4 months .

Etiology :
-Primary cause idiopathic .
-Secondary causes are :

 Primary motor dysfunction

associated with poor fusion .
 family history of strabismus .
 Born prematurely .
 A seizure disorder of hydrocephalus.
CONSISTANT FEATURES:
 Esotropia by 6 months.
 The angle >30 Δ eso and stable .
 Asymmetry OKN .
 Cross fixation .
 Abduction restriction .
 No clinical CNS involvement .
 Deviation same for N and D .
Associated features:
 IO overaction 60%.
 Nystagmus, DVD 50% > 1 year .
 Amblyopia 35%.
 AHP .
 It can be associated with systemic disease such as Down's
syndrome, albinism, cerebral palsy, or hydrocephaly.

• Differential diagnosis:
 bilateral congenital sixthnerve palsy .
 secondary (sensory) esotropia due to organiceye disease
 nystagmus blockage syndrome .
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  Duane syndrome .
 Mӧbius syndromes and strabismus fixus.

Initial treatment:

Early ocular alignment gives the best chance of the development

of some degree of binocular function. Ideally, the eyes should be
surgically aligned by the age of 12 months, and at the very latest
by the age of 2 years, but only after amblyopia and any significant
refractive error have been corrected.

• The initial procedure can be either recession of both medial

recti or unilateral medial rectus recession with lateral rectus
resection. Very large angles may require recessions of
6.5 mm or more. Associated significant inferior oblique
overaction should also be addressed.

• An acceptable goal is alignment of the eyes to within 10 Δ,

associated with peripheral fusion and central suppression
. This small-angle residual strabismus is often
stable, even though bifoveal fusion is not achieved.

Subsequent treatment:
• Undercorrection may require further recession of the
medial recti, resection of one or both lateral recti or
surgery to the other eye, depending on the initial
procedure.
• Inferior oblique overaction may develop subsequently, most
commonly at age 2 years The parents should
therefore be warned that further surgery may be necessary
despite an initially good result. Initially unilateral, it
frequently becomes bilateral within 6 months. Inferior
oblique weakening procedures include disinsertion, recession
and myectomy.
• DVD is characterized by up-drift with
excyclorotation (extorsion) of the eye when under cover, or
spontaneously during periods of visual inattention. When
the cover is removed the affected eye will move down
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without a corresponding down-drift of the other eye. It is
usually bilateral. Surgical treatment may be indicated for
cosmesis; options include superior rectus recession with or
without posterior fixation sutures and inferior oblique
anterior transposition.
• Amblyopia subsequently develops in about 50% of cases as
unilateral fixation preference commonly develops
postoperatively.
• An accommodative element should be suspected if the eyes
are initially straight or almost straight after surgery and then
start to reconverge. Regular refraction is therefore
important.

2. ESSENTIAL Acquired Esotropia

a. Basic
b. Convergence
c. Divergence Insufficiency
A. Basic Esotropia
- Comitant Esotropia.
- Amount of deviation is almost equal for distance and near in optically
corrected eye .
- Normal AC/A ratio .

Etiology
-Innervational imbalance in muscle
 Excessive Tonic convergence.
 Muscle Imbalance .
 Improper Muscle Tone .

CLINICAL FEATURES :
- Onset = after 6 months - 5 years
- Amount of Deviation = almost equal for distance and near Normal
AC/A ratio
- NPA within normal limit
- Refractive Error: Hyperopia or Emmetropia
-

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TREATMENT:
- No glasses or miotics are helpful .
- First treat amblyopia .
- Muscle Surgery (BL MR recession but depends on surgeon) .

B. Convergence ExcessEsotropia
- Comitant Esotropia
- More deviation at near than distance
- Divergence is normal ( Deviation at distance is neutralized)
- Not associated with any refractive error or High AC/A ratio

Etiology
- Increased Innervational Tone of Converging Muscle
Clinical Features
- onset - 1 to 5 years of age .
- AC/A ratio is normal.
- NPA is normal .
- Amount of Deviation is more at near than distance .
- Refractive Error may be Hyperopic or else emmetropic.

TREATMENT
- Muscle Surgery ( BL MR Recession but depends on surgeon)

C. Divergence Insufficiency Esotropia

- Comitant esotropia in which deviation is more in distance than
near and is associated with the weakening of the diverging
muscle.
- Convergence for near is normal
- Chances of amblyopia is high
Etiology
- Innervational imbalance in muscleaction
Clinical Features
- After 6 months to any age
- AC/A ratio is normal
- NPA is normal
- Amount of deviation is more at distance than near

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 - Refractive Error is not associated

TREATMENT
- Muscle Surgery is not reliable
- Spectacles with BO prisms are helpful
- Spectacle to be worn when distance vision is needed

B. ACUTE ACQUIRED COMITANT ESOTROPIA

- Comitant esotropia which is always associated with diplopia.

- It has acute onset and so can occur at any age.
- It is not associated with paralysis of muscle

1. Acute Strabismus After Artificial Interruption Of Fusion:

- Patients may have no history of Squint.

- Esotropia occurs after interruption of FUSION. Fusion breakdown
conditions are :
o Prolonged bandaging or Patching
o Occlusion in refractive amblyopia
o Swelling of eyelid followed by trauma
- Postulate ; initially patients have ESOPHORIA which was being
controlled by well self-functioning fusion.

CLINICAL FEATURES:
- Onset is acute , can occur at any age group.
- Diplopia is alwayspresent( Patient may close one or both eye to
avoid diplopia )
- Amount of Deviation is slightly more in near than distance
Associated with precipitating factors (Refractive Error or Systemic
Illness)
TREATMENT
- Refractive Error management.
- Systemic Illness management.
- Muscle Surgery:BL MR Recession or BL LR Resection.

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 - STRATEGY:Removal of Precipitating factors may dissolve deviation
in some cases. Unless, Surgery is done.
2. ACUTE STRABISMUS WITHOUT PRECEEDING
DISRUPTION OF FUSION:

Characteristics:
- Acute onset Diplopia .
- Relatively large angle of Esotropia.
- No sign of paralysis of muscle .
- No interruption in fusion is associated.
- Precipitating Factors: Prolonged illness .
CLINICAL FEATURES
- Onset is acute for all age group .
- Refractive error has minimal effect .
- Accommodative Element is minimal .
- Amount of deviation ranges from 20 – 60pd.

ETIOLOGY
- Idiopathic

TREATMENT
- Refractive Error management.
- Determination of angle by prism adaptation test.
- Muscle Surgery: BL MR Recession or BL LR Resection.

3.ACUTE ESOTROPIA OF NEUROLOGIC ORIGIN

Characterized by:
- It is always associated with neurological problems like:
o Hydrocephalus
o Brain Tumor
o Craniocervical junction anomaly
CLINICAL FEATURES
- Etiology neurologic origin .
- Onset is acute .
- Refractive error Influence is minimal .
- No certain associations, sign or symptoms .

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TREATMENT:
STRATEGY:Being a life threatening entity
( Refer to Neurologist):
Treatment may dissolve Esotropia, If Not Go for Surgery.

C. CYCLIC ESOTROPIA

Characterized by:
o A strabismic and no- strabismic phase of 24 hours each.
o This 48 hours of cycle is most common.
o However 72 and 96 hours cycle is also reported.
o Cycle may last from 4 months to several years.
o Unless treated , esotropia becomes constant.

CLINIAL FEATURES
 Onset - early infancy : Usually during early childhood.
 Amount of deviation for both Near and Distance ranges from 40-70
 Suppression in one eye .
 History of Amblyopia after being constant deviation .
 Fusional Amplitude is defective or absent.
Fusion and stereopsis are normal(Non strabismic phase)
 No manifest deviation, esophoria may be present.

Not related to:

- Visual Acuity
- General or Ocular fatigue
- Accommodation
- Disruption of sensory fusion
- Esotropia may be UL or BL.

ETIOLOGY
- Idiopathic

TREATMENT
- Muscle Surgery

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RECURRENT ESOTROPIA (Malignant Esotropia)

- An unusual form of esotropia which reoccurs of the same angle

even after multiple operations.
- No associations with conditions like :
o Increased uncorrected hyperopia .
o A deep seated ARC .
o Nystagmus blockage syndrome .
o An unstable AC/A ratio .
o Blind Spot Syndrome .

CLINICAL FEATURES
o Recurrent occurrence AC/A Normal Refractive Error
influence is minimal .
ETIOLOGY
o Idiopathic.
TREATMENT
o Initially Muscle Surgery .
o BI Prisms mounted on spectacle.

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EXOTROPIA

EXOTROPIA:
visual axis is deviated laterally and fovea rotated nasally.

Exodeviation

latentmanifest

controlled by fusion -intermittent or constant

-unilateral or alternating

Pseudoexotropia:
Appearance of exodeviation:
-wide interpupillary distance
-large positive angle kappa- hyperopia, ROP

Types:
A. COMITANT

- Primary
- Infantile exotropia
- Intermittent exotropia
- Secondary
- Sensory exotropia
- Consecutive exotropia
B.Incomitant

- Paralytic

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 - Restrictive
- Musculofascial innervational
anomalies.
Comitant Exotropia
 Constant Exotropia:
- Infantile Exotropia
- Sensory Exotropia
- Consecutive Exotropia
- End stage of decompensated intermittent exotropia
 Intermittent Exotropia

Essential infantile exotropia:

 It is a rare condition
 It occurs in patients with

 Craniofacial anomalies
 Ocular albinism
 Cerebral palsy
Features:
 Large angle constant exo deviation is mostly more
than 35PD
 Fusion will be poor
 Amblyopia> intermittent exotropia

Sensory exotropia:
 Poor vision in one eye leads to XT.
 Sensory esotropia or exotropia may occur.
 Secondary to some sensory deficit.
 Causes -Marked anisometropia E.g.; unilateral high myopia.
 Retinoblastoma(22% present with strabismus).
 Unilateral cataract .

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CONSECUTIVE EXOTROPIA:

 Formerly esotropic patient.
 Either spontaneously or after surgical
overcorrection.
Treatment:
o Correction of refractive error if
present.
o surgery(cosmetic).

Intermittent Exotropia:
 Outward drifting of either eye.
 Interspersed with periods of goodalignment
 Exodeviation less common than esodeviation in West.
 Female> Male.
 Exodeviation found areas with more sunlight.
 Frequently seen in neonatal period –
year of life )35-40%) .
 Often positive family history.
 Common with facial asymmetry and neurological defects.

Classic presentation:
 Begins as exophoria– shortly after birth
 –Binocular fixation and NRC
 –Progresses to intermittent exotropia( XT)
o Adults have diplopia
o Children develop hemiretinal suppression
o Periods of phoria and tropia
 Frequent pseudo-oblique dysfunction associated with tight laterals
Called “leash phenomenon”.

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 Natural History
 Progression occurs in 35% - 75% of pts.
 Improvement occurs in 16% - 65%
 Factors:
- Age:
o Decreasing tonic convergence
- Suppression sets in :
o The key to unlocking fusion
o Worsening seen at distance first
 Decreased accommodation.
 Orbital divergence from maturation of facial features.
 Most common form of divergent strabismus.
 Onset before 5 years of age.
 Manifest during:
o Visual inattention
o Fatigue
o Illness
o Daydreaming
o Drowsiness upon awakening

Symptoms
 Asymptomatic
 Transient diplopia
 Asthenopic symptoms
 Reflex closure of one eye in bright sunlight

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 Deviation Sensory

1- Exophoria a t distance, Asymptomatic

Orthophoria at near.

2-Intermittent exotropia for Symptomatic for distance

distance, orthophoria/ exophoria
at near.

3-Exotropia for distance, BV for near, suppress ion

exophoria or intermittent scotoma for distance
exotropia at near.

4-Exotropia at distance as well as Lack of binocularity.

near.

CLASSIFICATION:
- Burian has classified IDS into 4 types based on measurements
of the distance and near deviation.
1. Basic type: distance deviation and near deviation are within 10 PD
of each other.
2. Divergence excess type: distance measurement 10 PD or greater
than the near deviation.

3.Convergence insufficiency type: near deviation 10 PD greater

than the distance.
4. Simulated or pseudo divergence excess type: near deviation is
less than the distance deviation but it increases to within10 PD of
distance deviation after 30 - 60 minutes of monocular occlusion.

-Kushner has further modified this classification by taking into

account AC/A ratio. He introduced two new groups:

1-Pseudo divergence with tenacious proximal fusion (near deviation

increase after 60 minutes of monocular occlusion).

2-True Divergence excess with High AC/A ratio.

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Basic exotropia:
Burian and Kushner:
- Distance = Near - Normal AC/A

Convergence insufficiency exotropia:

•Burian :
Near 10 PD more than at Distance.

• Kushner:
- Normal AC/A
- Fusional convergence insufficiency.
-AC/A LOW.
-Accommodative convergence insufficiency.

 Patching increase distance deviation to match the near deviation

pseudo CI exotropia.

Divergence Excess:
•Burian:
Distance 15 PD more than at Near.

• Kushner:
- True Divergence Excess
- Normal AC/A RATIO
-HIGH AC/A RATIO
- Simulated:
 Tenacious proximal fusion.

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Examination:
• Comprehensive ophthalmologic examination .
• Check fusion and stereopsis beforeoccluding eyes for visual acuity
examination. So ARC and suppression do not set in.
• Check stereo acuity for distance and for near.
• Versions .
• Cover test.
• Important to obtain cycloplegic retinoscopy
• “Pseudoamblyopia”
- Exodeviation often manifests with fixation preference
- Misinterpreted as evidence of amblyopia
- Excellent fusion and stereopsis when eyes are aligned
- Patching may worsen situation and induce iatrogenic loss of fusion and
stereopsis.

Measurement of deviation:

1. Prolonged alternate cover test:

To maximally suspend the tonic fusional convergence during the ACT the
occluder must be placed in front of either eye for a sufficient duration
and alternated .
2. Patch Test: Mono ocular occlusion for 30 -60 minutes, It differentiates
true and pseudo divergence excess.
3.High AC/A ratio (Lens gradient test / +3.0 D test): This test helps in
diagnosing the patients with divergence excess due to a high AC/A ratio.
In such cases the near deviation increases by 20 PD or more on addition
of a +3.0 D lens.
4. Far distance measurement: Apart from the near and distance (20 feet)
measurement, the deviation must also be measured for far distance
(100 - 200 feet).

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EXOTROPIA RESPONSE PATTERNS FOR TESTS:

• Occlusion - Distance deviation increases

- If Near = Distance with occlusion → Simulated divergence excess
- Near <distance with +3.00 lens » True divergence excess(
High AC/A ratio or Normal AC/A).

FUSIONAL CONTROL:

The level of fusional control is an baseline evaluation and indicator of

progression.
1.Home control: percentage of waking hours when the squint is noticed
by the parents .
Deviation manifesting more than 50% of waking hours indicates poor
control.
2-Clinical control: fusional control can be assessed using cover test:
A. Good control: The patient resumes fusion rapidly without blinking or
re-fixation.
B. Fair control: Patient blinks or re-fixates to control the deviation.
C. Poor control: Patient breaks spontaneously without any disruption.

ASSESSING THE CONTROL:

Category of control of exodeviation:

135
3- Stereo-acuity: (mainly for distance) Indicator of both control of the
deviation and deterioration of fusion.
The distance stereoacuity can be assessed using Random dot E test.

Treatment:
-Two types:
•Non-surgical
•Surgical

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Various Non-Surgical Therapies for Intermittent Exotropia:

Corrective lenses for any significant RE

part time Alternate Occlusion

Minus lenses Therapy

Orthoptics (Including
Convergence exercises)
Therapeutic Base –
in prisms
Botulinum
Toxin

Spectacle correction of refractive error:

•Correction of significant myopia, astigmatism and hypermetropia.

•Correction of mild myopia .
•Mild to moderate degrees of hypermetropia not
routinely corrected.

Part-time patching of dominant eye:

•Converts intermittent exotropia to phoria .

•Done 4-6 hours/day.
•Advantage – Delays surgical intervention .
•Disadvantage - Prevents fusion & accelerate
progression .

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Overcorrecting minus lens therapy:

•Stimulates accommodative convergence &control exodeviation

•Usually 2-4 D beyond refractive error Correction with cycloplegiafor DE
with high AC/A.
• Advantage: Promotes fusion & delay surgery .
• Disadvantage: Asthenopia .

Active orthoptic treatments:

•Consist of antisuppression therapy .

•Fusional convergence training .
•Should be used as supplement to surgery .

Prism therapy:

•Base-in prism used .

•Promotes bifoveal stimulation .
• Disadvantage - Causes reduction in fusional vergence amplitude .

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Indications of Surgical Treatment:
•Gradual loss of fusional control .
•Increased frequency of manifest phase .
•Increase size of the basic deviation .
•Development of suppression .
•Decrease of Stereoacuity .

Surgery:
•Bilateral lateral rectus recession .
•Unilateral lateral rectus recession with
ipsilateral medial rectus resection .
•Unilateral lateral rectus recession .

Lateral rectus recession:

139
LR recession and MR resection:

Post-operative complications:

 Over Correction:
- Persistent esotropia 3-4 weeks after surgery.

Treatment:
•Correction of refractive error
•Part-time alternate patching
•Base-out prisms
•Botulinum toxin injection
•Reoperation

 Under Correction:
•Observation .
•Orthoptic exercise.
•Prism therapy.
•Reoperation.

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Alphabetical pattern deviation:
Patterns of Strabismus:
 A Pattern.
 V Pattern.

…A PATTERN:
- Relative convergence on up gaze and relative divergence on down
gaze.
- Minimum of 10-pd diopters difference between up gaze and down
gaze.

…V PATTERN:
- Relative divergence on up gaze and relative convergence on down
gaze.
- Minimum of 15-pd diopters difference between upgaze and down
gaze.
- This allows for a slight physiological V pattern.

Variants of A and V patterns include:

X pattern: There is relative divergence on both

up- and downgaze.
Y pattern: There is relative divergence on upgaze with no significant
difference between the primary position and downgaze.
λ pattern: There is relative divergence on downgaze with no significant
difference between the primary position and upgaze.

♦ pattern: There is relative convergence on both up- and downgaze .

A PATTERN V PATTERN

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why necessary:

- It is Common.
- Countless surgical overcorrections andundercorrections have
been made due tofailure to recognize patterns.

Must-know point:

… Anatomy of EOMs
- Only when there is integrity of a sensorimotor apparatus is there a
BSV.
- Any anomaly-no normal BSV.
- Origin of EOMs.
… Anatomical peculiarities of IO
- Only EOM that does not originate from the orbital apex
- Short tendon of less than 2 mm
- The tendon-insertion lies within 2 mm of macula
- Run shortest course
- Only muscle to come in contact with other two muscles:IR and LR.

AETIOLOGY:
- A great deal has been advanced as regards the role of
o Horizontal, vertical and oblique muscle dysfunctions
o Facial characteristics
o Abnormal muscle insertions
- …But no assent concerning pathophysiology has been obtained.
- … Several schools of thought have evolved and some of them
which are into acceptance arepresentedhere.

Horizontal school:
This theory was believed to be responsible for V-pattern strabismus, but
no convincing evidence supports it.
In V-pattern esotropia, the medial rectus muscle was believed to
overact, thereby increasing esotropia in downgaze, and, in V-pattern
exotropia, the lateral rectus muscle overaction was responsible for
increased exotropia in upgaze.

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-V pattern esotropia: OA of MR on downgaze
OA of LR on upgaze
-V pattern exotropia: OA of LR on upgaze
OA of MR on downgaze
- A pattern exotropia: UA of MR on downgaze
- A pattern esotropia: UA of LR on upgaze
- It has been found that there occurs an elevation or depression upon
adduction. And this is a common feature in A and V pattern.
- Villascea shared a view that although some vertical elements could be
present, the pattern strabismus could be treated with the horizontal
surgery only.

2-Vertical school

- Brown championed opinion that A or V pattern may be caused by

primary anomalies in vertical muscles which have adductive function in
tertiary action.
- A syndrome: with eyes looking up and elevators contracting, the
increased adduction of eyes could be caused by overaction SR and by
underaction IOs and with eyes looking down and the depressors
contracting the increased abduction could be due to overaction SOs and
underaction IR.
- V syndrome: the increased abduction of eyes when looking up would
be due to overaction IOs and the underaction SR and the increased
adduction in downgaze would be due to overaction of IR and
underaction of SOs.

Oblique school
- A syndrome: OA of SOs
- V Syndrome: OA of IOs

A syndrome:
Overaction of SOs Overaction may be primary or secondary to
underaction (paresis) of IOs. SO is abductor and its abducting factor will
be most noticeable in depression There occurs relative divergence of
eyes producing A pattern.

143
V syndrome:
Overaction of IOs Overaction may be primary or secondary to
underaction (paresis) of SOs. IO is abductor and its abducting factor will
be most noticeable in elevation There occurs relative divergence of eyes
producing V pattern.

Anatomical factors:
- Facial and orbital configuration.
- Urrets-Zavalia reported association of A esotropia (with UA IOs)
and V exotropia (with OA IOs) in patients with mongoloid features.
- Mongoloid features:
o Hyperplasia of malar bones
o Upward slanting of palpebral fissures
o Straight lower lid margin
- Urrets-Zavalia reported association of V esotropia (with OA IOs)
and A exotropia (with UA IOs) in patients with antimongoloid
features .
- Antimongoloid features:
o Hypoplasia of malar bones
o Downward slanting of palpebral fissures
o S-shaped contour of lid margin

Mongoloid feature A esotropia Antimongoloid feature V esotropia

- Coats reported the association of V patternstrabismus in 10 out of

14 cases of craniofacial synostosis .
- Paysse observed strabismus in 59% of patients with Spina bifida
and 47% of strabismic patients had A pattern strabismus.

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Muscle Insertion anomalies:

- Many have reported anomalies in the insertions of horizontal recti

muscles; thus, if the muscles insertions are higher or lower than
normal, adduction or abduction is subsequently increasedin
upgaze or downgaze.
- In V pattern, the MR insertions were higher than normal and the
LR insertions were lower than normal.
- Resulting in increased abduction of LR on elevation and increased
adduction of MR on depression.
- In A pattern, the LR insertions were higher than normal and the
MR insertions were lower than normal.
- Resulting in increased adduction of MR on elevation and
increased abduction of LR on depression.

Sensory Deprivation:

- Guyton hypothesized that poor binocular function may result in

pattern strabismus.
- Deficient fusion is a/w excyclotorsion of globe With
excyclotorsion, MR becomes a partial.
- elevator whereas SR has a reduced elevatingcomponent.

Effect of the pulley systems:

- Upward displacement of the pulley systems around the lateral

rectus muscle may cause V-pattern strabismus.

Prevalence:
- … Co-existence of A or V pattern with horizontal strabismus is
seen in 12.5% to 50% of cases.
- …According to 1964 American Academy of Ophthalmology: V
eSo> A eSo> V eXo> A eXo.
- … However, a somewhat different distribution was reported by
von Noorden and Oslon: V eXo> A eXo> V eSo> A eSo.

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 Clinical Features:
Symptoms:
- Age at presentation:
o 58% of patients had age of onset at 12 months or younger.
- If the pattern is small in magnitude it may not be recognized until
the early school when head posture becomes apparent or reading
difficulties are noted.
- Asthenopia and Diplopia.
- A exotropia and V esotropia.
- Anomalous Head Posture:
o 11% of patients with alphabet patterns.
o A esotropia and V exotropia have fusion in
the downward gaze. So usually have chin
elevation.
o V esotropia and A exotropia have fusion in
the upward gaze. So usually have chin
depression.
- Amblyopia.
o Ciancia found abnormal retinal
correspondence in 89% of cases of A or V
pattern.

Patients at high risk:

- Craniofacial anomalies likecraniosynostosis, spina
bifida.
- Antimongoloid lid fissures (A exotropia and V esotropia).
- Mongoloid lid fissures (A esotropia and V exotropia).
- Infantile esotropia (V esotropia).

Crouzon syndrome

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PSEUDOPATTERNS:
- Patients with accommodative esotropia may have Pseudo- V
pattern
- This is particularly apparent if the patient is examined without
hypermetropic correction as with
o Uncorrected hyperopia there is a tendency to
accommodate in the primary gaze and downgaze, thus
simulating a V pattern.

Clinical investigation:
Aims
- To detect and measure A/V patterns .
- To assess ocular movements to determine the reason if possible.
- To assess significance of A/V patterns for prognosis and
management.
 Observation AHP
 Ocular movement
o COVER TEST :primary positionAnd up gaze and down gaze
 Measure of deviation

Ocular movement:

- Grading of Inferior oblique muscle overaction

 Inferior oblique overaction is graded by observing the angle the
adducting eye makes with the horizontal line as it elevates and
abducts on lateral version to the opposite side.
o Grade 1- upto 15º angle with the horizontal line .
o Grade 2- upto 30º angle with the horizontal line .
o Grade 3- upto 60º angle with the horizontal line .
o Grade 4- upto 90º angle with the horizontal line .
Grading of Inferior oblique muscle over action
 For practical purposes, oblique over action is graded as
o Mild- if hyperdeviation is present in elevation.
o Moderate- if hyperdeviation is present adduction .
o Severe-if hyperdeviation is present in primary position.

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 Prism cover test:
 Measure patient's alignment in 25:up gaze and 25: down gaze
with the patient fixating an accommodative target at distance,
with fusion prevented.
 Measure patient's alignment in 25º upgaze and 35ºdowngaze with
the patient fixating an accommodative target at 33 cm.

 Full refractive correction should be worn and accommodation

should be well controlled toprevent the appearance of pseudo V
pattern.
 The position of elevation and depression may be achieved
o By moving the fusion target upwards or downwards,
o or By moving the patient's head downwards or upwards.
Criteria for diagnosis
 V pattern: minimum difference of 15 PD from up gaze to down
gaze.
 A pattern: minimum difference of 10 PD from upgaze to
downgaze.

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INCOMITANT STRABISMUS;
Definition: a strabismus where the angle or degree of the deviation
varies in different directions of gaze OR with each eye fixing (i.e. the
secondary deviation is greater than the primary).

Classification
 According to the underlying cause:
i. Neurogenic
ii. Mechanical
iii. myogenic
 Also may be congenital or acquired.

Congenital:
 Usually isolated defects in otherwise healthy individual.
 Sometimes familial.
 Specific cause unknown, presumed due to a developmental
anomaly in the anatomy or functioning of the extra-ocular muscles
or their innervating nerves.
 Some are associated with serious developmental neurological
defects e.g. hydrocephalus & cerebral palsy .
 Gradually become more comitant as patient gets older Not likely to
respond to orthoptic treatment .

Acquired:
 Caused by injury or disease of the ocular motor system e.g.
trauma, inflammation.
 Vascular.
 Space-occupying lesions.
 Metabolic disorders.
 NB It is vital that we distinguish between longstanding/ static
acquired disorders and recent onset/active ones.

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Paralytic strabismus:

 Movement of the eye, following contracture of a muscle can be

considered in terms of the action of an individual, isolated muscle.

 this does not aid in the diagnosis of the affected muscle in

paretic situation.
 the field of action of the muscle should be considered.
 This is the direction in which the muscle’s primary position action
has maximal effect.

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Terms:

 Agonist = prime mover or protagonist.

 Antagonist= muscle having the opposed action.
 Synergist = muscle having the same actions .
 Ipsilateral = on the same side.
 Contralateral = on the opposite side.
 Contracture = increased resistance against passive stretching of
the muscle, loss of elasticity.

Hering’s Law of Equal Innervation:

 equal and simultaneous innervation flows to the synergistic
muscles concerned with the desired direction of gaze(applies to
voluntary and involuntary eye movements).
 I.e. innervation of one eye is equal that of the other eye, resulting
in movements of the two eyes that are equal symmetrical and
parallel (normally).
 This law has great practical significance when used in the diagnosis
of paralytic strabismus.

Sheringtons Law of Reciprocal Innervation:

 concerned with the co-ordination of muscle pairs of one eye.

 Muscle contraction does not increase simultaneously in opposed
muscles.
 I.e. the contraction of each ocular muscle is accompanied by a
simultaneous andproportional relaxation of its antagonist.

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Sequelae of Ocular Muscle Palsy:

 Underaction of the primary affected muscle .

 Overaction of the contralateral synergist.
 Overaction of the ipsilateral (direct) antagonist.
 Underaction of the antagonist of thecontralateral synergist
(contralateral antagonist).
 Overaction of the ipsilateral synergist?

Overaction of the contralateral synergist:

 always present.
 This overaction occurs when the affected eye is fixing as a result of
increasedinnervation being required to rotate the affected muscle
into its field of action.
 Due to Hering's Law an overstimulation of the contralateral
synergist follows.
 This is always the largest overaction in the Sequelae.

Overaction of the ipsilateral (direct) antagonist:

 Can lead to a permanent contracture of the muscle and a loss of
elasticity.
 If the patient fixes with the non-involved eye within a few days a
contracture will develop in the direct antagonist muscle.
 Because the normal contracture of the direct antagonist is
unopposed by the weakmuscle.

Underaction of the antagonist of the contralateral

synergist (contralateral antagonist):
 with the involved eye fixing, the movement of the eye into the
field of action of theweak muscles antagonist requires less
innervation than normal due to the contracture.
 Therefore less innervation is supplied to the contralateral
antagonist which under-acts.
 For example in paralysis of the right superior rectus?
 underaction of right superior rectus .
 overaction of the left inferior oblique .
 overaction of the right inferior rectus .
 underaction of the left superior oblique .

152
For right eye read from the top:
Muscle Direct Contralateral Contralateral
Antagonist synergist antagonist
RMR RLR LLR LMR
RLR RMR LMR LLR
RSR RIR LIO LSO
RIR RSR LSO LIO
RIO RSO LSR LIR
RSO RIO LIR LSR

PARALYTIC SQUINT:

THIRD NERVE PALSY:

Diagnosis:
Signs of a left third nerve palsy :
- Weakness of the levator causing profound ptosis , due to which there is
often no diplopia .
-Unopposed action of the lateral rectus causing the eye to be abducted
in the primary position .
-The intact superior oblique muscle causes intorsion of the eye at rest ,
which increases on attempted down gaze .
-Normal abduction because the lateral rectus is intact .
-Weakness of the medial rectus limiting adduction .
-Weakness of the superior rectus limiting elevation .
-Weakness of inferior rectus limiting depression .
-Parasympathetic palsy causing a dilated pupil associated with defective
accommodation .
-Partial involvement will produce milder degrees of ophthalmoplegia .

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Treatment
1- non-surgical treatment:options include the use of Fresnel prisms if
the angle of deviation is small , uniocular occlusion to avoid diplopia ( if
ptosis is partial or recovering ) and botulinum toxin injection into the
uninvolved lateral rectus muscle to prevent its contracture before the
deviation improves or stabilizes.
2- surgical treatment: as with other ocular motor nerve palsies , should
be contemplated only after all spontaneous improvement has ceased .
This is usually not earlier than 6 months from the date of onset .

4TH NERVE PALSY TROCHLEAR NERVE PALSY SUPERIOR

OBLIQUE palsy:

INTRODUCTION:

 Thinnest and longest 75mm.

 Only CN that comes out from the dorsal aspect of the brainstem.
 Only CN that crosses completely to the opposite side. Thus
originates from the contralateral nucleus.
 Somatic motor component , innervates the superior oblique of the
contralateral orbit.

ANATOMY:
 From each nucleus, the nerve fibers run laterally and emerge. from
the dorsal aspect of the midbrain .
 Pass medially and decussate (X).
 Thus it crosses completely before passing
forward.
 Once the 4th CN exits from the brain from the
dorsal side it turns ventral and passes the
Posterior Cerebral Artery and Superior Cerebellar
artery.

154
  Then it pierces the arachnoid and enters the subdural
space on the posterior corner of the roof of the
cavernous sinus.

 In the cavernous sinus it runs on the lateral wall

below the Oculomotor nerve and above the 1st div of
5th CN.
 Before crossing the cavernous sinus it crosses the 3rd
nerve through the lateral part to enter the superior
orbital fissure.
 In the intraorbital part, the 4th CN doesn’t transverse
through the annulus of zinn, it projects anteriorly,
superiorly and medially to it.
 Travels temporal and inferior to innervate the
superior oblique muscle.

CAUSES OF AN ISOLATED 4TH NERVE PALSY:

I)CONGENITAL :
Congenital lesions are a common cause , although symptoms do not
develop until decompensation occurs in adult life. Children develop a
compensatory head tilt in order to compensate for underacting superior
oblique muscle, on the contralateral side.

II) ACQUIRED :
1.TRAUMA : trauma is an important cause of 4th nerve palsy accounting
for 30% of acquired 4th nerve palsies, 4 th nerve is the most commonly
involved nerve in a traumatic palsy. Trauma usually causes bilateral 4th
nerve palsies due to an impact in the area of the Anterior medullary
vellum, where the two nerves decusate.

2.IDIOPATHIC :In about 20% of cases the cause is unknown.

3.VASCULAR AND NEUROLOGICAL : These account for about 5 % of
trochlear nerve palsies , in older individuals microvasculopathy
secondary to diabetes atherosclerosis or hypertension may cause an
isolated 4th nerve palsy. Aneurysms and tumors are rare causes.

- Thyroid related orbitopathy and Myasthenia gravis may mimic as an

isolated4th nerve palsy due to fibrotic inferior oblique , superior rectus.

155
-Nuclear:
Most often due to stroke, less often neoplasm, and almost never
isolated; other causes include demyelinative disease and trauma.
-Fascicular:
Rare, same associations as nuclear; may get contralateral Horner’s
syndrome; trauma (especially near anterior medullary velum) may cause
bilateral CN IV palsies.
-Subarachnoid Space:
Usually due to closed head trauma; rarely tumor, infection or aneurysm.
-Intracavernous Space:
Due to cavernous sinus disease from inflammation
(sarcoidosis), infection (fungal), or neoplasm
(lymphoproliferative, meningioma, pituitary m
acroadenoma); usually associated with CN III, V, and
VI findings and sympathetic abnormalities.
-Orbital :
Trauma, inflammatory or tumor.

FEATURES OF 4TH NERVE PALSY:

The featu res of nuclear , fasicular and peripheral 4th nerve palsies are
clinically identical except that nuclear lesions produce CONTRALATERAL
superior oblique weakness.

SY MPTOMS :
DIPLOPIA : Acute onset of a vertical diplopia, which is more on
downward gaze ,it is noted by patients while coming down stairs and
while doing near work.

SIGNS :
1)HYPERTROPIA: the involved eye is higher as a result of weakness of
the superior oblique muscle, which becomes more prominent when the
head is tilted towards the ipsilateral shoulder.
2)RESTRICTED OCULAR MOVEMENTS: there is limitation of depression
on adduction.
3)ABNORMAL HEAD POSTURE: to avoid diplopia ,head takes
a posture towards the action of the superior oblique muscle,
face is slightly turned to the opposite side, chin is depressed,
and head is tilted towards the opposite side.

156
  bilateral involvement should always be suspected until proved
otherwise :
-Right hypertropia in left gaze , left hypertropia in right gaze .
-Greater than 10° of cyclodeviation on double Maddox rod test .
-V pattern esotropia .
-Bilaterally positive Bielschowsky test .

SPECIAL TESTS USED IN DIAGNOSIS OF 4TH NERVE PALSY :

1) PARKS -BIELSCHOWSKY THREE STEP TEST.

2) DOUBLE MADDOX ROD TEST.

 PARK-BIELSCHOWSKYTHREE STEP TEST:

STEP 1 : (to assess which eye is hypertropic in the primary gaze.) In case
of left hypertropia, the following four muscles could be involved:
1) Depressors of the left eye i.e. superior oblique and inferior rectus.
2) Elevators of the right eye i.e. the superior rectus or inferior oblique.
- In a 4th nerve palsy the involved eye is always higher.

STEP 2 :(which lateral direction has worse hypertropia )

If the left hypertropia increases on right gaze implicates a left superior
oblique or right superior rectus involvement. Increase in the left gaze
implicates that either the right inferior oblique or left inferior rectus are
involved. In 4th nerve palsy the deviation isWORSE ON OPPOSITE GAZE
(WOOG).

STEP 3:( in which head tilt direction is the hypertropia worse )

The head tilt test is performed with the patient fixating at a straight
ahead target at 3 mts. Increase in left hypertropia on left head tilt
implies the left superior oblique is involved , and increase in right
hypertropia on left head tilt indicates the right inferior rectus is involved.
In 4th nerve palsy the deviation is BETTER ON OPPOSITE TILT(BOOT).

- In Right SO palsy , on right head tilt RSR will work thus the eye will
move upwards.

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4TH CONFORMATORY STEP 4:(is the hypertropia worse in upgaze or
downgaze)
If the left hypertropia increases on down gaze it confirms that the left
superior oblique is involved. Helps to rule out mimickers like myasthenia
and thyroid disease.

 DOUBLE MADDOX ROD TEST:

A unilateral 4th nerve palsy is characterized by less than 10 degree of

cyclodeviation, while a bilateral palsywill have more than 10 degree of
cyclodeviation.
-Red and green Maddox rods , with the cylinders vertical , are placed one
in front of either eye .
- Each eye will therefore perceive a more or less horizontal line of light .
-In the presence of cyclodeviation , the line perceived by the paretic eye
will be tilted and therefore distinct from that of the other eye .
-One Maddox rod is then rotated till fusion ( superimposition ) of the line
is achieved .
-The amount of rotation can be measured in degrees and indicates the
extent of cyclodeviation .
-Unilateral fourth nerve palsy is characterized by less than 10° of
cyclodeviation whilst bilateral fourths may have greater than 20° of
cyclodeviation. This can also be measured with a synoptophore .
-The amount of rotation can be measured in degrees and indicates the
extent of cyclodeviation .
-Unilateral fourth nerve palsy is characterized by less than 10° of
cyclodeviation whilst bilateral fourths may have greater than 20° of
cyclodeviation. This can also be measured with a synoptophore .

MANAGEMENT:

Occlusion:Double vision is restricted to the downward gaze, occlude the

lower third of the spectacle lens before the affected eyewith semi
opaque tape.

158
Surgical treatment:
It is important to have a period of stable measurements of at least six
months before embarking on surgery. The surgical option depends on
the angle of deviation in primary position, area of maximum deviation
and presence of torsion.

Knapp classification:
This is a useful way of classifying IV nerve palsy as it helps planning
surgical treatment options.
- Class I: greatest hypertropia in ipsilateral inferior oblique
(contralateral up) field
- Class II: greatest hypertropia in ipsilateral superior oblique
(contralateral down) field .
- Class III: greatest hypertropia in entire contralateral field .
- Class IV: greatest hypertropia in entire contralateral field and
across the lower field .
- Class V: greatest hypertropia across lower field .
- Class VI: bilateral IV palsy .
- Class VII: traumatic paresis combined with Brown’s syndrome.

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SIXTH NERVE PALSY :

Introduction:

 The sixth cranial nerve is a somatic efferent nerve that innervates

ipsilateral lateral rectus (LR) muscle to elicit eye abduction.
 Effector organ : LR muscle
 Action: Eye abduction
 Also called as abducens nerve or abducent nerve or CNVI.
 Function:
 Solely to innervate the lateral rectus muscle and abduct the
eye.

Anatomy:

- The sixth nerve nucleus is located in the pons.

- The sixth nerve contains only somatic efferent fibers.
- Runs a long course from the brainstem to the lateral
rectus muscle, through the superior orbital fissure and
into the orbit through the annular ligament (annulus of
Zin) then to the lateral rectus.
- Functioning to abduct the eyes.
- 6th nerve: The longest subarachnoid course of all the
cranial nerve .
- The long course of the 6th nerve between the
brainstem and the eye makes it vulnerable to injury at
many levels.
- Close association between 6th nerve and 7th nerve
(facial) in the midbrain
•Facial muscle also been involved in some 6th nerve
palsies.

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What is the sixth nerve palsy?
- Limited ability of the affected eye to turn out (abduct) due to 6th
nerve lesion.
Why?
- Due to lesion anywhere along its course between the pons to the
lateral rectus muscle, which causes impaired eye
abduction(incomplete (paresis)or complete(palsy))→incomitant
esotropia and ipsilateral abduction deficiency.

 Classified under neurogenic-cause of incomitant strabismus It can
be congenital (rare) or acquired (common) .
 Can be unilateral or bilateral 6th nerve palsy.

Bilateral 6th nerve palsy:

Types Sixth nerve palsy:

-Total palsy ( paralysis):Presence of abduction
past the midline.

-Partial palsy (paresis):Presence of abduction past

the midline.

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INCIDANCE:
The sixth cranial nerve is the most commonly affected of the
ocular motor nerves based on some studies.
- But ranking second following fourth nerve palsy according to
other reports.

- Most patients who develop acute CN VI palsy are older than 50

years of age. This group often has a concurrent history of
hypertension and/or diabetes.
- Children are also prone to develop CN VI palsy. The causes may
range from benign (e.g., viral illness or trauma) to malignant
etiologies.
- Young adults aged 20to 50 years also can have CN VI palsy due to
neurologically complicated CN VI palsies involving additional
cranial nerves (such as III and IV) or other neurological signs (such
as ataxia or intention tremors.

Etiology:

 Lesions can affect any part of the nerve’s pathway.

 Usually due to direct damage of the sixth cranial nerve,
encephalon nuclei or less frequently diffuse axonal damage.
 It can be congenital (rare) or acquired (common).
 Identifying the causative factor is important for further
management.
 The four most common causes were idiopathic( 26 %)
,hypertension alone (19 %)coexistent diabetes and hypertension
(12 %(and trauma 12% ).

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163
 1- ADULT:
AQUIRED:

More common Less common

Idiopathic Multiple sclerosis

Vasculopathic (diabetes, Increased intracranial pressure

hypertension, atherosclerosis)

Trauma Sarcoidosis/vasculitis

Stroke (usually not isolated)

Lumbar puncture

Myasthenia Gravis

Giant cell arteritis

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2- Etiology in children:
Acquired:
•Traumatic
•Tumor
•Idiopathic
•Infection

Congenital:
- Very rare
- If occurs as an isolated finding in the first week, usually resolves
spontaneously. May represent one of following: Duane syndrome,
infantile esotropia, nystagmus blockage syndrome.

Differential diagnosis:

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 CLINICAL SIGNS AND SYMPTOMS:
A- MOST COMMON
1- Esotropia:
a. N›D.
b. Increase with the gaze at affected
side.
2- LIMITATIONT TO ABDUCTION:
a. In the affected eye.
b. Normal adduction.
3- HORIZONTAL BINOCULAR DIPLOPIA:
a. Worse at affected side and distance.
4- HEAD-TURN:
a. Toward the affected side.
b. To avoid diplopia.

B- LESS COMMON:
1- Loss of vision.
2- Pain
3- Hearing loss.
4- Headache.
5- Symptoms of vasculitis, particularly giant cell arteritis.

Clinical assessment and investigation:

166
Control diplopia
Patient adopt face turn towards the affected eye (Right Maintaining BSV
side)

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168
169
170
171
 OCCLUSION:

- Young children(‹8 years):

o To treat amblyopia;alternating daily between the two eyes
both to preserve vision
o To stimulate movement in the paretic eye to reduce the
potential for medial rectus contracture.
- Adult/older children:
o To eliminate diplopia if patient cannot adopt a face turn to
achieve single binocular vision.
Procedure:
o Binasal occlusion.
o Full monocular occlusion.

Binasal occlusion

 Type of sector occlusion

 Not as a permanent treatment
 Indication: Esotropia, amblyopia, diplopia, CE, DI
 Why recommended:
 Reduce double vision and direct patients to use their
peripheral system, helping them to locate objects and judge
distances more accurately .
 Material : Translucent material (opaque) , clear nail polish, black
tape .
 Sector size measurement:
 Patient wear the glasses, focus at distant target.

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  Binasal occluder (determine the degree of nasal).

Monocular occlusion
 Method of full patch covering affected eye.
 Purpose: Remove diplopia in lateral gaze .
 Material: Occluder with different grades (Bangerter foils).

Fresnel prism:

Botulinum toxin:

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Extraocular muscles surgery:
 Indicated if longstanding esotropia.
 Considered when the deviation has been stable for 6month.
 May include a combined medial rectus recession and lateral rectus
resection on the affected side.

Approximately half of all 6th nerve palsies recover:

 spontaneously approx. 3 months after onset.

 Patient with Vasculopathic 6th nerve palsy have a better chance of
recovery( 69 %to 86 %(recover more rapidly (4 to 6weeks( than
patient with 6th nerve palsy from other causes.
 A report of over 2000 patients with 6th nerve palsy of unknown
etiology found that 36 %recovered in (eight weeks to 2months)
and 84 %recovered in 4 months.

DUANES RETRACTION SYNDROME:

 Described by Stilling in 1887 and Turk in 1896 Hence in European
literature - referred to as the Stilling-Turk-Duane syndrome after
it’s early describers.
 In 1905, Duane emphasized that the retraction of the globe is an
essential clinical feature of this syndrome, thus the term “Duane’s
Retraction Syndrome” is deeply entrenched.
 Duane retraction syndrome is most likely a spectrum of
mechanical, anatomical, and innervational disorders of the
extraocular muscles.
 Mechanical Theory:
Mechanical disturbances can occur due to the presence of facial
bands, which are found in some cases of DRS. These bands act as a
leash to cause limitation of the eye movement.

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PATHOGENESIS:

Myogenic Theory:
This theory, suggested by earlier studies, indicates there is fibrosis or
inelasticity of the lateral rectus muscles and that the medial rectus
muscle inserts abnormally far posteriorly.

Neurogenic Theory:
A disturbance in embryologic development between weeks 4-8
results in an absent abducens nerve with anomalous innervations of
the lateral rectus muscle by a branch of the oculomotor nerve.
- Simultaneous activation of the medial and lateral rectus muscles, as
demonstrated by EMG studies, may be the cause of global
retraction.

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CLASSIFICATION (HUBERS):
Type I the most common, is characterized by:
• Limited or absent ABDUCTION.
• Normal or mildly limited adduction.
• In the primary position, straight or slight esotropia.

Type II, the least common, is characterized by:

• Limited ADDUCTION.
• Normal or mildly limited abduction.
• In primary position, straight or slight exotropia.

Type III is characterized by:

• Limited ADDUCTION AND ABDUCTION.
• In the primary position, straight or slight esotropia.

Type IVis a paradoxical .

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Duane’s Syndrome Type I:
OS limited abduction, retraction in adduction:

Duane’s Syndrome Type II:

OS limited adduction retraction in adduction:

Duane’s Syndrome Type III:

OS limited adduction and abduction retraction in adduction:

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EPIDEMIOLOGY:

- Prevalence of about 1/1000 in general population.

- Females (60%) > Males (40%) .
- Accounts for up to 4% of all strabismus cases.
- Most common type of congenital aberrant ocular innervation.
- 80% of cases occur unilaterally, with a LE predominance.

SYNDROMIC FORMS:

Goldenhar syndrome: malformation of the jaw, cheek and ear,

usually on one side of the face.
Moebius syndrome : congenital paresis of facial and abducens
cranial nerves.
Morning Glory syndrome: abnormalities of the optic disc.

- 70% of cases are isolated 30% of cases are associated with other
congenital anomalies.

ISOLATED CASES
- 90%occur sporadically and are commonly unilateral.
- Remaining 10% are inherited and these are commonly bilateral.

CLINICAL FEATURES
- Characterized by some or all of the following :
1) Complete, or less often partial, absence of outward movement
(abduction) of the affected eye.

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2) Partial, or rarely complete, deficiency of inward movement
(adduction) of the affected eye.

3) Retraction of the affected eye into the

orbit when it is adducted.

4) Partial closure of the eyelids (pseudoptosis) of the affected eye

when it is adducted.
5) A sharply oblique movement of the affected eye, either down and
in (downshoot) or up and in
(upshoot ), when it is adducted.

6) Deficiency of convergence, with the

affected eye remaining fixed in the
primary position while the other eye is converging.
7) Alphabetical patterns: A large incidence of increased innervation
of the lateral rectus in elevation or depression explains the
frequent observation of A, V, or X patterns in these patients.

8) Abnormal head posture is adopted to search for the direction of

gaze where there is no misalignment of the two eyes in order to
obtain binocularity. Longstanding torticollis (since birth) leads
commonly to craniofacial asymmetry.

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  Strabismus: 76% of individuals have frank strabismus in primary
gaze .
 Poor Binocular Vision .
 Reviews of DRS patients have shown hypermetropia of greater
than +1.50 in 71% of the patients.
 Amblyopia occurs in about 10% of individuals and will respond to
standard therapy if detected early .
 Anisometropia .

Differential diagnosis:
 Congenital sixth nerve palsy
 Infantile esotropia
 Mobius syndrome

MANAGEMENT:

A) NON SURGICAL
 Spectacles or contact lenses for refractive error.
 Prism glasses to improve the compensatory head position.
 Treat amblyopia with standard therapy.
 Botulinum Toxin: botulinum toxin decreases the amount of
deviation and leash phenomenon (upshoot or downshoot of globe
with adduction).

B) SURGICAL
The aims of surgery are:
 To correct a manifest strabismus.
 To centralize the field of binocular single vision.
 To overcome or reduce the need for a large compensatory head
posture.
 Avoid lateral rectus resection.

Surgery is indicated for the following reasons:

 Decompensation, giving rise to manifest strabismus.
 Abnormal head posture.
 Severe globe retraction with or without up- shoot and down-shoot.

 For types 1 and 3 with head turn: recession of medial rectus

muscle or horizontal transposition of vertical rectus muscles.

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  For types 1 and 3 with Leash Phenomenon and/or severe globe
retraction: recession of both medial and lateral rectus muscles
with possible Y- splitting of the lateral rectus muscle.

 For type 2 with head turn and fixation with uninvolved eye:
recession of ipsilateral lateral rectus muscle.
 For type 2 with head turn and fixation with involved eye:
recession of contralateral lateral rectus muscle.
 For type 2 with Leash Phenomenon: recession of lateral rectus
muscle with possible Y-splitting.

Complications of Surgery:

 Undercorrection of primary position esotropia and the

compensatory head turn .
 Overcorrection leading to secondary exotropia .
 New vertical deviations can occur after vertical rectus
transposition procedures.

BROWN SYNDROME:

 In 1950, Harold W. Brown first published on an unusual

motility disorder, characterized by limited ocular
elevation in adduction.
 Brown attributed the limited elevation to a short or tight
anterior superior oblique tendon sheath. He termed this as
superior oblique tendon sheath syndrome.
 He further hypothesized that the short tendon sheath was
due to a complete congenital paresis of the ipsilateral
inferior oblique muscle and secondary to sheath
contracture.
 In the mid 1970s, Parks and colleagues reported that a tight
tendon sheath was not the cause of Brown
syndrome;instead, it was a tight or short superior
oblique tendon.
 Subsequent studies confirmed the cause of the
syndrome tobe a tight or inelastic superior
oblique tendon.

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ETIOPATHOGENESIS:
Brown syndrome can be divided into congenital and acquired.

1- CONGENITAL BROWN SYNDROME:

A- Superior oblique Brown syndrome:

A tight or inelastic superior oblique tendon muscle complex would
restrict ocular elevation in adduction. Many theories for
the cause of the tight or inelastic tendon exist.

- Helveston theory of abnormal telescopingmechanism:

 Earlier, it was believed that the superior oblique tendon moves
through the trochlea much like a rope through a pulley.
 Through a detailed anatomical study, Helveston showed that the
superior oblique tendon appears to move in part by a telescoping
or slide-by fashion with only the central fibers of
the tendon making the total excursion.
 Congenital Brown syndrome could be caused by adevelopmental
abnormality of the elastic-crossed fibers thatnormally allow the
telescoping movement of the central tendonfibers.

- Wright hypothesis of congenital inelastic superior obliquemuscle-

tendon complex:

 In 1999, Wright described a computer simulation of

Brownsyndrome, using two specific models, as follows:
o a short superior oblique tendon, and
o a stiff superior oblique tendon (stretched sensitivity).
 The computer model showed that a tight or inelastic muscle
tendon complex was the best fit for the Brown syndromepattern
of deviation.

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B- Non superior oblique Brown syndrome:

Non superior oblique Brown syndrome or pseudo-Brownsyndrome is a

restriction of ocular elevation in adductioncaused by pathology other
than an abnormality of thesuperior oblique muscle or tendon.
 Congenital bands: Inferior orbital fibrous adhesions orfibrous
bands to the posterior globe are rare causes of restriction of
elevation in adduction.
 Congenital inferior location of lateral rectus muscle
pulley: Rare case of congenital Brown syndrome arecaused by
congenital inferior location of the lateral rectus muscle. In these
cases, the limitation of elevation in adduction is caused by the stiff
lateral rectus muscle that iscongenitally located inferior to the
normal position.

C-ACQUIRED BROWN SYNDROME:

 Acquired superior oblique Brown syndrome:

- Abnormal telescoping mechanism: Due to one of thefollowing:

vascular dilatation of the tendon sheath vessels and local edema
occurring within the confined area of the trochlea.
- Tight or inelastic superior oblique tendon A tight superioroblique
tendon can be caused by a mass that displaces thetendon, a
scleral buckling, or a superior oblique tendon tuck.
- A rareacquired fibrosis of the superior oblique muscle ispossibly
associated with thyroid disease or an intramuscular injection of
local anaesthetic.
- Stenosing tenosynovitis (trigger-thumb analogy theory)Chronic
movement of the superior oblique tendon throughthe trochlea
can result in a traumatic tenosynovitis with tendon-swelling and
stenosis of the surrounding tendonsheath. Trigger-thumb is a
congenital or acquired constriction or stenosis of the fibrous
sheath, which surrounds the tendon and causes secondary
enlargement ofthe tendon proximal to the constriction. The
combinationof a sheath-stenosis and tendon swelling
preventsmovements of the tendon.

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  Superior oblique click syndrome :
Inflammation produces a nodule on the superior obliquetendon, just
posterior to the trochlea. The nodule wouldhave difficulty entering the
trochlea, thus restricting tendonmovement.

 Peritrochlear scarring:

l Extensive scarring around the trochlea can result inrestriction of

the tendon movement in both ways, resultingin both a Brown
syndrome and a superior oblique palsy(canine tooth syndrome).
This can be caused by trauma,periocular surgery, and upper lid
blepharoplasty withremoval of periorbital fat with cautery.

 Acquired non superior oblique Brown syndrome:

 Inferior orbital fibrous adhesions to the posterior globe are

caused by the following: orbital floor fracture and fat adherence
syndrome associated with inferior orbitaltrauma.
 Superior nasal orbital mass: These patients usually demonstrate a
large vertical deviation in primary position often associated with
exotropia. Possible causes are a glaucoma drainage implant or a
neoplasm in the superiororbital quadrant.

EPIDEMIOLOGY:
 The incidence of this condition is 1 in 450 cases ofstrabismus.
 Approximately one in 20,000 live births.The actual incidence may
be higher as many cases are asymptomatic.
 There is equal predilection for both sexes in congenital
Brown syndrome.
 Wright noted that 5% cases are bilateral and idiopathicBrown
syndrome has a higher preponderance in females(63%) and
traumatic acquired Brown in males (82%).

CLINICAL FEATURES:

A left Brown syndrome has the following

characteristics:
MAJOR SIGNS:
• Usually straight with BSV in the primaryposition
• Limited left elevation in adduction

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• Limited left elevation on upgaze is common
• Normal left elevation in abduction
• Absence of left superior oblique overaction
• Positive forced duction test on elevating the globe in adduction.

VARIABLE SIGNS:
• Down-shoot in adduction.
• Hypotropia in primary position.
• AHP with chin elevation and ipsilateral head tilt

Brown syndrome has also been classified as:

a) mild - no hypotropia in primary or adducted position
b) moderate - hypotropia in adducted position
c) severe - hypotropia in primary position

A third classification was proposed by Jampolsky

a) True Brown syndrome - no hypotropia in primaryposition or down
gaze.
b) Brown syndrome plus - vertical deviation in primaryposition or
adduction ± head posture.

Differential diagnosis:
1)Isolated inferior oblique palsy: This is characterized by overaction
of the superior oblique muscle and positive Parks’ three step test.
Forced duction test is free in inferior oblique palsy.
2. Double elevator palsy: Limitation of elevation is present in both
adduction and abduction. In addition the patients have ptosis or
pseudoptosis.
3. Congenital fibrosis syndrome: The differences include
restricted elevation in abduction and esotropia onattempted upgaze.
4.Blow out fracture of the inferior orbital wall: The elevation
deficiency is more marked in abduction.
Imaging reveals a fracture and there may be associatedenophthalmos.
5. Thyroid ophthalmopathy: The elevation deficiency isworse in
abduction than adduction.
6. Adherence syndrome: During inferior oblique surgeryadhesions may
form due to fat prolapse and limit elevationin abduction.

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MANAGEMENT:
 The vision needs to be checked to rule out amblyopia.
 Abnormal head posture if present is indicative of thepresence of
fusion.
 Forced duction testing needs to be performed to confirm
the diagnosis.
 Spontaneous improvement is known to occur. Hence itmay be
prudent to observe cases where there is no threat to
binocularity.
 Elevation in adduction exercises can improve the conditionin
congenital cases or in cases where there is intermittentBrown
syndrome.
 Injection of corticosteroids has been reported to improvethe
Brown syndrome in patients with inflammatorydisease.
 Systemic treatment of the underlying disease may improvecases
of acquired Brown syndrome.

SURGICAL MANAGEMENT:

Indications:
 When there is a loss of binocularity, with the chance
ofdevelopment of amblyopia and the child does not developan
abnormal head posture, surgery is indicated.
 Mild Brown syndrome needs to be observed. If there ispresence of
primary position hypotropia andunacceptable downshoot on
adduction, surgery can beconsidered.
 Acquired cases due to the presence of a scleral explant or
aglaucoma filtering valve need to be operated.

TECHNIQUES:

Historical:Sheathectomy, Superior oblique and trochlearluxation.

Others:
- Superior oblique tenoctomy or tenotomy
- Z-tenotomy of the superior oblique
- Simultaneous inferior oblique recession
- Superior oblique tendon expander
- Chicken suture

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MONOCULAR ELEVATION DEFICIT(MED):
Monocular elevator palsy , sometimes also referred to as double
elevator palsy , is a rare sporadic condition . It is thought to be caused by
either a tight or contracted inferior rectus muscle or a hypoplastic or
ineffective superior rectus muscle .

Etiology:
MED can be congenital or acquired in onset:
Congenitalcases of MED occur sporadically but cases occurring in twins
have been reported .The causes include supranuclear defects, primary
SR paresis and primary IR restriction (congenital fibrosis of inferior
rectus).
Acquired MED is usually caused by cerebrovascular diseases like
hypertension, thromboembolism, arteritis. Other causes include
sarcoidosis, syphilis, and midbrain tumors like pineocytomas, acoustic
neuromas and metastatic tumors.

Clinical Features
 Deviation: There is hypotropia of the affected eye when the
normal eye is fixing and hypertropia of the normal eye when the
affected eye is fixing.
 Elevation deficit: Monocular limitation of up gaze above midline
(horizontal plane) is present in all the three horizontal positions,
i.e., abduction, primary position and adduction.

187
 Ptosis/Pseudoptosis: A hypotropic eye is associated with ptosis
because of the facial attachments between the levatorpalpebrae
superioris and the superior rectus muscle.

 Marcus Gunn phenomenon (MGP):may be present with variable

amount of severity.(Figure 5) It has been seen that up to 25%
cases of MED have associated MGP.

 Diplopia: MED with congenital onset usually has no complaints of

diplopia as the affected eye is usually amblyopic. In acquired MED
however, bothersome vertical diplopia is present.
 Abnormal Head Posture (AHP): If binocular fusion is present, a
chin elevation is usually seen.Taking fixation with the affected eye
is very rare, but has been reported. Patient may not have an AHP
if there is orthotropia in primary position or if the affected eye is
amblyopic.
 Upward Saccades: Upward saccades are slow/floating in cases of
SR palsy, absent above the midline in supranuclear deficiency, and
intact (coming to an abrupt halt) in cases associated with IR
restriction.
 A positive Forced Duction Test (FDT): is seen in patients of IR
restriction.

188
Classification:
 Type 1:
It includes patients with primary IR restriction or fibrosis. They are
often orthotropic in primary gaze. FDT demonstrates restriction of
upward rotation because of a tight IR. The upward saccades are
usually normal until stopped by tight IR preventing further upgaze.
Bells phenomenon is usually poor.

 Type 2:
This group includes cases of primary SR palsy and is characterized
by a forced duction test demonstrating no restriction to full
upward rotation of the eyeball. The upward saccades are slow
both below and above midline. Bell’s phenomenon is usually
absent in this type of MED.

 Type 3:
It is the supranuclear type of MED, which is usually congenital and
is characterized by intact or mildly reduced vertical saccadic
velocity below midline but abnormal or absent velocity above
midline. There is no resistance to upward rotation of the eyeball
on FDT.
Differential Diagnosis
 In Brown’s Syndrome:the limitation of elevation is worse
on adduction and improves on abduction. A V pattern
strabismus and superior oblique restriction on FDT is
characteristic.
 Congenital absence of superior rectus and or
inferioroblique often mimic MED but are usually
associated with craniofacial abnormalities.
 Congenital fibrosis of extraocular muscles affects inferior
recti initially and can be confused with MED. Bilateral
presentation and involvement of other extraocular
muscles are features that help distinguish it.
 A third nerve palsy may simulate the findings of MED.
Abnormal pupillary reactions and exotropia of the
affected eye are seen. A palsy of the superior division of
the third nerve affecting the SR and levator muscle is very
difficult to distinguish from MED.

189
Management:
includes both non-surgical and surgical components.
 The correction of underlying refractive error is done.
 amblyopia therapy is given if needed, followed by surgery
whenever indicated.
 Indications for surgery are significant vertical deviation in
primary gaze, significant abnormal head posture,
deviation-induced amblyopia, diplopia in primary gaze,
and restricted binocular fields.
 The goal of surgery is to improve the position of the
affected eye in primary gaze and to increase binocular
field of vision.

CONGENITAL FIBROSIS OF EXTRAOCULAR MUSCLES

(CFEOM):

 Congenital fibrosis Syndrome, is a group of congenital

disorders characterized by restriction of the extraocular
muscles and replacement of the muscles by fibrous tissue.
 It can be unilateral or bilateral, with the bilateral form
being more common.
 The spectrum ranges from isolated fibrosis of a single
muscle to B/L involvement of all EOMs.
 Familial disorder showing Autosomal Dominant
Inheritance.
 Congenital fibrosis syndrome has traditionally been
considered a primary muscle disorder.
 Recently, CFEOM has been accepted to be of neurogenic
origin similar to that of DRS but involving the III
cranialnerve complex.
 Co-contraction phenomenon resulting in globe retraction
has also been described in patients with CFEOM.
 But the exact mechanism & cause is unknown.

CLINICAL FEATURES OF CFEOM:

 Congenital non-progressive bilateral external

ophthalmoplegia
 Congenital non-progressive bilateral ptosis

190
  In the primary position each eye is fixed below the
horizontal by about 10°.
 The hypotropic eye may be secondarily exotropic,
esotropic or neutral.
 The degree of residual
horizontal movement varies
from full to absent.
 Vertical movements are
always severely restricted with
inability to elevate the eyes
above the horizontal plane.
 A subset of cases show unilateral fibrosis with
enophthalmos and ptosis
 Systemic associations:
o Mental retardation
o Facial palsy
o Dental anomalies
o Spina bifida

MANAGEMENT OF CFEOM :
 Surgery is difficult and requires release of the restricted
muscles (weakening procedures).
 Fibrosis of adjacent tissue may be present as well.
 A good surgical result aligns the eyes in primary position,
but full ocular movements cannot be restored.
 Outcome of such surgeries is always unpredictable.

MÖBIUS SYNDROME:

 Heterogeneous clinical disorder, which includes congenital

facial palsy with impairment of ocularabduction due to
sixth nerve palsy.
 Developmental disorder of the brainstem rather than an
isolated cranial nerve disorder.
 The ocular motility disturbances in Mobius syndrome are
frequently bizarre and asymmetrical, resembling more ofa
congenital fibrosis pattern than cranial nerve palsies.
 Most cases are sporadic.

191
  Neural Imaging studies have shown:
o Brain stem hypoplasia in the region of the sixth and
the seventh nerve & hypoplasia of extraocular
muscles and intraorbital motor nerves

CLINICAL FEATURES:

Systemic features :
 Bilateral facial palsy which is usually asymmetrical giving
rise to a mask-like facial expression andproblems with lid
closure.
 Paresis of the 12th cranial nerves which results in atrophy
of the tongue.
 Mild mental handicap.
 Limb & Chest wall anomalies.
Ocular features :
 Horizontal gaze palsy is present in 50% of cases.
 Bilateral 6th nerve palsy.
 Occasionally 3rd and 4th nerve palsy and ptosis.

MANAGEMENT:
Non-surgical management-
 Detection and treatment of amblyopia, corneal exposure
and refractive errors
Surgical management-
 No single surgery useful
 Medial rectus muscle recession is tried
 Transposition of vertical recti to insertion of LateralRectus
described.

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STRABISMUS FIXUS:
It is a rare congenital anomaly in which both eyes are fixed in either the
convergent position caused by fibrous tightening of the Medial Recti

(Convergent Strabismus Fixus):

DivergentStrabismus Fixus:

 No horizontal movement is possible.

 Diplopia does not occur because of suppression of image
from one eye.
 Amblyopia also does not develop because the patient
tends to use both eyes alternately.

TREATMENT OF STRABISMUS FIXUS-

 Involves recession of medial recti along with recession of
conjunctiva & tenon’s capsule, but abduction beyond
midline can never be achieved.

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VISION THERAPY

What is Vision Therapy?

•Vision Therapy is an individualized, supervised, treatment program
designed to correct visual-motor and/or perceptual deficiencies. Vision
Therapy sessions include procedures designed to enhance the brain's
ability to control :
 eye alignment.
 eye teaming.
 eye focusing abilities.
 eye movements.
 visual processing .
•Vision therapy is often requested for individuals with the following
visual dysfunctions:
 Accommodative disorders - focusing problems.
 Amblyopia - lazy eye.
 Ocular motility dysfunction - eye movement disorders.
 Strabismus - misalignment of the eyes.
 Vergence dysfunction - inefficiency in using both eyes
together.
 Visual rehabilitation after traumatic brain injury.


•Vision Therapy Consists of Two Broad Categories:
1. Orthoptic
2. Behavioral

1-Orthoptic Vision Therapy

•Non-surgical techniques to correct conditions which might be
responsible for eye fatigue and discomfort with close work.

•Used to correct:

- Convergence insufficiency :
•CI is one of the few ocular problems that can interfere with the physical
act of reading.

194
•It can cause blurring of vision and the sensation that letters and words
run together especially during times of prolonged reading or near work.
•Most common treatment for CI is pencil push-ups in which the patient
practices turning his/her eyes inward to converge on a near target such
as a pencil point.

• Also used to correct:

 Accommodative insufficiency ( the inability of the eye to focus
properly on an object) , After age 40 it is considered part of the
aging process. Usually seen in conjunction with convergence
insufficiency.
3. Heterophorias.
4. Refractive errors ( need for glasses).

- Note:Orthoptic can provide excellent results for patients who have

reading difficulty secondary to convergence and accommodative
problems.
- However these ocular disorders are the less common causes of true
reading disabilities.

2-Behavioral Vision Therapy:

•Eye movement and hand-eye coordination training
techniques which attempt to improve visual
processing skills, visual perception and visual-motor
integration.
• May also include the use of colored overlays or
filters and glasses for mild refractive errors with or
without prisms.
•Requires a number of office visits depending upon
the severity of the problem diagnosed by the vision
therapy provider.
•Typical length of the program ranges from several weeks to several
months and may include activities to perform at home.

•Note : There is NO consistent scientific evidence that supports the

use of behavioral vision therapy as an effective treatment for
learning disabilities or for the remediation of complex pediatric
neurological conditions such as autism spectrum disorders.

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SIGHT VERSUS VISION:

•6/6 eyesight is the ability to see a certain letter size on the eye chart
when standing 6 meter away. You can have 6/6 eyesight, but still have a
vision problem.
•This is because reading an eye chart is a static visual task, but most
daily activities require our eyes to perform more demanding, dynamic
functions.
•There are four aspects of vision that are important in daily activities
and learning.

Aspects of vision:
•Eye Tracking (Oculomotor).
•Eye focusing (Accommodation).
•Eye Teaming/Fusion (Binocularity).
•Visual Perception.

1-Eye Tracking (Oculomotor):

•Oculomotor dysfunction exists when both eyes do not move smoothly,

precisely or quickly.
•Skipping lines or words, misreading the beginnings of words and loss of
place are all sign of problems with eye tracking.
•An eye tracking problem inhibits the ability to sustain attention and
fixate onto a single target such as a word in a book or a ball in a sport
game.

2-Eye focusing (Accommodation):

•Accommodation is the focusing capability of the eye.

•The eye is equipped with a variable lens system that allows for changes
in focusing.
•Excess effort may be needed in order to maintain a clear image. As a
result, eyestrain, headaches, and intermittent blurry vision can occur.

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3-Eye Teaming/Fusion (Binocularity):

•Eye fusion is the ability of two eyes to work together to obtain a single
image.
•Many children maintain the use of both eyes working together;
however, it may come at the expense of excessive effort, fatigue and
sometimes confusion.
•Strabismus is the condition where both eyes fail to work together and
one or both of the eyes deviates instead of aiming at one location.
•The inability of both eyes to work together as a team can result in
double vision, reduced depth perception and poor physical coordination
in sports.

4-Visual Perception:

•This is the learned ability to interpret, perceive and correctly identify

information.
•It is the understanding of things that we cannot use our other senses
such as touch, taste, smell or hear for.
•Visual perception delays can result in letter reversals (such as b and d),
and poor spelling, reading comprehension and math abilities.

WHAT DOES VISION THERAPY INVOLVE?

•In order to treat the visual condition in an efficient and effective

manner, vision therapy usually involves weekly/ bi-weekly in-office
training of 30 -60 minutes duration, supplemented by daily home
therapy of approximately 20-30 minutes.
•The length of the program varies between several months to up to a
year depending on the severity of the condition.

The goal of vision therapy:

•The goal of vision therapy is to improve or correct diagnosed visual

dysfunctions.
•Vision therapy includes a wide range of nonsurgical optometric
treatment modalities.

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•Modalities include eye exercises, flashing light response exercises,
prisms, wearing tinted or colored lenses, filters, occluders, specialized
instruments, computer programs and other devices.

Vision Therapy work extensively in the following treatment

areas :
1-Learning-related Vision Problems:
Vision Therapy can help those individuals who lack
the necessary visual skills for effective reading,
writing, and learning (i.e., eye movement and
focusing skills, convergence, eye-hand activity,
visual memory skills, etc.).

2-Poor Binocular Coordination :

•Vision Therapy helps individuals develop normal coordination and
teamwork of the two eyes (binocular vision).
•When the two eyes fail to work together as an
effective team, performance in many areas can
suffer (reading, sports, depth perception, eye
contact, etc.

3- Strabismus and Amblyopia:

Vision Therapy programs offer much higher cure rates for turned eyes
and/or lazy eye when compared to eye surgery, glasses, and/or
patching, without therapy. The earlier the patient
receives Vision Therapy the better.

4-Stress-induced Visual Difficulties:

•21st century lifestyles demand more from our
vision than ever before. Children and adults in our
technological society constantly use their near vision at work and at
home.
•C.V.S. (Computer Vision Syndrome) is one of the
fastest growing health concerns in the workplace today.
Environmental stresses on the visual system (including
excessive computer use or close work) can induce
eyestrain, headaches, and/or visual difficulties which
can be effectively treated with corrective lenses and/or
Vision Therapy .

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5-Visual Rehabilitation for Special Populations:
•Vision can be compromised as a result of neurological
disorders or trauma to the nervous system (such as,
traumatic brain injuries, stroke, cerebral palsy,
multiple sclerosis, etc.).
•Vision Therapy can effectively treat the visual
consequences of trauma (including double vision) .

6-Sports Vision Improvement:

•Strong visual skills are critical to sports success. Not much happens in
sports until your eyes instruct your hands and body as to what to do!
•Accurate vision and athletic visual skills can be
measured, developed, and enhanced through
Vision Therapy.
•We can measure and successfully improve eye-
hand coordination, visual reaction time,
peripheral awareness, eye teaming, focusing,
tracking, and visualization skills.

Is Vision Therapy Only for Children?

•Vision therapy is not only for children. Many adults
find that vision therapy effects an improvement or
recovery of their vision impairment; even in cases in
which visual problems have been previously
pronounced or hopeless by other vision care
professionals.
•Most visual conditions which can be treated in a child
can be treated in an adult as well.
•For example, many cases of (amblyopia) can be successfully treated
with vision therapy at any age.
•For many years, it was thought that amblyopia was only amenable to
treatment during the "critical period". This is the period up to age seven
or eight years.
•Current research has demonstrated that effective treatment can take
place at any age, but the length of the treatment period increases
dramatically the longer the condition has existed prior to treatment.

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Methods of treatment:
1-The Brock String :

•The Brock String is a simple tool which gives the child a great deal of
visual feedback.
•It teaches the patient how to aim his eyes together
correctly for varying distances in space and allows
him to experience the difference between
convergent and divergent eye aims.
•It also allows the child to determine if he is
suppressing, and tells him where his eyes are aimed
and how far off his eye aim may be.
•This is usually one of the first techniques the child is
taught and is often assigned as home therapy.

2-Computers :

•Computers are an important part of vision therapy treatment.

•Orthoptic software can create a wide range of
visual stimuli and affords the variability to
individualize techniques to meet each child's specific
needs.
•The child can work on programs which train eye
movements, eye coordination, stereo vision, and
antisuppression techniques.
•Therapy always begins at a level where the patient
can succeed and gradually increases the visual
demands to stretch his range and skill.

3- Cheiroscope:

•It's used to assess binocular stability and alignment

and to detect the presence and extent of suppression.
•Suppression occurs when the patient's brain shuts off
an eye by blocking its visual input when the child loses
the ability to control his eye alignment.
•Suppression is an adaptive neurological response to
protect oneself from double vision.

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•Training on the cheiroscope gives the child important feedback that he
is suppressing and allows him an opportunity to gain the binocular
control necessary to correct his eye aim and eliminate suppression.

4-Aperture rule:

•The patient is asked to look through a window in a slide at a series of

targets placed at the end of the instrument.
•Each eye sees a different part of the target, and
the child learns to fuse the two images coming in
from his left and right eyes into a single picture.
•The therapist's role is to coach the child on ways
to adjust his visual system to achieve the goal of
clear, single vision.

5-Amblyoscope :

•The amblyoscope is a machine which trains a child to use his/her eyes

together.
•The goal of this instrument is to help the child
achieve binocular fusion, or normal two-eyed
single vision with depth perception.
•As the child progresses in skill, the therapist
increases the fusional demands to stretch and
normalize the patient's ability to efficiently use
his/her two eyes together.
•Amblyoscope also allows a child to know when
he/she is suppressing an eye; visual awareness is
the first step in successful training.

6- Neurological adaptation “Anti-suppression”:

•Children with unstable visual systems often learn a neurological

adaptation called suppression, in which their brains block the visual
input coming in from one eye.
•Children unconsciously learn to suppress at very young ages to keep
from seeing double.
•Suppression is never normal and is always a sign of an unstable visual
system.

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•Vision therapy trains the eyes to work together but to do so both eyes
have to be "on".
•Here a therapist works with a child using
special red-green lenses and a target with red-
green letters.
•One eye can only see the red letters, and the
other the green.
•If the visual system shuts off an eye, the child
won't be able to see all of the letters.
•Antisuppression activities such as these make the child aware of when
she is suppressing and allow her to gain control and learn to leave both
eyes on simultaneously.
•This is especially important for children with crossed eyes, and lazy
eyes .

7-Lenses and prisms:

•Lenses and prisms are always important in visual training.

•They modify the patient's world and allow him to create an appropriate
visual response.
•Here a child is working on a focusing technique
called accommodative rock.
•The "flippers" hold two different sets of lenses,
One is a pair of plus lenses; the other are minus.
•By rapidly alternating between the two sets of
lenses, the patient is forced to relax or increase
focusing accommodation in order to clearly see the
print, thus gaining greater facility and control over
his focusing system.
•Patients always begin with lower powered lenses and gradually
increase the strength at which they can successfully complete the task .

8-Mental minus:

•This child is working on another focusing technique

called "mental minus" that teaches him to control how
much he's focusing.
•Focusing problems cause children to see blurry print,
especially when they read small print for long periods or
have to make a lot of focusing shifts between the board and their desks.

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9-Vectograms :

•This patient is working with special polarized slides called Vectograms.

•These slides allow a child to work with a variety of
targets to train central or peripheral vision, flat fusion
or stereo fusion, and convergent or divergent eye
positions.
•The targets also help to control suppression, or the
patient's tendency to shut off an eye when his visual
system is stressed.

10-Tug exercises:

•Children with conditions called convergence insufficiency and exotropia

have difficulty turning their eyes inward at close
ranges.
•As a result, they often struggle in school because
they simply can't maintain the inward eye aim
required for reading and most close up activities.
•These children have to be taught to converge their
eyes.

11- The saccadic fixator:

•The saccadic fixator is an instrument which trains eye movements,

tracking, visual memory, peripheral awareness, and visual motor
integration.
•It allows the children to set goals for themselves
as they continually strive to improve their last
performance .
•Besides children with oculomotor dysfunctions,
this machine is particularly good for young
athletes; it improves their eye-hand-body
coordination and response time.

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12- The rotator:

•The rotator is a tracking instrument used to increased a

child's ability to control where she's moving her eyes.
•The child is asked to place golf tees in a rotating pegboard.
As the child's skill improves, the speed at which the
pegboard is rotating is gradually increase.
•This procedure is usually done while the patient is wearing
a patch over one eye. Strong monocular skills must be
gained before a child can achieve good binocular, two-eyed
skills .

13- The walking rotator:

•The walking rotator integrates the child's eye movements with his or
her body movements.
•The child is asked to find letters or pictures on the turning wheel as he
walks on a raised rail.
•This activity not only helps tracking skills, but it
also improves visual motor integration skills.
•Our visual systems are continually sending
information to our bodies to help control
movement, balance, coordination.
•Children who have poor control over their visual
systems often have poor control over their body
coordination.
•These children appear awkward and clumsy, do
poorly in sports, and may find it difficult to learn to ride a bike.
•Fine motor skills are also affected. Poor handwriting is a common
problem of children with poor eye-hand coordination .

Convergence insufficiency:

•Convergence insufficiency (CI) is a common binocular vision disorder

affecting school-age children and university students causing discomfort
with reading,
•CI has been shown to have a negative impact on the quality of life and
school performance in school-age children.

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Diagnosing of Convergence insufficiency Symptoms:

•Patients with symptomatic convergence insufficiency will often

complain of headaches, blurred vision, diplopia, loss of concentration
and sleepiness when reading.
•They often lose their place when reading, feel that the words move
around on the page and need to re-read frequently.
•In order to determine if these symptoms were significant for CI, the
Convergence Insufficiency Treatment Trial ―CITT‖ group developed a
valid and reliable questionnaire.

Diagnosing of Convergence insufficiency:

•Patients are asked to rank their responses to the 19 questions on a

scale from ―never‖ (0) to ―always‖ (4).
•The responses are then tallied and multiplied by the set multiplier. A
score ≥16 is considered significant.

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Cause of Convergence insufficiency:

•Convergence insufficiency can be either primary or secondary to an

underlying etiology.
•In primary CI, the deviation is comitant and the patient reports long-
standing symptoms with a negative health history.
•Whereas, a secondary CI (or, potentially, a convergence paralysis) may
be associated with precipitating factors such as a mild traumatic brain
injury, neuro-degenerative disease such as Parkinson’s disease, micro-
vascular event or secondary to accommodative insufficiency, also known
as a pseudo-convergence insufficiency.

Signs of Convergence insufficiency:

1.A receded near point of convergence (NPC) breakpoint .

Additional inclusion criteria used by the CITT Investigator group
included:
2. Exophoria greater at near than at distance by at least 4 prism diopters,
and
3. Positive fusional vergence that is insufficient to meet demands.
•It is recommended to repeat NPC measurements five times, as most of
the change occurs between the first and fifth measurement.
•Positive fusional vergence can be measured using two methods:

1.using the phoropter for evaluation of smooth vergences or,

2.using a prism bar in free-space and an accommodative (20/30) target
for evaluation of step vergences.

•The advantage of step vergence testing is that it can be administered

outside the phoropter, which may be beneficial when examining young
children.
•Expected findings are different for smooth versus step vergences.
•Expected minimum norms for positive fusional vergence are 17/21/11.

Treatment of Convergence insufficiency:

•Studies determined that the most efficacious form of treatment for CI

in school-age children was in-office vision therapy with home
reinforcement.
•In young adults, treatment is still effective, although less so.

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- In-office Vision Therapy
•The studies conducted by the CITT Investigator Group have shown that
in-office vision therapy is the only treatment for CI more effective.
•Therapy is typically comprised of a 45 or 60-minute session conducted
once or twice a week, with 15-30 minutes of home therapy performed
during the week.
•The CITT protocol was comprised of 12 weeks of 60-minute weekly
sessions in-office, with 15 minutes of home reinforcement on weekdays.
•It is prudent to consider any prior amblyopia and suppression present
prior to starting therapy.
•It is ideal for the appropriate refractive correction to be in place.
•While this should not be the case for a patient with symptomatic CI
exophoria, the presence of an intermittent or constant strabismus would
provide additional barriers that would compromise success.
•Please note that patients with preexisting strabismus and amblyopia
were excluded from the CITT studies.
•In general, the sequence of vision therapy is as follows:
1. Anti-suppression activities and development of physiologic diplopia
awareness.
2. Monocular activities to normalize accommodative amplitude and
facility.
3. Activities utilizing monocular fixation in a binocular field.
4. Fusional vergence training – both positive and negative.
5. Integration of fusional vergence training with binocular
accommodation, as well as free space fusion activities.

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•Although deep suppression is uncommon in an exophoric patient with
symptomatic CI, shallow, central, facultative suppression may still be
present.
•Thus, anti-suppression activities are still advisable during the earlier
sessions of vision therapy. Anti-suppression activities often utilize red/
green glasses, red lenses, and polarized filters to provide the patient
with visual cues regarding suppression.
•The cheiroscope can be used to train anti-suppression.
•The Brock String is also a common and convenient
tool used during these beginning stages of vision
therapy.
•Instruments, such as the stereoscopes can also
provide an artificial environment in which the
patient can be more easily anti-suppressed.
•Once suppression is broken, the patient can be
made aware of physiological diplopia.
•The next step in vision therapy includes training of monocular
accommodative amplitude and facility. These monocular activities often
involve the use of lens flippers, as well as varying distances of targets.
•Some examples of these include monocular distance-to-near Hart chart
rock, monocular lens sorting and monocular loose lens rock.
•Once suppression has been appropriately broken and accommodative
functions strengthened, fusional vergence training can begin.
•In general, all activities begin where fusion is strongest; in the case of a
patient with symptomatic CI, these activities would be at a greater
distance.
•The targets and tools would then be brought closer as
the patient’s convergence strengthens.
•The goals of fusional vergence training are to expand
both the positive and negative fusional vergence ranges
utilizing both the slow, smooth vergence system.
•There are a number of tools used during fusional
vergence procedures.
•For example, one could use vectograms or
tranaglyphs, which are available in either variable or
non-variable forms.
•Loose prisms can also be flipped or dipped‖ to
strengthen jump vergences and vergence facility.

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Home vision therapy:

1-Home-based pencil pushups:

•Although less effective as in-office vision therapy, the most common

treatment for convergence insufficiency to date has been home-based
pencil pushups (HBPP) and base-in prism reading glasses.
•To perform this technique, the patient is asked to place an index card
or other object on the wall in front of them to be used as a visual check
for suppression.
•The patient then holds a pencil approximately 40 cm in front of his or
her face, and brings the pencil towards the tip of the nose while trying to
maintain fusion.
•The pencil is only pushed away if the patient is unable to fuse the
diplopic images.
•The goal of this exercise is for the patient to be able to appropriately
view the pencil on the tip of his or her nose and sustain fusion for about
five seconds.

2-Base-in prism reading glasses:

•Of course, not all patients are a good fit for active treatment measures
such as vision therapy or HBPP.
•Thus, for this subset of patients with symptomatic CI, would base-in
prism reading glasses be a viable treatment option?
•On one hand, Scheiman et al., found that base-in prism reading glasses
were no more effective than placebo lenses and thus were not an
effective treatment for children with symptomatic CI.
•The amount of prism prescribed was based on Sheard’s criterion, with
the average amount of prism prescribed being approximately 4 prism
diopters of base in prism.
•Compliance to treatment was excellent, and both groups ; those with
base-in prism reading glasses and those wearing placebo glasses;
showed statistically significant decreases in symptoms.
•On the other hand, Pang et al., used base-in prism reading glasses to
treat presbyopic patients symptomatic for CI.
•Their results indicated that glasses were successful in managing
symptoms in this patient population, particularly if those with greater
near heterophorias and receded near points of convergence.

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•Overall, it appears that base-in prism glasses for managing
symptomatic CI offers passive, rather than active treatment.

Conclusion:

•Overall, CI is a treatable binocular vision disorder that can be

successfully managed with in-office vision therapy, ideally, as well as
with pencil push-ups and computer orthoptics software.
•It appears that patients continue to experience symptomatic relief as
well as improvement in positive fusional vergence and the near point of
convergence up to a year post-treatment.
• While base-in prism reading glasses offer the same amount of
symptomatic relief as placebo lenses in children, they may have a place
in management for symptomatic presbyopes.

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