Dr. Tintu Susan Joy presented on the approach to diplopia. Diplopia occurs when more than one image of an object is seen simultaneously. It can be binocular or monocular in nature. Binocular diplopia is caused by misalignment of the visual axes between the two eyes. Monocular diplopia can result from light diffraction, metamorphopsia, or cerebral polyopia. A thorough history and examination including assessment of eye movements is needed to localize the cause, which may be restrictive, paralytic, or supranuclear in nature. Management depends on the underlying etiology.

1. APPROACH TO DIPLOPIA
PRESENTED BY
DR TINTU SUSAN JOY
MODERATOR
DR PAVANA ACHARYA.

2. DIPLOPIA
 when more than one image ( two ) of the object of
regard are seen simultaneously, it is called
DIPLOPIA

3. BINOCULAR SINGLE VISION
 Perfect ( or near perfect ) alignment of the visual
axes simultaneously on the object of regard
 Perfect ( or near perfect ) retinal correspondence
 Perfect central ( or paracentral ) fusional capability.
 Perfect ( or near perfect ) alignment of the retinal
receptors
 Perfect ( or near perfect ) optics to allow only one
image to be formed on the retina and the same
single image to be formed on the other

4. WHEN DIPLOPIA OCCURS
 More than one image of the object of regard is
formed in the retinae of one or both eyes (
monocular diplopia)
 The eyes lose their simultaneous alignment with the
object of regard in one or more directions ( or
distances ) of gaze (incomitance of ocular
alignment – binocular diplopia)

5.  The eyes although aligned, send images of different
size to the brain which disallow fusion (
aniseikonia ( > 2.5 D, 5%)
 Local retinocerebral adaptations to misalignments
in early life go askew (paradoxical diplopia, loss of
suppression)
 Rarely, purely cerebral mechanisms

6. HISTORY
 Whether diplopia disappears or persists after closing one eye
(Binocular vs monocular diplopia)?
 PERSISTS EVEN AFTER CLOSING ONE EYE
MONOCULAR DIPLOPIA
QUESTION-1

7. MONOCULAR DIPLOPIA
 Monocular diplopia can result from
 Light diffraction,
 Metamorphopsia and
 Cerebral polyopia.

8.  Light diffraction causes images of a single object to fall on the
fovea and the extra-foveal retina of the same eye.
 The images are of different clarity
extra-foveal ghost-image overlapping the clear foveal image.
 Monocular diplopia due to light diffraction
resolves with viewing through a pinhole

9.  Metamorphopsia or distortion of retinal images
 Maculopathies such as macular edema or epiretinal
membrane
 Metamorphopsia does not resolve with viewing
through a pinhole.

10.  Cerebral polyopia is the perception of multiple
images due to pathologies in occipital cortex or
central visual pathway lesions.
 Monocular diplopia occurs bilaterally, the images
are of equal clarity and do not overlap.

11. CAUSES OF MONOCULAR DIPLOPIA
Refractive error High refractive error, irregular astigmatism; Edge
effect of spectacle or contact lens
Eyelid Mechanical compression on cornea chalazion,
tumor, hematoma, edema
Tear film Abnormalities of tear film causing light diffraction
mucus strand, foreign bodies, oil droplets
Cornea Opacity causing light diffraction: scar, edema,
corneal dystrophies; Abnormal corneal shape:
keratoconus, keratoglobus, megalocornea; Post
refractive surgery

12. Lens Opacity cataract, vacuoles, water cleft; Shape: lenticonus,
spherophakia; Position: ectopia lentis, intraocular
lens subluxation
Iris and pupil Iridodialysis, polycoria, peripheral iridotomy /
iridectomy
Vitreous Foreign bodies
Retina Macular edema; Central serous retinopathy
Cerebral
polyopia
Trauma, migraine, multiple sclerosis, encephalitis,
seizure

13. HISTORY….
 When and how did the double vision started?
 History of any trauma to eye, face, head or any
history of ocular surgery recent or in past.
 Associated symptoms with double vision if any like
–headache, difficulty with speech or swallowing,
facial or ocular pain?

14. EXAMINATION
 Slit lamp examination
 Retinoscopy
 Fundus examination
keratoconus

16. ALPORT LOWES

19. BINOCULAR DIPLOPIA
 Binocular diplopia is due to misalignment of the
visual axes.
 Images fall on non-corresponding parts of both
retinas.
 Image falls on the fovea of the fixating eye and
extra-foveal retina in the non-fixating eye. Both
images fall outside the Panum’s area of single
binocular vision.
 The separation of both images is greatest when the
object is viewed in the direction of paretic muscle.

21. CAUSES OF BINOCULAR DIPLOPIA
a) Orbital disorders
Trauma, mass or tumor, infection, thyroid-
associated ophthalmopathy.
b) Extraocular muscle restriction
Thyroid – associated ophthalmopathy, mass or
tumor, extraocular muscle entrapment, extraocular
muscle injury or hematoma due to ocular surgery.
c) Neuromuscular junction dysfunction
Myasthenia gravis, botulism.

22. d) Palsies of the third, fourth or sixth cranial nerves
Ischemia, haemorrhage, tumor or mass,
vascular malformation, aneurysm, trauma,
meningitis, multiple sclerosis.
e) Brain stem injury to cranial nerve nuclei
Stroke, haemorrhage, tumor or mass, trauma,
vascular malformation.
f) Supranuclear injury (pathways to and
between cranial nerve nuclei)
Stroke, haemorrhage, tumor or mass, trauma,
multiple sclerosis, hydrocephalus, syphilis,
Wernicke’s encephalopathy, neurodegenerative
disease.

23. WHETHER DEVIATION CHANGES WITH
DIRECTION OF GAZE???
BINOCULAR
DIPLOPIA
CONCOMITANT
INCOMITANT

24. COMITANT DEVIATIONS
 Comitant misalignment seen in congenital or early
onset strabismus.
 typically do not report diplopia because of
suppression
 BUT DIPLOPIA HAPPENS 
 Later in life, when the degree of ocular
misalignment changes.
 long-standing exophoria, develop horizontal
diplopia when accommodation and convergent
capacities wane( 5TH DECADE).
 Febrile illness or ill health – phorias becomes
tropia diplopia

25. DIVERGENCE INSUFFICIENCY
 Is a type of comitant deviation that manifests as an
esodeviation that is greater at distance than at near
but is comitant in right and left gaze.
 Uncrossed diplopia at distance
 Treatment – base out prism
CONVERGENCE INSUFFICIENCY
 Crossed Diplopia greater for near than for distance
.
 Treatment- orthoptic exercised n base in prism.

26. INCOMITANT DEVIATION
 It is most frequently acquired and usually causes
diplopia. If the deviation is very small, fusional
amplitudes may eliminate the diplopia.
 Normal fusional divergence 8-12 D for near ,4-6 D
for distance. Normal fusional convergence for near
35 D and distance 18D.
RESTRICTIVE
PARALYTIC

27. RESTRICTIVE PATHOLOGY
 The most common cause of restrictive strabismus is
thyroid-associated orbitopathy.
 inferior and medial recti most commonly affected
elevation and abduction of eye affected.
 associated with proptosis, chemosis, lid retraction, and
lid lag.
 Forced duction testing and measurement of differential
intraocular pressure (>5mmHg)
 CT-
RESTRICTIVE 1

28.  Blowout fractures of the orbit
 fracture of the inferior orbital floor with entrapment
of inferior rectus muscle.
 This entrapment produces the same pattern of
vertical strabismus( double diplopia)
 Less commonly, the medial rectus muscle becomes
entrapped.
RESTRICTIVE 2

29. Post-Cataract Extraction Restriction
 Injury or inflammation to the inferior rectus muscle
complex secondary to retrobulbar injection for
cataract (or other ocular) surgery can produce
vertical diplopia.
 The onset of vertical diplopia just after surgery
initially suggests nerve damage or possible
myotoxicity from the local anesthetic.
 Over time, extraocular muscle fibrosis occurs
leading to restricted movement of the eye. The
involved eye becomes hypotropic, and the
hypotropia increases in upgaze.
RESTRICTIVE 3

30. POST PTERYGIUM EXCISION
 Medial rectus muscle disinsertion following
pterygium surgery is characterized by a small to
moderate amount of exo deviation in the primary
position, mild to moderate limitation of adduction
with diplopia.
 Medial rectus muscle recession combined with scar
tissue removal is required to eliminate diplopia in
the primary position.

31. ORBITAL MYOSITIS
 Idiopathic inflammation of one or more extraocular muscles
typically produces ophthalmoplegia, pain, conjunctival
hyperemia, chemosis, and sometimes proptosis.
 The pain is intense and accentuated by eye movements.
 CT or MRI typically shows enlargement of one or more of the
extraocular muscles, with involvement of the tendon, and
often the inflammation extends into the orbital fat.
 Orbital myositis usually responds promptly to systemic
corticosteroid therapy.
 may be associated with systemic disease such as Wegener's
granulomatosis, systemic lupus erythematosus, or sarcoidosis
RESTRICTIVE 5

32. NEOPLASTIC INVOLVEMENT
 Infiltration of the orbit by cancer, from the
surrounding paranasal sinusesimpair eye
movements either because of extraocular muscle
infiltration or involvement of the ocular motor cranial
nerves.
RESTRICTIVE 6

33. PARALYTIC CAUSES
 Proper localization of the lesion is very important.
 Central lesions of the ocular motor cranial nerves
may involve supranuclear, internuclear, nuclear,
and fascicular structures within the brain stem.
 Peripheral lesions involve subarachnoid space, the
cavernous sinus, superior fissure, and orbit.

34.  Via Frontomesencephalic
pathway from these areas,
impulses travel down
 Pass through anterior limb
of internal capsule, medial
part of cerebral peduncle
 Cross to opposite side at
pontomesencephalic
junction
 End in paramedian pontine
reticular formation(PPRF)-
horizontal gaze 6th CN
 Rostral interstitial nucleus of
medial longitudinal
fasciculus (riMLF) in vertical
gaze 3, 4 TH CN

35. SUPRANUCLEAR -SKEW DEVIATION
 Acquired vertical misalignment of the eyes resulting
from asymmetric disruption of supranuclear input
from the otolithic organs.
 These organs sense linear motion and static tilt of
the head and transmit information to the vertically
acting ocular motoneurons, as well as to the
interstitial nucleus of Cajal.

36. SKEW DEVIATION
 Central causes of skew
deviation are common
and can occur
anywhere within the
posterior fossa (brain
stem and cerebellum).
 difficult to distinguish
presentation of skew
deviation from a fourth
nerve palsy,

37. ALTERNATING SKEW DEVIATION
 An alternating skew deviation usually manifests as
hypertropia of the abducting eye (ie, right
hypertropia on right gaze) that switches when gaze
is directed to the opposite side.( diff frm SO palsy)
 cerebellum or dorsal midbrain.

38. OCULAR TILT REACTION
 Ocular tilt reaction is a combination of a head tilt,
skewdeviation, and cyclotorsional abnormalities of
both eyes that can occur in tonic or paroxysmal
fashion.
 This syndrome typically develops because of loss
of otolithic input to the INC from a central lesion,
which may be in the medulla, pons, or midbrain.
 Such a lesion can alter one's sense of true vertical,
which in turn drives the head and rotates the eyes
toward the same side in a compensatory response
to correct to true vertical.( worsens in 4th nerve)

39. DORSAL MIDBRAIN SYNDROME/PARINAUD’S
 Bilateral disturbanc in vertical gaze.
 light near dissociation
 Diffective accommodation
 Lid retraction- ‘collier’s sign

40. THALAMIC ESODEVIATION
 Thalamic esodeviation is an acquired horizontal
strabismus that may be seen in patients with
lesions near the junction of the diencephalon and
midbrain.
 seen in younger patients with pineal tumors or
craniopharyngioma or in older patients with cerebral
hemorrhage.
 The esodeviation may develop insidiously or
acutely and, in the case of expanding tumors, may
be progressive.

41. INTERNUCLEAR OPHTHALMOPLEGIA
 "internuclear" lesion is one that disrupts the medial
Iongitudillal fasciculus (MLF) {connect the sixth
nerve nucleus on one side to the medial rectus
subnucleus (of the third nerve) on the opposite side
of the brain stem}.
 The cardinal feature of an INO is slowed
adducting saccadic velocity in one eye.
 This limitation mayor may not be associated with
nystagmus of the abducting eye.
 Convergence may be spared or disrupted.
 A skew deviation, ipsilateral to the lesion, may be
present.

43.  These patients may not report horizontal diplopia due to
adduction limitation but report vertical diplopia due to an
associated skew deviation and have difficulty tracking
fast-moving objects.( tennis)
 Bilateral lNO lesion near the third nerve nuclei (ie, the
"wall-eyed" bilateral INO, or WEBINO, syndrome)
vertical, gaze-evoked nystagmus that is best
appreciated in upgaze. Exo in primary position.
 The two most common causes of INO are demyelination
and stroke.
 Myasthenia gravis can produce pseudo-INO(tensilon)

44. ONE-AND-A-HALF SYNDROME
 The one-and-a-half syndrome shares the features
of a unilateral INO, plus conjugate limitation of
horizontal gaze to the same side as the lesion
 caused by a pontine abnormality large enough to
involve the MLF and the PPRF
 Stroke is the most common cause of this disorder.

45. NUCLEAR AND FASCICULAR
INVOLVEMENT
 Third nerve nucleus
 bilateral ptosis and contralateral superior rectus
muscles involvement(DAROFF RULE)
 Injury to the third nerve nuclear complex is
uncommon,
 occur secondary to reduced perfusion through a
small, paramedian penetrating blood vessel, which
causes unilateral damage to I nuclear complex.
 Brain stem tumors may also produce nuclear
lesions.

46. WEBERS
SYNDROME- +
contralateral
hemiparesis( ventral
mid brain- cerebral
peduncle)
BENEDIKT
SYNDROME -
contralateral ataxia
and/or tremor (red
nucleus and substantia
nigra).
CLAUDE SYNDROME
NOTHNAGEL SYNDROME

47. THIRD NERVE PALSY

48. 4TH CRANIAL NERVE NUCLEUS
 Microvascular or inflammatory lesions
 Feature of contralateral horners
syndrome(proximity of decending sympathetic
pathway)
 Damage to both trochlear nerve fascicles at their
decussation within the anterior medullary velum
usually results from trauma .

49. A fourth nerve palsy typically causes
diplopia that is worse in down gaze(
reading). V patten esotropia

50. 6TH CRANIAL NERVE NUCLEUS
 A selective lesion of
the sixth nerve
nucleus causes a
horizontal gaze palsy
(like a lesion of the
PPRF) and not an
isolated abduction
paresis in I eye, and
thus patients do not
report diplopia.
 ( LR n fibres of I/L
MLF)
FOVILLE
MILLARD
GUBLER

51. PONTINE LESIONS
 FOVILLE SYNDROME - Intra-axial lesions that involve
the fascicle of the sixth nerve may also damage the
fascicle of the seventh nerve, the tractus solitarius, and
the descending tract of the trigeminal nerve ipsilateral
abduction palsy, facial weakness, loss of taste over the
anterior two thirds of the tongue, and facial
hypoesthesia.
 MILLARD-GUBLER SYNDROME- Lesions of the
ventral pons can damage the sixth and seventh nerves
along with the corticospinal tract contralateral
hemiplegia and ipsilateral facial nerve palsy and
abduction deficit .

52. PERIPHERAL LESIONS OF THE OCULAR MOTOR CRANIAL NERVES INVOLVE
SUBARACHNOID SPACE, THE CAVERNOUS SINUS, SUPERIOR ORBITAL FISSURE.

53. CAUSES
ISOLATED CRANIAL MONONEUROPATHIES-
 microvascular disease of the vasa
nervorum( DM,HTN, elevated serum lipids)
 generally present acutely.
 Resolves with in 3 months.
 demyelination.
 Less common causes include aneurysmal
compression, tumor, inflammation
(sarcoidosis, vasculitis), infection
(meningitis), infiltration (lymphoma,
carcinoma), and trauma.

54. MULTIPLE-CAVERNOUS SINUS THROMBOSIS
 Febrile, Nausea , vomiting
 U/L Periorbital pain
 Adnexal edema
 Ptosis
 Chemosis and severe congestion.
 Proptosis
 Opthalmoplegia( 3, 4, 6 CN)
 Decreased visual acuity or blindness (Central retinal
artery/ vein occlusion secondary to ICA arteritis, septic
emboli, ischemic optic neuropathy)
 Initially unilateral  Bilateral

55. SUPERIOR ORBITAL FISSURE
SYNDROME
 Trauma Craniofacial fractures
 Syphilis
 Hematoma of retrobulbar space or cavernous sinus,
 Infection
 Neoplasm
CF
 Ptosis
 Proptosis
 Ophthalmoplegia
 Fixed dilated pupil
 Anaesthesia of upper eyelid and forehead.

56. TOLOSA HUNT SYNDROME
 Non specific granulomatous inflammation of
cavernous sinus or superior orbital fissure or orbital
apex.
 Diagnosis of exclusion
 Diplopia with ipsilateral periorbital or hemicranial
pain, ( steady, boring)
 3rd, 4th , 6th , & 1st division of trigeminal nerve are
involved
 Horner’s syndrome may be present
 Characterised by remission, relapses, high ESR&
response to steroid.

57. GIANT CELL ARTERITIS
 Granulomatous necrotising arteritis affecting large and
medium size arteries.
 Smoking, low BMI, early menopause are risk factors
 Rare < 50 yrs
 Female: male- 4:1
 Scalp tenderness
 Headache
 Jaw claudication( pathognomonic)
 Weight loss, fever, night sweats
 Double vision
SIGNS
 Thickened tender inflamed nodular non pulsatile arteries
 ocular motor palsies including pupil involving third nerve
palsy

58. HISTORY
AGE-
Children - transient Ophthalmoplegia following viral
infection or vaccination.
Ophthalmoplegic migraine,
Accomodation insuffiency,
Divergence insuffiency
Thalamic esotropia( pineal gland tumours)
Adults –
Thyroid ophthalmopathy,
Cranial nerve palsy due to aneurysms,
Divergence or convergence insuffiency,
Multiple sclerosis- internuclear opthalmoplegia,CN palsies

59. ELDERLY
 Mononeuropathies( DM,HTN)
 Giant cell arteritis
 CNS infarction or haemorrhage
 Tumours
GENDER
 FEMALE- thyroid eye disease, multiple sclerosis, giant
cell arteritis, myosthenia
 MALE- cranial nerve mononeuropathy
When and how did the double vision started?
 Sudden Ocular motor palsy, neurologic, trauma

60.  Is the diplopia constant, intermittent or variable?
 Intermittent
 Decompensating phorias and vergence problems,
ocular myasthenia,
 multiple sclerosis,
 internuclear ophthalmoplegia,
 superior oblique myokymia,
 transient ischemia involving the vertebrobasilar
system, ischemia of extra-ocular muscles (as in
temporal arteritis)

61. Is it constant in all gazes or more in a particular gaze
(comitant vs incomitant)?
 Yes Restriction/weakness of one or more extra-
ocular muscles
 No Decompensated deviation or phoria
Is it more for far or near fixation?
 Worse at distance Esotropia, lateral rectus
muscle problem (as in sixth nerve palsy)
 Worse at near Convergence insufficiency, medial
rectus muscles problem

62. Whether the images are horizontally, vertically or
obliquely separated?
 Horizontal diplopia  Impaired neural control or
function of medial or lateral rectus muscles, sixth
nerve, or both
 Vertical diplopia Weakness of inferior oblique and
superior rectus muscles, Weakness of superior oblique
and inferior rectus muscles. Fourth nerve palsy
 Oblique diplopia  Weakness of superior oblique or
inferior oblique. Vertical recti weakness. Third nerve
palsy cause.
 Orbital processes (e.g. orbital pseudotumour, orbital
cellulitis, fractures) can cause horizontal, vertical, or
oblique diplopia

63. Whether diplopia worsens at the end of the day?
 fatigability/ variability Yes Myasthenia gravis
 History of orbital trauma, eye surgery, or evidence
of orbital pathology such as enophthalmos or
proptosis. restrictive pathology
 Trauma  paralytic

64. ASSOCIATIONS
 Intermittent lid droopiness (worsens later in the
day) Myasthenia gravis
 Mild ipsilateral eye pain (subsides within a week)
Ischemic ocular motor cranial neuropathy
 Severe pain Temporal arteritis, subarachnoid
haemorrhages

65.  Painful third nerve palsy Aneurysms, Diabetes,
Hypertension, hyperlipidemia Ischemic ocular motor cranial
neuropathy
 Vertigo, speech difficulty Vertebrobasilar ischemia
 Lid, pupil, or eye movement involvement Horner’s
syndrome (ptosis with small pupil), third nerve palsy
(ptosiswith big pupil), inflammatory disease (e.g. Guillain–
Barré or Miller Fisher variant

66. PAST HISTORY
 History of any trauma to eye, face, head or any
history of ocular surgery recent or in past.
 Detailed history of systemic diseases like diabetes
mellitus, hypertension, thyroid disorders,
myasthenia gravis should be taken.

67. EXAMINATION
Abnormal head posture-
 The patient prefers a head posture in which the
ocular deviation is least and the images can be
fused.
(a) Chin elevation or depression (vertical)
(b) Face turn to right or left side (horizontal)
(c) Head tilt to right or left shoulder (torsional)

68. ORBITAL AND LID ABNORMALITIES
 Proptosis,
 Ptosis,
 Periorbital swelling,
 Ocular trauma,
 Lid retraction,
 Lid lag or other signs of thyroid associated
ophthalmopathy.
 Pupillary reactions ( esp.third nerve palsies )

69.  Abnormal ocular posture -
 Esotropia
 Exotropia
 Hypertropia or hypotropia
hirschberg test

70. PRISM BAR COVER TEST
 Measurement of angle of deviation to quantify the
amount of deviation in different gazes should be
done.
 done in all 9 positions of gaze with each eye fixing
and both for distance and near.

71. MADDOX ROD TEST
 This gives a
quantitative
information about
the degree and type
of ocular
misalignment.
 This test dissociates
the eyes, patients
with phoria may
report misalignment
of the visual axes.

72. DOUBLE MADDOX ROD TEST
 Maddox rods with
same orientation in
front of each eye
(vertically oriented
to produce a
horizontal streak)
can be used to
assess torsional
misalignment when
vertical diplopia is
present.

73.  Extraocular muscle movements – Ocular
movements ductions ,versions and vergences
should be checked in all nine positions of gazes.
 “Floating saccades” are suggestive of a nerve
palsy or paresis
 Normal saccadic velocity with limitation indicates a
restricted muscle

74. PARETIC VS RESTRICTIVE ETIOLOGY
 Forced Duction Test (FDT) – A forced duction test
helps to differentiate paretic from restrictive cause.
 Active Force Generation Test (AFGT)
 Differential IOP- Ocular movement restriction from
thyroid eye disease can also be judged by
measuring intraocular pressure in primary position
and in eccentric gaze.

75. DIPLOPIA CHARTING
 This test helps in recording the subjective deviation
by asking the patient to quantify the separation
between the double images , dissociated by red
green glasses.
 done in all 9 positions of gaze and both for distance
and near.
 Main points to be noted are:
 Distance of separation between images
 Position where maximum separation is present.
 See image from which eye is more deviated.
 Crossed or uncrossed/ higher or lower
 Tilted images.

76. LEFT LR

77. LEFT SR

78. LEFT MR

79. LEFT IO

80. LEFT IR

81. LEFT SO

82. RESTRICTIVE PATHOLOGY- ORBITAL
FLOOR FRACTURE

83. HESS CHARTING
 It is a subjective test of ocular deviation.
 Quantitative measurement of actions of extraocular
muscles
 Based on principle of haploscopy- presence of
NRC, two objects presented to two eyes will be
superimposed if they stimulate foveae of two eyes.
Prerequisites
 Good vision in both eyes
 Central fixation
 Normal retinal correspondence.

84. RIGHT LR

85. LEFT SO

86. THIRD NERVE PALSY

88. INVESTIGATIONS
 Blood sugar levels / HbA1C for Diabetes Mellitus
 Test for myasthenia gravis – electromyography
(EMG), nerve conduction studies with a repetitive
stimulation test and anti - acetylcholine receptor
antibodies
 T3, T4, TSH for thyroid eye disease
 CT scan / MRI of brain and orbit for thyroid eye
disease, any intracranial or orbital pathology.

90. TREATMENT
 Treat the underlying cause, wherever possible.
 Unilateral eye occlusion therapy with either an eye patch
or by blurring one lens of the patient’s glasses with
semi-opaque surgical tape.
 Prisms are used for optical correction of symptomatic
binocular diplopia. Fresnel prisms can be incorporated
on to the patient’s existing glasses
 Injection botulinum into the antagonist muscle during the
first three months appreciate fusion in primary gaze
without necessity for head turn, Prevents contracture of
antagonist muscle.
 Surgery for strabismus can be done to restore ocular
alignment after a period of observation for atleast 6
months.

92. REFERENCES
 American academy of ophthalmology.
 Duke Elder textbbok of ophthalmology
 A. k Khurana. Theory and practice of squint and
orthoptics.