diplopia

1. APPROACH TO DIPLOPIA
Dr Akhil Deshmukh

2. MUSCLES ACTIONS
•Primary Muscle Action is the main and most powerful
direction in which the eye moves when the muscle is
Contracted
• Secondary Muscle Action is the second direction in which
the eye moves when that muscle is contracted, but is not the
main or most important action
• Tertiary Muscle Action is the least powerful direction in
which the eye moves as a result of contraction of the muscle

3. MONOCULAR/
DUCTIONS
•1. Abduction
•2. Adduction
•3. Elevation
•4. Depression
•5. Intorsion
•6. Extorsion
BINOCULAR
•1. Versions
•2. Vergences

5. Version:
• Eye movements are paired, that is both eyes move in the
same direction simultaneously.
Vergence:
• Eyes move in the opposite directions simultaneously

9. 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

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

12. 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

13.  The eyes although aligned, send images of different
size to the brain which disallow fusion Aniseikonia

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

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

16.  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

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

18.  Cerebral polyopia is the perception of multiple
images due to pathologies in occipital cortex or
central visual pathway lesions.
-
-Cerebral infarction is the most common etiology,
although cerebral polyopia may also occur with
tumors, multiple sclerosis, encephalitis, seizures, and
migraine

19. 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

20. 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

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

22. ALPORT LOWES

25. BINOCULAR DIPLOPIA
 Image falls on the fovea of the fixating eye and
extra-foveal retina in the non-fixating eye. Both
images fall outside the area of single binocular
vision.
 The separation of both images is greatest when the
object is viewed in the direction of paretic muscle.

27. 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,diphtheria

28. 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.

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

30. COMITANT DEVIATIONS
It is a type of manifest squint in which the amount of
deviation in the squinting eye remains constant
(unaltered) in all the directions of gaze; and there is
no associated limitation of ocular movements.

31. INCOMITANT DEVIATION
It is most frequently acquired and usually causes
diplopia.
It is a type of heterotropia (manifest squint) in which the
amount of deviation varies in different directions
of gaze.
RESTRICTIVE
PARALYTIC

33. RESTRICTIVE PATHOLOGY
 The most common cause of restrictive
strabismus is Thyroid-associated orbitopathy.
• Post-Cataract Extraction Restriction
• Blowout fractures of the orbit
• Post pterygium excision
• Neoplasm of orbit
• Orbital myositis
RESTRICTIVE 1

34. 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.

35. SUPRANUCLEAR -SKEWDEVIATION
 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.

40. 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,

41. 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)

43. DORSAL MIDBRAIN SYNDROME/PARINAUD’S
 Upgaze palsy/skew deviation
 Light near dissociation
 Convergence retraction nystagmus
 Lid retarction( Colliers sign)
 Sunsetting sign.

44. 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.

46. 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}.
Ataxic nystagmus.
Associated skew deviation

48.  These patients may report horizontal diplopia due to
adduction limitation ,but report vertical diplopia due to
an associated skew deviation.
 Bilateral lNO lesion near the third nerve nuclei (ie, the
"wall-eyed" bilateral INO, or WEBINO, syndrome)
exotropia
 The two most common causes of INO are demyelination
and stroke.

49. NUCLEAR AND FASCICULAR
INVOLVEMENT
 Third nerve nucleus
 bilateral ptosis and superior rectus muscles
involvement
 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.

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

51. THIRD NERVE PALSY

52. 6TH CRANIAL NERVE NUCLEUS
 A selective lesion of
the sixth nerve
nucleus causes a
horizontal gaze palsy
FOVILLE
MILLARD
GUBLER

54. 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 .

56. PONTINE LESIONS
 FOVILLE SYNDROME -
 MILLARD-GUBLER SYNDROME
 RAYMOND SYNDROME

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

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

59. 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

60. SUPERIOR ORBITAL FISSURE
SYNDROME
 Trauma to 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.

61. 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.

62. GIANT CELLARTERITIS
 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

63. HISTORY
AGE-
Children - transient Ophthalmoplegia following viral
infection or vaccination.
Ophthalmoplegic migraine,
Accomodation insuffiency,
Adults –
Thyroid ophthalmopathy,
Cranial nerve palsy due to aneurysms,
Divergence or convergence insuffiency,
Multiple sclerosis- internuclear opthalmoplegia,CN palsies

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

65.  Is the diplopia constant, intermittent or variable?
 Intermittent
 PHORIAS, ocular myasthenia,
 multiple sclerosis,
 superior oblique myokymia,
 transient ischemia involving the vertebrobasilar
system, ischemia of extra-ocular muscles (as in
temporal arteritis)

66. Is it constant in all gazes or more in a particular gaze
(comitant vs incomitant)?
 Yes COMITANT
 No INCOMITANT
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 EXOTROPIA

67. 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

68. 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

69. Is the diplopia relieved by
covering either eye?

70. •Are the images separated
horizontally,vertically, or
obliquely?

71. •Is the distance between
images constant despite the
direction of gaze, or does it
vary?

72. •Is the diplopia worse for
near vision or for distance?

73. • Is one image tilted?
• Do the eyelids droop?

74. • Is the diplopia inluenced by
head posture?

75. •Are there associated
symptoms such as
headache, dizziness,
vertigo, or weakness?

76. Whether diplopia worsens at
the end of the day?

77. Lateral rectus muscle weakness causes
diplopia that is worse at distance and
worse on looking to the side
of the weak muscle.

78. superior oblique weakness causes
diplopia that is worse on looking
downward to the side opposite the weak
muscle and causes difficulty with tasks
such as reading, watching television in
bed, descending steps, and walking on
uneven ground.

79. Medial rectus muscle weakness
causes diplopia that is worse for near
than for distance vision and is worse to
the contralateral side

80. 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.

81. 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)

82. 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 )

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

84. 1.Cover uncover test

85. 2.Cross-cover test

86. 3.MADDOX ROD
TEST
 .

87. 4. Red glass test
the patient views a penlight while a
red filter or glass is placed, by
convention, over the right eye.
This allows easier identification of each
image; the right eye views a red light
and the left a white light

94. 5.Hirschberg corneal
reflex test
-Penlight held approximately 30 cm from the
patient’s eyes.
-1 mm of decentration is equal to 7 degrees of
ocular deviation.
-One degree is equal to approximately 2
prism diopters.

96. 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.

97. 6.Forced Duction Test
(FDT)

98. 7. Double Maddox Rod test
 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.

99. LEFT LR

100. 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.

102. TREATMENT
• Treat the underlying cause, wherever possible.
• Patching (occlusive) therapy is used mainly to
eliminate one image during the acute phase of
diplopia. In children younger than age 6, each eye
should be patched alternately to prevent
developmental amblyopia..

103.  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.

105. THANK YOU