DOUBLE VISION / DIPLOPIA

Dr. R. Handoko Pratomo, SpM

First Muscle Operations

1838 Stromeyer, an Orthopedic surgeon on a
cadaver Hanover, Germany
1839 J.F. Diffenbach in Berlin, by 1842 had
done 1,200 strabismus operations, which
consisted of tenotomy of the medial rectus
muscle

Double Vision=/=Diplopia
Diplopia = Seeing one object as two. Must
rule out Vertigo, Syncope, Hysteria, etc.
Double the Time
Double the Effort
Double the Cost
Double the reward

Questions to Ask

Does the DV go away by covering one eye

Abnormal head posture seen in old photos
Pain, facial numbness, circulatory issues
Eyelid malposition and endocrine disease
Fatigability, dysarthria, dysphagia, SOB
FH, Meds, MH, SH, smoking, ETOH, etc
Compliance and socioeconomic
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Work-up Diplopia

History, History, Histroy

Old Records and Studies
Compare Measurements
Impression(s)
Plan: Short and Long Term
Communication

Tools of the Trade

Patience, Efficiency and Insight

Lensometer readings
Best Corrected Vision, Pinhole
Stereopsis
Prism Bars, Occluder, Pupil Light
Clip-ons, Trial Set, Cycloplegia

Basic Review

Anatomy
Eye Movements
Binocular Vision
Strabismus
Motor Evaluation
Sensory Evaluation

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SENSORY
Simultaneous perception- brains ability to perceive
images from OU at same time
Suppression-brain shuts off information
Fusion- cortical integration of separate retinal
images into single sensory perception
Stereopsis- to perceive the relative distance of
objects

Tests for stereopsis

Titmus

Polaroid spectacles
Figures seen in 3-D

TNO random dot test

Red-green spectacles
Hidden shapes seen

Lang

Frisby

No spectacles
Hidden circle seen

No spectacles
Shapes seen

Tests for sensory anomalies

Worth four-dot test

a - Prior to use of glasses

b - Normal or ARC
c - Left suppression
d - Right suppression
e - Diplopia

Bagolini striated glasses

a - Normal or ARC
b- Diplopia
c - Suppression
d - Small suppression scotoma

Synoptophore

Grading of binocular vision

Detection of suppression and ARC
Measurement of angle
Measurement of fusional amplitudes

Hirschberg test
Rough measure of deviation
Note location of corneal light reflex
1 mm = 7 or 15

Reflex at border of pupil = 15

Reflex at limbus = 75

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Motility tests

Tests versions and ductions

Grades under/overaction

Left inferior oblique overaction

Left lateral rectus underaction

Cover tests

Cover test detects heterotropia

Uncover test detects heterophoria

Prism cover test measures tropia

Alternate measures total tropia and phoria

Alternate cover test detects total deviation

Amblyopia

Strabismus
Anisometropic (sph or cyl) > 1.5 D
Deprivation (media opacity >1 mm in size
or ptosis < 1 mm margin reflex distance)
Cost Effectiveness Tx gain from $2053 to
$2509 ($/ QALY) <20K especially good
www:aao.org/ppp cost-utility analysis

The Pediatric Eye Disease

Investigator Group (PEDIG)

Randomized multicenter clinical study

Patching regimens part vs full time
2 hr/day for moderate cases(20/40-80)
Atropine 1% vs patching(6hr/day) ages 3- 7
24% recurrence < 8 years age within one year
cessation either method
27% improvement age 3-7 anisometropia Rx
50% >2 lines age 7 to 12 either method, age 13
-17 47% benefit no prior vs 16% prior Tx
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Types of Turns

ESODEVIATION
EXODEVIATION
A and V Patterns
Cyclovertical

Monocular Diplopia

Signs of chalazion (meibomian cyst)

Painless, roundish, firm lesion

within tarsal plate

May rupture through conjunctiva

and cause granuloma

Morphological classification of keratoconus

Nipple cone

Oval cone

Small and steep curvature

Larger and ellipsoidal

Globus cone

Largest

Progressive iris atrophy

Progressive stromal iris atrophy

Broad-based PAS

Displacement of pupil
towards PAS

Isolated familial ectopia lentis

Autosomal recessive

Pupil may be normal

Pupil may be displaced in opposite

direction (ectopia lentis et pupillae)

Classification according to maturity

Immature

Hypermature

Mature

Morgagnian

Implant displacement
Decentration

May occur if one haptic is inserted

into sulcus and other into bag
Remove and replace if severe

Optic capture

Reposition may be necessary

Binocular Diplopia

No Misalignment

INCOMITANT

Mechanical (Restrictive)
Diplopia

Graves Ophthalmopathy
Browns Syndrome
Orbital Pseudotumor
Ocular Myositis
Orbital Mass Lesions
Orbital Trauma

Signs of eyelid retraction

Occurs in about 50%

Bilateral lid retraction

No associated proptosis

Bilateral lid retraction

Bilateral proptosis

Unilateral lid retraction

Unilateral proptosis

Lid lag in downgaze

Restrictive myopathy
Occurs in about 40%
Due to fibrotic contracture

Elevation defect - most common

Depression defect - uncommon

Abduction defect - less common

Adduction defect - rare

Optic neuropathy
Occurs in about 5%
Early defective colour vision
Usually normal disc appearance

Caused by optic nerve compression

at
orbital apex by enlarged recti

Often occurs in absence of significant

proptosis

Brown syndrome (right)

Normal elevation in
abduction

Straight in primary position

Limited elevation in
adduction

Idiopathic orbital inflammatory disease (IOID)

Non-neoplastic, non-infectious orbital lesion (pseudotumour)

Involves any or all soft-tissue components

Presentation - 20 to 50 years with abrupt painful onset

Usually unilateral
Periorbital swelling and chemosis
Proptosis
Ophthalmoplegia

Clinical course and treatment of IOID

1. Early spontaneous remission without sequelae
Treatment - nil

2. Prolonged intermittent activity with eventual remission

Treatment options - steroids, radiotherapy or cytotoxics

3. Severe prolonged activity causing a frozen orbit

Left involvement resulting in ophthalmoplegia and ptosis

Orbital myositis

Subtype of IOID
Involvement of one or more extraocular muscles
Clinical course is usually short - treat with NSAIDs
Presentation - sudden onset of pain on ocular movement

Underaction of left lateral rectus

Worsening of pain on attempted left gaze

CT shows fusiform enlargement

of left lateral rectus

Cavernous haemangioma
Most common benign orbital tumour in adults
Usually located just behind globe
Female preponderance - 70%
Presents - 4th to 5th decade

Slowly progressive axial proptosis

May cause choroidal folds

Treatment - surgical excision

Pleomorphic Lacrimal Gland Adenoma

Presents - 4th to 5th decade

Painless and very slow- Posterior extension may Smooth, encapsulated

growing, smooth mass in cause proptosis and
outline
Excavation of lacrimal gland
ophthalmoplegia
lacrimal fossa
Inferonasal globe
fossa without destruction
displacement

Lacrimal gland carcinoma

Presents - 4th to 6th decades
Very poor prognosis

Posterior extension may cause proptosis,

ophthalmoplegia and episcleral
congestion
Trigeminal hypoaesthesia in 25%

Painful, fast-growing mass in

lacrimal fossa
Infero-nasal globe displacement

Management

Biopsy
Radical surgery and radiotherapy

Optic nerve glioma

Typically affects young girls
Associated neurofibromatosis -1 is common
Presents - end of first decade with gradual visual loss

Gradually progressive proptosis

Optic atrophy

Treatment
Observation - no growth, good vision and good cosmesis
Excision - poor vision and poor cosmesis
Radiotherapy - intracranial extension

Sphenoidal ridge meningioma

Presents with gradual visual loss and reactive hyperostosis

Proptosis

Fullness in temporal fossa Hyperostosis on plain x-ray

Lymphoma
Presents - 6th to 8th decades

Affects any part of orbit and Anterior lesions are rubbery May be confined to
may be bilateral
on palpitation
lacrimal glands

Treatment

Radiotherapy - localized lesions

Chemotherapy - disseminated disease

Direct carotid-cavernous fistula

Defect in intracavernous part of internal carotid

Rapid flow shunt
Causes
Head trauma - most common
Spontaneous rupture - in hypertensive females

Ptosis, chemosis and conjunctival injection

Ophthalmoplegia
Raised intraocular pressure

Direct carotid-cavernous fistula

Pulsatile proptosis with bruit Retinal venous congestion and haemorrhages

and thrill
Abolished by ipsilateral
carotid compression

Indirect
carotid-cavernous fistula (dural shunt)
Indirect communication between meningeal branches of internal
or external carotids and cavernous sinus
Slow flow shunt
Causes
Congenital malformations
Spontaneous rupture

Dilated episcleral vessels

Raised intraocular pressure with
wide pulsation

Occasional ophthalmoplegia
and mild proptosis

Incomitant Misalignment

Tensilon Test
Tensilon (Edrophonium HCL) 10 mg/ml fast
acting anti-cholinesterase
Neostigmine (Prostigmin) IM (0.02mg/kg)
alternative
Have injectable Atropine Sulfate ready

Ophthalmic Signs of Myasthenia

Gravis

Ptosis
EOM Palsies
Pseudogaze Palsies
Pseudointernuclear Ophthalmoplegia
Pseudoconvergence Paresis
Lid Twitch
Quiver Movements
Orbicularis Weakness
Nystagmus

Myasthenia Gravis
1. Clinical features

Uncommon, typically affects young women

Weakness and fatiguability of voluntary musculature
Types: Neonatal, Congenital, Ocular, System

2. Investigations
ICE Test
Tensilon test (edrophonium) or Prostigmine
Antibodies to acetylcholine receptors 3 types, MuSK
(muscle-specific receptor tyrosine kinase)
CT or MRI for presence of thymoma

3. Treatment options

Medical - AChE inhibitor, steroids, immunomodulators

Thymectomy, prisms, strabismus surgery

Ocular myasthenia
Ptosis

Insidious, bilateral but asymmetrical

Worse with fatigue and in upgaze
Ptotic lid may show twitch and
hop signs

Diplopia

Intermittent and usually vertical

Edrophonium test
Before injection

Positive result

Measure amount of ptosis or

diplopia before injection

Inject i.v. atropine 0.3 mg

Inject i.v. test dose of edrophonium

(0.2 ml-2 mg)
Inject remaining (0.8 ml-8 mg) if no
hypersensitivity

Cranial Neuropathy

Oculomotor (3rd) Cranial Nerve

Trochlear (4th) Cranial Nerve
Abducen (6th) Cranial Nerve
Adult, Child, TITS

Anatomy of third nerve

Oculomotor nucleus
Pituitary gland
Red nucleus

Carotid artery

Cavernous sinus

Pons

III nerve
Post cerebral artery

Clivus

Basilar artery

Applied anatomy of pupillomotor nerve fibres

Blood vessels on pia mater supply surface
of the nerve including pupillary
fibres ( damaged by
compressive lesions )

Vasa nervorum supply part

of nerve but not pupillary
fibres ( damaged by medical
lesions )
Pupillary fibres lie dorsal and peripheral

Signs of right third nerve palsy

Ptosis, mydriasis and cycloplegia Normal abduction

Abduction in primary position

Limited adduction

Intorsion on attempted
downgaze

Limited elevation

Limited depression

Important causes of isolated third nerve palsy

Idiopathic - about 25%
Vascular disease - hypertension, diabetes
Trauma
Posterior communicating aneurysm
Extradural
haematoma

Aneurysm
Chiasm

Midbrain
pushed
across
Edge of
tentorium

Prolapsing
temporal
lobe

Third nerve

Posterior cerebral
artery

Anatomy of fourth nerve

Internal carotid artery
Postr. communicating
artery
III
VI
Postr.cerebral artery
Supr.cerebellar artery
Basilar artery
IV

Only cranial nerve to emerge dorsally

Crossed cranial nerve
Very long and slender

Signs of right fourth nerve palsy

Right hyperdeviation in primary

position when left eye fixating
Excyclotorsion

Right underaction on depression

in adduction
Vertical diplopia

Right overaction on left gaze

Positive Bielschowsky test in right fourth nerve pal

Increase in right
hyperdeviation on ipsilateral
head tilt

Absence of right
hyperdeviation on
contralateral head tilt

Anatomy of sixth nerve

Basilar artery
Medial
lemniscus

Pituitary gland
Carotid artery

4th ventricle

Cavernous sinus

Petroclinoid
ligament
Vestibular
nucleus

Clivus
Pyramidal tract

VI nerve

Old right sixth nerve palsy

Straight in primary position due to partial

recovery

Limitation of right abduction and

horizontal diplopia

Normal right adduction

Important causes of isolated sixth nerve palsy

Vascular - hypertension, diabetes
Raised intracranial pressure
Acoustic neuroma
Dilated
ventricles

Petrous
tip

Brainstem pushed downwards

SUPRANUCLEAR DISORDERS OF
EYE MOVEMENT
1. Horizontal gaze palsies
Internuclear ophthalmoplegia
Combined internuclear and PPRF
(one-and-a-half syndrome)
MLF

2. Vertical gaze palsies

Parinaud dorsal midbrain syndrome
Progressive supranuclear palsy

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Internuclear ophthalmoplegia
Lesion involving left MLF

Defective left adduction and ataxic

nystagmus of right eye

Normal left gaze

Convergence intact if lesion discrete

Important causes

Demylination - usually bilateral

Vascular disease
Tumours of brainstem

One-and-a-half syndrome
Combined lesion of left MLF and PPRF

Paralytic Pontine Exotropia

Ipsilateral (left) gaze palsy

Defective left adduction

Normal right abduction with ataxic
nystagmus

Parinaud dorsal midbrain syndrome

Supranuclear upgaze palsy

Large pupils with light-near dissociation Convergence weakness

Lid retracton (Collier sign)

Normal downgaze
Convergence-retraction nystagmus

Important causes

In children: aqueduct stenosis, meningitis and pinealoma

In young adults: demylination, trauma and a-v malformations
In elderly: vascular accidents and posterior fossa aneurysms

Progressive supranuclear palsy

( Steele-Richardson-Olszewski syndrome )
Affects elderly

Pseudobulbar palsy

Extrapyramidal rigidity

Gait ataxia

Dementia

Initially involves downgaze

Subsequent defective up and

horizontal gaze

Medial wall blow-out fracture

Signs

Periorbital subcutaneous emphysema

Ophthalmoplegia - adduction and abduction

if medial rectus muscle is entrapped

Treatment
Release of entrapped tissue
Repair of bony defect

COMITANT

Review History
Decompensated Phoria
Accomodative Esotropia
Acute Esotropia of Childhood
Vergence Paresis
Skew Deviation
Foveal Displacement Syndrome
Central Disruption of Fusion

Decompensated Phoria
latent ocular misalignment due to lose of
single binocular fusion
associated with febrile illness, head trauma,
changing refractive needs, asthenopia
presence of adaptive head posture and large
fusional amplitudes

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Refractive accommodative esotropia

Presents between 18 months - 3years

Initially intermittent
Normal AC/A ratio
Excessive hypermetropia

Fully accommodative

Partially accommodative

Esotropia greater for near

Straight for distance

Straight for distance and near

Esotropia for near

Non-refractive accommodative esotropia

Presents between 18 months to 3years

High AC/A ratio
- due to increased AC (convergence excess)
- due to decreased A (hypoaccommodative)
No significant refractive error
Signs

Straight for distance

Esotropia for near

Recent right sixth nerve palsy

Right esotropia in primary position due to

unopposed action of right medial rectus

Marked limitation of right abduction due to

right lateral rectus weakness

Skew Deviation
vertical misalignment of visual axes due to
imbalance of prenuclear inputs
vertical diplobia cannot be isolated to a
single EOM(s)
Hypertropia varies with gaze associated with
downbeat nystagmus
brainstem and cerebellar disease, MS, INO,
increased ICP
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Assessment after photocoagulation

Poor involution

Good involution

Persistent neovascularization

Regression of neovascularization

Haemorrhage

Re-treatment required

Residual ghost vessels or

fibrous tissue
Disc pallor

Choroidal neovascularization (CNV)

Less common than atrophic AMD but more serious

Metamorphopsia is initial symptom
Most lesions are not visible clinically

Suspicious clinical signs

Pinkish-yellow subretinal lesion

with fluid

Subretinal blood or lipid

Idiopathic premacular fibrosis

Macular pucker

Cellophane maculopathy

Translucent epiretinal
membrane
Fine retinal striae and mild
vascular distortion

Severe retinal wrinkling and

vascular distortion
Pucker emanating from
epicenter

Opaque epiretinal membrane

May be associated with
macular pseudo-hole

Recession

Resection

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Summary

What is patients real complaint ?

Disease process, work up, time frame
Trial of prisms
Is surgery an option?
Are other referrals or treatments necessary?
Communication between all parties
Evidence-Based Medicine

Evidence-based Medicine
the conscientious, judicious,explicit use of
the best available evidence from clinical
care research in making health care
decisions
Harvard Health Policy Review 2007: 8:145-155 Montori
and Guyatt: Corruption of the evidence as threat and
opportunity for evidence-based medicine
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VISION THERAPY
1) Orthoptic VT helpful for convergence
insufficiency and binocular function
2) Behavioral-Perception VT unproven for
visual processing and perception
3) Prevention or correction of Myopia
unproven
* Eye excercises do not treat learning
disabilities
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Learning Disabilities
15-20% of the population affected with
reading, math, foreign langauge problems,
organizing written and spoken language
reading disorder different from dyslexia
85% have dyslexia, whereby, loosing place
reading due to difficulty decoding letter(s) or
word combinations and/or lack of
comprehension, not because of a tracking
abnormality
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