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DOUBLE VISION, ACQUIRED, and
CONGENITAL STRABISMUSRobert Cordero, M.D., F.A.C.S
Central Florida Eye Specialists, P.L.
October 30, 2010
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• www.theeyespecialists.com• www.aapos• www.aao• Google
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New, Updated, Revised, Better• potions, purification, diet, lancets
• Hammurabi’s Code 1800 B.C.
• Egyptian Papyrus 1600 - 1300 B.C.
• Susruta father of Hindu surgery
• Hebrew Talmud 1300 B.C.- 70 A.D.
• Greece, Alexandria, and Rome
• Middle Ages (395-1492) and Renaissance 14-16th century
Georg Bartisch (1535-1606)
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Chevalier John Taylor 1739
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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
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Eye Massager 1890
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
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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
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 stereopsisTitmus
• Red-green spectacles
TNO random dot test
• ‘Hidden’ shapes seen • Polaroid spectacles• Figures seen in 3-D
Lang
• No spectacles
Frisby
• ‘Hidden’ circle seen
• No spectacles• Shapes seen
Tests for sensory anomaliesWorth four-dot test
a - Prior to use of glassesb - Normal or ARCc - Left suppression
Bagolini striated glasses
a - Normal or ARCb- Diplopiac - Suppression
d - Right suppressione - Diplopia
d - Small suppression scotoma
Synoptophore
• Measurement of fusional amplitudes
• Detection of suppression and ARC• Measurement of angle
• Grading of binocular vision
Hirschberg test• Rough measure of deviation
• Note location of corneal light reflex
Reflex at border of pupil = 15 Reflex at limbus = 75
• 1 mm = 7 or 15
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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 • Prism cover test measures tropia• Alternate measures total tropia and phoria
• Alternate cover test detects total deviation
• Uncover test detects heterophoria
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
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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
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 Globus cone
Small and steep curvature Larger and ellipsoidal Largest
Progressive iris atrophy
Progressive stromal iris atrophy
Broad-based PAS Displacement of pupil towards PAS
Isolated familial ectopia lentisAutosomal recessive
Pupil may be normal Pupil may be displaced in opposite direction (ectopia lentis et pupillae)
Classification according to maturity
Immature Mature
Hypermature Morgagnian
Implant displacementDecentration
• May occur if one haptic is inserted into sulcus and other into bag
• Reposition may be necessary
• Remove and replace if severe
Optic capture
Binocular Diplopia
No Misalignment
INCOMITANT
Mechanical (Restrictive) Diplopia
• Grave’s Ophthalmopathy
• Brown’s 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
• Lid lag in downgaze • Unilateral lid retraction • Unilateral proptosis
• Occurs in about 40% • Due to fibrotic contracture
Restrictive myopathy
Elevation defect - most common Abduction defect - less common
Depression defect - uncommon 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)
• Usually unilateral• Periorbital swelling and chemosis• Proptosis• Ophthalmoplegia
• Non-neoplastic, non-infectious orbital lesion (pseudotumour)• Involves any or all soft-tissue components
• Presentation - 20 to 50 years with abrupt painful onset
Clinical course and treatment of IOID1. Early spontaneous remission without sequelae
2. Prolonged intermittent activity with eventual remission
Treatment - nil
3. Severe prolonged activity causing a ‘frozen orbit’
Treatment options - steroids, radiotherapy or cytotoxics
Left involvement resulting in ophthalmoplegia and ptosis
Orbital myositis
• Underaction of left lateral rectus
• Clinical course is usually short - treat with NSAIDs
• Subtype of IOID• Involvement of one or more extraocular muscles
• Presentation - sudden onset of pain on ocular movement
• Worsening of pain on attempted left gaze
• CT shows fusiform enlargement of left lateral rectus
Cavernous haemangioma
• Presents - 4th to 5th decade
Slowly progressive axial proptosis
• Most common benign orbital tumour in adults• Usually located just behind globe• Female preponderance - 70%
May cause choroidal folds
Treatment - surgical excision
Pleomorphic Lacrimal Gland Adenoma
• Painless and very slow- growing, smooth mass in lacrimal fossa• Inferonasal globe displacement
• Posterior extension may cause proptosis and ophthalmoplegia
• Smooth, encapsulated outline• Excavation of lacrimal gland fossa without destruction
Presents - 4th to 5th decade
Lacrimal gland carcinoma
• Biopsy
• Painful, fast-growing mass in lacrimal fossa• Infero-nasal globe displacement
• Posterior extension may cause proptosis, ophthalmoplegia and episcleral congestion• Trigeminal hypoaesthesia in 25%
Management
• Radical surgery and radiotherapy
• Presents - 4th to 6th decades• Very poor prognosis
Optic nerve glioma
• Presents - end of first decade with gradual visual loss
• Observation - no growth, good vision and good cosmesis• Excision - poor vision and poor cosmesis• Radiotherapy - intracranial extension
• Typically affects young girls• Associated neurofibromatosis -1 is common
Gradually progressive proptosis Optic atrophy
Treatment
Sphenoidal ridge meningioma
Presents with gradual visual loss and reactive hyperostosis
Fullness in temporal fossa Hyperostosis on plain x-rayProptosis
LymphomaPresents - 6th to 8th decades
Affects any part of orbit and may be bilateral
Anterior lesions are rubbery on palpitation
Treatment
May be confined to lacrimal glands
• Radiotherapy - localized lesions• Chemotherapy - disseminated disease
Direct carotid-cavernous fistula
• Head trauma - most common• Spontaneous rupture - in hypertensive females
Causes
• Ptosis, chemosis and conjunctival injection• Ophthalmoplegia• Raised intraocular pressure
• Defect in intracavernous part of internal carotid• Rapid flow shunt
Direct carotid-cavernous fistula
• Pulsatile proptosis with bruit and thrill• Abolished by ipsilateral carotid compression
• Retinal venous congestion and haemorrhages
• Dilated episcleral vessels• Raised intraocular pressure with wide pulsation
Causes
• Occasional ophthalmoplegia and mild proptosis
Indirect carotid-cavernous fistula (dural shunt)• Indirect communication between meningeal branches of internal or external carotids and cavernous sinus• Slow flow shunt
• Congenital malformations• Spontaneous rupture
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
• Uncommon, typically affects young women1. Clinical features
•ICE Test•Tensilon test (edrophonium) or Prostigmine
2. Investigations
• Medical - AChE inhibitor, steroids, immunomodulators3. Treatment options
• Weakness and fatiguability of voluntary musculature• Types: Neonatal, Congenital, Ocular, System
• Antibodies to acetylcholine receptors 3 types, MuSK (muscle-specific receptor tyrosine kinase)• CT or MRI for presence of thymoma
• Thymectomy, prisms, strabismus surgery
Ocular myasthenia
• Insidious, bilateral but asymmetrical• Worse with fatigue and in upgaze
Ptosis
• Ptotic lid may show ‘twitch’ and ‘hop’ signs
• Intermittent and usually vertical
Diplopia
Edrophonium test
• 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
Before injection Positive result
Cranial Neuropathy
• Oculomotor (3rd) Cranial Nerve
• Trochlear (4th) Cranial Nerve
• Abducen (6th) Cranial Nerve
• Adult, Child, TITS
Anatomy of third nerveOculomotor nucleus
Pituitary gland
Carotid artery
Cavernous sinus
III nerveClivus
Basilar artery
Post cerebral artery
Red nucleus
Pons
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 partof nerve but not pupillaryfibres ( damaged by medicallesions )
Pupillary fibres lie dorsal and peripheral
Signs of right third nerve palsy
• Ptosis, mydriasis and cycloplegia• Abduction in primary position
• Limited depression • Limited adduction
• Normal abduction
• Limited elevation
• Intorsion on attempted downgaze
Important causes of isolated third nerve palsy
Idiopathic - about 25%
Vascular disease - hypertension, diabetesPosterior communicating aneurysmTrauma
Extraduralhaematoma
Prolapsingtemporallobe
Edge oftentorium
Aneurysm
Chiasm
Third nerve
Posterior cerebralartery
Midbrainpushedacross
Anatomy of fourth nerve
• Only cranial nerve to emerge dorsally• Crossed cranial nerve• Very long and slender
Internal carotid artery
Postr. communicating artery
IIIVI
Postr.cerebral arterySupr.cerebellar artery
Basilar arteryIV
Signs of right fourth nerve palsy
• Right overaction on left gaze
• Right underaction on depression in adduction • Vertical diplopia
• Right hyperdeviation in primary position when left eye fixating• Excyclotorsion
Positive Bielschowsky test in right fourth nerve palsy
Absence of right hyperdeviation on contralateral head tilt
Increase in right hyperdeviation on ipsilateral head tilt
Anatomy of sixth nerve
Basilar artery
Pituitary gland
Carotid artery
Cavernous sinus
VI nerve
Petroclinoidligament
Clivus
Pyramidal tract
Vestibularnucleus
Mediallemniscus
4th ventricle
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 palsyVascular - hypertension, diabetes
Acoustic neuromaRaised intracranial pressure
Dilated ventricles
Petroustip
Brainstem pushed downwards
SUPRANUCLEAR DISORDERS OF EYE MOVEMENT
1. Horizontal gaze palsies
2. Vertical gaze palsies
• Internuclear ophthalmoplegia• Combined internuclear and PPRF (‘one-and-a-half syndrome’)
• Parinaud dorsal midbrain syndrome• Progressive supranuclear palsy
MLF
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Internuclear ophthalmoplegia
• Demylination - usually bilateral • Vascular disease
Important causes
• Tumours of brainstem
Defective left adduction and ataxic nystagmus of right eye
Normal left gaze
Convergence intact if lesion discrete
Lesion involving left MLF
‘One-and-a-half syndrome ’
Paralytic Pontine Exotropia
• Ipsilateral (left) gaze palsy • Defective left adduction• Normal right abduction with ataxic nystagmus
Combined lesion of left MLF and PPRF
Parinaud dorsal midbrain syndrome
• In young adults: demylination, trauma and a-v malformations
• In children: aqueduct stenosis, meningitis and pinealoma
• Supranuclear upgaze palsy
• Large pupils with light-near dissociation
• Lid retracton (Collier sign)
Important causes
• Normal downgaze
• Convergence weakness
• Convergence-retraction nystagmus
• In elderly: vascular accidents and posterior fossa aneurysms
Progressive supranuclear palsy
• Affects elderly
Initially involves downgaze
Subsequent defective up and horizontal gaze
• Pseudobulbar palsy
• Extrapyramidal rigidity
( Steele-Richardson-Olszewski syndrome )
• Gait ataxia
• Dementia
Medial wall blow-out fracture
Signs
• Release of entrapped tissue• Repair of bony defect
Periorbital subcutaneous emphysema Ophthalmoplegia - adduction and abduction if medial rectus muscle is entrapped
Treatment
COMITANT
• Review History
• Decompensated Phoria
• Accomodative Esotropia
• Acute Esotropia of Childhood
• Vergence Paresis
• Skew Deviation
• Foveal Displacement Syndrome
• Central Disruption of Fusion
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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
Refractive accommodative esotropia
Fully accommodative
• Normal AC/A ratio• Excessive hypermetropia
Straight for distance and near
Partially accommodative
Esotropia for near
• Presents between 18 months - 3years• Initially intermittent
Esotropia greater for near Straight for distance
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
Esotropia for near Straight for distance
Signs
Recent right sixth nerve palsy
Right esotropia in primary position due to unopposed action of right medial rectus
Marked limitation of right abduction due toright lateral rectus weakness
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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
Assessment after photocoagulation
• Persistent neovascularization
• Haemorrhage
Poor involution
• Re-treatment required
• Regression of neovascularization• Residual ‘ghost’ vessels or fibrous tissue
Good involution
• Disc pallor
Choroidal neovascularization (CNV)
• Metamorphopsia is initial symptom• Most lesions are not visible clinically
Suspicious clinical signs
Pinkish-yellow subretinal lesion with fluid
Subretinal blood or lipid
• Less common than atrophic AMD but more serious
Idiopathic premacular fibrosis
• Pucker emanating from epicenter
• Opaque epiretinal membrane
• May be associated with macular pseudo-hole
• Severe retinal wrinkling and vascular distortion
Macular pucker
• Translucent epiretinal membrane• Fine retinal striae and mild vascular distortion
Cellophane maculopathy
ResectionRecession
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Summary
• What is patient’s 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
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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”
References:• Burde RM, Savino PJ, Trobe JD. Cliinical Decisions in Neuro-
Ophthalmology, 2nd ed. St. Louis: Mosby-Year Book Inc., 1992.• Gorin G, History of Ophthalmology. Delaware:Publish or Perish, 1982
• Miller KM, Capo H, Mallette RA, Guyton DL. Ocular Motility and Binocular Vision. St. Louis: C.V. Mosby Co., 1989.
• Pediatric Ophthalmology and Strabismus, Section 6, Basic and Clinical Course. San Francisco: American Academy of Ophthalmology,1990-1.
• Taylor D. Pediatric Ophthalmology. Cambridge: Blackwell Scientific Publications, Inc, 1990.
• Wright KW. Text Book of Ophthalmology. Baltimore: Williams P. Wilkins, 1997.
• Kanski JJ, Bolton A. Illustrated Tutorials in Clinical Ophthalmology.
• Butterworth-Heinemann, 2001.
• American Orthoptic Journal, Volume 60, 2010
• FocalPoints Advances in the Management of Amblyopia, Kerr,NC 2010
• FocalPoints Practical Management of Amblyopia, Keech,RV Mar 2000
• FocalPoints Diplobia:Diagnosis and Management, Lee,MS Dec 2007
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