Diplopia strabismus ppt-talk_10-2010
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The document discusses different types of double vision including acquired and congenital strabismus. It provides a brief history of eye surgery beginning in ancient times and discusses important early developments such as the first muscle operations in the 1830s-40s. The remainder of the document focuses on evaluating and diagnosing double vision, including questions to ask patients, important examination tools, and distinguishing types of misalignments that can cause double vision.
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Diplopia strabismus ppt-talk_10-2010
- 1. DOUBLE VISION, ACQUIRED, and CONGENITAL STRABISMUS Robert Cordero, M.D., F.A.C.S Central Florida Eye Specialists, P.L. October 30, 2010
- 2. • www.theeyespecialists.com • www.aapos • www.aao • Google 2 2
- 3. 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 3
- 5. Chevalier John Taylor 1739 5
- 6. 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 6
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- 8. Eye Massager 1890 8
- 9. 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
- 10. 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 10
- 11. Work-up Diplopia • History, History, Histroy • Old Records and Studies • Compare Measurements • Impression(s) • Plan: Short and Long Term • Communication
- 12. 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
- 14. Basic Review • Anatomy • Eye Movements • Binocular Vision • Strabismus • Motor Evaluation • Sensory Evaluation
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- 21. 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 •
- 22. Tests for stereopsis Titmus TNO random dot test • Polaroid spectacles • Red-green spectacles • Figures seen in 3-D • ‘Hidden’ shapes seen Frisby Lang • No spectacles • No spectacles • ‘Hidden’ circle seen • Shapes seen
- 23. Tests for sensory anomalies Worth four-dot test Bagolini striated glasses a - Prior to use of glasses a - Normal or ARC b - Normal or ARC b- Diplopia c - Left suppression c - Suppression d - Right suppression d - Small suppression scotoma e - Diplopia
- 24. Synoptophore • Grading of binocular vision • Detection of suppression and ARC • Measurement of angle • Measurement of fusional amplitudes
- 25. 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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- 29. Motility tests • Tests versions and ductions • Grades under/overaction Left lateral rectus underaction Left inferior oblique overaction
- 30. Cover tests • Cover test detects heterotropia • Prism cover test measures tropia • Alternate measures total tropia and phoria • Uncover test detects heterophoria • Alternate cover test detects total deviation
- 31. 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
- 32. 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 32
- 33. Types of Turns • ESODEVIATION • EXODEVIATION • A and V Patterns • Cyclovertical
- 35. Signs of chalazion (meibomian cyst) Painless, roundish, firm lesion May rupture through conjunctiva within tarsal plate and cause granuloma
- 36. Morphological classification of keratoconus Nipple cone Oval cone Globus cone Small and steep curvature Larger and ellipsoidal Largest
- 37. Progressive iris atrophy Progressive stromal iris atrophy Broad-based PAS Displacement of pupil towards PAS
- 38. Isolated familial ectopia lentis Autosomal recessive Pupil may be normal Pupil may be displaced in opposite direction (ectopia lentis et pupillae)
- 39. Classification according to maturity Immature Mature Hypermature Morgagnian
- 40. Implant displacement Decentration Optic capture • May occur if one haptic is inserted • Reposition may be necessary into sulcus and other into bag • Remove and replace if severe
- 42. No Misalignment
- 43. INCOMITANT
- 44. Mechanical (Restrictive) Diplopia • Grave’s Ophthalmopathy • Brown’s Syndrome • Orbital Pseudotumor • Ocular Myositis • Orbital Mass Lesions • Orbital Trauma
- 45. Signs of eyelid retraction Occurs in about 50% • Bilateral lid retraction • Bilateral lid retraction • No associated proptosis • Bilateral proptosis • Unilateral lid retraction • Lid lag in downgaze • Unilateral proptosis
- 46. Restrictive myopathy • Occurs in about 40% • Due to fibrotic contracture Elevation defect - most common Abduction defect - less common Depression defect - uncommon Adduction defect - rare
- 47. Optic neuropathy • Occurs in about 5% • Early defective colour vision • Usually normal disc appearance Caused by optic nerve compression at Often occurs in absence of significant orbital apex by enlarged recti proptosis
- 48. Brown syndrome (right) Normal elevation in Straight in primary position Limited elevation in abduction adduction
- 49. Idiopathic orbital non-infectious orbitaldisease (IOID) • Non-neoplastic, inflammatory 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
- 50. 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
- 51. 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 • CT shows fusiform enlargement of left lateral rectus • Worsening of pain on attempted left gaze
- 52. 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
- 53. 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 lacrimal fossa ophthalmoplegia • Excavation of lacrimal gland • Inferonasal globe fossa without destruction displacement
- 54. Lacrimal gland carcinoma • Presents - 4th to 6th decades • Very poor prognosis • Posterior extension may cause proptosis, • Painful, fast-growing mass in ophthalmoplegia and episcleral lacrimal fossa congestion • Infero-nasal globe displacement • Trigeminal hypoaesthesia in 25% Management • Biopsy • Radical surgery and radiotherapy
- 55. 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
- 56. Sphenoidal ridge meningioma Presents with gradual visual loss and reactive hyperostosis Proptosis Fullness in temporal fossa Hyperostosis on plain x-ray
- 57. 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
- 58. 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
- 59. Direct carotid-cavernous fistula • Pulsatile proptosis with bruit • Retinal venous congestion and haemorrhages and thrill • Abolished by ipsilateral carotid compression
- 60. 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 • Occasional ophthalmoplegia • Raised intraocular pressure with and mild proptosis wide pulsation
- 62. Tensilon Test • Tensilon (Edrophonium HCL) 10 mg/ml fast acting anti-cholinesterase • Neostigmine (Prostigmin) IM (0.02mg/kg) alternative • Have injectable Atropine Sulfate ready
- 63. Ophthalmic Signs of Myasthenia Gravis • Ptosis • EOM Palsies • Pseudogaze Palsies • Pseudointernuclear Ophthalmoplegia • Pseudoconvergence Paresis • Lid Twitch • Quiver Movements • Orbicularis Weakness
- 64. 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
- 65. Ocular myasthenia Ptosis Diplopia • Insidious, bilateral but asymmetrical • Intermittent and usually vertical • Worse with fatigue and in upgaze • Ptotic lid may show ‘twitch’ and ‘hop’ signs
- 66. Edrophonium test Before injection Positive result • Measure amount of ptosis or • Inject i.v. test dose of edrophonium diplopia before injection (0.2 ml-2 mg) • Inject remaining (0.8 ml-8 mg) if no • Inject i.v. atropine 0.3 mg hypersensitivity
- 67. Cranial Neuropathy • Oculomotor (3rd) Cranial Nerve • Trochlear (4th) Cranial Nerve • Abducen (6th) Cranial Nerve • Adult, Child, TITS
- 68. Anatomy of third nerve Oculomotor nucleus Pituitary gland Red nucleus Carotid artery Cavernous sinus Pons III nerve Post cerebral artery Clivus Basilar artery
- 69. 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
- 70. Signs of right third nerve palsy • Ptosis, mydriasis and cycloplegia • Normal abduction • Abduction in primary position • Intorsion on attempted downgaze • Limited adduction • Limited elevation • Limited depression
- 71. Important causes of isolated third nerve palsy Idiopathic - about 25% Vascular disease - hypertension, diabetes Trauma Posterior communicating aneurysm Extradural Aneurysm haematoma Chiasm Midbrain pushed across Edge of tentorium Prolapsing temporal Posterior cerebral artery lobe Third nerve
- 72. 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
- 73. Signs of right fourth nerve palsy • Right hyperdeviation in primary • Right underaction on depression position when left eye fixating in adduction • Excyclotorsion • Vertical diplopia • Right overaction on left gaze
- 74. Positive Bielschowsky test in right fourth nerve pal Increase in right Absence of right hyperdeviation on ipsilateral hyperdeviation on head tilt contralateral head tilt
- 75. Anatomy of sixth nerve Basilar artery Medial Pituitary gland lemniscus Carotid artery 4th ventricle Cavernous sinus Petroclinoid ligament Vestibular Clivus VI nerve nucleus Pyramidal tract
- 76. Old right sixth nerve palsy Straight in primary position due to partial recovery Limitation of right abduction and Normal right adduction horizontal diplopia
- 77. Important causes of isolated sixth nerve palsy Vascular - hypertension, diabetes Raised intracranial pressure Acoustic neuroma Dilated ventricles Petrous tip Brainstem pushed downwards
- 78. 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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- 80. Internuclear ophthalmoplegia Lesion involving left MLF Defective left adduction and ataxic Normal left gaze nystagmus of right eye Convergence intact if lesion discrete Important causes • Demylination - usually bilateral • Vascular disease • Tumours of brainstem
- 81. ‘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
- 82. Parinaud dorsal midbrain syndrome • Supranuclear upgaze palsy • Normal downgaze • Large pupils with light-near dissociation • Convergence weakness • Lid retracton (Collier sign) • 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
- 83. Progressive supranuclear palsy ( Steele-Richardson-Olszewski syndrome ) • Affects elderly • Pseudobulbar palsy Initially involves downgaze • Extrapyramidal rigidity • Gait ataxia • Dementia Subsequent defective up and horizontal gaze
- 84. Medial wall blow-out fracture Signs Ophthalmoplegia - adduction and abduction Periorbital subcutaneous emphysema if medial rectus muscle is entrapped Treatment • Release of entrapped tissue • Repair of bony defect
- 85. COMITANT • Review History • Decompensated Phoria • Accomodative Esotropia • Acute Esotropia of Childhood • Vergence Paresis • Skew Deviation • Foveal Displacement Syndrome • Central Disruption of Fusion
- 86. 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 86
- 87. 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
- 88. 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
- 89. Recent right sixth nerve palsy Right esotropia in primary position due to Marked limitation of right abduction due t unopposed action of right medial rectus right lateral rectus weakness
- 90. 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 90
- 91. Assessment after photocoagulation Poor involution Good involution • Persistent neovascularization • Regression of neovascularization • Haemorrhage • Residual ‘ghost’ vessels or fibrous tissue • Re-treatment required • Disc pallor
- 92. 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 Subretinal blood or lipid with fluid
- 93. Idiopathic premacular fibrosis Cellophane maculopathy Macular pucker • Translucent epiretinal • Severe retinal wrinkling and • Opaque epiretinal membrane membrane vascular distortion • Fine retinal striae and mild • Pucker emanating from • May be associated with vascular distortion macular pseudo-hole epicenter
- 94. Recession Resection
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- 96. 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
- 97. 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 97
- 98. 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 98
- 99. 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” 99
- 100. 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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