Diplopia strabismus ppt-talk_10-2010


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Diplopia strabismus ppt-talk_10-2010

  1. 1. DOUBLE VISION, ACQUIRED, andCONGENITAL STRABISMUS Robert Cordero, M.D., F.A.C.S Central Florida Eye Specialists, P.L. October 30, 2010
  2. 2. • www.theeyespecialists.com• www.aapos• www.aao• Google 2 2
  3. 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
  4. 4. Georg Bartisch (1535-1606)
  5. 5. Chevalier John Taylor 1739 5
  6. 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. 8. Eye Massager 1890 8
  9. 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. 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. 11. Work-up Diplopia• History, History, Histroy• Old Records and Studies• Compare Measurements• Impression(s)• Plan: Short and Long Term• Communication
  12. 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
  13. 13. Basic Review• Anatomy• Eye Movements• Binocular Vision• Strabismus• Motor Evaluation• Sensory Evaluation
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  20. 20. 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•
  21. 21. 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
  22. 22. Tests for sensory anomalies Worth four-dot test Bagolini striated glassesa - Prior to use of glasses a - Normal or ARCb - Normal or ARC b- Diplopiac - Left suppression c - Suppressiond - Right suppression d - Small suppression scotomae - Diplopia
  23. 23. Synoptophore• Grading of binocular vision• Detection of suppression and ARC• Measurement of angle• Measurement of fusional amplitudes
  24. 24. Hirschberg test • Rough measure of deviation • Note location of corneal light reflex • 1 mm = 7 or 15Reflex at border of pupil = 15 Reflex at limbus = 75
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  28. 28. Motility tests • Tests versions and ductions • Grades under/overaction Left lateral rectus underactionLeft inferior oblique overaction
  29. 29. 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
  30. 30. 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
  31. 31. 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
  32. 32. Types of Turns• ESODEVIATION• EXODEVIATION• A and V Patterns• Cyclovertical
  33. 33. Monocular Diplopia
  34. 34. Signs of chalazion (meibomian cyst)Painless, roundish, firm lesion May rupture through conjunctivawithin tarsal plate and cause granuloma
  35. 35. Morphological classification of keratoconus Nipple cone Oval cone Globus coneSmall and steep curvature Larger and ellipsoidal Largest
  36. 36. Progressive iris atrophy Progressive stromal iris atrophyBroad-based PAS Displacement of pupil towards PAS
  37. 37. Isolated familial ectopia lentis Autosomal recessivePupil may be normal Pupil may be displaced in opposite direction (ectopia lentis et pupillae)
  38. 38. Classification according to maturity Immature Mature Hypermature Morgagnian
  39. 39. 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
  40. 40. Binocular Diplopia
  41. 41. No Misalignment
  42. 42. INCOMITANT
  43. 43. Mechanical (Restrictive) Diplopia• Grave’s Ophthalmopathy• Brown’s Syndrome• Orbital Pseudotumor• Ocular Myositis• Orbital Mass Lesions• Orbital Trauma
  44. 44. 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
  45. 45. Restrictive myopathy • Occurs in about 40% • Due to fibrotic contractureElevation defect - most common Abduction defect - less commonDepression defect - uncommon Adduction defect - rare
  46. 46. Optic neuropathy • Occurs in about 5% • Early defective colour vision • Usually normal disc appearance Caused by optic nerve compressionat Often occurs in absence of significant orbital apex by enlarged recti proptosis
  47. 47. Brown syndrome (right)Normal elevation in Straight in primary position Limited elevation inabduction adduction
  48. 48. 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
  49. 49. Clinical course and treatment of IOID1. Early spontaneous remission without sequelae Treatment - nil2. Prolonged intermittent activity with eventual remission Treatment options - steroids, radiotherapy or cytotoxics3. Severe prolonged activity causing a ‘frozen orbit’ Left involvement resulting in ophthalmoplegia and ptosis
  50. 50. 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
  51. 51. Cavernous haemangioma • Most common benign orbital tumour in adults • Usually located just behind globe • Female preponderance - 70% • Presents - 4th to 5th decadeSlowly progressive axial proptosis May cause choroidal folds Treatment - surgical excision
  52. 52. 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
  53. 53. 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
  54. 54. Optic nerve glioma • Typically affects young girls • Associated neurofibromatosis -1 is common • Presents - end of first decade with gradual visual lossGradually progressive proptosis Optic atrophy Treatment • Observation - no growth, good vision and good cosmesis • Excision - poor vision and poor cosmesis • Radiotherapy - intracranial extension
  55. 55. Sphenoidal ridge meningiomaPresents with gradual visual loss and reactive hyperostosis Proptosis Fullness in temporal fossa Hyperostosis on plain x-ray
  56. 56. Lymphoma Presents - 6th to 8th decadesAffects any part of orbit and Anterior lesions are rubbery May be confined tomay be bilateral on palpitation lacrimal glands Treatment • Radiotherapy - localized lesions • Chemotherapy - disseminated disease
  57. 57. Direct carotid-cavernous fistula• Defect in intracavernous part of internal carotid• Rapid flow shuntCauses• Head trauma - most common• Spontaneous rupture - in hypertensive females • Ptosis, chemosis and conjunctival injection • Ophthalmoplegia • Raised intraocular pressure
  58. 58. Direct carotid-cavernous fistula• Pulsatile proptosis with bruit • Retinal venous congestion and haemorrhages and thrill• Abolished by ipsilateral carotid compression
  59. 59. 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
  60. 60. Incomitant Misalignment
  61. 61. Tensilon Test• Tensilon (Edrophonium HCL) 10 mg/ml fast acting anti-cholinesterase• Neostigmine (Prostigmin) IM (0.02mg/kg) alternative• Have injectable Atropine Sulfate ready
  62. 62. Ophthalmic Signs of Myasthenia Gravis• Ptosis• EOM Palsies• Pseudogaze Palsies• Pseudointernuclear Ophthalmoplegia• Pseudoconvergence Paresis• Lid Twitch• Quiver Movements• Orbicularis Weakness
  63. 63. Myasthenia Gravis1. Clinical features • Uncommon, typically affects young women • Weakness and fatiguability of voluntary musculature • Types: Neonatal, Congenital, Ocular, System2. 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 thymoma3. Treatment options • Medical - AChE inhibitor, steroids, immunomodulators • Thymectomy, prisms, strabismus surgery
  64. 64. 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
  65. 65. 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
  66. 66. Cranial Neuropathy• Oculomotor (3rd) Cranial Nerve• Trochlear (4th) Cranial Nerve• Abducen (6th) Cranial Nerve• Adult, Child, TITS
  67. 67. Anatomy of third nerve Oculomotor nucleus Pituitary glandRed nucleus Carotid artery Cavernous sinus Pons III nerve Post cerebral artery Clivus Basilar artery
  68. 68. 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
  69. 69. 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
  70. 70. Important causes of isolated third nerve palsy Idiopathic - about 25% Vascular disease - hypertension, diabetes Trauma Posterior communicating aneurysm Extradural Aneurysm haematoma ChiasmMidbrainpushedacross Edge of tentorium Prolapsing temporal Posterior cerebral artery lobe Third nerve
  71. 71. Anatomy of fourth nerveInternal carotid arteryPostr. communicatingartery III VIPostr.cerebral arterySupr.cerebellar artery Basilar artery IV • Only cranial nerve to emerge dorsally • Crossed cranial nerve • Very long and slender
  72. 72. 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
  73. 73. Positive Bielschowsky test in right fourth nerve pal Increase in right Absence of right hyperdeviation on ipsilateral hyperdeviation on head tilt contralateral head tilt
  74. 74. Anatomy of sixth nerve Basilar artery Medial Pituitary gland lemniscus Carotid artery4th ventricle Cavernous sinus Petroclinoid ligament Vestibular Clivus VI nerve nucleus Pyramidal tract
  75. 75. Old right sixth nerve palsy Straight in primary position due to partial recoveryLimitation of right abduction and Normal right adductionhorizontal diplopia
  76. 76. Important causes of isolated sixth nerve palsy Vascular - hypertension, diabetes Raised intracranial pressure Acoustic neuroma Dilated ventricles Petrous tip Brainstem pushed downwards
  77. 77. SUPRANUCLEAR DISORDERS OF EYE MOVEMENT1. Horizontal gaze palsies • Internuclear ophthalmoplegia • Combined internuclear and PPRF (‘one-and-a-half syndrome’) MLF2. Vertical gaze palsies• Parinaud dorsal midbrain syndrome• Progressive supranuclear palsy
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  79. 79. Internuclear ophthalmoplegia Lesion involving left MLFDefective left adduction and ataxic Normal left gazenystagmus of right eye Convergence intact if lesion discrete Important causes • Demylination - usually bilateral • Vascular disease • Tumours of brainstem
  80. 80. ‘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
  81. 81. 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
  82. 82. Progressive supranuclear palsy ( Steele-Richardson-Olszewski syndrome ) • Affects elderly • Pseudobulbar palsyInitially involves downgaze • Extrapyramidal rigidity • Gait ataxia • DementiaSubsequent defective up andhorizontal gaze
  83. 83. Medial wall blow-out fracture Signs Ophthalmoplegia - adduction and abductionPeriorbital subcutaneous emphysema if medial rectus muscle is entrapped Treatment • Release of entrapped tissue • Repair of bony defect
  84. 84. COMITANT• Review History• Decompensated Phoria• Accomodative Esotropia• Acute Esotropia of Childhood• Vergence Paresis• Skew Deviation• Foveal Displacement Syndrome• Central Disruption of Fusion
  85. 85. 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
  86. 86. 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
  87. 87. 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
  88. 88. Recent right sixth nerve palsyRight esotropia in primary position due to Marked limitation of right abduction due tunopposed action of right medial rectus right lateral rectus weakness
  89. 89. 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
  90. 90. Assessment after photocoagulation Poor involution Good involution• Persistent neovascularization • Regression of neovascularization• Haemorrhage • Residual ‘ghost’ vessels or fibrous tissue• Re-treatment required • Disc pallor
  91. 91. Choroidal neovascularization (CNV) • Less common than atrophic AMD but more serious • Metamorphopsia is initial symptom • Most lesions are not visible clinically Suspicious clinical signsPinkish-yellow subretinal lesion Subretinal blood or lipidwith fluid
  92. 92. Idiopathic premacular fibrosisCellophane 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
  93. 93. Recession Resection
  94. 94. 9595
  95. 95. 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
  96. 96. 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
  97. 97. 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
  98. 98. 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
  99. 99. 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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