Approach to vision loss

A brief discussion and clinical approach to vision loss in adults

1. Approach to Vision Loss Dr Kirat S Grewal

2. Headings Definition and aspects Approach to vision loss Patterns of vision loss Transient Monocular Vision Loss Persistent Monocular vision Loss Binocular vision loss Cerebral vision loss Functional vision loss

3. Aspects of Vision Loss * Visual standards, Resolution of the International Council of Ophthalmology (2002)

4. Grades of Visual Impairment * Visual standards, Resolution of the International Council of Ophthalmology (2002)

5. Causes of Vision Loss Cause World South-Asia Refractive error 20.62 (18.62 - 22.55) 36.76 (34.29 - 39.05) Cataract 34.47 (25.69 - 43.35) 35.15 (27.18 - 43.16) Age-related macular Degeneration 8.30 (2.85 - 15.42) 5.66 (2.05 - 10.35) Glaucoma 5.64 (1.33 - 11.72) 2.40 (0.65 - 4.83) Corneal opacity 3.46 (0.53 - 7.77) 2.64 (0.47 - 5.82) Diabetic retinopathy 1.07 (0.15 - 2.44) 0.18 (0.03 - 0.38) Trachoma 0.98 (0.80 - 1.16) 0.04 (0.01 - 0.07) Other causes/unidentified 25.46 (9.82 - 44.20) 16.72 (5.97 - 30.58) Percentage of blindness by cause for all ages in 2015 Flaxman, SR, Bourne, RRA, Resnikoff , S et al. Global causes of blindness and distance vision impairment 1990–2020: a systematic review and meta-analysis. Lancet Glob Health. 2017

6. Age-standardised prevalence of blindness in adults aged 50 years and older from 1990 to 2015

7. Approach to vision loss Age : Degenerative and vascular disorders seen in adults Neoplasms / tumor types are age dependent Sex : Optic neuritis and giant cell arteritis are more prevalent in females

8. Approach to vision loss Is the visual loss monocular/ binocular ? Monocular vision loss : abnormality in the eye itself or in the optic nerve anterior to the chiasm Binocular vision loss result from bilateral anterior lesions or more likely chiasmal / retrochiasmal lesion Is the visual loss transient/ persistent ? Neuro -Ophthalmology : Diagnosis and Management Grant T. Liu, Nicholas J. Volpe

9. Approach to vision loss What is the pattern and degree of vision loss ? What is the tempo of onset ? Is the visual loss static /progressive/ fluctuating/resolving? What are the associated symptoms/signs or if any triggers ?

10. Painful Vision Loss Causes Characteristics and Associations Vascular visual loss ICA dissection( CRAO /AION) Carotid occlusion Neck Pain, Horner Syndrome Ocular ischemic syndrome Orbital pain , Iris neovascularization Iridocyclitis , retinal hemorrhages Giant cell arteritis Jaw claudication , Systemic symptoms Optic neuritis Periorbital /Pain on eye-movement Angle-closure glaucoma Nausea,vomiting,conjunctival injection Orbital apex syndrome Periorbital pain Other cranial nerve i nvolvement Ocular trauma H/O Trauma Pituitary Apoplexy Sudden temporal headache/ Periorbital pain , rapidly worsening v isual loss

11. Visual field Interpretation- Pattern of vision loss Monocular vs Binocular Central vs Peripheral Hemianopic or not Congruous vs Incongruous Homonymous hemianopia

12. Anatomical aspects- Retina

13. Anatomical aspects- Retina

14. Anatomical aspects- Chiasma

15. Chiasmal Vision Loss- Junctional Scotoma Trobe JD, Glasser JS: The visual field manual: a practical guide to testing and interpretation

16. Anatomical aspects- Chiasma

17. Anatomical aspects- Optic radiations

18. Visual Field defects: Visual cortex

19. Visual field defects

20. Bacigalupi , Michael. (2006). Amaurosis Fugax -A Clinical Review. I J Allied Health Sci Pract

21. Transient Monocular Vision Loss

22. Transient Monocular Vision Loss Ocular causes Neurologic causes Acute angle closure Glaucoma Migraine Anterior Ischemic ON Transient visual obscurations / Papilledema Impending CRVO Uhthoff phenomenon Hyphema Psychogenic

23. Amaurosis Fugax Acute onset, brief partial or complete monocular vision loss Brief, usually <15 minutes and rarely > 30 minutes, most patients are affected for only 1–5 min Usually begins in the upper field :Altitudinal vision loss with a shade /curtain effect seen in 15- 20% Mungas JE, Baker WH. Amaurosis fugax . Stroke 1977

24. Amaurosis Fugax Donders RC, Dutch TMB Study Group Clinical features of transient monocular blindness. J Neurol Neurosurg Psychiatry. 2001 Clinical Feature Implication Age > 45 years: Ischemic cause likely < 40 years: Benign migrainous cause likely Frequency of events Isolated events may be d/t embolism Repeated events d/t hypoperfusion in arterial stenosis Onset Over seconds: more likely Embolic/ vasospastic Over minutes: Hypoperfusion events Duration Lasting seconds : ocular , orthostatic hypotension 2- 30 minutes: Ischemic event Minutes to hours: Vasospastic / Migrainous event

25. Amaurosis Fugax Goodwin JA . Symptoms of amaurosis fugax in atherosclerotic carotid artery disease. Neurology 1987 Clinical Feature Implication Monocular/binocular Monocular: Occlusive Retinal / Carotid artery condition Binocular : Posterior circulation disturbances Description of event White-out/ Frosted Glass : Hemodynamic TMB Blackness/ darkness: Embolic TMB Positive phenomena: Migrainous / ocular event Carotid artery stenosis > 75% Altitudinal: More likely carotid/ cardiac embolic source Pain Headache: Migraine Chronic ocular/ retrobulbar pain: Carotid stenosis

26. Amaurosis Fugax Goodwin JA . Symptoms of amaurosis fugax in atherosclerotic carotid artery disease. Neurology 1987 Clinical Feature Implication Precipitating factor Posture/Exercise/ Meals : Hemodynamic TMB Bright Light: Hemodynamic TMB/ High Grade stenosis Hypovolemia / low cardiac output: Bilateral Gaze evoked: Orbital tumors Associated symptoms /signs Malaise/ Jaw claudication : Giant cell arteritis Encephalopathy/ HTN: Malignant HTN Horners syndrome: Carotid dissection

27. Hayreh S.S., Zimmerman M.B. Amaurosis fugax in ocular vascular occlusive disorders: prevalence and pathogeneses. Retina. 2014

28. Amaurosis Fugax Comprises approximately 20-25% of TIAs Annual incidence of stroke was 2% / four times greater than a normal population TMVL secondary to carotid artery stenosis , the 3-year ipsilateral stroke rate (10%) was half that for hemisphere TIAs (20%) -NASCET The risk of death in patients with TMVL and atheromatous carotid stenosis is around 4%/yr, mainly related to myocardial infarction KIine LB. The natural history of patients with amaurosis fugax . Ophthalmol Clin North Am 1996 PooleCJM , RossRussell RW: Mortality and stroke after amaurosis fugax ./ Neurol Neurosurg Psychiatry1985

29. Amaurosis Fugax

30. 3-year absolute reduction of risk of stroke with carotid endarterectomy in presence of 3 risk factors was 14.3% Benavente O et al. Prognosis after transient monocular blindness associated with carotid-artery stenosis . N Engl J med. 2001

31. Transient Binocular Vision Loss Transient visual obscurations ( b/l optic disc edema ) Visual migraine aura Cerebral hypoperfusion (vasospasm, systemic hypotension, thromboembolism , hyperviscosity ) Seizures PRES/ Posterior reversible encephalopathy syndrome Head trauma

32. Transient Binocular Vision Loss Clinical Feature Migraine Occipital Seizure Vertebrobasilar TIA Duration 20-30 minutes Variable Seconds to minutes Headache Frequent headaches Occur after vision loss During or after vision loss During or after vision loss Typical visual symptom Hemifield marching Hemifield stationary Hemifield or total Positive phenomena Fortification scotoma Formed images Common Uncommon Rare Common Rare Uncommon Associated features Nausea, Photophobia Paresthesias,Dysphasia Eye deviation, automatisms, loss of consciousness S/S Brainstem dysfn . Dizziness, ataxia, diplopia , numbness, dysarthria

33. Sudden monocular vision loss: Clinical scenario 42 year old male presented with sudden onset of painless blurring of vision in right eye since past 7 days He also complains of distortion of images and micropsia . On examination, visual acuity is 6/24 in right eye, with a RAPD and central scotoma on visual field testing

34. Fundus

35. Fundus

36. Whether the visual loss a result of a lesion of the Optic nerve or a lesion of the macula ? SIMILARITIES 1. Decreased visual acuity 2. Central scotomas on visual fields 3. RAPD can occur in both* 4. Color vision can be affected in both*

37. Differences: ON vs Macula Symptom Optic nerve abnormality Macular abnormality Metamorphopsia Rare Common Pain Usually present in optic neuritis Absent Color vision/ dyschromatopsia More affected (for the degree of VA Deficit) Less affected Photopsia Rare Common Darkening of vision Common Rare Recognition of peripheral field loss Common Rare Glare/ Light sensitivity Rare Sometimes TVO Occasionally Rare

38. Differences Sign/Investigations Optic nerve abnormality Macular abnormality RAPD Common Rare Ophthalmoscopy Swollen pale or normal optic nerve Macular abnormality Pale optic nerve +/- Visual field defects Central, Cecocentral , nasal, arcuate , altitudinal Positive Central scotoma Recovery following bright light exposure Normal Abnormal ERG/OCT Normal Nerve fibre layer thinning +/- Abnormal VEP Large latency delay Small latency delay

39. RAPD- Pupillary reflex

40. RAPD Result of consensual and bilateral nature of the light reflex Unilateral or asymmetrical bilateral disruption of the afferent limb of light reflex Detected by swinging flash light test Can quantitate the severity of retinal ganglion cell and optic nerve damage

41. RAPD- Localization Optic nerve disease ( U/L or if B/L-Asymmetric) Macular/retinal lesions (CRAO/BRAO, Large retinal detachments) Optic tract disease ( contralateral RAPD) Unilateral dorsal midbrain lesion ( contralateral RAPD)

42. The relative afferent pupillary defect (RAPD) was measured in ten patients, each of whom had a dense cataract in one eye only. All patients with mature or nuclear cataracts had a measureable RAPD in the other eye May be due to increased intraocular scatter of light by the cataract RAPD in the same eye as a unilateral cataract, likely to be a major defect of the anterior visual pathway in that eye.

43. The ‘better’ eyes had optic nerve or retinal dysfunction. The eyes with worse visual acuity but no afferent pupillary defect had an abnormality of the ocular media.

44. Monocular vision loss Corrects with Pin hole No

45. Sudden Monocular Vision Loss with Progression Optic neuritis Leber’s hereditary optic neuropathy Anterior ischemic optic neuropathy ( arteritic / nonarteritic )

46. CRAO Painless sudden monocular vision loss; usually embolic etiology (commonly Carotid artery atherosclerotic disease ) Prudent to rule out giant cell arteritis ( if also age>50 yrs) Vascular emergency ; evaluate on lines of cerebral infarction Fundus may be normal in acute stages; repeat examination necessary

47. Fundus

48. Characteristics of retinal emboli

49. In similar setting, which condition would this fundus appearance represent?

50. Annual risk of stroke in patients with visible asymptomatic retinal cholesterol emboli : 8.5% vs 0.8% controls ( RR 9.9; 95% CI ( 2.3 to 43.1 ); P = 0.002 ) Stroke occurred in 15.0% RAO group vs 8.0% controls ( P < 0.001). RAO was associated with an increased risk of stroke occurrence (hazard ratio, 1.78; 95% confidence interval, 1.32–2.41) Risk of stroke Bruno A, Vascular outcome in men with asymptomatic retinal cholesterol emboli. A cohort study. Ann Intern Med. 1995 Rim TH, et al. Retinal Artery Occlusion and the Risk of Stroke Development: Twelve-Year Nationwide Cohort Study. Stroke. 2016

51. Prognosis of CRAO is considered dismal, with some studies reporting as few as 8% experiencing a recovery in visual acuity All patients with CRAO should be admitted for immediate workup and initiation of secondary prevention. MR brain may detect concomitant cerebral ischemia in 25% pts. Of CRAO Intraarterial thrombolysis or intravenous thrombolysis are of limited benefit . ??? In one metanalysis , systemic fibrinolysis (<4.5 hours onset) resulted in rate of recovery is nearly 3 times that in the natural history cohort ( P  < .001), with a 32.3% absolute RR and a NNT of 4.0 Management Lee J, et al. Co-occurrence of acute retinal artery occlusion and acute ischemic stroke: diffusion-weighted magnetic resonance imaging study. AM J Ophthalmol . 2014 Ahn SJ, : Efficacy and safety of intra-arterial thrombolysis in central retinal artery occlusion. Invest Ophthalmol Vis Sci 2013

52. Classic features of a unilateral optic neuropathy Central visual loss Clear view through the ocular media to the optic nerve Relative afferent pupillary defect Swollen or pale optic nerve head Exceptions – N-AION: Visual Acuity good despite altitudinal vision loss Retrobulbar optic neuritis : Disc is normal for 4-6 weeks

53. Ischemic optic neuropathies Most common optic neuropathies in patients >50 yrs age Involvement of posterior ciliary arteries: atherosclerosis or vasculitis AION (90% of total cases) more common than PION Nonarteritic ischemic optic neuropathy is more common than arteritic ION Repka MX. Clinical profile and long-term implications of anterior ischemic optic neuropathy. Am J Ophthalmol . 1983

54. Ischemic optic neuropathies Parameter Arteritic AION NAION Age (years) >65 45- 70 Sex F:M ( 3:1) M=F Systemic symptoms + Headache/pain >50% : Polymyalgia rheumatica 25% : Isolated visual s/s Absent Amaurosis Fugax Common ( 32%) Uncommon (2.5%) ESR and CRP Raised (ESR normal in 12%) Normal HayrehSS . Anterior ischaemic optic neuropathy: differentiation of arteritic from non- arteritic type and its management.Eye.1990

55. Ischemic optic neuropathies Parameter Arteritic AION NAION Degree of vision loss Severe 70% < 6/60 Less severe 50% Better than 6/18 Arteriosclerotic Risk Factors According to Age Present Binocular involvement 30-50% Interval often <1 week 20-30% Interval rarely < 6 months Improvement Rare 25% HM+ / worse 30% improvement Ophthalmoscopy Pallid edema , Cotton wool spots Disc hemorrhages Disc edema , hemorrhages Disk at risk FFA Segmental Choroidal hypoperfusion Normal, Delayed disc filling

56. Fundus NAION Arteritic AION

57. 37-year-old woman Four weeks prior to presentation, she noticed painless decreased vision in the inferior visual field in the right eye, which worsened over 4 to 5 days. She had a brain MRI that showed no optic nerve enhancement, but showed one small nonenhancing periventricular T2 high signal lesion. She did not receive treatment. Her vision failed to improve during the following 4 weeks. On neuro -ophthalmic examination, visual acuity was 6/6 left and 6/24 in right eye and mild red desaturation was present in the right eye. RAPD + Case vignette

58. Fundus At 1 week At 6 weeks

59. Visual field

60. NAION Vs Optic neuritis Parameter NAION Optic neuritis Age (years) , Sex >50, M=F <40, F>M Pain Absent 90% of presentations Onset Acute / One time event Few cases have progression Progressive Recovery Static ( >2/3 rd no improvement) Good recovery Optic disc Pale disc, Disc at risk Peripapillary hemorhages + 33% disc edema Visual fields Altitudinal/nerve fibre bundle defect Central FFA Delayed disc filling Normal MR Brain No Optic nerve enhancement Enhancement + 84% Rizzo JF, Lessell S. Optic Neuritis and Ischemic Optic Neuropathy Overlapping Clinical Profiles. Arch Ophthalmol . 1991

61. Altitudinal disc swelling and Hemorrhage on the swollen disc was more common in AION than in ON AION was the clinical diagnosis 82 % of the cases with altitudinal edema, 81 % of the cases with disc hemorrhages 93 % of the cases with pallid edema 90% of the cases with arterial attenuation

62. Glaucoma, CRAO and ION were correctly identified by atleast 1/5 observers with accuracy >80% Helpful features in differentiating entities: Retinal arteriolar attenuation and sheathing in CRAO , AION Segmental temporal pallor in hereditary (bilateral) and ON (unilateral) Pathological disc cupping for glaucoma

63. Optic Neuritis Classical Features Female , Age 77% , 32 +/- 6.7 years Onset to peak Hours to days ( upto 2 weeks) Ocular Pain 92% precedes vision loss , Usually lasts 3- 5 days Swollen optic disc 35% Visual Acuity 55% (6/7.5 to 6/60) Recovery Untreated : Vision stops getting worse at 7 days, starts improving in 80% within 3 weeks ; most recovery in 4 wks ; 70% recover 6/6 Treated : No difference ,except recovery faster within first 2 weeks Recurrence Cumulative probability over 5 years: 19% : affected eye, 17% :unaffected eye, and 30% for either eye Conversion to MS (15 year) No brain lesion: 25%, One or more lesions: 72% Beck RW, Cleary PA, Anderson MM Jr , et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med 1992

64. Typical Vs Atypical ON Optic Neuritis Atypical ON/ Red flags Young Adults (Mean age 32 years) Predominantly Females (77%) Age > 45 years Subacute visual loss over hours to days Progression of visual loss after 2 weeks Presence of Pain (90%) Absence of Pain/ persistent pain Predominantly Unilateral involvement Bilateral involvement Optic disc edema (35%) Severe disc edema , Vitreous cells and hemorrhage , Macular star Optic atrophy at presentation Photopsia / phosphenes (1/3) Positive phenomena : Retinal mimic Good recovery Monophasic course Lack of partial recovery within 4 weeks of onset of vision loss Relapse after stopping steroids

65. Differential diagnosis of ON

66. Differential diagnosis of ON

67. Case scenario 26 year female presented with C/C of right upper limb radicular pain and neck pain 1.5 months PTA Right eye vision loss , inferior altitudinal at onset, 4 weeks prior to presentation with complete loss 14 days post onset Horizontal diplopia , more on focussing to right side Painful left eye vision loss 2 weeks PTA with complete loss 7 days after onset Headache , bifrontal and moderate grade since 2 weeks PTA

68. Fundus

69. MR Brain

70. Optic disc edema vs. Papilledema Clinical features Optic disc edema / Papillitis Papilledema Laterality Unilateral > Bilateral Bilateral, may be asymmetric Early central vision loss (visual acuity impaired) Common Uncommon Color vision Abnormal Preserved until late Typical visual field defect Central or paracentral scotoma , arcuate or altitudinal defect Enlarged physiologic blind spot, arcuate defect, nasal step, inferotemporal loss, concentric constriction Friedman, D.I. Papilledema and idiopathic intracranial hypertension. Continuum ( Minneap Minn ). 2014

71. Optic disc edema vs. Papilledema Clinical features Optic disc edema Papilledema Spontaneous venous pulsations May be present Absent Afferent pupillary defect Present if unilateral or asymmetric vision loss Usually absent unless asymmetric visual loss Disc leakage on fluorescein angiogram May be present Yes Associated symptoms Pain on eye movement, other symptoms specific to etiology Headache, diplopia, photophobia, nausea, vomiting, meningismus

72. Repeat MR Brain and spine

73. Papilledema Optic disc swelling secondary to raised ICP Secondary to blockage of axoplasmic flow in nerve fibres An intracranial mass lesion and malignant hypertension should be excluded CSF opening pressure: Abnormal values are >28 cm H20 in children and >25 cm H20 in adults (Normal of 6cm to 25cm H20 – 95%CI ) 1. Avery RA, Shah SS, Licht DJ, et al. Reference range for cerebrospinal fluid opening pressure in children. N Engl J Med 2010. 2. Lee SC, Lueck CJ. Cerebrospinal fluid pressure in adults. J Neuroophthalmol 2014

74. Spontaneous venous pulsations Present in 90% of normal subjects SVPs occurred only in patients with CSF pressures below 19 cm H 2 O and in the absence of optic disc edema In IIH ,CSF pressure often fluctuates and may even be normal at times. SVPs may hence be present at times Levin BE . The clinical significance of spontaneous pulsations of the retinal vein. Arch Neurol 1978;35:37–40

75. Transient Visual Obscurations Brief episodes (lasting seconds) of monocular or binocular black-outs/gray-outs of vision in patients with optic disc edema Precipitated by postural changes / valsalva maneuvres /eye movement TVOs may be the only symptom of raised ICP, which is their most likely cause Due to transient decreased perfusion of the optic nerve head Biousse V, Trobe JD. Transient monocular visual loss. Am J Ophthalmol 2005

76. Etiology of Papilledema Common Causes Uncommon IIH (44%) Dural sinus AV Malformation Intracranial mass Lesion (21%) OSA Hydrocephalus (17%) GBS Venous sinus thrombosis (9%) CIDP Intracranial Hemorrhage Spinal cord tumors Meningitis Craniosynostosis Neuro -Ophthalmology at a Tertiary Eye Care Centre in India. Sharma,Pradeep MD; Saxena , Rohit MD, Journal of Neuro -Ophthalmology 2017

77. IIH: Clinical features Features IIHT (n=165) AIIMS (n= 89) Mean Age 29(7.4) years 29.9(11) Females 97.6% 82% BMI 39.9(8.3) (88%obese) 27.1 ± 5.4 (67% obese) Headache TVO Tinnitus Diminution of vision Binocular diplopia 84% 68% 52% 32% 18% 92% 53% 13% 62% 24% Recent gain in weight 45% 11% CSF Opening pressure;cm 34.3(8.6) 27.2(7.3) M. Wall, The idiopathic intracranial hypertension treatment trial: clinical profile at baseline, JAMA Neurol. 71 (2014) Agarwal A, Vibha D, Prasad K, Bhatia R, Singh MB, Garg A, et al. Predictors of poor visual outcome in patients with idiopathic intracranial hypertension Clin Neurol Neurosurg . 2017

78. Papilledema vs. Pseudopapilledema Features Papilledema Pseudo- Papilledema Disc colour Hyperemic Pink , yellowish pink Disc Margins Indistinct early at superior and inferior pole Irregularly blurred, may be lumpy Vessels Normal distribution, Fullness SVP Absent Emanate from centre Frequent anomalous pattern SVP +/- Nerve fiber layer Dull as a result of edema No edema Hemorrhages Splinter Subretinal , retinal, vitreous

79. Cerebral blindness Complete loss of visual sensation, including light and dark perception Loss of reflex lid closure to bright illumination/ threatening gestures; Retention of the pupillary light reaction and near response; Integrity of normal retinal structures; Normal extraocular movements Fraser JA, Newman NJ, Biousse V. Disorders of the optic tract, radiation and occipital lobe. Handb Clin Neurol 2011

80. Higher Cortical Visual deficits

81. Deficit Localization Achromatopsia / Dyschromatopsia Bilateral Lesions of Lingual Gyri Apperceptive visual form agnosia Lateral occipital cortex Associative visual agnosia Left or b/L lesions of the parahippocampal , fusiform , and lingual gyri Prosopagnosia Right or b/l fusiform gyri Pure alexia Left occipitotemporal lesions Ventral stream: Visuo -perception

82. Visual agnosia

83. Deficit Localization Akinetopsia B/L Lateral occipitotemporal cortex Simultanagnosia Medial occipitoparietal junction, cuneus Optic ataxia Inferior parietal lobule/Superior occipital cortex Acquired ocular motor apraxia B/L lesions of the parietal eye fields, FEF Astereognosis B/L occipitoparietal lesions Dorsal stream: Visuo -motor

84. Simultanagnosia

85. Functional vision loss: Finger touching test

86. Functional vision loss: Optokinetic nystagmus

87. Functional vision loss: Prism shift test

88. Functional vision loss: Visual field constriction

89. Prospective cohort study done in Department of Neurology at King George Medical University, Uttar Pradesh, Lucknow over a span of 2 years (October 2011-September 2013) 64 patients were included in the study: 27 cases were male and 37 cases were female

90. DIAGNOSIS Percentage of patients Demyelinating /inflammatory/ischemic Optic neuropathy 37.5% Chronically raised ICP 37.5% Compressive Optic neuropathy 9.4% Cortical vision impairment 15.6% Distribution of etiology

91. Neuro -Ophthalmology at a Tertiary Eye Care Centre in India . Sharma,Pradeep MD; Saxena , Rohit MD, Journal of Neuro -Ophthalmology Retrospective study (Jan 2015 – December 2015) at RPC/AIIMS 1597 patients (5% of total) were referred for neuropthalmology evaluation (out of which 1334 were deemed valid) Mean age of presentation was 30.8 ± 19.5 years (range: 3months–88 years) M:F : 2.02 Sixteen percent (n = 263) of patients were incorrect referrals including retinal dystrophy, maculopathy , cataract, and refractive error

92. Neuro -Ophthalmology at a Tertiary Eye Care Centre in India DIAGNOSIS Percentage of patients Optic nerve disorders Disc edema + 63.8% (1020) 33% (335) Disc edema -- 67% (635) Cranial nerve palsies 7% Cortical visual impairment 6.5% Others 6% Incorrect referrals 16%

93. Neuro -Ophthalmology at a Tertiary Eye Care Centre in India