Visual field assessment is important in the evaluation of lesions involving the visual pathways and should be performed at baseline and periodically in the follow-up. Standard automated perimetry has been shown to be adequate in neuro-ophthalmic practise and is now the technique of choice for a majority of practitioners.

1. Approach to Disc Pallor and
Automated Fields in Neuro-
ophthalmology
Dr.Shah-Noor Hassan FCPS,FRCS(Glasgow)

2. Approach to Optic disc pallor
Types of optic atrophy
• Primary
• Secondary
• Consecutive
• Temporal pallor
• Glaucomatous

3. Primary optic atrophy
• cause not detected ophthalmoscopically
• eg, pituitary tumor, optic nerve tumor, traumatic optic
neuropathy, multiple sclerosis ,toxic/nutritional
• Fundus features of disc
 Color-chalky white
 Margins-sharp
 Demarcated cup
 Cup may be enlarged
 normal retinal vessels

4. Secondary optic atrophy
• eg, papilledema, papillitis
• Damage due to swelling of the disc with glial proliferation
• Fundus features of disc
 Color-yellow waxy/dirty white
 Margins-blurred
 Obliterated cup
 Perivascular sheathing
 Retinal vessels attenuated

5. classification
Pathologic classification
• Ascending optic atrophy - follows damage to
RGC/nerve fibre layer
• Descending optic atrophy - retrolaminar optic
nerve/chiasma/optic tract
• Trans-synaptic degeneration- seen in patients with
occipital damage incurred either in utero or in early
infancy.

6. Unilateral optic atrophy
Ischemic (anterior ischemic optic neuropathy, retinal
occlusive disease)
Compressive (orbital, anterior fossa)
Inflammatory (demyelinating, infectious,
Autoimmune, sarcoid)
Traumatic
Infiltrative

7. Bilateral optic atrophy
Glaucoma
Secondary to retinal degeneration
Post-papilledema
Congenital anomalies: hypoplasia, coloboma
Methyl alcohol toxicity
Inherited ON : LHON, Auto dominant
Nutritional/toxic

8. Optic Atrophy
• Varies from temporal pallor to chalky white
• Due to changes in blood supply, axonal loss,
glial tissue
• Also nature and extent of injury/damage

9. Differentials
• Axial myopia
• Optic nerve hypoplasia
• Brighter-than-normal luminosity
• Optic nerve pit
• Myelinated nerve fibers
• Scleral crescent
• Optic disc drusen
• Tilted disc

10. Myelinated nerve fibers

11. Optic nerve hypoplasia

12. Optic atrophy
• Slight, moderate, severe
• Diffuse or sectoral

13. Optic atrophy
• Color of disc not indicative of atrophy
• Often temporal side of disc has less color than
nasal side
• O.A diagnosis is based on
-color of disc,changes in vessels,nf layer
- v.a, color vn, VF, pupils,VER

14. 0ptic atrophy
• In AION – Limited to upper and lower quad
• Chiasmal lesions – temp and nasal
pallor(bowtie or band atrophy) due to
crossing nasal fibres being involved
Also seen in eye contralateral to unilateral
optic tract lesion

15. Causes of primary optic atrophy
Idiopathic
Demyelination
Post inflammatory
Toxic
Inflammation of orbit, sinus and meninges
Compressive
Nutritional
Hereditary

16. Causes of secondary optic atrophy
• Anterior ischaemic optic neuropathy
• Papllitis
• Papilledema
• Metabolic diseases (Diabetes)

17. Optic disc pallor
Clinical approach
• Demographic profile
–Age
- Gender
- Race
• Clinical history

18. Optic disc pallor
Demographic profile
• Age – most important of demographic
parameters
• No watertight compartments
• Significant overlaps between age groups
• Glaucoma can present with pallor at any age

20. Optic disc pallor
• Gender can guide in favour of a diagnosis but
not always
• Male: LHON, Traumatic ON,Tapetoretinal
deg,ToxicON,Occupational(heavy metal
exposure), lead, arsenic,Nutritional(chronic
alcoholism)
• Female: MS, Meningioma,
Autoimmune/collagen vasc dis.,Sheehan synd,
ecclampsia

21. Optic disc pallor- Racial differences
• Blacks – lower incidence of Ischaemic ON,
better visual fn in IIH
• Caucasians more likely for MS than Hispanics
and Asians
• Overall Optic atrophy more in blacks than
whites

22. Optic disc pallor- Clinical history
• Onset –over hrs or days- Optic neuritis,
Iscemic ON, Traumatic ON
Subacute- over few days – in demylenating,
compressive
• Course- resolved naturally, recurrent
episodes- demyelinating
residual poor vn ,progressive,protracted
course- other pathologies

23. Optic disc pallor -History
• Laterality
- Unilateral – Typical ON
NAION
Traumatic ON
Compressive
- Bilateral - Toxic,
Nutritional,Hereditary,Arteritic AION, Atypical
Optic neuritis

24. Optic disc pallor - History
• Systemic – fever, jaw claudication,
palpitations, dyspnoea,
hypertension,diabetes,thyroidTB etc
• Ocular painful eye movements, diplopia,
proptosis
• CNS –Headache, vomiting,TIAs, motor deficits,
paraesthesias etc.
• Trauma
• Family history
• Medications- for toxic

25. Optic disc pallor –Ocular Exam
• V.A.
• Visual Fields
• Color Vision
• Pupils
• Fundus – Disc color, cup, margins,
vascularity(Kestebaum count -10 capillaries on
disc. In optic atrophy<6)
• RNFL Defects – Red free green filter exam

26. Optic disc pallor – diagnosis by
optic disc appearance
• Ischaemic – pallid edema
- arterial
attenuation,sheathing
- superior /inferior disc
pallor
- Haemorrhages
- fellow eye small cup-disc
ratio(disc at risk)

27. Inferior disc oedema
Dilated inferior veins
Disc at risk

28. Optic disc pallor - Infective
• Macular star
• Mild pallor or oedema

29. Disc pallor- Toxic/nutritional
• Temporal disc pallor, bilateral

30. Disc pallor-LHON/DOA
• Temporal, occasionally diffuse

31. Optic disc pallor- Chiasma/tract
lesion
• Bowtie/band atrophy
Glaucomatous
Nonglaucomatous

32. Optic disc pallor
• Compressive neuropathy
– unilateral or bil edema
– painless progressive
pallor
– shunt vessels

33. Optic disc pallor- papilloedema
• Dirty grey pallor, bilateral, blurred margins,
obscured cup and gliosis, attenuation of
vessels

34. Papilloedema -stages

35. Disc pallor – systemic exam
Look for
• Nutritional deficiency
• B.P
• Anemia
• Lymph nodes
• CVS /CNS

36. Optic disc pallor-Ocular
investigations
At baseline and followup
• V.A
• Color Vn
• Contrast sensitivity
• VF
• FFA(if necessary)
• OCT
• VER/ERG

37. Optic disc pallor- Investigations
First line
1.Haemogram,peripheral smear,TLC,DLC
2.ESR
3.Mx
4.Chest Xray
5.MRI Head and Orbit with thin cuts and fat
suppression
6.VDRL
7. LP(if reqd)

38. Optic disc pallor- Investigations
1.Sarcoidosis-Serum ACE, serum Ca, CT chest
2.Collagen dis- Immunology workup;ANA,RF
3.Nutritional- Serum B12, Folate levels
4.Toxic-heavy metal screening
5.TORCH
6.Hereditary-LHON mutation(full mitochondrial
sequencing or common mutations
11778,3460,14484)
7.NMO ab for Devic’s. MRI Spine
8. Thyroid functions- T3,T4 and TSH levels

39. VISUAL FIELD EVALUATION

40. VF testing strategies
• Confrontation
• Goldmann kinetic or static
• Humphrey static automated

41. Confrontation fields

42. Presentation Outline
1. General aspects of automated perimetry
2. Components and basics of interpreting visual field reports
3. Physiological basis of visual field defects in neurological afflictions
4. Clinical examples discussing the topographic representation of
visual fields
5. Visual field alterations in neuro-ophthalmological afflictions
6. Algorithm for field assessment and interpretation
7. Review of various field defects

43. Why choose automated perimeters:
Humphrey perimeter
Advantages of Automated Perimetry
•Provides more sensitive and reproducible results
•Provides quantitative information
•Provides results in a more timely and precise manner
•Experienced perimetrist is not required
Advantages of Static Perimetry
•Scotomas better defined
•Temporal summation of stimulus possible
•Less dependence on Perimetrist

44. Patient Information
• Name
• Age
• Refractive Error
• Visual acuity
• Pupil Diameter
• Stimulus/Target
• Strategy
• Fixation
• Gaze monitor
Reliability Indices
• Fixation Losses
• False Positive
• False Negative
• High fixation losses maybe
pseudolosses due to misalignment
or true in cases of central vision
loss
• High FP rates almost always
indicate unreliable test
• High FN rates in abnormal fields
are common in perfectly attentive
patients
• In normal visual field it shows
patient was inattentive
Test Parameter

45. • Any Patient with visual loss unexplained on
Ocular or refractive basis should have a visual
field examinatin as the very next test.

46. Extent of normal visual field
• Nasally 60 degrees
• Superiorly 60 degrees
• Inferiorly 70 to 75 degrees
• Temporally 100 to 110 degrees

47. Interpretation of Humphrey visual Field

48. Why is the Grey scale plot suited for field
assessment in Neuro-ophthalmology cases
• Optic nerve diseases are more likely to result in absolute field
losses
• Absolute field defects are very clearly demarcated on grey
scale plots
• These visual fields often respect the vertical meridians and
these are well defined on grey scale plots
• Orientation of scotoma with respect to the blind spot is best
appreciated on the grey scale plots

49. Effects of distortion or obscuration
• Of light entering eye
by eyebrows, skin of lid
Lens rim, spectacle power(high
plus/minus),incorrect lenses
• By eyelids and media
Pupil size,opacities in media

50. Basis of visual field defect
• Anatomical structure of retinal nerve fibres-
which has 4 groupings which enter Optic disc
a.Inf. Ret n. fibres subserve Sup. visual field
b.Sup. Ret. N. fibres – Inferior visual field
c.Fibres bet macula & optic disc(papillomac
bundle)- central Vn
d.Nasal fibres which enter disc in wedge
shaped manner

51. Basis of field defect
• Superior and Inferior fibres form arcuate
bundles around papillomacular bundle to
enter optic nerve at 12 o’ clock and 6 o’ clock
• Peripherally in retina they join horizontal
raphe. Fibres do not cross horizontal raphe.
• Arcuate n.f.bundle –arcuate field defect. Nasal
extent is hor. Meridian
• Pap-mac bundle-central or centrocaecal
scotoma
• Nasal wedge-temporal defect

52. Basis of field defects
• Optic disc lesions will produce VF defects
identical to those of retina
• Posteriorly fibres rotate 90degrees
• Macular fibres occupy central core of Optic
nerve
• Hence retrobulbar optic nerve lesions produce
more central scotomas.

54. Basis of Visual Field Defects in
Neuro-Ophthalmology

55. Arrangement of nerve fibres along the course
of visual pathway
Lateral Geniculate Body
Upper retina fibers - medial part
Lower retina fibers - lateral part
Macular fibers -posterior 2/3

56. Preview of field
defects seen in
neuro-ophthalmology

57. Topographic principle of visual field
alterations in ret vasc dis
CRVO (Non-ischemic)
BRVO
BRAO
PRP done for Diabetic Retinopathy

58. Visual Field alterations in nerve fibre layer affliction

59. Visual field changes in neuro-ophthalmology
1. Optic disc pit
2. Tilted optic disc
3. Optic disc drusen
4. Anterior ischemic optic neuropathy
5. Papilledema
6. Hereditary optic atrophy
7. Toxic optic neuropathy
8. Optic neuritis
9. Optic nerve meningioma
10. Pituitary adenoma
11. Craniopharyngioma
12. Optic tract and LGB lesions
13. Optic radiation afflictions
14. Visual cortex lesions
15. Miscellaneous field alterations

60. Optic disc pit
Tilted optic disc
Crater like optic disc pit
Optic Disc Drusen
60° field
Optic Disc Drusen
Optic Disc Drusen
30° field

61. AION with cecocentral sparing
Typical AION
Maculopapular ischemia

62. Papilledema (IIH)
Hemorrhagic Papilledema
Papilledema secondary to astrocytoma

63. Principle behind
cecocentral scotoma
Hereditary optic nerve atrophy
Toxic optic neuropathy

64. Visual Field defects in optic
neuritis
Central
Diffuse depression
Altitudnal
Nasal hemianopia
Nerve fibre bundle defects
Combined defects

65. Orbital apex meningioma –alt
defect
Optic nerve sheath meningioma
Sphenoid ridge meningioma with left
orbital apex involvement

66. Field alterations in
chaismal and
perichiasmal lesions
Junctional scotoma in a case of
sphenoid meningioma

67. Pituitary Adenoma
Early stage of pituitary adenoma

68. Late stage pituitary adenoma- Hemianopia and subtotal defects

69. Craniopharyngioma Chiasmal meningioma

70. Field alterations in optic tract and lateral geniculate body lesions
Basal Ganglia neoplasm: Incongruent
Hemianopia

71. Field alterations in lesions involving optic radiations
Astrocytoma of left temporal lobe
Substance
defects in
left brain
Infarct of left occipital and parietal lobe

72. Complete hemianopia in total involvement of all
optic radiations
Hemianopia with sparing of fixation in subtotal in
involvement of all optic radiations
Involvement of all optic radiations after left cystic
tissue defect following neurosurgery

73. Incongruent field losses in occipital lobe infarct
affecting the optic radiations asymmetrically
Incongruent field losses in multiple sclerosis
seen in a 30-2 field
Incongruent field losses in multiple sclerosis are
better demarcated in this 10-2 field

74. Field alterations in afflictions of the visual cortex
Congruent homonymous hemianopia with macular sparing
Occipital lobe infarct with complete homonymous defects
Occipital lobe infarct with incomplete homonymous
defects

75. Miscellaneous Field Defects
Peripheral field defects
• May be out of field for 30-2
• A fast 60-2 protocol used
Bilateral homonynous hemianopia
• Seen in vascular lesions
• May have both congruent
and incongruent areas

76. Miscellaneous Field Defects
Central homonymous hemianopia
• Seen in occipital lobe
abscess
• Also called reading scotoma
Functional visual field loss
• No organic lesion

77. Localisation of homonymous
hemianopia
• Macular sparing
• Congruity
• Pupillary response – normal in Op Radiation
• Asymmetric OKN -Parietal
• Saccadic pursuit to side of lesion-parietal

78. Algorithm for Field Assessment and
Interpretation

79. • References
1. Field charts referenced from Atlas of Computerized
Perimetry by Weber and Caprioli, Published by W.B.
Saunders Co.Philadelphia,2000
2.Clinical Neuro-Ophthalmology by Ulrich Scheifer et
al,Publishers,Springer

80. THANK YOU