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OPTIC ATROPHY
Optic Atrophy
Optic atrophy refers to the ophthalmoscopic
appearance of the optic disc that may result from
damage to any portion of the ganglion cells from their
cell bodies to their synapse at the lateral geniculate
body.
It represents permanent loss of retinal ganglion cell
axon in conjunction with retinal ganglion cell death.
Optic atrophy
• It should be considered a pathologic end point
that is clinically discernible but does not imply
cause.
Optic atrophy
• Optic atrophy sets in 4-6 weeks after axonal damage.
• Severe damage with chalky white optic disc is easily
identified.
• Milder forms are identified by:
- comparison of colour of the 2 discs.
- evaluation of surface vasculature of the disc.
- evaluation of the peripapillary nerve fibre layer.
Optic atrophy
Types:
Primary
Secondary
Consecutive
Glaucomatous
Types:
Ascending/Upstream
Descending/Downstream
Primary optic atrophy
• Primary optic atrophy results from the loss of
optic nerve fibres with otherwise minimum
disturbance of optic nerve head
microanatomy.
Primary optic atrophy
• Ophthalmoscopic features:
-Pale to white disc.
-Clearly defined disc
margins.
-Decrease in capillaries on
the disc.
-Arteriolar narrowing.
Primary Optic atrophy
• Results from any injury to the retinal ganglion cell
or its axon , anywhere in its course.
• Common causes:
-AION( Ant ischaemic optic neuropathy)
-Compressive lesions of the optic nerve
-Other ischaemic ,inflammatory and lesions
- Less common- PION
Trauma
Granulomatous inflammation of the
optic nerve
Secondary optic atrophy
• It represents disorganised appearance of the
optic disc usually as a result of severe disc
edema/ papilledema, severe inflammation at
the optic nerve head ( papillitis/neuroretinitis)
or, long standing severe orbital inflammation.
Secondary optic atrophy
• Ophthalmoscopic appearance:
-Disc-grayish
-Disc margin blurred
-Raised disc surface
-Glial proliferation on the
surface
-Arteriolar narrowing
Consecutive optic atrophy
Optic atrophy due to destruction of ganglion
cells resulting from the extensive diseases of
the retina is called consecutive optic atrophy.
Examples:
Pigmentary retinal dystrophy
Central retinal artery occlusion
Consecutive optic atrophy
Glaucomatous optic atrophy
• The condition is characterised by enlargement
and excavation of the optic disc cup.
Glaucomatous physiological cup Glaucomatous optic atrophy
Optic atrophies: comparison
Fundus Primary Secondary Consecutive Glaucomatous
Disc
colour
Pale/
White
gray Waxy Pale/
White
Margin Sharp Blurred Sharp/blurred Sharp
Cup unremark
able
full unremarkable Deep,
cavernous
BV on
the disc
decreased decreased decreased decreased
Retina Normal May show
gliosis
Retinal
disease
Normal
Clinical presentation
Diminution of vision
Impaired colour perception
Impaired contrast sensitivity
Pupillary signs
Approach to a case of optic atrophy
• Tailored to the clinical inputs.
• History
• General and systemic examination.
Examination and investigations
• Vision
• IOP
• Pupil
• Fundus
• Systemic Exam
• Investigations including neuroimaging
Toxic/nutritional optic neuropathies
• These include a number of conditions in which
optic nerve fibres are damaged due to
exposure to exogenous poisons or nutritional
deficiencies.
• Many of them have similar clinical picture
because of their common pathways.
Toxic/nutritional optic neuropathies
Etiology
• Dietary deficiency : Vitamin B ₁₂, folate,
thiamine.
• Toxic exposure: Ethambutol, isoniazid,
hydroxyquinoline, cisplatin, vincristine.
• Substance abuse: Ethanol
Symptoms
• In the early stages symptoms and signs are minimal
• Subtle depression of VF within 10⁰ fixation region
,noticed on Amsler's grid.
• With progression visual acuity and colour vision
• suffers.
• Central field defect
• Fundus: Normal initially/optic atrophy finally.
Test of central field with Amsler grid
Diagnosis
• History of exposure to toxin , drug intake,
substance abuse.
• Blood test for serum B12 ,transketolase for
thiamine deficiency.
• Neuroimaging
Differential diagnosis
• Subtle maculopathies
• Hereditary, compressive , demyelinating,
infiltrative optic neuropathies
Course and prognosis
• Untreated deficiency optic neuropathy can
lead to profound visual loss.
• Correction of deficiency reverses the deficit
within few months.

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optic atrophy.pptx

  • 2. Optic Atrophy Optic atrophy refers to the ophthalmoscopic appearance of the optic disc that may result from damage to any portion of the ganglion cells from their cell bodies to their synapse at the lateral geniculate body. It represents permanent loss of retinal ganglion cell axon in conjunction with retinal ganglion cell death.
  • 3. Optic atrophy • It should be considered a pathologic end point that is clinically discernible but does not imply cause.
  • 4. Optic atrophy • Optic atrophy sets in 4-6 weeks after axonal damage. • Severe damage with chalky white optic disc is easily identified. • Milder forms are identified by: - comparison of colour of the 2 discs. - evaluation of surface vasculature of the disc. - evaluation of the peripapillary nerve fibre layer.
  • 6. Primary optic atrophy • Primary optic atrophy results from the loss of optic nerve fibres with otherwise minimum disturbance of optic nerve head microanatomy.
  • 7. Primary optic atrophy • Ophthalmoscopic features: -Pale to white disc. -Clearly defined disc margins. -Decrease in capillaries on the disc. -Arteriolar narrowing.
  • 8. Primary Optic atrophy • Results from any injury to the retinal ganglion cell or its axon , anywhere in its course. • Common causes: -AION( Ant ischaemic optic neuropathy) -Compressive lesions of the optic nerve -Other ischaemic ,inflammatory and lesions - Less common- PION Trauma Granulomatous inflammation of the optic nerve
  • 9. Secondary optic atrophy • It represents disorganised appearance of the optic disc usually as a result of severe disc edema/ papilledema, severe inflammation at the optic nerve head ( papillitis/neuroretinitis) or, long standing severe orbital inflammation.
  • 10. Secondary optic atrophy • Ophthalmoscopic appearance: -Disc-grayish -Disc margin blurred -Raised disc surface -Glial proliferation on the surface -Arteriolar narrowing
  • 11. Consecutive optic atrophy Optic atrophy due to destruction of ganglion cells resulting from the extensive diseases of the retina is called consecutive optic atrophy. Examples: Pigmentary retinal dystrophy Central retinal artery occlusion
  • 13. Glaucomatous optic atrophy • The condition is characterised by enlargement and excavation of the optic disc cup.
  • 14. Glaucomatous physiological cup Glaucomatous optic atrophy
  • 15. Optic atrophies: comparison Fundus Primary Secondary Consecutive Glaucomatous Disc colour Pale/ White gray Waxy Pale/ White Margin Sharp Blurred Sharp/blurred Sharp Cup unremark able full unremarkable Deep, cavernous BV on the disc decreased decreased decreased decreased Retina Normal May show gliosis Retinal disease Normal
  • 16.
  • 17. Clinical presentation Diminution of vision Impaired colour perception Impaired contrast sensitivity Pupillary signs
  • 18. Approach to a case of optic atrophy • Tailored to the clinical inputs. • History • General and systemic examination.
  • 19. Examination and investigations • Vision • IOP • Pupil • Fundus • Systemic Exam • Investigations including neuroimaging
  • 20. Toxic/nutritional optic neuropathies • These include a number of conditions in which optic nerve fibres are damaged due to exposure to exogenous poisons or nutritional deficiencies. • Many of them have similar clinical picture because of their common pathways.
  • 21. Toxic/nutritional optic neuropathies Etiology • Dietary deficiency : Vitamin B ₁₂, folate, thiamine. • Toxic exposure: Ethambutol, isoniazid, hydroxyquinoline, cisplatin, vincristine. • Substance abuse: Ethanol
  • 22. Symptoms • In the early stages symptoms and signs are minimal • Subtle depression of VF within 10⁰ fixation region ,noticed on Amsler's grid. • With progression visual acuity and colour vision • suffers. • Central field defect • Fundus: Normal initially/optic atrophy finally.
  • 23. Test of central field with Amsler grid
  • 24. Diagnosis • History of exposure to toxin , drug intake, substance abuse. • Blood test for serum B12 ,transketolase for thiamine deficiency. • Neuroimaging
  • 25. Differential diagnosis • Subtle maculopathies • Hereditary, compressive , demyelinating, infiltrative optic neuropathies
  • 26. Course and prognosis • Untreated deficiency optic neuropathy can lead to profound visual loss. • Correction of deficiency reverses the deficit within few months.