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Optic Neuritis, Papilledema
Normal optic disc
2
Optic Neuritis
Definition: Inflammation of the optic nerve,
impairing nerve conduction.
Secondary to demyelination, infection or
autoimmune pathology.
3
Aetiology
• Idiopathic
• Demyelinating disorders
• Multiple Sclerosis
– Presenting feature in 25% patients
– 70% cases occur in established disease
– Recurs in same/ opposite eye in 25% patients
– Uhthoff”s phenomenon: impairment of vision more
with increased body temperature
– Pulfrich phenomenon: altered perception of moving
objects
4
Aetiology
• Neuromyelitis optica (Devic’s disease): acute,
bilateral optic neuritis in young patient with
paraplegia
• Post-viral: mumps, measles, chicken pox, whooping
cough,following immunization
• Metabolic/Nutritional deficiency:
B1, B6, B12, B2, Folic acid deficiency
Thyroid dysfunction, diabetes
• Hereditary optic neuritis (Leber's disease) 5
Aetiology
• Toxic amblyopia:
Chloroquine, Ethambutol
Tobacco, Ethyl alcohol, methyl alcohol
Lead, Arsenic.
• Ischaemic: Giant cell arteritis, Takayasu's disease,
PAN, SLE
• Granulomatous inflammation:
Sarcoidosis, tuberculosis, syphilis
6
Classification
A. Papillitis
B. Retrobulbar neuritis
– Acute
– Chronic (toxic
amblyopia)
C. Neuroretinitis
D. Perineuritis
7
Symptoms
• Idiopathic/demyelinating : 20-40 years of age
• Viral: children
• Uniocular sudden/rapid diminution of vision
• Visual loss, usually maximum by end of second week,
improves by 1-4 weeks
• Discomfort/pain behind eyeball especially when moved
superiorly
8
Signs
• Visual Acuity: Usually 6/60 or less
• Local tenderness
• Pupillary reaction: Sluggish, ill-sustained or RAPD
• Impaired coloured vision: Red desaturation
• Impaired contrast sensitivity
• Delayed dark adaptation
• Visual Field: central, centrocaecal or paracentral scotoma,
more pronounced for coloured fields
• Visually evoked response (VER)-reduced amplitude and
delay in transmission time
9
Ophthalmoscopic findings
• Optic neuritis: MC in children,
engorged, oedematous optic
disc with obliteration of optic cup,
small haemorrhages on disc
• Retrobulbar neuritis: MC in
adults
• Neuroretinitis:
Optic neuritis+ macular star
10
Differential diagnosis
• Papilloedema
• Pseudopapillitis
High hypermetropia,
Myelinated nerve fibres,
Optic nerve head drusen
(blurred margin, disc not significantly
elevated, no vascular changes, stationary)
11
Investigations
• MRI brain and orbit:
demyelinating lesions,
SOL
• VEP: reduced
amplitude and delayed
transmission time
(P100 latency
increased)
Right optic neuritis
12
13
Advanced case of optic neuritis
14
Course and prognosis
• Recovery takes 4-6 weeks
• 90% recover normal VA, but colour vision
defects may persist
• No correlation between initial visual loss
and final visual outcome
• 10% secondary or post-neuritic optic
atrophy
• Better outcome in young, unilateral cases
15
Treatment
• Of cause e.g. anti-infective therapy
• Intravenous methyl prednisolone 20
mg/kg/day(250 mg QID) for 3 consecutive days
followed by oral prednisolone 1-1.5 mg/kg x 11
days.
• Dexamethasone 200 mg OD pulse for 3-5 days
is a cheaper alternative
• Interferon theraphy
• Supportive therapy 16
Papilloedema
• Definition: Bilateral, non-inflammatory
passive swelling of optic disc due to raised
Intracranial pressure.
• Does not develop if optic nerve is atrophic
17
CSF circulation
18
Foster-Kennedy syndrome : contralateral
papilloedema with ipsilateral pressure atrophy of
optic nerve
Due to - frontal lobe tumour, olfactory meningioma
19
D/D: Causes of 'disc oedema'
• Inflammations-Papillitis, neuroretinitis
• Ocular hypotony
• Infiltrative conditions-leukaemias,lymphomas
• Orbital causes-orbital cellulitis,Optic Nerve
glioma, meningioma
• Vascular causes-CRVO,AION,uremia,diabetic
papillopathy
20
Etiopathogenesis of papilloedema
1.Congenital conditions - Aqueductal stenosis,
craniosynostosis
2. lntracranial space-occupying lesions (ICSOLs) -
Brain tumours, abscess, tuberculoma, gumma,
subdural haematoma and aneurysms
3. Intracranial infections such as meningitis and
encephalitis
4. Intracranial haemorrhages. CerebraI as well as
subarachnoid haemorrhage 21
6. Tumours of spinal cord
7. ldiopathic intracranial hypertension (IIH) also
known as pseudotumour cerebri.
8. Systemic condilions include malignant
hypertension, pregnancy-induced hypertension (PIH),
cardiopulmonary insufficiency, blood dyscrasias and
nephritis.
9. Diffuse cerebral oedema from blunt head trauma.
10. Cerebral venous sinus thrombosis
22
Aetio-Pathogenesis
• Elevated Intracranial pressure due to any cause
• Prelaminar Optic Nerve is affected by changes in tissue
pressure, IOP and CSF pressure
• Increased CSF pressure increases tissue pressure
hampering axoplasmic flow
• This further increases pressure on pre-laminar capillaries
and small veins causing vasodilatation and tortuosity
• Venous drainage compromise further increases
congestion 23
24
General Symptoms
• Headache, made worse by coughing or
straining
• Vomiting
• Focal neurological deficit with/without
changes in level of consciousness
25
Ocular symptoms
• VA may be normal until late stages
• Amaurosis fugax in some
• In 25% patients, visual symptoms occur
only in severe, advanced papilloedema
• Pupillary reactions are normal until
secondary atrophy sets in
26
1. Early (incipient) papilloedema
2. Established (fully developed)
papilloedema
3. Chronic or long standing papilloedema
4. Atrophic papilloedema
27
Signs
• Early papilloedema-
– Blurring of nasal>superior>inferior margins of
disc
– Disc hyperemia and dilated capillaries
– Spontaneous venous pulsation absent
– Splinter haemorrhages at/just off disc margin
– Normal optic cup preserved
28
29
Established papilloedema
• Margins indistinct and cup
obliterated
• Surface elevated upto more
than +3 D with direct
ophthalmoscope
• Flame-shaped haemorrhages,
cotton-wool spots
• Venous engorgement and
peripapillary oedema
• Paton's Lines-radial lines
cascading from optic disc
• Macular star
• Hard exudates
30
With progression
• Chronic papilloedema
– Central cup remains
obliterated
– Haemorrhagic and exudative
components resolve gradually
– 'Champagne cork' appearance
31
• Atrophic
papilloedema
– Retinal vessels attenuated
with perivascular sheathing
– Dirty white colour due to
reactive gliosis
– Leads to secondary optic
atrophy
32
Visual fields
• Early-no changes
• Established stage- enlarged blind spot
• Chronic- peripheral constriction of field
with nerve fibre bundle defects
• Finally- total loss of visual field
33
Fundus photo, FFA , OCT
34
Papilloedema Optic neuritis
History Headache, vomiting Rapid DV preceded by
fever/respiratory infection
Laterality usually bilateral usually unilateral
VA normal till late stage severely reduced <6/60
Pain/tenderness of eyeball absent may be present
Pupil reaction normal RAPD (Marcus-Gunn's pupil)
Disc swelling >+3 D in established +2D to +3D
Haemorrhage, exudates More, in established relatively less
Visual fields Enlarged blind spot,
later gradual
constriction
Central or centrocaecal scotoma
Colour vision No effect Affected
CT/MRI SOL Demyelinating disorder
Recovery of vision May not be complete
even after treatment
Usually complete after adequate
treatment
35
36
Treatment
• Urgent neuroimaging ( CT scan / MRI)
• Treat Cause
• Acetazolamide 250 mg 4 times a day
• Surgical decompression of optic nerve to
preserve vision
37
Thank you
38

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830_Optic_nerve_final copy 2.pptx

  • 3. Optic Neuritis Definition: Inflammation of the optic nerve, impairing nerve conduction. Secondary to demyelination, infection or autoimmune pathology. 3
  • 4. Aetiology • Idiopathic • Demyelinating disorders • Multiple Sclerosis – Presenting feature in 25% patients – 70% cases occur in established disease – Recurs in same/ opposite eye in 25% patients – Uhthoff”s phenomenon: impairment of vision more with increased body temperature – Pulfrich phenomenon: altered perception of moving objects 4
  • 5. Aetiology • Neuromyelitis optica (Devic’s disease): acute, bilateral optic neuritis in young patient with paraplegia • Post-viral: mumps, measles, chicken pox, whooping cough,following immunization • Metabolic/Nutritional deficiency: B1, B6, B12, B2, Folic acid deficiency Thyroid dysfunction, diabetes • Hereditary optic neuritis (Leber's disease) 5
  • 6. Aetiology • Toxic amblyopia: Chloroquine, Ethambutol Tobacco, Ethyl alcohol, methyl alcohol Lead, Arsenic. • Ischaemic: Giant cell arteritis, Takayasu's disease, PAN, SLE • Granulomatous inflammation: Sarcoidosis, tuberculosis, syphilis 6
  • 7. Classification A. Papillitis B. Retrobulbar neuritis – Acute – Chronic (toxic amblyopia) C. Neuroretinitis D. Perineuritis 7
  • 8. Symptoms • Idiopathic/demyelinating : 20-40 years of age • Viral: children • Uniocular sudden/rapid diminution of vision • Visual loss, usually maximum by end of second week, improves by 1-4 weeks • Discomfort/pain behind eyeball especially when moved superiorly 8
  • 9. Signs • Visual Acuity: Usually 6/60 or less • Local tenderness • Pupillary reaction: Sluggish, ill-sustained or RAPD • Impaired coloured vision: Red desaturation • Impaired contrast sensitivity • Delayed dark adaptation • Visual Field: central, centrocaecal or paracentral scotoma, more pronounced for coloured fields • Visually evoked response (VER)-reduced amplitude and delay in transmission time 9
  • 10. Ophthalmoscopic findings • Optic neuritis: MC in children, engorged, oedematous optic disc with obliteration of optic cup, small haemorrhages on disc • Retrobulbar neuritis: MC in adults • Neuroretinitis: Optic neuritis+ macular star 10
  • 11. Differential diagnosis • Papilloedema • Pseudopapillitis High hypermetropia, Myelinated nerve fibres, Optic nerve head drusen (blurred margin, disc not significantly elevated, no vascular changes, stationary) 11
  • 12. Investigations • MRI brain and orbit: demyelinating lesions, SOL • VEP: reduced amplitude and delayed transmission time (P100 latency increased) Right optic neuritis 12
  • 13. 13
  • 14. Advanced case of optic neuritis 14
  • 15. Course and prognosis • Recovery takes 4-6 weeks • 90% recover normal VA, but colour vision defects may persist • No correlation between initial visual loss and final visual outcome • 10% secondary or post-neuritic optic atrophy • Better outcome in young, unilateral cases 15
  • 16. Treatment • Of cause e.g. anti-infective therapy • Intravenous methyl prednisolone 20 mg/kg/day(250 mg QID) for 3 consecutive days followed by oral prednisolone 1-1.5 mg/kg x 11 days. • Dexamethasone 200 mg OD pulse for 3-5 days is a cheaper alternative • Interferon theraphy • Supportive therapy 16
  • 17. Papilloedema • Definition: Bilateral, non-inflammatory passive swelling of optic disc due to raised Intracranial pressure. • Does not develop if optic nerve is atrophic 17
  • 19. Foster-Kennedy syndrome : contralateral papilloedema with ipsilateral pressure atrophy of optic nerve Due to - frontal lobe tumour, olfactory meningioma 19
  • 20. D/D: Causes of 'disc oedema' • Inflammations-Papillitis, neuroretinitis • Ocular hypotony • Infiltrative conditions-leukaemias,lymphomas • Orbital causes-orbital cellulitis,Optic Nerve glioma, meningioma • Vascular causes-CRVO,AION,uremia,diabetic papillopathy 20
  • 21. Etiopathogenesis of papilloedema 1.Congenital conditions - Aqueductal stenosis, craniosynostosis 2. lntracranial space-occupying lesions (ICSOLs) - Brain tumours, abscess, tuberculoma, gumma, subdural haematoma and aneurysms 3. Intracranial infections such as meningitis and encephalitis 4. Intracranial haemorrhages. CerebraI as well as subarachnoid haemorrhage 21
  • 22. 6. Tumours of spinal cord 7. ldiopathic intracranial hypertension (IIH) also known as pseudotumour cerebri. 8. Systemic condilions include malignant hypertension, pregnancy-induced hypertension (PIH), cardiopulmonary insufficiency, blood dyscrasias and nephritis. 9. Diffuse cerebral oedema from blunt head trauma. 10. Cerebral venous sinus thrombosis 22
  • 23. Aetio-Pathogenesis • Elevated Intracranial pressure due to any cause • Prelaminar Optic Nerve is affected by changes in tissue pressure, IOP and CSF pressure • Increased CSF pressure increases tissue pressure hampering axoplasmic flow • This further increases pressure on pre-laminar capillaries and small veins causing vasodilatation and tortuosity • Venous drainage compromise further increases congestion 23
  • 24. 24
  • 25. General Symptoms • Headache, made worse by coughing or straining • Vomiting • Focal neurological deficit with/without changes in level of consciousness 25
  • 26. Ocular symptoms • VA may be normal until late stages • Amaurosis fugax in some • In 25% patients, visual symptoms occur only in severe, advanced papilloedema • Pupillary reactions are normal until secondary atrophy sets in 26
  • 27. 1. Early (incipient) papilloedema 2. Established (fully developed) papilloedema 3. Chronic or long standing papilloedema 4. Atrophic papilloedema 27
  • 28. Signs • Early papilloedema- – Blurring of nasal>superior>inferior margins of disc – Disc hyperemia and dilated capillaries – Spontaneous venous pulsation absent – Splinter haemorrhages at/just off disc margin – Normal optic cup preserved 28
  • 29. 29
  • 30. Established papilloedema • Margins indistinct and cup obliterated • Surface elevated upto more than +3 D with direct ophthalmoscope • Flame-shaped haemorrhages, cotton-wool spots • Venous engorgement and peripapillary oedema • Paton's Lines-radial lines cascading from optic disc • Macular star • Hard exudates 30
  • 31. With progression • Chronic papilloedema – Central cup remains obliterated – Haemorrhagic and exudative components resolve gradually – 'Champagne cork' appearance 31
  • 32. • Atrophic papilloedema – Retinal vessels attenuated with perivascular sheathing – Dirty white colour due to reactive gliosis – Leads to secondary optic atrophy 32
  • 33. Visual fields • Early-no changes • Established stage- enlarged blind spot • Chronic- peripheral constriction of field with nerve fibre bundle defects • Finally- total loss of visual field 33
  • 34. Fundus photo, FFA , OCT 34
  • 35. Papilloedema Optic neuritis History Headache, vomiting Rapid DV preceded by fever/respiratory infection Laterality usually bilateral usually unilateral VA normal till late stage severely reduced <6/60 Pain/tenderness of eyeball absent may be present Pupil reaction normal RAPD (Marcus-Gunn's pupil) Disc swelling >+3 D in established +2D to +3D Haemorrhage, exudates More, in established relatively less Visual fields Enlarged blind spot, later gradual constriction Central or centrocaecal scotoma Colour vision No effect Affected CT/MRI SOL Demyelinating disorder Recovery of vision May not be complete even after treatment Usually complete after adequate treatment 35
  • 36. 36
  • 37. Treatment • Urgent neuroimaging ( CT scan / MRI) • Treat Cause • Acetazolamide 250 mg 4 times a day • Surgical decompression of optic nerve to preserve vision 37