This document provides information on optic neuritis, including its definition, etiology, pathology, clinical features, diagnosis, and treatment. Some key points: - Optic neuritis is an inflammatory condition of the optic nerve that can cause visual loss. Common causes include multiple sclerosis, infections, and autoimmune disorders. - Clinical features include sudden visual loss or blurring in one eye, pain with eye movement, and abnormal pupil response to light. Diagnosis is made based on symptoms and MRI findings. - Treatment involves corticosteroids via IV or oral administration. The Optic Neuritis Treatment Trial found IV methylprednisolone can help delay conversion to multiple sclerosis.

1. OPTIC
NEURITIS
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2. OPTIC NERVE
• Forms innermost strata of the retina.
• Continuation of Axon From ganglion Cells (Second Order Neuron)
• Unmyelinated intra-retinally.
• Converge at optic disc (blind spot) & then acquires myelin.
• Exits through lamina cribrosa of the sclera.
• Optic Disc To Optic Chaisma
• 50mm in length
• Extraocular part is surrounded by meninges
• Saltatory Conduction Via the cell membrane

5. DEFINITION
• Includes inflammatory and demyelinating disorders of the optic nerve

8. ETIOLOGY
• Idopathic
• Hereditary optic neuritis ( Lebers disease )
• Demyelinating disorders –
a) Multiple sclerosis (MC)
b) Devics disease
c) Schilder disease

9. • Parainfectious optic neuritis –
associated with measles , mumps, chicken pox or following
immunisation
• Infectious –
sinus related (ethmoiditis) , cat scratch fever , syphilis , lyme disease
, cryptococcal meningitis

10. • Autoimmune disorders associated with optic neuritis:
sarcoidosis, SLE, PAN, Guillain barre syndrome, wegeners
granulomatosis
• Toxic optic neuritis

13. PATHOLOGY
Perivascular infiltrate of inflammatory cells
Destruction of myelin
Removal of disintegrated myelin by phagocytic cells
Proliferative gliosis

15. Typical & Atypical ON
TYPICAL ATYPICAL
• Associated with demyelination Associated with causes other
than demyelination
• Particularly Multiple sclerosis eg. infectious

16. Clinical features
• Visual loss - typical
sudden, monocular, progressive and profound visual loss.
• Dark adaptation lowered
• Visual obscuration in bright light - typical
• Impairment of colour vision (dyschromatopsia)- always present
• Movement phosphenes and sound induced phosphenes – may be perceived
(visual flashing sensations brought about by side-to-side eye movement or sound)
• Uhthoff’s symptom- episodic transient obscuration of vision
• Pulfrich’s symptom – depth perception impaired

18. • Pain :
- mild dull eyeache more marked in retrobulbar neuritis than
papillitis.
- aggravated by ocular movements esp. in upward or downward
direction due to attatchment of some fibres of SR muscle to
duramater.

19. Signs
• Visual acuity markedly reduced
• Colour vision severly impaired (typically red saturation)
• Pupil shows ill sustained constriction to light
MARCUS GUNN pupil – indicates relative afferent pupillary defect (RAPD )
detected by swinging flash light test

20. This is a common case in pupillary examination.
The swinging light test shows abnormal light response of the affected eye (initial dilatation followed by constriction).
For example,
if the left eye were abnormal, both pupils constrict when the light is shown into the right eye.
When the light is swung to the left eye, both pupils dilate.
When the light is swung back to the right eye both pupils again constrict.
This reaction indicates a defect in the afferent pupillary fibres from the left eye.

21. • Ophthalmoscopic features
1. Disc edema and physiological cup obliteration (2-3 D)
2. Retinal veins congested and tortous
3. Splinter hemorrhages and fine exudates may be seen on disc
4. Slit lamp examination may reveal inflammatory cells in vitreous
5. macular star formation – neuroretinits
6. In retobulbar neuritis fundus appears normal , ocassionally temporal
pallor of disc may be seen

23. 7. visual field defects : MC defect is a relative central or centrocaecal scotoma
8. Contrast sensitivity is impaired
9. Visually evoked response (VER) shows reduced amplitude and delay
in transmission time
10. Fundus fluroscein angiography reveals mild to moderate leak in early
phase which increases with time

25. Differenial diagnosis
Papillitis vs papilledema
Acute retrobulbar neuritis vs indirect optic neuropathy, cortical blindness

26. Diagnosis
• The diagnosis of optic neuritis is clinical, based on the history and
physical findings.
• Investigations
• Brain MRI
• Serological tests: ESR, syphilis, antinuclear antibody (ANA),
antineutrophil cytoplasmic antibodies (ANCA)
• CSF analysis (lumbar puncture) : Presence of oligoclonal band,
elevated IgG level suggest MS.

27. Brain MRI
• MRI of the brain and orbits with gadolinium contrast has become the
cornerstone of the evaluation in patients with optic neuritis
• To confirm the clinical diagnosis (look for additional plaques of
demyelination)
• Offers very strong prognostic information about the risk of future
demyelinating events and MS
• For treatment decision

28. A gadolinium-enhanced fat-saturated T1-weighted scan will show a
bright enhancement of the inflamed optic nerve (upper left red arrow).
Additionally, bright spots characteristic of multiple sclerosis may also be
seen in the brain (lower right red arrow).
White matter lesions in
brain MRI denote a
higher risk of
developing MS

29. TREATMENT
• Treat the undelying cause
• No effective treatment for idiopathic and hereditary optic neuritis and that
associated with demyelinating disorders
• CORTICOSTEROID therapy may shorten the period of visual loss, but will not
influence the ultimate level of visual recovery in patients with optic neuritis.
• Interferon therapy reduces the recurrences in patients with MS , costly with
unknown long term benefits

30. OPTIC NEURITIS TREATMENT TRIAL (ONTT)
1. Oral prednisolone therapy alone is C/I in treatment of acute ON
since it was associated with risk of new attacks of ON.
2. IV methylprednisolone –
A pt presenting with AON should have brain MRI scan
- if it show lesions supportive of multiple sclerosis
regardless of severity of vision loss, each should receive immediate iv
methyl prednisolone
Regimen
IV methylprednisolone
1g daily for 3 days followed by oral steroid as prednisone (1mg/kg/day) for 11 days
and then tapered over 4 days
This therapy will delay conversion to clinical MS over the next 2 years.

31. Indiactions for IV methylprednisolone in AON with normal brain MRI scan
• Visual loss in both eyes simultaneously or subsequently within hours or
days of each other.
• When the only good eye is affected
• When the slow progressive visual loss continues to occur

32. The most common side effects associated with Corticosteroids in the
ONTT were :
• mood changes
• facial flushing
• sleep disturbances
• weight gain
• dyspepsia.