Optic neuritis is inflammation of the optic nerve that can be caused by demyelination, infection, or other autoimmune processes. It is classified based on location of inflammation (retrobulbar, papillitis, neuroretinitis) and etiology. Common symptoms include sudden unilateral vision loss, eye pain on movement, and color vision changes. Examination may reveal reduced acuity, afferent pupillary defect, and optic disc swelling or atrophy. Brain MRI and lumbar puncture help diagnose underlying causes like multiple sclerosis. For demyelinating optic neuritis, high-dose intravenous steroids can hasten recovery of vision lost.

1. Optic neuritis
=INFLAMMATION,INFECTION OR
DEMYELINATION OF OPTIC NERVE

2. Optic Neuritis - Outline
• Definition
• Classification
▫ Ophthalmoscopic
▫ Aetiological
• Clinical Features
• Investigations
• Principle of Management

3. CLASSIFICATION:
Can be classified both ophthalmoscopically and
etiologically:
 Retrobulbar neuritis
 Papillitis (most common)
 Neuroretinitis
 Demyelinating **
 Parainfective
(rubella,mumps&chicken pox)
 Infective
(sinusitis.syphilis,cat-scratch fever)
 Autoimmune
OPHTHALMOSCOPICALLY
ETIOLOGICALLY

4. • Retrobulbar neuritis
 Optic nerve is affected more posteriorly with no disc swelling.
• Papillitis
Affect optic nerve head (hyperaemia & oedema of optic disc) +
peri-papillary flame-shaped haemorrhages
• Neuroretinitis
Characterized by papillitis with inflammation of the retinal nerve
fiber layer. A macular star figure composed of hard exudates
may present. Least common and most frequently associated with
viral infections and cat-scratch fever, Syphilis and Lyme disease.
Usually self-limiting which resolves 6-12 months.
Neuroretinitis is rarely a manifestation of demyelination.

5. Ophthalmoscopical Classification
Retrobulbar neuritis Papillitis Neuroretinitis
 Optic nerve affected
behind the eyeball
 Optic nerve head affected  Concomitant swelling of
optic nerve head
(papillitis) and macula
(inflammation of retinal
nerve fibre layer)
 The optic disc appears
normal
 The condition may be truly
described as ‘ the patient
sees nothing and the
doctor sees nothing.’
 Hyperaemia and oedema
of the optic disc
 May be a/w peripapillary
flame-shaped
haemorrhages
 Macular star
(exudates that form
around the macula give
the appearance of the
star)
 Most frequent type in
adults
 Frequently a/w multiple
sclerosis (MS)
 Most common type in
children
 Least common type
 Rarely a manifestation of
demyelination
 Due to viral infection,cat-

6. Normal optic disc, primary optic atrophy. The condition may be truly described
as ‘ the patient sees nothing and the doctor sees nothing.’
Retrobulbar neuritis

7. swollen disc with blurring and hyperaemia of disc margin; venous dilation and
engorgement ; vitreous haziness because of inflammatory exudates and cells that
invaded the vitreous( mild vitritis); Flame-shaped hemorrhages and cotton wool
spot (soft exudates) on and around the disc; secondary optic atrophy
Papillitis

8. Macular star
(Exudates in a star-shaped
pattern radiating from the
macula)
Neuroretinitis
Diffuse Unilateral Subacute
Neuroretinitis - Nematode

9. Aetiological Classification (causes)
1. Demyelinating
 Pathological process: the normally myelinated nerve fibres lose
their insulating myelin layer (The myelin is phagocytosed by
microglia and macrophages,subsequent to which astrocytes lay
down fibrous tissue (plaque) -> distrupts nerve conduction w/in
white matter tracts( brain,brainstem,spinal cord)
 Ages: 20-50 years old, F:M = 3:2
 Most common cause (eg. Multiple sclerosis)
 Optic disc is normal (retrobulbar neuritis)

10. DEMYLINATING DISEASE CAUSES OCULAR PROBLEMS:
1. Isolated optic neuritis
2. Multiple sclerosis
3. Devic disease (neuromyelitis optica) : bilateral optic neuritis -> transverse
myelitis
4. Schilder disease : bilateral; progressive generalised disease (onset prior to
10y/o death within 1-2yrs)
a) visual p/way-> lesion commonly involve optic nerves and cause optic
neuritis
b) Brainstem-> lesions result in gaze palsies, ocular motor cranial nerve
palsies, trigeminal , facial nerve palsies and nystagmus

11. Multiple sclerosis (MS)
• A remitting idiopathic
demyelinating disease in CNS
• Autoimmune rxn : T-cell
activation => attack&destruct
myelin

12. 2. Parainfectious
 Common in children
 Occurs d/t exposure of antigens of certain infectious agents
eg. measles, mumps, chickenpox, rubella,whooping
cough,glandular fever
 Following viral infection, immunization
 Usually 1-3 weeks following viral infection with acute severe
visual loss
 Usually bilateral papillitis occur
(occasionally: neuroretinitis or the discs may be normal)
 Spontaneous recovery within few weeks
 May be a/w other neurological features eg. headache,
seizures or ataxia (meningoencephalitis)

13. 3. Infectious
 Sinus-related optic neuritis
 a/w Cat-scratch fever, syphilis, Lyme disease, cryptococcal
meningitis in patients with AIDS and herpes zoster.
4. Non-infectious
 Sarcoidosis- optic nerve head exhibit lumpy appearance,
inflammatory reaction in vitreous
 Systemic autoimmune diseases –retrobulbar neuritis
 eg. SLE, polyarteritis nodosa, other vasculitides (vasculitis)

14. Clinical Features of Optic Neuritis

15. Clinical Presentations
• Usu. women aged btw 20-40 (mean around 30 years)
• Acute unilateral loss of vision, may progress over a few days,
then slowly improve
• Pain exacerbated on eye movement (retrobulbar neuritis) b/c rectus
contraction pulls on the optic nerve sheath; painless (papillitis)
• Dyschromatopsia (change in color perception) in affected eye
• Flashes of light/ phosphenes (tiny white or coloured flashes or
sparkles) induced by eye movement or loud sounds
• Relapsing( most common)/ Progressive (10%)

16. • A preceding H/O viral illness in some cases
• Vision loss exacerbated by heat or exercise (Uhthoff
phenomenon).
• 40-70% of patients will have other neurological symptoms
(such as parasthesia, weakness, incontinence, Lhermitte sign)
to suggest a diagnosis of demyelination (multiple sclerosis)

17. Examinations
• Reduced visual acuity
• Reduced color vision
• RAPD (Relative afferent pupillary defect) : reduced
optic nerve conduction
• Central scotoma
• Normal disc: retrobulbar neuritis ; Swollen disc:
papillitis

18. 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.

19. 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

20. 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

21. Principle of Management
TREAT THE
UNDERLYING
CAUSE

22. Management: Demyelinating Optic
Neuritis
• In most cases (mild vision loss, no significant visual field
loss, no enhancing lesions on brain MRI) - no treatment
• Vision slowly recovers over several weeks even w/o treatment
(spontaneously)
• Treatment Indicated
▫ Visual acuity worsen than 6/12
▫ Treatment hasten the recovery process, but no effect on
long-term visual outcome

23.  Regimen
▫ IV corticosteroid (eg. methylprednisolone)
 1g daily for 3 days followed by oral steroid as prednisone
(1mg/kg/day) for 11 days and then tapered for 3 days
▫ IM interferon beta-1a
 Reducing the development of clinical MS over the
following 3 years in patients at high risk (based on the
presence of subclinical brain MRI lesion)
NB. Oral prednisolone alone is contraindicated b/c it does not affect
the speed of recovery and is a/w a significantly higher recurrence rate.
Corticosteroids S/E
• Mood changes
• Facial flushing
• Weight gain
• Dyspepsia