Optic neuritis is inflammation of the optic nerve that commonly presents as sudden, unilateral vision loss. It affects young females predominantly and is often the initial presentation of multiple sclerosis. Treatment with intravenous steroids followed by oral steroids accelerates visual recovery but provides no long-term benefit over oral steroids alone. Early treatment of multiple sclerosis after an initial demyelinating event such as optic neuritis can reduce future relapse rates and disability progression.

1. OPTIC NEURITIS

2. DEFINITION
 Optic neuritis refers to
inflammation of the optic
nerve
 Occurs in about 50 % of pts
with multiple sclerosis and is
presenting feature in 20%

3. EPIDEMIOLOGY
 1/1,00,000
 5:1- female:male ratio
 Young age (20-40 years old)

4. ETIOLOGY

5.  Idopathic
 Demyelinating disorders –
a) Multiple sclerosis
b) Devics disease
c) Schilder disease
d) acute disseminated
encephalomyelitis

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

7. CLINICAL TYPES
 Papillitis – involvement of optic
disc
 Neuroretinitis – involvement of
optic disc and surrounding retina in
macular area
 Retrobulbar neuritis –
involvement of optic nerve behind
the eyeball

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

10. CLINICAL FEATURES
 HISTORY
 A prodromal viral illness may
occur.
 Orbital pain and pain with eye
movement prior to visual
changes. The pain can be
excruciating or very mild like a
foreign body sensation.

11. SYMPTOMS
 Sudden profound U/L vision loss
 Pain aggravated by ocular
movements – especially upward or
downward ( due to attachment of
fibres of superior rectus to dura )
 Visual obscuration in bright light
 Impaired dark adaptation
 Reduced vividness of saturated
colours

12.  Movement phosphenes and sound
induced phosphenes
 Uthoff phenomenon – transient
obscuration of vision on exertion
and on exposure to heat
 Pulfrich phenomenon – altered
depth perception for moving objects

13. SIGNS
 Decreased visual acuity
 Decreased color vision (red
desaturation) and/or decreased
contrast/brightness sense
 RAPD unless both eyes are affected
or RAPD was present prior in
contralateral eye

14.  Disc edema (only 35% noted in
ONTT, thus lack of disc edema does
not rule out acute optic neuritis)
 Retinal vascular sheathing, pars
planitis (periphlebitis occurs in 5-
10% of multiple sclerosis patients)

15.  Any scotoma on Amsler grid and/or
confrontation visual fields or formal
visual field testing – most common
is a central or centrocecal scotoma
 VEP shows reduced amplitude and
delayed transmission time

16. TYPICAL OPTIC NEURITIS
 Predominantly affects females
 15-45 years
 Unilateral
 Acute , painful vision loss over
hours to days

17.  Retrorbital pain worse with eye
movments
 Peak visual loss within 2 weeks
after which improvement occurs
 Poor color vision , contrast
sensititivity
 Any type of visual field defect
 VEP- prolonged latency , decreased
amplitude

18. ATYPICAL OPTIC NEURITIS
 Painless visual loss
 Extremes of age
 Bilateral
 Disc hemorrhage , cotton wool
spots
 Progression of visual loss beyond 2
weeks
 Fails to improve with treatment

19. D/D
PAPILLEDEMA PAPILLITIS PSEUDO-
PAPILLITIS
LATERALITY B/L U/L U/L OR B/L
VA BLURRED
VISION
SUDDEN
PRFOUND LOSS
OF VISION
BLURRED
VISION
PAIN ON
OCULAR
MOVEMENTS
NIL YES NIL
MEDIA CLEAR VIT CELLS CLEAR

20. PERIPAPILLARY
EDEMA , VENOUS
ENGORGEMENT,
RETINAL HRAGE ,
EXUDATES
MARKED LESS MARKED ABSENT
FIELD
DEFECT
ENLARGED BLIND
SPOT
CENTRAL
SCOTOMA
NIL
FFA LEAKAGE OF
DYE++
MINIMAL
LEAKAGE
NIL

21. INVESTIGATIONS
 Routine Ix are not required in a
case of typical optic neuritis
 Required in the following conditions
A) Atypical optic neuritis
B)Recurrent optic neuritis
C)Acute optic neuritis in children
D)Presence of systemic
inflammatory disease

22.  CBC
 Chest x ray
 ANA , dsDNA
 FTA-ABS , VDRL
 Serology and culture for bartonella
 PCR for viral infections
 CSF tap

23. MRI CRITERIA FOR
DIAGNOSING MS
 Atleast 3 lesions and two of the
following should be present
 1) lesions abutting the lateral
ventricles
 2)lesions with diameters greater
than 5 mm
 3)lesions present in the posterior
fossa

24. TREATMENT
 Optic neuritis treatment trial
(ONTT)
 OBJECTIVES
To evaluate efficacy
of corticosteroids in
Rx of acute optic
neuritis
To investigate
relationship b/w optic
neuritis and multiple
sclerosis

25.  INCLUSION CRITERIA
 Age 18-46 yrs
 Acute U/L optic neuritis for 8 days
or less
 A RAPD and a visual field defect in
the affected eye
 No previous corticosteroid
treatment for optic neuritis or MS
 No systemic disease other than MS
that might be cause of optic neuritis

26. Pts were randomised to one of 3
groups
ORAL PREDNISOLONE
1MG/KG FOR 14 DAYS
IVMP (250MG/6HRS) FOR 3
DAYS FOLLOWED BY ORAL
PREDNISOLONE 1MG/KG
FOR 11 DAYS
ORAL PLACEBO FOR 14
DAYS

27. RESULTS
 Routine Ix are of limited value in
diagnosing optic neuritis in a patient
with typical optic neuritis
 Brain MRI is a powerful predictor of
early risk of MS after optic neuritis
 Visual recovery begins within 2 weeks
and continues upto 1 yr
 Probability of recurrence of optic neuritis
in either eye within 5 yrs is 28 %

28.  Treatment with high dose IV
steroid followed by oral steroid
accelerated visual recovery but
provided no long term benefit to
vision
 Treatment with oral
prednisolone alone did not
improve visual outcome and was
associated with increased rates of
new attacks of optic neuritis

29.  Dyschromatopsia , defective
stereoacuity , RAPD , delayed
latencies on VEP , pulfrich and
uthoff phenomenon may remain as
residual deficits after an attack of
optic neuritis

30.  Four large scale clinical trials have
been conducted to determine
whether early treatment following
first demyelinating episode can
delay the second event
 1)CHAMPS AND CHAMPIONS
 2)ETOMS
 3)BENEFIT
 4)PRECISE

31. CONTROLLED HIGH RISK AVONEX
MULTPLE SCLEROSIS TRIAL- CHAMPS
STUDY
•TO STUDY WHETHER INTERFERON BETA 1a TRAETMENT
WOULD BENEFIT PTS HAVING FIRST DEMYELINATING
EVENT AND MRI ABNORMALITIES IN REDUCING THE
INCIDENCE OF CDMS
OBJECTIVES
•ALL PTS RECEVIED IVMP FOR 3 DAYS F/B ORAL
PREDNISOLONE FOR 11 DAYS PLUS
•GROUP 1 – RECIVED WEEKLY INJECTION OF IFN BETA 1
a
•GROUP 2 RECEIVED PLACEBO INJECTION
MATERIAL
AND
METHODS
•AT THE END OF 3 YRS PROBABILITY OF DEVELOPING
CDMS WAS 50 % IN PLACEBO GROUP AND 35% IN IFN
BETA TREATED GROUP
•TREATMENT WITH AVONEX (IFN BETA 1 a)REDUCED 2
YRS LIKELIHOOD OF FUTURE NEUROLOGICAL EVENTS
RESULTS

32. Controlled high risk avonex multiple
sclerosis prevention surveillance -
 CHAMPIONS STUDY – compared
outcomes of those who had been
given drug from start of CHAMPS
study versus those who switched
from placebo after about 30 months
 Those who were started on Rx
immediately had fewer relapses and
fewer MRI brain lesions than
delayed treatment group

33.  Early treatment of multiple
sclerosis study – ETOMS
 IFN B 1a treatment at an early
stage had significant positive clinical
and MRI outcomes

34.  Betaseron in newly emerging
multiple sclerosis for initial
teratment study – BENEFIT
 Early initiation of Rx with IFN B 1b
prevents development of disability
supporting its use after first
manifestation of relapsing remitting
MS

35.  PreCISe study
 Early treatment with Glatiramate
acetate is efficacious in delaying
conversion to CDMS in patients
presenting with CIS and brain
lesions detedcted by MRI

36. COURSE
 Typically visual acuity and color vision
is lost over 2-5 days
 Recovery starts within 2 weeks and
takes 4-6 weeks
 75-90% cases get good visual
recovery
 Reccurent attacks of retrobulbar
neuritis develop primary optic atrophy
and pts with recuurent papillitis get
postneuritic optic atrophy