Referat :

OPTIC NEURITIS
By :
Widjayanti 17360157
Preceptor : dr. Rahmat Syuhada, sp.M
 Optic Nerve:
Anatomy
Second Cranial Nerve
50mm in length
Forms innermost strata of the retina

Optic Nerve Parts :

Visual Nerve Pathways :
Impressions of light >>
cornea >> COA >> pupil
>> COP >> lens >> corpus
vitreus >> retina >> optic
nerve >> optic chiasma >>
optic tracts >> lateral
geniculate bodies >> optic
radiation >> occipital
cortex (area 17)
 Optic neuritis is the inflammation or demyelination of
the optic nerves cause by various diseases.

Definition Optic neuritis is classified into :

1. papillitis
2. retrobulbar neuritis
 Papillitis: Papillitis is a swelling of the discus opticus
caused by inflammation in the part of optic nerve
(intraocular). Can be seen with fundoscopic
examination.
Retrobulbar Neuritis: Retrobulbar neuritis is a
inflammation in the part of optic nerve
(ekstraocular/intraorbital). Which located on the back of
the eyeball, there is no abnormalities optical discus
with ophthalmoscopy, but there is decreased of vision.
 Demyelinatif (ruptured of the myelin sheath on
neurons) :
- Idiopathic
- Multiple Sclerosis
- Neuromielitis optica
Etiology Immune-mediated :
- Optic neuritis after viral infection (ex : morbilli, mumps,
varicella, influenza, mononucleosis infeksiosa)
- Optic neuritis post immunization
- Acute disseminated encephalomyelitis
- Acute idiopathic polyneuropathy (guillain-barre
syndrome)
- Eritematosus lupus systemic
- Leber disease
Direct infection :
- Herpes zoster, syphilis, tuberculosis, crytococcosis,
cytomegalovirus
Granulomatous optic neuropathy :
- Sarcoidosis
- idopathic
 Inflammatory local disease :
- Intraocular inflammation
- Orbita disease
- Sinus diseases, including mucormikosis
- Intracranial diseases (meningitis, enchepalitis)
Exogenous intoxication :
- tobacco, alcohol etyl, alcohol metyl
Metabolic disease :
- diabetic, anemia, pregnancy, avitaminosis
 Most common pathology inflammatory
demyelination of optic nerve.(similar to that of acute
multiple sclerosis (MS) plaques in the brain)
Perivascular cuffing, edema in the myelinated nerve
sheaths, and myelin breakdown.
Pathophysiology Inflammation of the retinal vascular endothelium can
precede demyelination and is sometimes visibly
manifest as retinal vein sheathing .
Myelin loss exceeds axonal loss.
Hypothesized by Immune mediated demyelination.
Specific mechanism and target antigen(s) are
unknown.
Systemic T cell activation is identified at symptom
onset and precedes changes in the CSF.
Systemic changes also normalize earlier (within 2-4
weeks) than central changes.
T cell activation leads to the release of cytokines and
other inflammatory agents.
 B cell activation against myelin basic protein
not seen in peripheral blood
but can be demonstrated in the CSF.

As with MS, a genetic susceptibility for optic neuritis is

suspected , supported by an over-representation of certain
human leukocyte antigen (HLA) types among patients with
optic neuritis.
 Acute:
symptoms of optic neuritis are usually monocular, but
can affect both eyes especially in children
a sudden loss of vision for several hours to several
days
Symptoms eye pain (especially during ocular movement)
afferent pupillary defect (Relative Afferent Pupillary
Defect examination)
field of view defects may be secocentral or
paracentral
color blindness in affected eye (88% of patients)
Chronic :
Persistent loss of vision
afferent afferent pupil defect persisted in 25% of
patients two years after the initial symptoms
denaturation of color, especially red color, when
viewing with affected eyes into pink or orange
uthoff phenoma (occurs temporary exacerbations of
visual impairment arising from elevated body
temperature)
optical discs are smaller and pale, especially in
temporal areas. The pale discus extends to the
boundary of the discus to the peripheral retinal fibers.
Clinical Features
of Optic Neuritis
General
description
 Anamnesis
based upon the history and examination findings.

physical examination
A detailed ophthalmologic examination - an
Diagnosis essential feature of the clinical evaluation.

supporting examination
directed toward excluding other causes of visual loss
in atypical cases and in assessing the risk of
subsequent multiple sclerosis (MS).
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 swing to the left eye, both pupils dilate.
When the light is swing back to the right eye both pupils again
constrict.
This reaction indicates a defect in the afferent pupillary fibres
from the left eye.
Normal appearance :

Optic Neuritis : Fundus appearance

 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

Management treatment (spontaneously)

Treatment Indicated
Visual acuity worsen
Treatment hasten the recovery process, but no
effect on long-term visual outcome
 Corticosteroids S/E
Mood changes
Facial flushing
Weight gain
Dyspepsia

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)
 Loss of vision in optic neuritis can occur
permanently.
MS-induced neuritis has the distinctive
Complications features of recurrence and remission. An
increase in body temperature may exacerbate
disability (uthoff phenomenon), especially
visual disturbances
 The healing and recovery process of vision acuity
occurs in 92% of patients. Rarely who experience
Prognosis progressive loss of vision. Although, vision can
not be completely normal.