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OPHTHALMOLOGY
1.2A DISORDERS OF THE OPTIC NERVE

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OUTLINE
Anatomy of the Optic Nerve
Evaluation of Patients with Optic Nerve Disorders
Optic Nerve Disorders
ANATOMY

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Optic nerve
Optic chiasma
Optic tract
Lateral geniculate body
Optic radiation
Visual cortex
Superior colliculus of the midbrain
Putamen
Long association bundle - inferior occipitofrontal fasciculus
Pulvinar of the thalamus
Calcarine fissure
Posteroinferior horn of the lateral ventricle

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1.2A DISORDERS OF THE OPTIC NERVE

Swinging Flashlight Test
Ophthalmoscopy
ANISOCORIA

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Approx 50mm long

Approx 1.2M axons (from the retinal ganglion cells)
2 portions

Anterior (Intraocular): can be visualized using an

ophthalmoscope

~1mm long

Posterior (Retrobulbar): covered by myelin

Intraorbital (~30mm long)

Intracanalicular (~6mm long)

Intracranial (~10mm long)

Papilla: short intraocular portion
Intraorbital segment

Longest

S-shaped

Encircled by dura, arachnoid and pia mater

PATIENT EVALUATION
Hx and Sx
Ocular exam
a. VA
b. Pupils
c. Ophthalmoscopy
Ancillary Tests
a. Perimetry
b. Others
History and Symptoms

Eye pain?

Headache?

Unilateral/bilateral involvement?

Past medical, family, social, personal history & other

contributory factors

Common complaint: BOV

Ocular Exam
Check for Visual Acuity

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1.2A DISORDERS OF THE OPTIC NERVE

Ancillary Tests

- Visual Field Test

THE COMS GRADING SCHEME : GRADED FEATURES

Optic disc edema is seen as blurring of the disc margins.
The University of Iowa is a participant in the Collaborative Ocular
Melanoma Study (COMS), a multicerter randomized trial sponsored by
The National Eye Institute and The National Cancer Institute of the
National Institutes of Health.
- Visual Field Defects

confrontation visual fields are useful at the bedside when

combinations of techniques are used.
Standard automated perimetry provides adequate testing of the
visual field in a majority of neuro-ophthalmic patients.
Goldmann perimetry is useful in patients with severe visual and
neurological deficits or patients with "isolated peripheral visual
field defects".

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1.2A DISORDERS OF THE OPTIC NERVE

Variable results in patients with optic neuritis. Note the variation from
near normal to near complete hemianopia (Reproduced with permission
of the American Medical Association. From Wall et al.[14] Copyright
1998. American Medical Association. All rights reserved.)

ANCILLARY TEST: OTHERS

Color vision test
Contrast sensitivity
Visual evoked response
Imaging studies

Ultrasound

CT scan

MRI
OPTIC NERVE DISORDERS
Papilledema
Optic neuritis
Anterior ischemic optic neuropathy
Toxic optic neuropathy
Optic atrophy
Leber hereditary optic neuropathy
PAPILLEDEMA
Swelling of optic nerve head secondary to raised CSF pressure
Causes:

Brain tumors, intracranial trauma, meningitis,

hydrocephalus, subarachnoidal hemorrhage, etc

Visual field defects in idiopathic intracranial hypertension. (a) Enlarged

blind spot. (b) Nasal step. (c) Biarcuate scotoma. (d) Severe visual field
constriction

Almost always bilateral

Severity increase in intracranial pressure

Enlargement of physiologic blind spot = early VF defect

Treatment is directed in the underlying cause

If untreated, will lead to optic atrophy and permanent visual

loss

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1.2A DISORDERS OF THE OPTIC NERVE

OPTIC NEURITIS
Inflammatory edema of the optic
nerve
Foremost symptom: severe
visual loss
Eye pain aggravated by eye
movement
Usu. Unilateral
RAPD detected
Swollen hyperemic optic disc

with blurred margins

Papillitis: localized anterior to
optic disc
Retrobulbar neuritis: posteriorly
behind eyeball
neuroretinitis : extended to the
adjacent retina
Demylenating etiology is always
considered, like MS
Meticulous neurologic history and exam is mandatory

Occlusion of the posterior ciliary arteries resulting to optic disc

edema and altitudinal field defect

Non-arteritic: HTN, DM, dyslipedemia, coronary heart

disease; mngt is directed towards the predisposing
medl problem

Arteritic (less common): temporal and giant cell

arteritis; steroids is necessary
NON-ARTERITIC AION
Presentation
- Age: 45 to 65 years
- Altitudinal field defect
- Eventually bilateral in 30% (give aspirin)
Affects about 25% of untreated patients with giant cell arteritis
Severe acute visual loss
Treatment - steroids to protect fellow eye
Bilateral in 65% if untreated
ACUTE SIGNS

LATE SIGNS

Color

photograph of a patient with acute anterior

optic neuritis (papillitis)

Spontaneous resolution of visual loss may occur

Corticosteroid preferably given IV may shorten clinical course

CLASSIFICATION OF OPTIC NEURITIS

Retrobulbar neuritis
Papilitis (hyperaemia
Neuroretinitis
(normal disc)
& edema)
(papillitis and macular
star)

Pale disc with diffuse or

sectorial oedema
Few, small splinter-shaped
haemorrhages
Subsequent optic atrophy

Resolution of oedema and

haemorrhages
Optic atrophy and variable
visual loss

FA in acute non-arteritic AION

Demyelination most common

Sinus-related
(ethmoiditis)
Lyme disease

Viral infections and

immunization in
children (bilateral)
Demyelination
(uncommon)
Syphilis

Cat-scratch fever
Lyme disease
Syphilis

Localized hyperfluorescence

Increasing localized
hyperfluorescence

Generalized hyperfluorescence

ANTERIOR ISCHEMIC OPTIC NEUROPATHY

SUPERFICIAL TEMPORAL ARTERITIS

Presentation
- Age: 65 to 80 years
- Scalp tenderness
- Headache
- Jaw claudication
- Polymyalgia rheumatica
- Superficial temporal arteritis
- Acute visual loss
Special investigations
- ESR - often > 60, but normal in 20%
- C-reactive protein - always raised
- Temporal artery biopsy

Sudden painless, non-progressive blurring of vision in patients

over 50 years of age

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1.2A DISORDERS OF THE OPTIC NERVE

HISTOLOGY OF GIANT CELL ARTERITIS

Granulomatous cell infiltration

Disruption of internal elastic
lamina
Proliferation of intima
Occlusion of lumen

High-magnification shows
giant cells

THE MOST COMMON CAUSES OF TOXIC OPTIC NEUROPATHY

Tobacco / ETOH amblyopia

Antitubercular drugs: Ethambutol, Isoniazid, Streptomycin

Chloramphenicol

Chlorpropamide

Disulfiram

Arsenic

Heavy metals: Lead. mercury, Thallium

Alcohols: Methanol, ethylene glycol (antifreeze)

Antiarrhythmic agents: Digitalis, Amiodarone

Antimalarials: Chloroquine / Quinine

Radiation

Antibiotics: Chloramphenicol, sulfonamides, linezolid

Anticancer agents: Vincristine, methotrexate

Others: Carbon monoxide, tobacco

Disc pallor in a 44-year-old female with ethambutol toxicity.

She was treated with ethambutol for 2 months for tuberculoma
brain.
OPTIC ATROPHY

TOXIC OPTIC NEUROPATHY

Symptoms
- Diminution of vision: bilaterally symmetrical, painless,
gradually progressive
- Dyschromatopsia
Signs
- Pupils: sluggish, no RAPD
- Optic disc: normal, swollen, or hyperemic in early stages;
temportal optic disc pallor later
- Visual field defect: centrocaecal scotoma

A result of a severe long standing damage or injury to the optic

nerve
Pallor optic disc = Degeneration of the nerve axons
Leads to vision loss and poor prognosis

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1.2A DISORDERS OF THE OPTIC NERVE

LEBER HEREDITARY OPTIC NEUROPATHY

Maternal mitochondrial DNA
mutations
Presents:
- Typically in males - third decade
- Occasionally in females - any age
- Initially unilateral visual loss
- Fellow eye involved within 2 months
- Bilateral optic atrophy
Signs:
- Disc hyperaemia and dilated capillaries
(telangiectatic microangiopathy)
- Vascular tortuosity
- Swelling of peripapillary nerve fibre layer

END OF TRANX

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