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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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Ophthalmology
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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Ophthalmology
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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Ophthalmology
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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Ophthalmology
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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Ophthalmology
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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Ophthalmology
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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