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OPTIC NERVE
LESIONS
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ANATOMY
Begins:
Optic disc (Anatomically)
Ganglion cells of retina (physiologically)
ANATOMY
First part of ON
Approx. 1.0-1.2 M ganglion cells
ANATOMY
Intraorbital
Extends approx. 25-30mm to
Intracranial
10-20mm
LESIONS
PAPILLEDEMA
Swelling of the optic disc from increased intracranial
pressure
head
PAPILLEDEMA CAUSES
Space occupying lesion (tumor, hemorrhage)
Decreased CSF drainaige or absorption (obstructive
cerebri)
DIAGNOSIS
Fundus exam - noting disc swelling (usually bilateral
Fluorescein Angiography
Perimetry (enlarged blind spots)
CT or MRI (preferred) (can be noted as flattening of
Lumbar puncture
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nerve cupping in the right eye with posterior scleral flattening and
protrusion of optic nerve papilla into the globe (arrow)
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PAPILLITIS
Inflammation or infarct of the optic nerve head
Usually unilateral
(+) Visual abnormalities (color, VA)
Optic nerve head swelling
Disc hemorrhages
Causes:
Optic neuritis
Multiple sclerosis
Infarct or nerve head
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PAPILLEDEMA VS PAPILLITIS
Papilledema
Papillitis
Definition
Laterality
Bilateral
Unilateral
Cause
Increase in ICP
Vision loss
Not usual
COMMON (cardinal
symptom)
Color perception
Unchanged
Depressed
RAPD
No
Yes
Hemorrhages
Around disk
Treatment
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WHICH IS WHICH?
Papillitis
Papilledem
a
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pseudopapilledema).
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beneath it
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TREATMENT
No treatment necessary (normal physiologic variant)
Visual prognosis for is generally good
Currently no effective treatment for patients that have gradual loss of
visual fields
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TRAUMATIC OPTIC
NEUROPATHY (TON)
Most common cause: Indirect injury to the optic nerve
85% of patients are male, ave age of 34 (International Optic Nerve Trauma Study)
Symptoms:
Decreased central visual acuity
Depressed color vision
RAPD
Visual field deficits
Signs
The optic nerve head will appear normal initially, but optic atrophy can be seen
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History:
A history consistent with TON
Vision loss after blunt or penetrating trauma that could not be
explained by slit lamp or dilated fundus findings.
Often, patients complain of acute unilateral decrease in vision, color
vision deficits, or visual field deficits.
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PATHOPHYSIOLOGY OF TON
The optic nerve dura is continuous with the orbital periosteum, leaving the
optic nerve, which can cause axonal injury or disturb the blood supply of
the optic nerve.
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PROGNOSIS
Visual acuity improvement of >3 lines was seen in 57% of patients
Use of steroids did not result in significant difference in outcome
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ARTERITIC ANTERIOR
ISCHEMIC OPTIC
NEUROPATHY
(AAION)
Acute and painless optic neuropathy
of cases)
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PATHOGENESIS
Inflammatory and thrombotic involvement of the short
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DIAGNOSIS
Severe visual acuity loss
(+) RAPD
Pallor of the optic disc, which may be severe, chalky-white is the hallmark
of AAION
characteristic of AAION
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TREATMENT
Early treatment is essential.
High dose systemic corticosteroid are standard.
IV methylprednisolone at 1g/day for the first 3 days has been
Oral prednisone in the range of 60-100mg/day may be used initially and for
beginning taper.
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PROGNOSIS
Without treatment, visual loss occurs in 54-95%, typically
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insufficiency
Up to 97% of patients with NAION have small optic discs with small or
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scotoma)
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DIAGNOSTICS
ESR
CRP
Temporal artery biopsy is recommended to rule out GCA and AAION
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TREATMENT
There is no effective treatment for NAION
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PROGNOSIS
Vision can worsen over 2 weeks after initial presentation
Natural history of visual outcome showed approximately 50% of
patients had a visual acuity of 20/30 or better and nearly onequarter were 20/200 or worse.
Vision in the affected eye will typically stabilize within two months
Progression or recurrence more than two months after initial
years
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DIABETIC PAPILLOPATHY
Occurs in both DM type 1 or 2
No symptoms or have nonspecific symptoms of"blurred vision'' or
papillopathy
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PROGNOSIS
resolve slowly over 2-l 0 months. Optic atrophy occurs in 20% of cases, but
the visual
retinopathy.
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Fundus Triad
(AAO 2015):
1. Hyperemia and elevation of the optic disc, with thickening of the peripapillary
retina; although the disc appears swollen, it does not leak on fluorescein
angiography ("pseudoedema'')
2. Peripapillary telangiectasia
3. Tortuosity of the medium-sized retinal arterioles
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TREATMENT
No effective treatment
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PROGNOSIS
Unaffected eye becomes symptomatic within weeks to months
Vision loss is usually permanent
Recovery of vision occur in 10%-20% of cases over several
years
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AUTOSOMAL DOMINANT
OPTIC ATROPHY (ADOA)
Most common hereditary optic neuropathy (1:50,000)
Autosomal dominant
First decade of life
Insidious vision loss
Bilateral and symmetric
Color vision loss
No treatment available
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develops in 25%-75%
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embryonic fissure
depending on severity
be present
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of retinal vessels
or worse
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POSTERIOR OPTIC
NEUROPATHIES:
RETROBULBAR OPTIC
NEURITIS
Typically in young females (30s)
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TREATMENT
Corticosteroids failed to demonstrate long term benefit for visual acuity
Corticosteroids may speed up recovery by a few weeks
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NEUROMYELITIS OPTICA
AKA Devic Syndrome
Optic neuritis and acute myelitis
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TREATMENT
Mainstay treatment for acute period is high
dose steroids IV
IV Ig or plasmapheresis can be done on
patients who do not respond to steroids
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PROGNOSIS
Visual prognosis for NMO patients are poorer vs MS
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OPTIC PERINEURITIS
Inflammation of optic nerve sheath
Acute painful vision loss
Female predilection
Patients are generally older >50 y/o
Vision loss and pain progresses over weeks unless
treate
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DIAGNOSIS
Orbital MRI will show
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TREATMENT
Responds rapidly to corticosteroids, but relapses are common
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INTRAORBITAL COMPRESSIVE
OPTIC NEUROPATHY
Slow progressive vision loss
RAPD
Monocular visual field loss (central of diffuse)
Other signs of orbital disese
Proptosis
Ptosis
Retraction
Lag
Edema
Optic disc might be normal or with some edema
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DIAGNOSIS
MRI
Thin section CT scan
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Optociliary shunt
vessel
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Ring sign
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TREATMENT
Fractionated radiation therapy is the modality
patients
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nerve
May involve optic nerve, chiasm or both
First decade of life
Men = Women
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DIAGNOSIS
Proptosis (94%)
Vision loss (87.5%)
Optic dic pallor (59%)
Disc edema (35%)
Strabismus (27%)
RAPD usually present
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DIAGNOSIS
MRI shows diffuse enlargement and
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TREATMENT
Observation may be indicated for stable
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PROGNOSIS
Blindness usually 2-4 months after start of
vision loss
Death usually within 6-12 months
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TOXIC OR NUTRITIONAL
OPTIC NEUROPATHY
Gradual progressive vision loss
Painless
Bilateral and symmetric
Central scotoma
Decrease in VA and color vision
Disc edema
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COMMON MEDICATIONS
IMPLICATED
Ethambutol
Linezolid
Isoniazid
Chloramphenicol
Hydroxyquinolines
Penicillamine
Cisplatin
Vincristin
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PROGNOSIS
Slow resolution of nerve edema over months of
discontinuation of substance
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INFILTRATIVE OPTIC
NEUROPATHY
Infiltration of ON with neoplastic or inflammatory cells
Progressive, sever vision loss
Often with pain
Unilateral or bilateral
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USUAL CAUSES
Leukemia
Lymphoma
Sarcoidosis
Syphilis
TB
Fungal
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DIAGNOSIS
Neuro imaging
CSF evaluation
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Metastasis of
Leukemia to the
Optic nerve head
Note ill defined
yellowish
infiltrates
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PROGNOSIS
Metastatic:
Poor even with aggressive therapy
Infectious/Inflammatory:
damage may be partially reversed
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