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OPTIC DISC

SYMPTOMS OF THE OPTIC NERVE


DISEASES
Loss of vision
Defective color vision
Visual field defect.
TVO( transient visual obscurations

Clinical evaluation of the optic nerve


diseases

Visual acuity
Color vision
Visual fields defects
Contract sensitivity
Light Brightness appreciation.
Pupilary reactions
PAPILLEDEMA

Papilledema is optic disc swelling that is caused by


increased intracranial pressure. The swelling is usually bilateral

TEN HALLMARKS

There are 10 hallmarks of papilledema:


1. Blurring of the disc margins
2. filling in of the optic disc cup
3. anterior bulging of the nerve head
4. Edema of the nerve fiber layer
5. Retinal or choroidal folds
6. Congestion of retinal veins
7. Peripapillary hemorrhages
8. Hyperemia of the optic nerve head
9. Nerve fiber layer infarcts
10. Hard exudates of the optic disc

PATHOPHYSIOLOGY
As the optic nerve sheath is continuous with
the subarachnoid space of the brain , increased
pressure is transmitted through to the optic nerve.
However, the anterior end of the optic nerve stops
abruptly at the eye. Hence the pressure is
asymmetrical and this causes a pinching and
protrusion of the optic nerve at its head.
PSEUDO PAPILLEDEMA
Hypermetropia
Optic nerve head drusens

CAUSES

1. Pseudo-tumor cerebri.
2. Space-occupying intracranial lesions.
3. Microbial infection: meningitis, encephalitis.
4. Hypertensive encephalopathy
5. Intracranial vascular lesions: sub-arachnoid
hemorrhage, sagittal sinus thrombosis, etc.
6. Head-injury - long standing contusions,
carotid-cavernous fistula
7. Metabolic disorders: Addison's disease, , hypo-
parathyroidism, etc.
8. Blood dyscrasias : leukemia, polycythemia, etc.
Choroidal plexus tumour by hypersecretion.
9. Miscellaneous; serum sickness, status epilepticus,
sarcoidosis etc.
SYMPTOMS

General symptoms :
Headache - bifrontal/occipitonuchal, worse in the
morning and by coughing or straining.
Vomiting without nausea and without loss of appetite.
Focal neurological deficit with changes in level of
consciousness may be present.

Ocular symptoms:
Visual acuity remains fairly normal or decreased in
established papilloedema and grossly affected in
atrophic stage.
Amaurosis fugax - a transient, black out of vision for
few seconds may be present in some patients usually in
late stages due to enormous increase ICT.

SIGNS

Pupillary reactions are normal, until


secondary optic atrophy has set in.
Ophthalmoscopy: The Ophthalmoscopic features in the
different stages of the disease are:

Early Papilledema:
Earliest change is disc hyperemia and dilated capillaries.
Blurring of disc margins
Spontaneous venous pulsation is absent (does not
confirm papilledema because it is not present in 20 % of
normal population.)
Splinter hemorrhages at or just off the disc-margin.

ESTABLISHED PAPILLEDEMA:

Disc margins become indistinct and central cup is


obliterated.
Disc surface is elevated above the retinal plane (more
than + 3D (1mm) with direct ophthalmoscope).
Peripapillary edema.[Paton's lines, present temporal to
the disc].
Venous engorgement . Flame-shaped hemorrhages
and 'cotton-wool' spots around the disc.
Hard exudates in radiating pattern around the macula,
[macular star]

(c) CHRONIC PAPILLEDEMA OR VINTAGE


PAPILLEDEMA:

Disc edema resolves, but margins are blurred


Hemorrhagic and exudative components
gradually resolve. Optic disc appears pale like
a champagne cork. White spots - corpora amylacea
may be seen on the disc.

d) ATROPHIC PAPILLEDEMA
Peripapillary retinal vessels are attenuated and
sheathed.
Dirty-white appearance of the optic disc.
Secondary optic atrophy.

Definition

Optic neuritis is
inflammationdisintegration and
demyelinaton of the optic nerve.

Causes

Demylinating diseases.
Multiple sclerosis
Device Disease4
Schilders Disease
Post Infectious
Post vaccination

Epidemiology

Incidence: 1-5 per 100 000 per year

Highest incidence in
Caucasians
Countries with high latitudes: genetics?
Springtime
Ages 20-49
Women
CLINICAL FEATURES
Sub-acute, monocular visual loss

Clinical features
Painful extraocular movements

CLINICAL FEATURES
Decreased contrast sensitivity

CLINICAL FEATURES

Central scotomas

Paracentral scotomas

Altitudinal defects

Visual Field Defects


Demyelination is the most common cause

No need for laboratory investigation


i.e. ESR, ANA

Need to do MRI of the brain


Assess MS risk
CLASSIFICATION
ANTERIOR ISCHEMIC OPTIC NEUROPATHY

De: Characterized by pallid disk swelling associated


with acute loss of vision. The disorder is due to
occlusion or decreased perfusion of the short
posterior ciliary arteries.

CAUSES
Etiology
1.Local vascular lesion of papilla
2.Hypotension of eye or total body
3.Blood viscosity
4.High
5.Ocular hypertension

CLINICAL FEATURES
CLINICAL MANIFESTATION:

symptomssuddenpainlessnonprogressive visual loss.


signs
visionmoderate loss
pupilafferent pupillary defect
Fundus: pale disc swelling often involving only a
segment of the disc, flame-shaped hemorrhages, optic
atrophy after the edema resolves
Visual field: altitudinal or central visual field defect

Clinical types
Areritic Anterior ischemic optic neuropathy: due to giant
cell arteritis
nonAreritic Anterior ischemic optic neuropathy 5060
years
TREATMENT
Treat systemic disease
General application of corticosteroid
vasodilator
Decrease IOP
Optic nerve sheath decompression

Toxic/Nutritional optic neuropathies


Causes
Causes of nutritional optic neuropathy
include tobacco, ethanol, thiamine, and
vitamin B-12.
Causes of toxic optic neuropathy include
chemicals and drugs, such as methanol,
ethylene glycol, ethambutol, isoniazid,
digitalis, cimetidine, vincristine,
cyclosporine, toluene, and amiodarone.
LEBERS HEREDITARY OPTIC
NEUROPATHY

Bilat./ Symmetrical/ irreversible/ painless VA


No RAPD
Optic nerve pallor
Colour vision defect
VF
ERG, VEP, PERG
Onset: insidious (except LHON)/ congenital-late
Intra-, inter- familial variability (EXAMINE family!!)