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NEURO-OPHTHALMOLOGY

Chuanbao-Li

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Introduction

As demonstrated by their common embryological origin, theretinas and anterior visual pathways (optic nerves, opticchiasm, and optic tracts) are an integral part of the brain,

providing a substantial proportion of total sensory input.

They frequently give important diagnostic clues to centralnervous system disorders.

Intracranial disease frequently causes visual disturbancesbecause of destruction of or pressure upon some portion of theoptic pathways.

Cranial nerves III, IV, and VI, which control ocularmovements, may be involved, and nerves V and VII are alsointimately associated with ocular function.

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Clinical Examination

Visual Acuity

Colour Vision

Visual Fields

Pupils

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Normal Optic Disc

Cupped disc

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The swollen optic disc

Papilloedema

Papillitis

Malignant hypertension

Ischaemic optic neuropathy

Diabetic optic neuropathy

CRVO

Intraocular inflammation

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The pale optic disc

Congenital

Secondary to

raised IOPvascular

retinal disease

optic

neuritis

optic nerve

compression

trauma

Glaucoma

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Ocular motility

abnormalities Third nervepalsy

Double vision

Eye turned down & out Ptosis

Dilated pupil &

headache

Sixth nerve palsy

Double vision

Eye turned in

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shows the types of field defects causedby lesions in various locations ofthe pathway.

Lesions anterior to the chiasm (ofthe retina or optic nerve) causeunilateral field defects;

lesions anywhere in the visualpathway posterior to the chiasmcause contralateral homonymous

defects. Chiasmal lesions usually cause

bitemporal defects.

Localising the lesion

visual pathway

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Optic Neuritis

swollen optic disc

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Optic Neuritis

Symptoms

Loss of vision deteriorating over hours (rarely) to days(most commonly), with the nadir approximately 1 week

after onset. Visual loss may be subtle or profound. Usually unilateral,

but may be bilateral.

Age typically 18 to 45 years. Orbital pain, especially with

eye movement. Acquired loss of color vision. Reduced perception of light

intensity.

RAPD(Relative afferent pupillary defect )

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Optic Neuritis

RAPD(Relative afferent pupillary defect )

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Optic Neuritis

Etiology

Idiopathic.

MS(multiple sclerosis) : Frequently optic

neuritis is the initial manifestation of MS.

Childhood infections or vaccinations.

Other viral infections: e.g., herpes zoster.

Contiguous inflammation of the orbit

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Optic NeuritisTreatment

If patient seen acutely with no prior history of MS or opticneuritis:

If MRI reveals at least one typical area of demyelination, offer

pulsed intravenous injection steroid in the following regimenwithin 14 days of decreased vision

Methylprednisolone 1 g/day i.v. for 3 days, then

Prednisone 1 mg/kg/day p.o. for 11 days, then

Taper prednisone over 4 days (20 mg on day 1, 10 mg on days

2 and 4).Antiulcer medication (e.g., ranitidine 150 mg p.o., b.i.d.) forgastric prophylaxis.

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Optic NeuritisTreatment

If MRI shows two or more characteristic

demyelinating lesions, treat with the

aforementioned steroid regimen. Refer to

neurologist for possible treatment

With a negative MRI, the risk of MS is low

In a patient with diagnosis of prior MS or optic

neuritis:

Observation.

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Optic NeuritisNote

NEVER use oral prednisone as a primarytreatment because of increased risk ofrecurrence.

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