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Evaluation of optic nerve disease

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Page 1: Optic nerve 2

Evaluation of optic nerve disease

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Clinical features of optic nerve dysfunction

• Reduced visual acuity

• Afferant pupillary defect

• Dyschromatopsia

• Diminished light brightness sensitivity

• Diminished contrast sensitivity

• Vsual field defects

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Optic disc changes1 –Normal disc2-Disk swelling 3-optico-ciliary shunts4-optic atrophy

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Optic atrophyprimary optic atrophy

• A; causes • Following retrobulbar

neuritis• Compressive lesions

such as tumors and aneurysms

• hereditary optic neuropathies

• Toxic and nutritional optic neuropathies

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Disc appearance

• White flat disk with clearly delineated mar gins

• Reduction in number of blood

• Crossing the disk • Attenuation of

prepapillary vessels

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Secondary optic atrophy

Causes papilloedema

papillitis

AION

Disc appearance white

slightly raised

poorly delineated margin

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Special investigation

Automated perimetry

MRI

Visual evoked potential

Fluorescein angiography

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Classification of optic neuritis• 1-Ophthalmoscopic classification

• a; retrobulbar neuritis

• b; pappillitis

• c; neuroretinitis

• 2-Aetiological classification• a; demyelinating

• b; parainfectious

• c; infectius

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Optic neuriotis and demyelination

• VISUAL PATHWAY LESIONS

• BRAIN STEM LESION

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Demyelination diseases

• Isolated optic neuritis

• Multiple sclerosis

• devic disease

• Schilder disease

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Systemic feature of MS

• Spinal cord lesion

• Brain stem lesion

• Hemisphere lesion

• Transient phenomena

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Special investigation

• Lumbar puncture• VEP• MRI

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Optic neuritis

• 70% of women and 30% of men develop MS

• Evidance of optic neuritis in 70% of MS

• In 70% of isolated optic neuritis abnorml MRI

• Risk of MS winter onset HLA DR2 & uthuff

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presentation

• Sudden onest of visul loss

• discomfort in or around the eye

• Frontal headache tenderness of globe

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signs

• Normal disc in two-thirds (retrobulbar)

• Diminished visual acuity (very mild –very sever)

• Impairment of visual acuity & contrast sensitivity

• Visual field defect (central scotoma)

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Clinical course

• Impairment of visual acuity becomes maximum after 1-2 weeks (6/18-6/60)

• Recovery takes 4-6 weeks usually

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Prognosis

• Excellent in 75% (V/A 6/9)

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treatment

• In mild visual loss treatment is probably unnecessary

• When visual acuity in the first week of symptom is worse than 6/12 treatment may speed up recovery

• Intravenous methylprednisolon sodium succinat

• Treatment dose not appear to have any long term benefit on final visual acuity

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Other causes of optic neuritis

• Parainfectious ON (Viral)• Infectios ON (sinus related,syphlis,lyme,…

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signs

• Pale disc

• Diffuse or sectoral edema

• Localized disc hyperfluorescence

• V/A in 1/3 of patient is normal in remainder have moderate to sever impairment

• Visual field defect is typically altitudinal

• Color vision is diminished

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managment

• Serologic study

• Fasting lipid profile

• Blood glucose, fibrinogen & packed cell volume

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Treatment

• Treatment of any underlying diseases

• Stop smoking

• Low-dose aspirin

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Arteritic anterior ischemic optic neuropathy: clinical features of

giant cell arteritis• Scalp tenderness• Jaw claudification• Polymyalgia rheumatica• Neck pain, weight loss,

anorexia fever, night sweets, malaise depression

• Superficial temporal arteritis

• Arteitis of other arteries• Occult arterritis

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Arteritic anterior iscxhemic optic neuropathy

• Uniocular sudden and profound loss of vision

• Periocular pain

• Transient visual obscuration

• Flashing lights

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Signs

• pale and swollen optic disc

• Splinter hemorrhages• Finaly optic atrophy

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Special investigation

• ESR• C-reactive protein • Temporal artery

biopsy

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treatment

• Intravenous methylprednisolon 1g/day for 3 day together with oral prednisolon 80 mg

• After 3 days 60 mg for 3 day than 40 mg/days

• Than daily dose reduced 5 mg weekly

• Maintanance is 10 mg

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Papillodemacauses

• Space-ocupaying lesion

• Blockage of the ventricular system

• Obstruction of CSF absorption

• Benign intracranial hypertention, diffuse cerebral edema, sever hypertention

• Hypersecretion of CSF

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Early papillodema

• Visual symptom are absent ,V/A normal

• Hyperaemia and mild elevation in optic disc

• Indistinct disc margin• Absent spontaneous

venous pulsation• Nasal margin is

blured in first

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Estabilished papillodema

• Transient visual osscuration• V/A is normal or reduced • Sever hyperemic optic disc• Smal vessele obscured• Venous engorgment flam

shap hemorrhage• Cotton-wool spots• Hyperfluorescence• Retinal fold• Hard exudates• Enlarge blind spot

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Long standing papillodema

– V/A variable– V/F constriction– Cotton-wool and

hemorrhage absent– Optociliary shunts

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Atrophic papillodema

• V/A sever diminish• White optic disc

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Differential diagnosis

• Malignant hypertention

• Bilateral papilitis

• Bilateral compressive thyroid orbitopathy

• Bilateral simultaneousanteriorischemic optic neuropathy

• Bilateral compromisedvenous drainage

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Congenital optic nerve anomalies

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