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 lateral ventricle ventricle
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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
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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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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
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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". BEI SAMONTE ☺
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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.)
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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 α 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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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
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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
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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
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photograph of a patient with acute anterior optic neuritis (papillitis) •
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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)
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Pale disc with diffuse or sectorial oedema Few, small splinter-shaped haemorrhages Subsequent optic atrophy
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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
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Viral infections and immunization in children (bilateral) Demyelination (uncommon) Syphilis
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Cat-scratch fever Lyme disease Syphilis
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Localized hyperfluorescence
Increasing localized hyperfluorescence
Generalized hyperfluorescence
ANTERIOR ISCHEMIC OPTIC NEUROPATHY •
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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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HISTOLOGY OF GIANT CELL ARTERITIS
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Granulomatous cell infiltration Disruption of internal elastic lamina Proliferation of intima Occlusion of lumen
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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 •
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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
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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 BEI SAMONTE ☺
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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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