Optic Nerve Trilogy Patricia A. Modica, OD; FAAO Course Description: Acute and chronic abnormalities of the optic nerve are commonly encountered by eyecare clinicians. Since many are associated with serious underlying systemic or neurologic disease, appropriate work-up and accurate diagnosis is important. There are three optic neuropathies that have particular significance to the eyecare clinician. These optic neuropathies are important due their more common prevalence, and because new perspectives are now being brought into play that have important diagnostic and management implications. The clinical presentations of papilledema, optic neuritis and ischemic optic neuropathy are presented along with current literature updates that impact management. Learning Objectives: 1. To understand the clinical presentation of the most common optic neuropathies and their differential diagnoses 2. To understand the diagnostic work-up of optic neuritis, ischemic optic neuropathy and papilledema. 3. To understand the optometric and systemic management of these optic neuropathies. Course Outline: Optic Neuritis: I. Definition—Optic Neuritis II. Historical Overview III. Clinical Profile—Typical Acute Optic Neuritis (From the Optic Neuritis Treatment Trial) A. Sex B. Age C. Pain D. Optic nerve appearance E. Visual field defects F. MRI findings G. Visual Acuity IV. Optic Neuritis and Multiple Sclerosis A. MRI as a predictor B. Clinical Considerations C. Lumbar puncture V. Atypical Optic Neuritis A. Falls outside typical age range B. Painless C. Bilateral and simultaneous D. Worsens beyond 14 days E. Clinical evidence of other systemic disease F. Other ocular inflammatory signs VI. Optic Neuritis in Children A. Presentation B. Visual prognosis C. Systemic prognosis VII. Management of Optic Neuritis A. Typical versus atypical B. The Optic Neuritis Treatment Trial C. CHAMPS (Controlled High-Risk Subjects Avonex Multiple Sclerosis Prevention Study) VIII. Future implications of current scientific studies Ischemic Optic Neuropathy: I. Definition—Ischemic Optic II. Clinical Presentation A. Symptoms B. Optic nerve appearance a. Pallid swelling b. Arterial attenuation c. Flame hemorrhages d. NFL infarcts e. Macular star C. Optic nerve function a. Dyschromatopsia b. Afferent pupillary defect D. Visual fields III. Pathogenesis A. Hypoperfusion of the posterior ciliary arterial supply to the anterior optic nerve head B. Role of Mechanical factors C. Role of atherosclerotic disease D. Other predisposing factors a. Hypovolemia b. The Viagra connection IV. Risk Factors 1. -Hypertension 2. -Diabetes 3. -Atherosclerotic disease 4. -Small optic nerves 5. -Giant cell arteritis The first four are risk factors for the non-arteritic form while the fifth is a risk factor for the arteritic form V. Arteritic vs. Non-arteritic AION A. Age B. Visual presentation C. Systemic associations D. Optic nerve E. Prodrome VI. Arteritic Symptoms -Scalp tenderness -Jaw claudication -Mild fever -Arthralgias; myalgias VII. Visual Prognosis A. Ateritic vs. non-arteritic VIII. Management A. Rule out GCA -ESR; C-reactive protein -Temporal artery biopsy B. Rule out systemic disease -Hypertension, diabetes and other disorders that increase risk of vascular compromise C. Appropriate information should be communicated with the patient’s physician Treatment for AION -There is no treatment for non-arteritic AION; arteritic GCA is best treated with high dose corticosteroids (preferably IV) and this should be undertaken immediately Papilledema: I. II. Papilledema—Definition Disc edema secondary to increased intracranial pressure. Clinical Presentation a. Symptoms i. Headache ii. Tinnitis iii. Diplopia iv. Transient Visual Obscurations b. Signs i. Early vs. late ii. Acute vs. chronic c. Diagnostic Work-up i. Neuro-imaging ii. Lumbar puncture iii. Laboratory studies III. Important Etiologies a. Intracranial Mass or Neoplasm b. Intracranial Infection i. Meningitis ii. Encephalitis c. Intracranial Inflammatory Disease d. Pseudotumor Cerebri i. Systemic disease ii. Exogenous Agents iii. Sleep Apnea iv. Idiopathic IV. Hypercoagulable States and PTC a. Intracranial Venous Sinus Thrombosis and Related Systemic Disorders b. Diagnostic work-up i. Lab Studies ii. Magnetic Resonance Venography V. Idiopathic Intracranial Hypertension a. Patient profile b. Pathophysiologic Mechanism c. Treatment and Treatment pitfalls i. Carbonic Anhydrase Inhibitors ii. Weight loss iii. Surgical Techniques