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