This document provides an overview of optic neuropathy, including its causes, clinical approach, and treatment. It discusses various types of optic neuropathy such as inflammatory optic neuritis, non-arteritic and arteritic anterior ischemic optic neuropathy, traumatic optic neuropathy, infiltrative optic neuropathy from tumors, compressive optic neuropathy from lesions, and hereditary and nutritional optic neuropathies. For each type, it describes the symptoms, signs, investigations, and management approach. The document is a comprehensive review of the etiology, diagnosis, and management of optic neuropathies.

1. OVERVIEW OF OPTIC
NEUROPATHY
DR KHUDA BUKHSH SALEEMI
PGR1 OPHTHALMOLOGY

2. OPTIC NERVE
CNII
1.2 million special afferent nerve fibres (SSA)
Originates from the Ganglion Cell Layer of Retina
50mm long from the globe to Chiasm
Covered by meninges. Part of CNS

3. ANATOMICA
L
SUBDIVISIO
NS
IntraOcular: shortest (1mm), ophthalmoscopically
visible
IntraOrbital: longest (25-30mm)
IntraCanalicular: 6mm
IntraCranial: 5-16mm. Vulnerable to damage by
adjacent structural lesions

5. OPTIC NEUROPATHY
IS DAMAGE TO THE OPTIC NERVE FROM ANY CAUSE
Frequent cause of vision loss The diagnosis is made on clinical
grounds.
The history often points to the
possible etiology of the optic
neuropathy.

6. CAUSES
Rapid
onset
Inflammatory
Non-arteritic Ischemic
Arteritic Ischemic
Traumatic
Gradual
onset
Infiltrative
Compressive
Hereditary
Radiation
Paraneoplastic
Toxic/nutritional

7. CLINICAL
APPROACH
History
1. The MODE OF ONSET of visual loss is an
important clue to the etiology of the optic
neuropathy. i.e.
• Rapid onset is characteristic of optic neuritis,
ischemic optic neuropathy, inflammatory (non-
demyelinating) and traumatic optic neuropathy.
• Gradual onset over months is typical of
compressive toxic/nutritional optic neuropathy.
• History over years is seen in compressive
and hereditary optic neuropathies.

8. CLINICAL
APPROACH
2. ASSOCIATED SYMPTOMS
• In young patient H/O pain associated
with eye movement, paresthesia, limb
weakness, and ataxia is suggestive of
demyelinating optic neuritis.
• In elderly patients transient visual loss,
diplopia, temporal pain, jaw
claudication, fatigue, weight loss and
myalgia suggestive of AION.

9. CLINICAL
APPROACH
• Symptoms such as diplopia and facial
pain are suggestive of multiple cranial
neuropathies seen in inflammatory or
neoplastic lesions of the posterior orbit
or parasellar region.
• Transient diplopia and headache should
raise the suspicion of increased intra-
cranial pressure.

10. CLINICAL
APPROACH
3. DRUG HISTORY
Ethambutol, amiodarone, alcohol
Immunosuppressive medications such as
methotrexate and
Cyclosporine
4. MEDICAL HISTORY
DM, HTN and hypercholesterolemia is
common in patients with nonarteritic
ischemic optic neuropathy (NAION).

11. OPTIC
NEURITIS
Inflammation of the optic nerve, which is
associated with swelling and destruction of the
myelin sheath covering the optic nerve.
Seen in 70% cases of Multiple Sclerosis (MS)
presenting symptom in 20% cases.
The majority are middle-aged (20-50) females
(♀:♂ 3:1).

12. OPTIC NEURITIS
Symptoms:
• Monocular (Central Vision loss)
•Pain (eye movement)
•Altered colour vision
•Flashes

13. PHYSICAL SIGNS
Decreased visual
acuity
VF defect
(Central/Altitudinal
29% )
Dyschromatopsia
Afferent Pupil
Defect (RAPD)
Optic disc swelling
35%
Optic disc pallor
Abnormal Contrast
Sensitivity
Altered depth
perception

15. TREATMEN
T
Steroid regimen
• I/V methylprednisolone sodium
succinate 1 g daily for 3 days,
followed by oral prednisolone (1
mg/kg daily) for 11 days,
subsequently tapered over 3 days.
Other immunomodulatory
treatment options
• Interferon beta
• teriflunomide

16. OTHER
INFLAMMATORY
CAUSES
Optic disc swelling frequently
occurs with posterior uveitis and
retinitis.
Optic neuropathy can also occur in
the context of orbital inflammatory
disease (orbital pseudotumor).

17. NON
ARTERITIC
ANTERIOR
ISCHEMIC
OPTIC
NEUROPATHY
(NAAION)
Caused by occlusion of the short posterior
ciliary arteries resulting in partial or total
infarction of the optic nerve head.
Risk Factors
• Age > 50 yr
• Structural crowding of optic nerve head
• Hypertension
• Diabetes Mellitus
• Hyperlipidaemia
• Collagen vascular disease

18. NAAION
Symptoms:
Sudden painless monocular visual loss; this
is frequently discovered on awakening
Signs:
• moderate to severe visual impairment
• Visual field defects are typically inferior
altitudinal
• Dyschromatopsia is usually proportional to
the level of visual impairment
• Diffuse or sectoral hyperaemic disc swelling

19. NAAION
Investigations:
• blood pressure
• fasting lipid profile
• blood glucose

20. NAAION
Treatment:
• There is no definitive treatment
• Any underlying systemic predispositions
should be treated
• Aspirin is effective in reducing systemic
vascular events
• Aspirin is frequently prescribed in
patients with NAION

21. ARTERITIC ANTERIOR ISCHAEMIC OPTIC
NEUROPATHY (AAION)
caused by giant cell
arteritis (GCA)
Age: Fifty years of
age or older at
onset
Gender : 3 times
more common in
women than in men
New onset of
localized headache
Temporal artery
pulse
Elevated ESR
Positive temporal
artery biopsy.

22. OCCULAR
SIGNS OF
AAION

24. ARTERITIC
ANTERIOR
ISCHAEMIC
OPTIC
NEUROPATH
Y (AAION)
Diagnostic work up
1. Erythrocyte sedimentation rate (ESR) >47mm
2. C-reactive protein >2.45 mg/dL
3. Fluorescein fundus angiographic (FFA):
Critical diagnostic test for A-AION during the
early stages shows thrombosis and
occlusion of the posterior ciliary artery in
GCA
4. Temporal Artery Biopsy
5. Clinical Signs: Jaw Claudication, Neck Pain

25. ARTERITIC
ANTERIOR
ISCHAEMIC
OPTIC
NEUROPATH
Y (AAION)
Treatment: (steroid therapy)
 It is aimed at preventing blindness of the fellow eye
 High dose systemic corticosteroid (IV
methylprednisolone & oral
prednisolone) for several months.
 Intravenous methylprednisolone, 500 mg to 1 g/day
for 3 days followed by
oral prednisolone 1–2 mg/kg/day. After 3 more days
the oral dose is reduced
to 50–60 mg (not less than 0.75 mg/kg) for 4 weeks
or until symptom
resolution and ESR/CRP normalization.
 Prognosis-POOR

26. TRAUMATIC
OPTIC
NEUROPATHY
Caused by craniofacial trauma
but occasionally mild orbital or
eye injury.
most common site of injury of the
optic nerve is the intracanalicular
portion of the nerve

27. DIAGNOSIS
• CT scan of the orbit is recommended to
detect any bony fractures, fractures of
the optic canal,and acute orbital
hemorrhages

28. TRAUMATIC
OPTIC
NEUROPATH
Y
Treatment:
High-dose steroid therapy
Was adopted as a treatment because of
their beneficial effect in studies on spinal
cord injuries.
May be harmful to the optic nerve if
started 8 hours after the injury

29. INFILTRATIVE OPTIC NEUROPATHY
Tumors
Primary(optic gliomas,
capillary hemangiomas,
and cavernous
hemangiomas)
Secondary(nasopharyngeal
carcinoma, lymphoma,
and leukemia)
Inflammation (sarcoidosis) infections

30. COMPRESSIVE OPTIC NEUROPATHY
orbital and intracranial meningiomas
pituitary adenomas
intracranial aneurysms
Craniopharyngiomas
gliomas of the anterior visual pathway

31. HEREDITARY OPTIC NEUROPATHIES
manifest as symmetric bilateral central visual loss
Leber’s hereditary optic neuropathy (LHON)
Dominant optic atrophy (Kjer syndrome)

32. NUTRITIONAL OPTIC NEUROPATHIES
Thiamine
(vitamin B1)
Cyanocobalamin
(vitamin B12)
Pyridoxine
(vitamin B6)
Niacin (vitamin
B3)
Riboflavin
(vitamin B2)
Folic acid

33. TOXIC OPTIC NEUROPATHIES
Amiodarone ethambutol Methanol Cyanide
Isoniazid Lead Triethyl tin
Carbon
monoxide

34. FIELD DEFECTS OF OPTIC NEUROPATHIES
Demyelinating Central, cecocentral, arcuate
Non-arteritic Ischemic Arcuate, altitudinal
Arteritic Ischemic Arcuate
Inflammatory Arcuate, central, cecocentral
Hereditary Central, cecocentral
Traumatic Arcaute, central or hemianopic
Infiltrative Arcuate, hemianopic
Compressive Arcuate, hemianopic
Toxic/nutritional Central, cecocentral

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