Optic Disc Disorders

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Optic nerve disorders

GHADA ELNADY
Optic nerve anatomy
The ON carries 1.2 million afferent nerve fibers.
one third of the fibers subserve the central 5 degree of the visual
field.(papillomacular bundl).
80% are visual fibers and 20% are pupillary fibers for light reflex.
The ON is surrounded by myline sheath and 3 meningeal layers :
◦ Inner pia mater,archanoid and dura mater.

CSF
Anatomical subdivisions
1- intraocular: (optic nerve head) 1mm.
2- intraorbital: 25-30 mm,extends from globe to the optic foramen.
Its diameter 3-4 mm because of the addition of myelin sheath.
At the orbital apex the ON is surrounded by the annulus of zinn.
3- intracanalicular: 6mm.
4- intracranial :10 mm,joins the chisma.
Clinical Classification
1- optic disc

2- Retrobulbar optic nerve

functions of optic nerve


Light reflex
RAPD
Signs of ON dysfunction
1- Reduced VA.
2- RAPD.
3- Dyschromatopsia.(red,green).
4- Diminished contrast sensitivity.
5- Visual field defects.
Central scotoma,altitudinal defects acc to the underlying pathology.
6- delayed counduction of the VEP.
Classification of the optic neuropathy
1- Inflammatory: optic neuritis (demyelinating,infectious).
2- Ischaemic: arteratic and non arteratic optic neuropathy
Diabetic papillopathy
3- congenital hereditary optic neuropathy:leber ,morning glory and
optic nerve hypoplasia.
4- papilloedema: secondry to rasied intracranial pressure.
5- Nutritional and toxic.
6- Glaucomatous.
7- Traumatic optic neuropathy.
8- Compressive optic neuropathy. TED,Orbital myositis
9-Infltrative optic neuropathy: eg sarcoidosis and tumors.

Optic atrophy
acute optic neuropathy
1-optic neuritis:
- papilitis
- retrobulbar neuritis

2- ischemic optuc nuropathy:


- arteritic optic nuropathy
- Non artertic optic nuropathy
optic Neuritis
Inflamation of the optic nerve fibers
causes
1- Non infectious causes:
Demyelinating disorders (MS)
Middle aged female

2- Infectious causes:viremia ,vaccination,organism from nearby sinus or


menengies .usu in children.
Symptos, signs and Investigation
1- acute sever drop of vision and decrease in contrast sensitivity.
2- Dyschromatopsia esp for red and green
The colour is washed out
3- RAPD and pain
4- Disc oedema and hyperemia esp in papilitis.
Most cases ocure in children
Bilaltral
Good prognosis
Field of vision
Central and centrocaecal scotomas are most frrquent due to
affection of papillomacular bundle first by MS.
MRI

Demylination plaques.
VEP
It is the action potential of the visual cortex evoked by visual
stimulus.
Course of ON
Vision warsens over days to 3 weeks ,begins to improve over 6-12 ms
More than 90% of pts recover VA to 6/9 .

Coulor vision and contrast sensitivity may remain abnormal.

10% develop chronic optic neuritis end with optic atrophy and visual
loss.
Treat or not? ONTT
457 pts with acute optic neuritis randomized to 3 groups
- 250 mg IV methylpred/6h x 3 days,then oral steroid over 11
days and taper.
- Oral prednisolone 1mg/kg per day fo 14 days.
- Oral placebo for 14 days.
Outcomes are assessed over 6ms (VA,colour,contrast sensitivity and
visual field ).
outcomes
Visual functions recovered faster in IV steroid group.

Oral prednisolone alone associated with increased risk of optic


neuritis recurrence.
IV methylprednisolone 1 gm daily for 3 days followed by oral
predenisolone :1 mg /kg daily)for 11 days then tapered over 3 days.

Disease modifying therapies for MS : Interferon and monoclonal ABS.


Home messages from ONTT
It is acceptable to give or withhold IV steroids.

Steroides only accelerate recovery with no affection in long term


visual outcome.

There is no role for moderate dose oral steroids(1mg/kg/day)


It can increase recurrence of ON.
Ischemic optic neuropathy
1-Non arteritic ischemic optic neuropathy

2-Arteritic ischemic optic neuropathy


Non arteritic ischemic optic neuropathy
Caused by occlusion of the short post ciliary arteries resulting in
partial or total infarction of the optic nerve.

HTN,DM,HYPERLIPIDEMIA
Sudden hypotensive events,sleep apnea
Diagnosis

Age :50 ys
c/o sudden painless monocular visual loss usu discovered on
awakening.
Altitudinal visual field defect.
Dyschromatopsia usu proportional to the visual impairment.
Difuse or sectoral hypermic disc swelling followed by pallor 3-6 ws.
IX
Systemic work up
BP
FBS
Lipid profile
Referal to control the systemic predisposition
Prognosis of NAION
Improvment of vision is common
50% can achieve 6/9
25% will reach 6/60 0r worse

Involvment of the fellow eye occurs in 15% after 5 years


Arteritic ischemic optic nuropathy
it is caused by GCA
Inflamation (necrotizing arteritis) with predilection for large and
medium sized arteries
Superficial temporal artry,aortic branches and post ciliary artries
50% of pt have polymyalagia rheumatic
Diagnosis
Age 70-80 rare under 50ys
Female to male 4:1
Sever headache and scalp tenderness
Jaw claudication (pathognomonic): cramp like pain on chewing
Thickned ,tender superfacial temporal artery
Sever visual loss not preceded by amaurosis fugax
Start with altitudinal visual field defect then progressing
Pale (chalky white) disc oedema
The course is very aggressive end with optic atropy

The fellow eye will be involved in more than 30% of cases within
days to 1 week.
IX
Increased ESR and CRP
Temporal artery biopsy TAP

Pseudo Foster Kenedy syndrome


TREATMENT
IV methylprednisolone 1 gm/day for 3 days then oral dose 1-2 mg/kg
per day for 4ws or until ESR&CRP normalization
Taper along 1 -2 ys
Some pts may need maintenance therapy.
Referal and systemic work up due to complications
Myocardial infarction,aortic incompetence,renal failure and brain
stroke.
papillioedema
papilloedema
Disc swelling scondry to raised ICP (bilateral)
All pts with papilloedema should do MRI to exclude tumors
Causes: idiopathic ICH
Obstruction of the ventricular system
space ocuupying lesion
Diagnosis
Headache early in the morning increase with head bending
Nausea,vomiting
Vision is preserved till late of the disease
Transient visual obscurations pp by bending,caugh,vulsalva
manoeuver
Horizontal diplopia due to 6th N palsy
MRI
VF :enlarged blind spot
Treatment : of the cause

Foster Kenedy syndrme


Optic atrophy
Types
1- Primary optic atrophy
Occurs without previous swilling of the optic disc
Flat white disc with delinated margins
Reduction of number of small blood vessles
Causes: optic neuritis,hereditary optic neuropathies
Compression by tumors and aneurysms
Toxic and nutritional optic neuropathy and truma
2- secondry optic atrophy
Preceded by swilling of the optic n head
White greyish disc with poorly delinated margins
Sheathing of arterioles and venous tortuosity
Causes: papillitis
papillioedema
AION
3-Consecutive optic atrophy
Caused by disease of the retia or its blood supply
Obvious on fundus examination (RP,CRRO)
The disc appers waxy
4- Glaucomatous optic atrophy
Visual field defects in optic neuropathies
1- central scotom:
- demyelination
- toxic and nutritional
- compression
2- enlarged blind spot : papilloedema
3- altitudinal ,respect horizontal meridian:
ischemic ON,Glaucoma

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