Lecture on Optic Neuritis & Papilledema For 4th Year MBBS Undergraduate Students By Prof. Dr. Hussain Ahmad Khaqan

1. Optic Neuritis & Papilledema
Prof. Dr. Hussain Ahmad Khaqan
 MD
 FRCS(Glasgow)
 FCPS(Ophth.)
 FCPS(Vitreo Retina)
 MHPE (KMU)
 CICO(UK)
 CMT(UOL)
 Fellowship in Medical Retina (LMU, Munich)
 Fellowship in Vitreo Retinal Surgery (LMU, Munich)
 Consultant Ophthalmologist & Retinal Surgeon
Professor of Ophthalmology
Lahore General Hospital, Lahore
Ameer Ud Din Medical College, Lahore
Post Graduate Medical Institute, Lahore
Shaukat Khanum Memorial Cancer Hospital & Research Centre ,Lahore

2. OPTIC NEURITIS

3. DEFINITION
• The term optic neuritis is typically reserved for optic
nerve inflammation that may be associated with
demyelinating disease.

4. TYPES
Inflammation of the optic nerve may be divided into:
1. Papillitis (where the disc is swollen).
2. Retrobulbar neuritis (where the disc is spared).
3. Neuroretinitis (with retinal involvement, ‘macular star’).
Inflammation of the optic disc with adjacent retinal
exudation is referred to as neuroretinitis

5. Figure: Papillitis Figure: Retrobulbar Neuritis
Figure: neuroretinitis with macular star exudation

6. SYMPTOMS
• Abrupt and progressive vision loss.
• Orbital pain
• Loss of color vision
• Photopsia
• Body temperature

7. SIGNS
• Dyschromatopsia
• Decreased contrast sensitivity
• Relative afferent pupillary defect in unilateral or
asymmetric cases
• central, cecocentral, arcuate, or altitudinal visual field
defects.
• Swollen disc with or without peripapillary flame-shaped
hemorrhages, retinal exudates and mild vitritis.

8. CAUSES
• Idiopathic.
• Multiple sclerosis
• Childhood infections or vaccinations: Measles, mumps,
chickenpox and others.
• Other viral infections: Mononucleosis, varicella zoster,
encephalitis, and others.
• Contiguous inflammation of the meninges, orbit, or sinuses.
• Granulomatous inflammations: Tuberculosis, syphilis,
sarcoidosis, cryptococcus and others.

9. DIFFERENTIAL DIAGNOSIS
• Ischemic optic neuropathy
• Acute papilledema
• Severe systemic hypertension
• Orbital tumor compressing the optic nerve
• Intracranial mass compressing the afferent visual pathway
• Leber hereditary optic neuropathy
• Toxic or metabolic optic neuropathy: secondary to alcohol, malnutrition,
various toxins (e.g. , ethambutol, chloroquine, isoniazid,
chlorpropamide, heavy metals), anemia, and others.

10. INVESTIGATIONS
• MRI of the brain and orbits with gadolinium and fat suppression
• Visual field test
• Laboratory test: Full blood count (FBC), Erythrocyte sedimentation
rate (ESR), C-reactive protein (CRP), Urine examination (U+E), Liver
function tests (LFTs), Angiotensin converting enzyme (ACE),
Antinuclear antibody (ANA), syphilis serology, genetic testing for
LHON (Leber hereditary optic neuropathy), Lumber puncture (LP)
• Chest x-ray or CT.
• Optical coherence tomography (OCT)

11. TREATMENT
• Intravenous methylprednisolone treatment.
• Oral prednisone alone (without intravenous methylprednisolone)
• If MRI reveals at least one typical area of demyelination, offer pulsed
intravenous steroid in the following regimen within 14 days of decreased
vision:
Methylprednisolone 1 g/day i.v. for 3 days, then Prednisone 1
mg/kg/day p.o. for 11 days, then taper prednisone over 4 days.

12. • Antiulcer medication (e.g., omeprazole 20 mg p.o. Daily or ranitidine 150
mg p.o. b.i.d.) for gastric prophylaxis.
• Refer to neurologist or neuro-ophthalmologist for possible treatment with
interferon-beta, glatiramer acetate, fingolimod, dimethylfumarate, or
teriflunomide.
TREATMENT

13. OTHER TREATMENTS
• In experimental models of Multiple sclerosis, intravenous immunoglobulin
G (IVIG) has been shown to promote remyelination of the central nervous
system.

14. PAPILLEDEMA

15. DEFINITION
• Optic disc edema, usually bilateral, which results
from increased intracranial pressure.

16. SYMPTOMS
• Visual obscurations (transient visual acuity (VA) few
seconds’ duration, up to 30×/d, uni-/bilateral, may
be precipitated by posture/straining, etc.)
• Headache (often worse lying down/straining)
• Double vision
• Nausea
• Vomiting
• Pulsatile tinnitus.

17. SIGNS
The five mechanical clinical signs of optic disc edema are:
• Blurring of the optic disc margins.
• Filling in of the optic disc cup.
• Anterior extension of the nerve head (3 diopters =1 mm of elevation).
• Edema of the nerve fiber layer.
• Retinal or choroidal folds or both.

18. The five vascular clinical signs of optic disc edema are:
• Venous congestion of arcuate and peripapillary vessels.
• Papillary and retinal peripapillary hemorrhages.
• Nerve fiber layer infarcts (cotton-wool spots).
• Hyperemia of the optic nerve head.
• Hard exudates of the optic disc.
SIGNS

19. SIGNS
ASSOCIATED FEATURES:
• Gross elevation of the optic nerve head.
• Engorged and dusky veins.
• Peripapillary splinter hemorrhages.
• Occasionally choroidal folds and retinal striae.
• Loss of venous pulsations

20. GRADES OF PAPILLEDEMA
GRADES:
• Grade 1 papilledema is characterized by a C-shaped halo with a temporal gap.
• Grade 2 papilledema is characterized by circumferential halo.
• Grade 3 papilledema is characterized by obscuration of one or more major blood
vessels leaving the disc.
• Grade 4 papilledema is characterized by obscuration of major vessels on the disc.
• Grade 5 papilledema is characterized by obscuration of all vessels on and leaving
the disc.

21. Figure: Grades of Papilledema

22. CAUSES
• Primary and metastatic intracranial tumors.
• Hydrocephalus.
• Idiopathic intracranial hypertension
• Subdural and epidural hematomas.
• Subarachnoid hemorrhage:
• Arteriovenous malformation.
• Brain abscess
• Meningitis
• Encephalitis
• Cerebral venous sinus thrombosis.

23. DIFFERENTIAL DIAGNOSIS
• Disc edema without increased intracranial pressure and Pseudo
papilledema (e.g. , optic disc drusen or congenitally anomalous
disc)
• Other causes: compressive optic neuropathies, papillitis, anterior
ischemic optic neuropathy, juvenile diabetic papillopathy, and optic
disc vasculitis, Hypertensive optic neuropathy, Infiltration of the
optic disc (e.g. , sarcoid or tuberculous granuloma, leukemia,
metastasis, other inflammatory disease or tumor), Leber hereditary
optic neuropathy, Orbital optic nerve tumors, Thyroid-related optic
neuropathy, Uveitis (e.g. syphilis or sarcoidosis), Amiodarone
toxicity.

24. WORK-UP
• History and physical examination, including blood pressure measurement.
• Ocular examination, including a pupillary examination and assessment for
dyschromatopsia, posterior vitreous evaluation for white blood cells, and a
dilated fundus examination.
• Emergency MRI with gadolinium and magnetic resonance venography
(MRV) of the head are preferred. CT scan (axial, coronal, and parasagittal
views) may be done if MRI not available emergently.

25. • If MRI/MRV or CT is unrevealing, perform LP (Lumber puncture) with CSF
(cerebrospinal fluid) analysis and opening pressure measurement if no
contraindication.
• Optical coherence tomography (OCT)
• Automated visual fields such as Humphrey (HVF) are most important in assessing
visual status.
• FFA (fundus fluorescein angiography) (if diagnostic uncertainty): late leakage from
dilated disc capillaries.
WORK-UP

26. Figure: OCT in papilledemaFigure: FFA in papilledema

27. Figure: MRI brain and orbit

28. TREATMENT
• The treatment of papilledema associated with visual
loss depends in large part on the cause, symptoms,
signs, and progression of the problem.
• Medical treatment usually consists of diuretics,
especially carbonic anhydrase inhibitors such as
acetazolamide and, in cases of IIH (idiopathic
intracranial hypertension), weight reduction.