UNILATERAL
• Papillitis
• Anterior Ischemic optic neuropathy
• Neuroretinitis
• Papillophlebitis
• Ischemic CRVO
• Anterior compressive optic neuropathies (orbital tumors)
• Infiltrative optic neuropathies
• Ocular hypotony
• Foster-Kennedy syndrome
BILATERAL
• Papilledema
• Hypertension
• Diabetic papillopathy
• Advanced Graves disease
• Cavernous sinus thrombosis
• Carotid cavernous fistula
• Leber hereditary optic neuropathy

PAPILLEDEMA: “optic disc swelling”

1. Intracranial space occupying lesion
 neoplasm (location of the tumor is more important than size)
 abscess/inflammatory mass
 hemorrhage/infarct
 A-V malformation
2. Obstruction of ventricular system
3. Cerebral edema
4. Impaired CSF absorption by arachnoid villi:
 Meningitis
 Raised venous pressure
 SAH/trauma
 Communicating hydrocephalus
5. Severe systemic hypertension
6. Idiopathic (pseudo tumor cerebri):
7. Decreased size of cranial vault:
 Craniosynostosis
 Thickening of skull
8. Hypersecretion of choroids plexus tumor

SYMPTOMS
CLINICAL FEATURES
Ocular:
 Visual acuity-normal in early ,decreased when established and grossly affected when atrophic
 Amaurosis fugax(spasm of arteries)
 Central vision affected late(selective loss of peripheral neurons)
 Diplopia(assoc. 6th cranial nerve palsy in raised ICT)
General:
 Headache (bifrontal/occipital) more in the morning,
 aggravated by coughing straining
 Projectile vomiting
 Loss of consciousness/ focal neurological deficits

CLINICAL FEATURES
SIGNS
1. PUPILLARY REACTION -normal until optic atrophy sets in
2. FUNDOSCOPY
EARLY PAPILLEDEMA
 Hyperemia/elevation of disc
 Blurred margins
 Loss of SVP
 Superficial hemorrhage

CLINICAL FEATURES
ESTABLISHED/FULLY DEVELOPED PAPILLEDEMA:
 Engorged & tortuous veins
 Numerous flame shaped hemorrhages
 Cotton wool spots, hard exudates
 Peripapillary edema (paton’s lines)
 Retinal folds/macular star

CLINICAL FEATURES
CHRONIC/VINTAGE PAPILLEDEMA :
 Optic disc pale & elevated (champagne cork appearance)
 Disc obliterated
 Opticociliary shunts

CLINICAL FEATURES
ATROPHIC PAPILLEDEMA:
 Pale grey disc with reactive gliosis
 Narrow and sheathed vessels
 Retina shows pigmentary changes and
 choroidal folds

CLINICAL FEATURES
3. FIELD CHANGES
 Early-normal
 Established-enlargement of blind spot
 Chronic-peripheral constriction
 End stage-total loss
4. FLUORESCEIN ANGIOGRAPHY
 To differentiate true and pseudopapilledema
 Dilatation of surface capillaries and leakage of dye
 in the late phase
5. NEUROIMAGING
 Features of raised ICT-silver beaten appearance with erosion of posterior clinoid process and dorsum sellae
 Cause of raised ICT may be identified.

– Asymmetric
– Foster Kennedy syndrome
Seen in patients with frontal lobe/olfactory lobe tumors, meningiomas of olfactory groove/sphenoidal wing, characterized by optic atrophy on the side of the tumor caused by direct pressure on the nerve and papilledema on the opposite side because of raised ICT.
– Prior optic atrophy, congenital abnormality in disc, high myopia

Or Benign Intracranial hypertension
Defined by 4 criteria
1. Increased intracranial pressure
2. Normal or small ventricles
3. No evidence of intracranial mass lesion
4. Normal CSF composition
Usually idiopathic seen in young obese women

Endocrine causes
• Addison’s disease
• Hypoparathyroidism
• Hyperthyroidism
• Hypothyroidism
• Menopause
• Menarche
• Pregnancy
Drugs
• Vitamin A
• Tetracycline
• Steroids
• OCP
• Phenytoin
• Indomethacin
• Growth hormone
• lithium

• Weight loss
• Acetazolamide
• Lumbar puncture
• Surgical decompression (ventriculo-peritomeal shunt)

DIFFERENTIAL DIAGNOSIS - Ocular
Papillitis Papilledema
1.Presentation
2.Vision
3.Pupil
U/L
Sudden loss
RAPD present
B/L
Unimpaired initially
RAPD absent
4.Media
Hazy near posterior vitreous
5.Pain/tendeness of eyeball Present
Media clear
Absent
6.Hemorrhages/exudates
7.Disc swelling
8.Field defects
9.X-ray skull
10.CT/MRI
Less
+2 to +3D central/centrocaecal scotoma
Normal
Demyleinating
More(in established)
>+3D
Enlargement of blind spot, later peripheral constriction.
Silver beaten appearance, erosion of dorsum sellae,post clinoid
ICSOL etc.

DIFFERENTIAL DIAGNOSIS - Ocular
• Hypermetropia:
Crowded nerve fibers at disc. More in children, no enlargement of blind spot
• Astigmatism
• Optic nerve head drusen:
Calcium containing refractile bodies within substance of optic nerve head.
Seen in USG. Autofluorescence
• Hazy media

DIFFERENTIAL DIAGNOSIS - Ocular
3. AION/LHON/TOXIC AMBLYOPIAS
4. OCULAR HYPOTONY
Effusion from choroidal vessels
5. RAISED INTRAOCULAR PRESSURE :
Obliteration of peripapillary vessels by raised IOP
6. CRVO

1. IDIOPATHIC
2. DEMYELINATING (Always
Retrobulbar)
3.
Isolated
– a/w multiple sclerosis
– neuromyelitis optica
– schilder’s disease

• INFECTIOUS AND PARAINFECTIOUS
– LOCAL:
• Orbital cellulites
• Sinusitis
•
Teeth, tonsil
•
Meninges, brain or base of skull.
–
SYSTEMIC:
•
VIRAL-measles, mumps, rubella, chickenpox, herpes, CMV and EBV.
•
BACTERIAL-T.B,syphilis,cat scratch disease,lyme’s
• FUNGAL-cryptococcosis,histoplasmosis
• PARASITImalaria,pneumocystis,toxoplasma,toxocara,cystice rcosis
– VACCINES:BCG,DPT,TT,HepB,variola and influenza

4.
IMMUNE RELATED
LOCAL
Uveitis, sympathetic ophthalmitis.
SYSTEMIC sarcoidosis, Wegener’s polyarteritis nodosa, SLE etc.
5.
METABOLIC
Anemia
Diabetes
Starvation
6.
DRUGS AND TOXINS
INH, ethambutol, etanercept, INFa, tobacco, alcohol, quinine.

Commonly unilateral, more in females and mean age is 30-35 yrs.
SYMPTOMS
Triad of
Loss of central vision
Eye pain
Decreased colour vision
Other
Altered perception of moving objects
Worsening of symptoms with elevation of body temperature(uhthoff sign)

SIGNS
• Decreased visual acuity
• Tenderness
• Marcus gunn pupil (RAPD)
• Decreased colour vision and contrast sensitivity
• Visual field defects: classically central/centrocaecal scotoma but other defects can also occur
• Fundus changes
1. Papillitis: edema, hyperemia, blurred margins, dilated tortuous vs, few exudates and vitreous haze
2. Retrobulbar neuritis: normal
3. Neuroretinitis: macular star with exudates
• VEP-Delayed latency and decreased amplitude
• FAG to differentiate from other causes-dilated and telangiectatic vs with leak from capillaries

Field defects in optic neuritis Papillitis
Neuroretinitis

To determine cause for optic neuritis
1.Complete Hemogram
2. CRP, ESR, Mantoux
3. VDRL
4. Serology-ANA, Toxoplasma, Lymes
5. PNS X-ray, chest x ray(sarcoidosis)
6. X ray skull, CT
7. MRI(demyleinating plaques-2 or more predictive of deveplopment of MS)
8. Lumbar puncture-CSF pleocytosis and oligoclonal bands

1. ONTT Regimen - Intravenous methylprednisolone 250mg q
6 h for 3 days followed by
Oral prednisolone 1 mg/kg/day for 11 days, tapered with 20mg on 15th day and 10mg on 16th and 18th day
2. Posterior sub-tenon injection of triamcinolone
3. Vitamin B12
4. Treatment of identifiable cause

 Infarction of prelaminar or laminar portions of optic nerve caused by occlusion of posterior ciliary artery.
 Seen in >50 yrs.
 H/s/o giant cell arteritis or predisposing factors like
DM/HT
 Pale swollen disc with splinter hemorrhages
 Altitudinal scotoma
Classified as
Arteritic & Non-Arteritic

Features
Age
Sex Ratio
Vision loss
Laterality
Optic disc
Assoc. Signs
ESR
FAG
Treatment
Prognosis
Arteritic AION
>60yrs
F>M
Severe
Fellow eye affected in
95% within days to wks
Pale edema, may be sectoral
Scalp tenderness, palpable tender, non-pulsatile temporal artery
>40 mm in 1 st hr
Disc and choroidal filling delay
IV methylprednisolone
Poor
Non Arteritic AION
40-60yrs
F=M
Moderate (>6/60)
Fellow eye affected in <30% in months or yrs
Hyperemic or pale edema
Assoc. HT – 40%, DM – 24%
Shock, nocturnal hypotension
20-40mm in 1 st hr
Disc filling delay
? Levadopa-carbidopa
Improvement in upto 43%