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Inflammatory Optic Neuropathy
Inflammatory Optic Neuropathy
Optic Neuritis
Background: historically
Blindness a divine punishment for sin Optic neuritis may have accounted for miraculous spontaneous cures
Defination
Inflammation of optic nerve is known as optic neuritis , Characterized by sudden loss of vision in affected eye, often accompanied by pain
Demylinating disorders
Isolated
Local
Uveitis Sympathetic
ophthalmitis
Systemic Sarcoidosis,wegeners
Epidemology
Incidence -3-5 /lakh per year Prevalence -115 per 1lakh Majority of patients are between the age of 20-50 yr Females are more affected than males Acute demyelinating is the most common form of optic neuritis May be the initial presentation of Multiple Sclerosis
Ocular manifestations
Visual acuty -Subtle or profound visual loss
,usually unilateral may be b/l
VEP
Prolonged latency is seen
Dyschromatopsia
Ophthalmoscopic types-Papillitis
Approx 35 % cases of optic neuritis Inflammation is located anterior to nerve First hyperemic disc , then blurred margins , swelling & edema ,torturous & distorted veins Disc swelling does not exceed 2-3 D colour vision, contrast sensitivity ,stereo acuity diminished . Central Vn spared
Neuroretinitis
Entity characterized by optic disc edema & macular star(ODEMS). 3-4 th decade of age. Sudden decrease in vision not associated with pain Vision ranges from PL- 6/9 RAPD Oedma precedes macular star , which may not be presnt at the presentation
Neuroretinitis
Etiology Papilitis with retinal exudates which are in retinal nerve fiber layer & radially oriented to form macular fan or star .
50% cases are idiopathic Following a viral syndrome 2/3rd of neuroretinitis Cat Sratch Disease Toxoplasmosis Toxocariasis and helminths . Lyme disease, Syphilis, especially secondary syphilis as part of a meningitis
Investigations
Every case of neuro retinitis should be investigated for infectious etiology
Routine haemogram, X-ray (Chest), Mantoux, FTA-ABS & VDRL for syphilis, serology and culture for bartonella Serology for toxoplasmosis Blood culture
FA in neuroretinitis
Treatment
No treatment is also option as there is spontaneously But treatment may speed recovery & shorten duration
Diagnosis
Visual acuity
Colour vision
Fundus
Stereoacuity
Contrast sensitivity
Visual fields
Central scotomas
Paracentral scotomas
Altitudinal defects
Optic nerve sheath enhancement with Gad Periventricular whire matter lesion on MRI
To determine whether the cause is compressive inflammatory , infectious . To determine prognosis or risk for subsequent development of MS in mono symptomatic cases. To confirm the diagnosis & to access the other white matter lesion
Fluorescein Angiography-Papillitis
OCT
Predicting the subset of optic neuritis patients who will suffer from persistsant visual disfunction Poor visual outcome who had RNFL thickness less than 75 um in 3-6 months duration .
Left: OCT-showing average retinal nerve fiber layer measurements in affected eye at time of presentation, measuring 111 m in right eye (top) and 99 m in left eye (bottom). Right: thinning of average retinal nerve fiber layer in right eye (top), which now measured 44 m 6 months after acute optic neuritis event.
Old patients Bilateral Progression of visual loss beyond 2 week Patients fail to improve with treatment Disc haemorrhages and cotton wool spots can occur. spots can occur
Systemic Investigation
Routine hemogram X-ray (Chest) Mantoux FTA-ABS & VDRL for syphilis serology and culture for bartonella Serology for toxoplasmosis Markers of viral infection Serum electrolytes and FBS MRI Lumbar puncture and CSF tap (IgG index and oligoclonal bands) Blood culture ANA,dsDNA
AION Age Pain Pupil Defect Optic disc >50 yr Unsual +RAPD Altitudinal
Edema 100% may Edema 33 % hyperemic be pale Common Delayed disc filling No optic nerve enhansment Unsual No delayed disc filling
MRI scan
Papilloedema Present
Normal till late stages despite sever disc edema Normal till late stages
Usually decreased
Severely decreased
Present only if optic Always present atrophy sets in Shows demyelinative MRI Shows lesions in periventricular causative lesion ventricles region and enlargement
Optic neuritis in MS
Unless otherwise specified .the term optic neuritis implies an idiopathic or demylinating syndrome associated with multiple sclerosis Optic Neuritis occurs in about 50% of patients with MS Is presenting feature in about 20%. Occurrence of retro bulbar neuritis should always arouse suspicion of multiple sclerosis ONTT has shown that 10-year risk of development of multiple sclerosis is 38%.
Typical lesion s on MRI One or more typical lesions Risk of developing MS 56%
No lesions
22%
Pathophysiology
Autoreactive abs & T-Cells cross blood-brain barrier & damage myelin demyelination Genetic & environmental factors predispose to an autoimmune response
Genetic: HLA-Dw2; HLA-DR2 Environmental: Infection, stress, systemic antigens & metabolites
Differential diagnosis
Lebers optic neuropathy lack of pain, circumpapillary telangiectatic microangiopathy, absence of leak on FA & maternal pattern of inheritance.
Figure 1 Acute fundal appearance in Leber hereditary optic neuropathy showing disc hyperaemia, swelling of the parapapillary retinal nerve fibre layer and retinal vascular tortuosity
Sarcoidosis
Granulomatous inflammation of optic nerve Disc has characteristic lumpy white appearance ,d/t granulomatous inflammation . Rapid recovery with corticosteroid therapy but recurrence on steroid tapering is characteristic Which is unusual for demylinating optic neuritis
syphilis
U/L or B/L Vitreous cellular reaction is typical feature to diffn from demylinationg ON where vitreous humor is usually clear CSF VDRL iv Penicillin
Diffuse disc edema ,nerve fiber layer hamorrage , cotton wool spots ,stellate macullar exudates
Treatment Infection usually selflimiting May be treated with oral doxycycline or erythromycin, with or without rifampicin when infections are severe or sight threatening1
toxoplasmosis
Most important protozoan cause of intraocular inflammation Retinochoroiditis ,pappilitis , neuroretinitis, Focal necrotising retinitis , atropic scars Oval or circular lesions over cream coloured retina, retinal thickening
457 pts: acute unilateral ON & MS 18-46 yrs of age; 77% ; 85% caucasian
3 treatment groups: (1) IV methyl prednisolone 250mg Q6hrs x 3 days 11 days Oral prednisone (1mg/kg) (2) Oral prednisone (1mg/kg) x 14 days (3) Placebo Baseline gadolinium-enhanced MRI of brain/orbits 1 visual outcome measures: visual acuity, color vision, contrast sensitivity & visual field; 2 outcome measure: development of CDMS
Recommendations
IV methyl prednisolone dose of 250 mg IV slowly over 30-60minutes repeated for 6 hrs for 3 days , Followed by 11 days of oral prednisolone ,1 mg/ kg /day
Never use oral prednisolone alone ,as it may recurrence rate are significantly higher
If MS is already diagnosed or suffered from prior episode of optic neuritis ---- observation is rule .
CHAMPS:
Objectives
Group 1
Whether interferon
beta la (Avonex)
treatment would benefit patients who had experienced a first acute demyelinating event involving the optic nerve, brain stem/cerebellum, or spinal cord, and who displayed MRI brain abnormalities
Placebo injections
e
ETOMS
Champions Study
Controlled High Risk Avonex Multiple Sclerosis Prevention Surveillance Objective: Compared outcomes in those who had given drug from the start of the CHAMPS study (Immediate treatment or IT group) versus those who had switched from placebo after about 30 months (delayed treatment or DT group). Results: IT group had significantly fewer relapses and fewer MRI brain lesions than the DT group.
Newer modalities ; Copolymer-1 T-Cell Receptor Peptide Immunization Anti-CD4 Monoclonal Antibody Azathioprine (Imuran) Cyclophosphamide (Cytoxan) Oral Myelin Methotrexate Cladribine Intravenous Immunoglobulin G
th
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