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Optic neuritis

Optic neuritis is inflammation of the optic nerve that commonly presents as sudden, unilateral vision loss. It affects young females predominantly and is often the initial presentation of multiple sclerosis. Treatment with intravenous steroids followed by oral steroids accelerates visual recovery but provides no long-term benefit over oral steroids alone. Early treatment of multiple sclerosis after an initial demyelinating event such as optic neuritis can reduce future relapse rates and disability progression.

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OPTIC NEURITIS
DEFINITION  Optic neuritis refers to inflammation of the optic nerve  Occurs in about 50 % of pts with multiple sclerosis and is presenting feature in 20%
EPIDEMIOLOGY  1/1,00,000  5:1- female:male ratio  Young age (20-40 years old)
ETIOLOGY
 Idopathic  Demyelinating disorders – a) Multiple sclerosis b) Devics disease c) Schilder disease d) acute disseminated encephalomyelitis
 Parainfectious optic neuritis – associated with measles , mumps, chicken pox or following immunisation  Infectious – sinus related (ethmoiditis) , cat scratch fever , syphilis , lyme disease, cryptococcal meningitis
CLINICAL TYPES  Papillitis – involvement of optic disc  Neuroretinitis – involvement of optic disc and surrounding retina in macular area  Retrobulbar neuritis – involvement of optic nerve behind the eyeball
PATHOLOGY  Perivascular infiltrate of inflammatory cells  Destruction of myelin  Removal of disintegrated myelin by phagocytic cells  Proliferative gliosis
CLINICAL FEATURES  HISTORY  A prodromal viral illness may occur.  Orbital pain and pain with eye movement prior to visual changes. The pain can be excruciating or very mild like a foreign body sensation.
SYMPTOMS  Sudden profound U/L vision loss  Pain aggravated by ocular movements – especially upward or downward ( due to attachment of fibres of superior rectus to dura )  Visual obscuration in bright light  Impaired dark adaptation  Reduced vividness of saturated colours
 Movement phosphenes and sound induced phosphenes  Uthoff phenomenon – transient obscuration of vision on exertion and on exposure to heat  Pulfrich phenomenon – altered depth perception for moving objects
SIGNS  Decreased visual acuity  Decreased color vision (red desaturation) and/or decreased contrast/brightness sense  RAPD unless both eyes are affected or RAPD was present prior in contralateral eye
 Disc edema (only 35% noted in ONTT, thus lack of disc edema does not rule out acute optic neuritis)  Retinal vascular sheathing, pars planitis (periphlebitis occurs in 5- 10% of multiple sclerosis patients)
 Any scotoma on Amsler grid and/or confrontation visual fields or formal visual field testing – most common is a central or centrocecal scotoma  VEP shows reduced amplitude and delayed transmission time
TYPICAL OPTIC NEURITIS  Predominantly affects females  15-45 years  Unilateral  Acute , painful vision loss over hours to days
 Retrorbital pain worse with eye movments  Peak visual loss within 2 weeks after which improvement occurs  Poor color vision , contrast sensititivity  Any type of visual field defect  VEP- prolonged latency , decreased amplitude
ATYPICAL OPTIC NEURITIS  Painless visual loss  Extremes of age  Bilateral  Disc hemorrhage , cotton wool spots  Progression of visual loss beyond 2 weeks  Fails to improve with treatment
D/D PAPILLEDEMA PAPILLITIS PSEUDO- PAPILLITIS LATERALITY B/L U/L U/L OR B/L VA BLURRED VISION SUDDEN PRFOUND LOSS OF VISION BLURRED VISION PAIN ON OCULAR MOVEMENTS NIL YES NIL MEDIA CLEAR VIT CELLS CLEAR
PERIPAPILLARY EDEMA , VENOUS ENGORGEMENT, RETINAL HRAGE , EXUDATES MARKED LESS MARKED ABSENT FIELD DEFECT ENLARGED BLIND SPOT CENTRAL SCOTOMA NIL FFA LEAKAGE OF DYE++ MINIMAL LEAKAGE NIL
INVESTIGATIONS  Routine Ix are not required in a case of typical optic neuritis  Required in the following conditions A) Atypical optic neuritis B)Recurrent optic neuritis C)Acute optic neuritis in children D)Presence of systemic inflammatory disease
 CBC  Chest x ray  ANA , dsDNA  FTA-ABS , VDRL  Serology and culture for bartonella  PCR for viral infections  CSF tap
MRI CRITERIA FOR DIAGNOSING MS  Atleast 3 lesions and two of the following should be present  1) lesions abutting the lateral ventricles  2)lesions with diameters greater than 5 mm  3)lesions present in the posterior fossa
TREATMENT  Optic neuritis treatment trial (ONTT)  OBJECTIVES To evaluate efficacy of corticosteroids in Rx of acute optic neuritis To investigate relationship b/w optic neuritis and multiple sclerosis
 INCLUSION CRITERIA  Age 18-46 yrs  Acute U/L optic neuritis for 8 days or less  A RAPD and a visual field defect in the affected eye  No previous corticosteroid treatment for optic neuritis or MS  No systemic disease other than MS that might be cause of optic neuritis
Pts were randomised to one of 3 groups ORAL PREDNISOLONE 1MG/KG FOR 14 DAYS IVMP (250MG/6HRS) FOR 3 DAYS FOLLOWED BY ORAL PREDNISOLONE 1MG/KG FOR 11 DAYS ORAL PLACEBO FOR 14 DAYS
RESULTS  Routine Ix are of limited value in diagnosing optic neuritis in a patient with typical optic neuritis  Brain MRI is a powerful predictor of early risk of MS after optic neuritis  Visual recovery begins within 2 weeks and continues upto 1 yr  Probability of recurrence of optic neuritis in either eye within 5 yrs is 28 %
 Treatment with high dose IV steroid followed by oral steroid accelerated visual recovery but provided no long term benefit to vision  Treatment with oral prednisolone alone did not improve visual outcome and was associated with increased rates of new attacks of optic neuritis
 Dyschromatopsia , defective stereoacuity , RAPD , delayed latencies on VEP , pulfrich and uthoff phenomenon may remain as residual deficits after an attack of optic neuritis
 Four large scale clinical trials have been conducted to determine whether early treatment following first demyelinating episode can delay the second event  1)CHAMPS AND CHAMPIONS  2)ETOMS  3)BENEFIT  4)PRECISE
CONTROLLED HIGH RISK AVONEX MULTPLE SCLEROSIS TRIAL- CHAMPS STUDY •TO STUDY WHETHER INTERFERON BETA 1a TRAETMENT WOULD BENEFIT PTS HAVING FIRST DEMYELINATING EVENT AND MRI ABNORMALITIES IN REDUCING THE INCIDENCE OF CDMS OBJECTIVES •ALL PTS RECEVIED IVMP FOR 3 DAYS F/B ORAL PREDNISOLONE FOR 11 DAYS PLUS •GROUP 1 – RECIVED WEEKLY INJECTION OF IFN BETA 1 a •GROUP 2 RECEIVED PLACEBO INJECTION MATERIAL AND METHODS •AT THE END OF 3 YRS PROBABILITY OF DEVELOPING CDMS WAS 50 % IN PLACEBO GROUP AND 35% IN IFN BETA TREATED GROUP •TREATMENT WITH AVONEX (IFN BETA 1 a)REDUCED 2 YRS LIKELIHOOD OF FUTURE NEUROLOGICAL EVENTS RESULTS
Controlled high risk avonex multiple sclerosis prevention surveillance -  CHAMPIONS STUDY – compared outcomes of those who had been given drug from start of CHAMPS study versus those who switched from placebo after about 30 months  Those who were started on Rx immediately had fewer relapses and fewer MRI brain lesions than delayed treatment group
 Early treatment of multiple sclerosis study – ETOMS  IFN B 1a treatment at an early stage had significant positive clinical and MRI outcomes
 Betaseron in newly emerging multiple sclerosis for initial teratment study – BENEFIT  Early initiation of Rx with IFN B 1b prevents development of disability supporting its use after first manifestation of relapsing remitting MS
 PreCISe study  Early treatment with Glatiramate acetate is efficacious in delaying conversion to CDMS in patients presenting with CIS and brain lesions detedcted by MRI
COURSE  Typically visual acuity and color vision is lost over 2-5 days  Recovery starts within 2 weeks and takes 4-6 weeks  75-90% cases get good visual recovery  Reccurent attacks of retrobulbar neuritis develop primary optic atrophy and pts with recuurent papillitis get postneuritic optic atrophy
Optic neuritis