Optic neuritis-M.B

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Optic neuritis-M.B

  1. 1. Optic neuritis Dr. Meenank
  2. 2. Optic Neuritis (ON) • Inflammation of optic nerve - ON • Associated with swollen disc – papillitis/ anterior ON • Normal disc – retro bulbar ON/ neuritis • Absence of any signs of M.S/ systemic illness – monosymptomatic/ idiopathic/ Clinically isolated ON • Subtle clinical signs + electrophysiological evidence – asymptomatic ON
  3. 3. Two variants 1. Neuroretinitis – infla. Of intraocular + Peripapillary retina –> disc swelling + retinal oedema + Hx + hard exudates + macular star 2. Optic peri-neuritis – infla. Of optic nerve sheet only –> disc swelling with out Vn complications + large blind spot • D/D papilledema Demographic • 2.2 -2.6 per 100,000 cases (or) 115 / 100,00 cases per year • white population • Northern latitude • Females ( 77%) • Age – 15 to 50yr , (children – 10 to 20 ) • Mean age – 33yrs
  4. 4. initial attack – unilateral Triad of symptoms • Vision loss • Ipsilateral eye pain • dyschromotopsia Associated Symptoms • • • • Movement phosphens Sound induced phosphens Visual obscuration's in bright light Uhthoff’s syndrome
  5. 5. Loss of vision • Rapid / abrupt loss of vision • According to ONTT • • • • With in hrs – 29% In 1 to 2 days – 20% In 3 to 7 days – 23 % In 1 to 2 weeks – 7 % • Variant : • Ch. Demyelination of optic neuropathy characterized by slow progressive vision loss – due to macro-plaques optic nerve – impairment of vision • Micro-plaques chiasma – chiasmal optic neuritis ( rare symptom)
  6. 6. Pain • • • • • • • • • Freq. of Ipsilateral eye pain in unilateral ON – 55% to 92% Character – dull aching ass. With generalized / periocular headache aggravated by – EOM / touch Pain precedes vision loss Max severity – 24 to 36 hr subsides with in 48 to 72 hrs Pain = vision loss Pain in retro-bulbar > papillitis > AION ( 93%> 90% > 12% ) Atypical presentation = pain more than 7 days
  7. 7. Dyschromatopsia • Impaired color vision = 94% • Desaturation • – eg: red = dark/ beached • Distinguishes b/w macular lesion
  8. 8. Phosphens • • • • Ring of light ONTT = 30% positive 3 observation Sparkles sparkles Motion induced flashes • Due to disc oedema • Stimulation of Peripapillary retina • Motion induced • Before / during / months after • Most common – dim illumination, horizontal gaze, closed eyes • Rapid eye movement's – decrease phosphens Sound induced flashes
  9. 9. • Cause : spontaneous discharge of the partially demyelinated spinal chord axons in min. stress condt. • Sound induced • Loud noise at rest = phosphens • Pathological variant of hypnogogic hallucinations
  10. 10. Uhthoff’s symptoms Isolated ON (rare) / M.S. Quick recovery Hot baths /climate Transient blurring • Generalized blurring for 2- 20 min • Cool down vision back with in 5min to 24 hrs ( rare) • Not common in ON but seen in compressive toxic inflammatory LHON In ½ of isolated ON Shows recurrence , sporadic
  11. 11. Clinical Sign’s • • • • • • Acuity Dyschomatopsia Contrast sensitivity Afferent pupillary defect Optic disc Retinal finding • Acuity • Varying degree of visual acuity can be seen ranging from 6/9 to NLP
  12. 12. Dyschromatopsia • Unilateral Dyschomatopsia with good V.A → ON • Can be detected using • Hardy Rand Ritter • Ishihara pseudo=isochomatic plates • Fans-worth Munsell 100-hue Test • Ishihara - 20/280 • Hardy Randy Ritter – 20/ 100 • Color sensitivity > V.A • Contrast sensitivity = V.A Dyschromatopsia
  13. 13. Contrast sensitivity Recovered ON with 6/6 but, imperfect Vn Physiological test • Contrast sensitivity test – Pelli-Robson and Sloan low contrast Detect hidden vision loss • ONTT 98% abr • Pelli- Robson Contrast chart (Sensitivity) • Distance – 1 • Chart – 16 triplet of same letter • Contrast – 96% 10 1% • Sloan low Contrast acuity Chart (acuity) • Low contrast, light grey • Like snellen chart - good for subclinical ON - cannot diff. b/w ON/ maulopathy/ organic (or) non- organic
  14. 14. Stereoacuity • Stereoacuity and snellen’s and in linear relationship • Normal Stereoacuity with impaired snellen’s • Snellen's incorrect • Non-organic vision loss • Pulrich effect • Damaged optic nerve delays transmission to visual cortex from the unilateral eye • Oscillating target on the front plane is perceived as elliptical due to stereo –illumination due to impulse delay
  15. 15. • Magnitude of stereo – illumination • • • • Velocity of target Diff. between retinal illumination b/w two eyes Basic level of retinal illumination Distance between the observer and target • Pulrich – more sensitive indicator of optic nerve dis.
  16. 16. Visual fields • • • • ONTT = all patients show V.F abnormalities in acute phase Vn loss – central ⁺⁺⁺, peripheral⁺, particular region⁺ If Vn severely impaired – confrontation test Vision improved – • Multi-isotropic kinetic Goldman Perimetry ( only central scotoma) • Computer Assisted automated static Perimetry ( Diffused and focal ) • Octopus Perimetry • Focal defect – • Altitudinal • Arcate • Nasal step defect 42%
  17. 17. Afferent pupillary defect • In the absence of an optic nerve lesion in the fellow eye RAPD can be demonstrated by swinging flash light • RAPD can be graded by neutral density filters – 0.3, 0.6, 0.9, 1.2 • -ve RAPD in recurrent attacks
  18. 18. Optic disc • • • • • • Normal – ⅔ Optic disc oedema Oedematous - ½ Temporal pallor – 10% , suggestive of preceding attack Disc Oedema is without Hx / lipids/ cotton wool Disc changes α multiple sclerosis Recovered ON – optic disc • Normal 40% • Temporal pallor 30% • Total pallor 20% • M.S without ON can have pale optic nerves
  19. 19. Retinal Findings • Retinal venous sheathing • Small ill-defined/ round confluent white exudates along the peripheral veins • Most common – systemic illness ( M.S. , sarcoidosis) • Also in asymp. Eye of M.S as an isolated B/l finding • Recurrence – post complete resolution • RNFL atrophy • Disc atrophy is seen in all types of optic neuropathy • M.S – incidious RNFL atrophy with visual symptoms of optic nerve dysfuntion • RNFL defects in ON/ M.S – from axonal atrophy
  20. 20. • Seen as a slit in the nerve fiber striation in the arcate fiber bundle • Slits – M.S 70% - normal eye of ON – 2 sub-clinical optic nerve lesions • RNFL defects – focal / diffused atrophy Diagnosed through 1. 2. 3. 4. monochromatic red free ophthalmoscopy Red free light magnifying fungus photography OCT Heidelberg retinal tomography • RNFL thickness - α neurological function test - ⅟α contrast sensitivity test
  21. 21. RNFL Normal RNFL Loss of RNFL
  22. 22. Differential diagnosis • Unilateral ON • NAION • Infectious/ inflammatory • • • • • • • • • • • • Neuroretinitis Viral Post- viral Fungal Syphilis Toxoplasmosis Lyme Herpes zoster Sarcoidosis T.B. Collagen vascular disease Autoimmune ON • Leber’s hereditary ON • Compressive • • • • Meningioma Glioma Metastasis PNS mass • Infiltrative • Multiple myeloma • Leukemia • Cā meningitis • Retinopathies • Paraneoplastic ON • Cone dystrophy
  23. 23. • M.C occurring optic neuropathies AION and idiopathic ON • Difficult to distinguish on the basis of • Age, initial presentation, progression, V.F defects, optic nerve Optic neuritis AION demographics Mean age, yrs 33 ( 5- 70) 66 ( 11 – 90 ) Gender, % female 70% 45% Annual incidence, per 100,000 2 -6 1- 6 Symptoms Pain 92% 10% Progression 70% 30% - 45% Improvement >90% >40% Signs Acuity 6/6 to NPL 6/6 to NPL Field defects Central scotoma Inferior altitudinal Disc oedema 35% 100%
  24. 24. Rhinogenous ON • From the sinus – posterior ethmoidal (or) sphinodal • Mimics unilateral idiopathic ON • Seen in – recurrent attacks of Vn loss with sever head-ach/ febrile illness • Diff. diagnosis – • Rx – steroids • Can lead to steroid sensitive ON
  25. 25. Lyme disease • Lyme borreliosis ehrlichosis rarely cause optic neuropathy • Early stages – optic nerve swollen • Lyme meningitis- disc swelling – papilledema/ optic perineuritis • Diagnosis – serological test (imp. In endemic cases) • Rx – oral / I.V steroids
  26. 26. Acute syphilitic neuritis • Manifestation of 2⁰ syphilis – uni/ bi lateral Vn loss • Acc. by intraocular inflammation – uveitis , retinal vasculits • 2⁰ syphilis –> meningeal inflammation –> syphilitic optic perineuritis inflammation of the optic nerve sheet swelling of the optic disc • 2⁰ syphilis – tertiary syphilis Slow prog. Vn loss with optic atrophy without inflammation • Check for – palmar and truncal rash ( 2⁰ syphilis)
  27. 27. • Diagnosis • VDRL • PRP (plasma rapid reagent) positive for 2⁰ syphilis normal for tertiary syphilis • Immunocompetent + syphilis = +ve for life for • Microhemaglutten assay for treponema pallidum (MHA-TP) • Florescent treponemal antibody absorption test ( FTA-AB) • CSF – normal / inc. WBC
  28. 28. Neuro-retinitis • ON + swollen disc + macular oedema (ME) • Resolved ME –> macular star • Vitreous cells ± mid peripheral choroditis • Neuroretinitis due to infec./ infla • Cat-scratch dis • Syphilis • Lyme • Toxoplasmosis • Sarcoidosis • Prognosis – good
  29. 29. Cancer Paraneoplastic • Acute and sub-acute – Vn loss • Auto-antibodies –> retina / &, optic nerve – uni/bi Vn loss with in 1 week • Optic disc – normal to swollen, vitreous cells • Neurological defects – ataxia, peripheral neuropathy, movement disorders • Optic nerve – show (CRMP-5) IGg • Antibodies to Collapsing response mediated protein -5 • Tumors associated with Paraneoplastic optic neuropathy • Small cell Ca. lung • Thymoma • Thyroid Ca.
  30. 30. Bilateral (or) Simultaneous • Leber’s hereditary ON (LHON) • Chiasmal syndrome • Nutritional • B₁₂ deficiency • Tobacco – alcohol amblyopia • Toxic • • • • Linezolid Ethambutol Amiradone Tumor necrosis alpha inhibitors • Neuromylitis optica (NMO) • Papilledema
  31. 31. Neuromylitis Optica (NMO) • AKA Devic’s diseases • Rare, all ages, bilateral (91%) • Inflammatory CNS demyelinating diseases • Optic nerve • Spinal chord ( only 3 vertebrae ) • • • • • • • In NMO, ON –> transverse myelitis ( weeks) Acute stage – CSF proteins – CSF pleocytosis Pleocytosis – predictor of out come Don’t show oligoclonal bands No white matter lesions Incomplete neurological recovery NMO IGg antibodies – 70% sensitive , 100% specific to NMO
  32. 32. SLE • Affinity - 1% • Vision loss • Acute progressive • Corticosteroid Rx – sub-acute to slow prog. – steroid dependent and suggestive of collagen vascular disorder • Lab – ANA , anti-cardiolopin (increased) • Biopsy of non-exposed tissue • Peri-vascular infiltrates • Immune-complex deposits • Rx – prolong steroid thx in the dermis
  33. 33. Tobacco – alcohol amblyopia • • • • • • AKA Tobacco/ ON of chronic alcohol/ malnutrition ON Vision loss – slow progressive Visual field defect – B/L centro-coecal scotoma Dietary deficiency Rx – thiamine, B₁₂, folate Vision imp. Inspite of abuse Jamaican optic neuropathy • Vn 6/60 ↓, B/l dense central scotoma, W. Africa & Carrabinan immigrant's • Patient – well nourished, non-toxic, VDRL non-reactive • Rx – no Tx relief, no spontaneous recovery • Cause – unknown
  34. 34. Leber’s hereditary ON (LHON) • • • • • 1st disease to inherit mitochondrial mutation in DNA Maternally inherited 1 young men, white ( 80% -90% ) with 50% Vn loss Japanese's Symptoms • Sub-acute painless bilateral Vn loss • Central (or) ceco-central scotoma • Onset- all ages • Most common -12 yr to 30 yrs • Vn loss –permanent profound , with in weeks -1 month - 8yrs • Rare – monocular Vn loss • Uhthoff's symptoms ⁺
  35. 35. • Nadir of visual acuity, commonly 6/60 and ↑ • Fundus – depending on the stage / normal • Acute • • • • circumpapillary telangiectic microangiopathy with disc hyperemia Swelling of Peripapillary NFL Vascular tortuosity F.A – absence of leak from disc • Late • Telangiectic microangisums –resolved • Optic atrophy • Loss of NFL striations in papillomacular bundle • Associated with cardiac anomalies • Diagnosis – DNA analysis • Rx – L-carnitine, Succinate, Vit. B, Vit. E, co-enzyme Q₁₀, idebenon
  36. 36. ON in children Adults ⅓ • Disc oedema Children (50% - 75%) bilateral + optic nerve swelling • MRI - normal to large enhance white matter lesions • Acute disseminated encephalomyelitis • Rx – IVMP 1-4 gm./ kg/ day x 3-5 day oral prednisolone 1mg/ kg/ day (taper @ 4 wks) • Child with ant ON – relapse with steroid • Progress – 80% • Pediatric ON –> M.S, very low (4yrs to 9yrs)
  37. 37. Investigations Visual evoke potential • ON detects • Sub-clinical abnormalities • Difference between organic and non-organic origin • Test the central and para-foveal visual field • Flash VEP – areas 17, 18, 19 • Wave form VEP – triphasic • P100 - +ve peak • N75 with N45 - -ve peaks • Prolong P100 (latency) => changes with ON • P100 (amplitude) => visual acuity, not reliable
  38. 38. • Absolute latency @ P100, > 9 ms = optic nerve dysfunction • Delay in P100 permanent after an attack • Prolong latency in VEP • Compression • Glaucoma • Dopamine def. in central neurodegenerative dis. • Altered amplitude and latency in normal individuals • Defocusing • Looking away
  39. 39. Pattern Electro-retino-gram • PERG is used to evaluate the function of the macula or central retina • PERG refines VEP’s abnormal interpretations • To R/o the cause isn’t from a ant. Lesion • Waves – P50 (+ve), N95( large –ve), N35 ( small early –ve) • In ON – • Delayed VEP P100 latency • Near-normal PERG N50 amplitude • Small/ absent PERG N95 amplitude • Ant. Visual pathway dysfunction/ maculopathy – • Delayed/ small P100 • Reduced P50 • Normal N95
  40. 40. Magnet Resonance Imaging • Not always imp. but, help R/o other disorders • MRI brain and orbit with fat suppression and gadolinium • In ON – • Optic nerve – abr STIR signals • Gadolinium enhancements • Single white matter lesion in AMON – high risk for M.S • Abnormality > 3mm, oval, in peri-ventricular white matter, radially oriented towards the ventricular spaces on a unenhanced MRI
  41. 41. Revised McDonalds Criteria DISSEMINATION IN SPACE DISSEMINATION IN TIME One or more gadolinium enhanced lesions/ 9 hyper intense white matter lesion Gadolinium enhanced lesion > 3month post initial evaluation One or more infra-tentorial lesion New T2 lesion > 30 days after baseline MRI Three/ more prei-ventricular lesions A spinal chord lesion can substitute for one infra-tentorial lesion Need to fulfill atleast 3 Lesion should be 3mm or more
  42. 42. Prognosis and Recurrence Prognosis • although 85% show irreversible nerve damage • Visual out come is in 92% - 6/9 • Recurrence • Two group’s • Existing M.S – 45% • People using oral prednisolone
  43. 43. Multiple Sclerosis • MS is an inflammatory demyelinating disorder of the CNS white matter • Ophthalmic presentation • ON, inter-nuclear ophthalmaoplegia, nystagmus • Uncommon presentation – homonymous V.F loss, gaze palsy, isolated ocular motor palsy • Diagnostic – • Two or more lesions in nervous system in separate locations occurring at diff. time – separation of time and space, with no explanation • MRI - New gadolinium enhancement > 3months after ON attack • CSF - oligoclonal bands in the gamma-globulin region of the fractioned protein • Also seen in – neurosyphilis, neurosarcoidosis, meningitis • Abnormal IGg index
  44. 44. Treatment Corticosteroid's • ONTT (optic neuritis treatment trial) 3 groups 1. 2. 3. Oral prednisolone (1mg/kg) daily for 14 days Oral placebo (1mg/kg) daily for 14 days IVMP (1gm/d) for 3 days followed by oral prednisolone (1mg/kg) for 11 days • Faster recovery with IVMP, but no diff. in final result • Recurrence with oral prednisolone • IVMP – 50% reduction in development to M.S
  45. 45. Interferon therapy • CHAMPS – Controlled High Risk Subjects Avonex M.S. prevention • Multicenter , randomized, double-blinded, placebo-controlled clinical trial • Inclusion – abnormal MRI + 2 white matter lesions • Rx – systemic corticosteroids + weekly IM (interferon beta 1a) IFNβ1-a (or) placebo • Result @ 3yrs – 35% of IFNβ developed MS , no progression in MRI abnormalities • BENEFIT – Beteferon in Newly Emerging MS for Initial Treatment • Subcutaneous IFNβ1b reduces conversion ( 45%)

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