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Optic neuritis
- 1. OPTIC NEURITIS Kaushal RajKafle Intern Department Of Ophthalmology
- 2. OPTIC NERVE: ANATOMY • SecondCranial Nerve • Afferent Fibres though termed tract are equivalent to white matter of brain • Continuation of Axon From ganglion Cells (Second Order Neuron) • Optic Disc To Optic Chaisma • 50mm in length
- 3. OPTIC NERVE: COVERING MeningealSheath Innermost: vascular pia mater Outermost : Arachnoid mater Tougher Duramater continuous with sclera Subarachnoid Space and sub dural space is continuous with brain and contains CSF
- 4. OPTIC NERVE: MICROSCOPY • 1.2million each of 2-10µm in diameter • 600 bundles →2000 fibres, fibrous septae derived from the pia mater • unmyelinated axons traverse and acquire myelin sheaths outside the globe • one-third of the fibres = central 5° of the visual field (:. macular disease and disease of optic nerve can mimic) • No Neurilemma Hence No Regeneration • Contains Astrocyte, Oligodendrocyte and Microglia
- 5. OPTIC NERVE: PHYSIOLOGY Neural Signals:myelinated fibres Saltatory Conduction Via the cell membrane Conduction Velocity(m/s) = 6 x diameter of fibre Axoplasmic flow : Orthograde axoplasmic transport (from the eye to the brain) Slow: proteins, enzymes Intermediate : mitochondria Rapid : Sub cellular components Retrograde axoplasmic transport Intermediate: lysosomes and mitochondria
- 6. OPTIC NERVE: BLOOD SUPPLY PialNetwork Of vessels Central retinal artery : end artery that enters the optic nerve approximately 1 cm behind the globe Optic Nerve Head Surface layer: Capillaries of Retinal Arterioles Prelaminar Region: Centripetal Branches of Peripaplillary Choroid Lamina Cribrosa: Branches from Posterior Ciliary artey and arterial Circle of Zinn Retrolaminar Part : centrifuagl branches of central retinal artery and Centripetal Branches of plial Plexus
- 7. OPTIC NERVE: PARTS Intracanalicular 1mm 1.5 mm in vertical diameter Starts from optic disc Pierces choroid and sclera in Lamina cribrosa Visible in fudus examination Intra orbital 25-30 mm 3-4mm in diameter (Myelin sheath of nerve fibre) From globe To Optic Foramen Surrounded by Annulus of Zinn and the origin of 4 recti S shaped Partly adherent with superior rectus sheath Anteriorly free with orbital fat Intra ocular 6mm Optic canal Dura fused to periosteum Related to Ophthalmic artery: inferolaterally →crosses obliquely →medially Sphenoid and posterior ethmoidal sinuses medially : thin lamina papyraceae 10mm (5-16mm) Above cavernous sinus Converses with C/L optic nerve over diaphragm sellae Forms Optic Chaisma Long segment Intra cranial
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- 9. OPTIC NEURITIS Inflammation, demyelination orinfection of optic nerve
- 10. OPTIC NEURITIS :EPIDEMIOLOGY Caucasians F:M :: 2:1 Young adults (20-45), atypical in elderly Unilateral Sweden and Denmark : 4-5cases/100000 person/year (incidence) Medscape
- 11. OPTIC NEURITIS :ETIOLOGY Infection Most common • Multiple Sclerosis (70%) •Neuromyelitis Optica •Diffuse periaxial encephalitis of Schilder Parainfectious Bilateral and children VIRAL INFECTION •Measles •Mumps •Chicken Pox •Herpes Zooster •Whooping cough •Glandular fever IMMUNIZATION Demyelinating Sinusitis (Acute ethmoiditis) Catscratch disease Syphillis Lyme disease Cryptococcal infection (AIDS) Systemic Autoimmune disease : SLE, PAN, Vasculitides Sarcoidosis Toxic Optic Neuritis Lebers Hereditary Optic Neuritis Idiopathic Non Infectious
- 12. Optic disc Usually unilateral Children (1/3of cases) Papillitis Neuroretinitis Optic Nerve head with cointagious retinal Inflammation OPTIC NEURITIS: ANATOMICAL TYPES Optic Nerve behind eye ball No fundal changes: lately pale fundus Most common in adult (2/3 cases) Assosciated with MS Retrobulbar
- 13. OPTIC NEURITIS :CLINICAL FEATURES Asymptomatic Symptoms : Pain Mild dull aching ; with ocular movement Visual loss: Profound, sudden and progressive Visual Obscuration in bright light Reduced dark adaptation Impaired color vision Movement Phosphenes Uhthoffs Symptom Pulrich’s Phenomenon History Similar previous episode of loss of vision Facial or extremity weakness Positive family history
- 14. OPTIC NEURITIS :SIGNS Reduced visual acuity Afferent pupillary defect: Marcus Gunn Pupil Dyschromatopsia Diminished light brightness sensitivity Diminished contrast sensitivity Visual field defects: Classical: Central Scotoma, centrocaecal scotomas, nerve fibre bundle defect ONTT : altitudinal, arcuate and nasal field defect
- 15. OPTIC NEURITIS : SIGNSOpthalmoscopy Papillitis: Hymeremia of disc Blurred margins Obliterated physiological cup with edematous disc Congested tortous retinal veins Sphinter hemorrhage Fine exudates Neuroretinitis Plus Macular star formation Retrobulbar Neuritis “Neither Ophthalmologist Nor patient sees anything” Visually Evoked Response :
- 16. OPTIC NEURITIS :DIFFERENTIAL DIAGNOSES Papillitis Papilledema Ischemic Optic Neuropathy Pseudo pailledema Anterior orbital compression neuropathy Acute retrobulbar neuritis Malingering Hysterical Blindness Indirect optic Neuropathy Medscape
- 17. OPTIC NEURITIS :NATURAL HISTORY AND PROGNOSIS Visual acquity and color vision lost progressively over 2-5 days Recovery (characteristic) : Slower than progression and starts at 2 weeks and over 4-6 weeks 75% of patients recover visual acuity to 6/9 or better 1 Colour vision, contrast sensitivity and light brightness appreciation often remain abnormal 10% of patients develop chronic optic neuritis 1 1 Kanski
- 18. RELATION TO MULTIPLE SCLEROSIS Mostcommon presenting feature of MS (15–20% )1 75% of female and 35 % of patient ULTIMATELY develop MS 2 Optic neuritis occurs at some point in 50% of patients with established MS 1 Normal finding MRI 16% develop MS (5 year follow up ) 1 ONTT reported 10 year risk of MS 56% with atleast 1 MR T2 lesion1,2 those with no lesions have a 22% risk 1 The overall 10 year risk of developing MS following an acute episode of optic neuritis is 38%. In a patient with optic neuritis, the subsequent risk of MS is increased with winter onset, HLA-DR2 positivity and Uhthoff phenomenon 1 1 Kanski 2 Medscape
- 19. OPTIC NEURITIS :INVESTIGATION Exclude other cause CSF :myelin basic protein, oligoclonal bands with raised IgG >15% Neuromyelitis Optica (NMO) IgG specific autoantibody marker MRI Highly Sensitive and Specific (0.3T) Gandolium enhancement ONTT reported 10 year risk of MS 56% with atleast 1 MR T2 lesion VEP Abnormal even with normal MRI findings Mrked prolonged latency period
- 20. OPTIC NEURITIS :TREATMENT ONTT : Strong evidence against ISOLATED USE OF ORAL STERIOD (increased rate of recurrence) Intravenous methylprednisolone sodium succinate 1g daily for 3 days followed by oral prednisolone (1 mg/kg daily) for 11 days and then tapered over 3 days. No prognostic benefit only hasten the recovery of visual function
- 21. ONTT Prospective Study Randomized clinicaltrail 448 eligible patient (presenting with U/L vision defect in last 8 days) Four of the trial's major findings the prevalence of fellow eye abnormalities types of visual field defects, adverse effects of oral corticosteroid treatment, delay in onset of MS in patients treated with intravenous corticosteroids—were all unanticipated.
- 22. OPTIC NEURITIS :TREATMENT Controversy : Wait and watch without steroid VS IV steroid therapy Newer approaches Intramuscular interferon beta-1a (generally used after second attack) Plasma exchange in acute severe optic neuritis Erythropoietin Rituximab for NMOSD
- 23. REFERENCES Kansi Bowling ClinicalOphthalmology 7e Khurana AK- Comprehensive Ophthalmology 5e Parsons disease of Eye 21e Medscape The Optic Neuritis Treatment Trial : A Definitive Answer and Profound Impact With Unexpected Results, JAMA Ophthalmology, Vol 126, No. 7 http://archopht.jamanetwork.com/article.aspx?articleid=420680
Editor's Notes
- #5 whereas true peripheral nerves possess Schwann cells, fibroblasts and macrophages. As with white matter of the brain, the optic nerve has no powers of regeneration The axons of the optic nerve acquire myelin sheaths proximal to the lamina cribrosa and do not possess a neurilemma. Like other parts of the central nervous system, the optic nerve is covered with pia, arachnoid and dura mater as soon as the nerve leaves the eyeball.
- #6 Orthograde axoplasmic transport (from the eye to the brain) has a slow component (proteins and enzymes) that progresses at 0.5-3.Omm/ day, an intermediate component (mainly mitochondria) and a rapid component (subcellular organelles) that moves at 200-1000 mm/day. Retrograde axoplasmic transport of lysosomes and mitochondria (from the brain to the eye) also occurs at an intermediate rate.
- #7 The central retinal artery is an end artery that enters the optic nerve approximately 1 cm behind the globe Retinal capillaries supply the inner two-thirds of the retina, with the outer third being supplied by the choriocapillaris
- #12 1 Demyelinating, which is by far the most common cause. 2 Parainfectious, which may follow a viral infection or immunization. 3 Infectious, which may be sinus-related, or associated with cat-scratch fever, syphilis, Lyme disease, cryptococcal meningitis in patients with AIDS and herpes zoster. 4 Non-infectious causes include sarcoidosis and systemic autoimmune diseases such as systemic lupus erythematosus, polyarteritis nodosa and other vasculitides. myelin is phagocytosed by microglia and macrophages, subsequent to which astrocytes lay down fibrous tissue in plaques
- #13 1 Demyelinating, which is by far the most common cause. 2 Parainfectious, which may follow a viral infection or immunization. 3 Infectious, which may be sinus-related, or associated with cat-scratch fever, syphilis, Lyme disease, cryptococcal meningitis in patients with AIDS and herpes zoster. 4 Non-infectious causes include sarcoidosis and systemic autoimmune diseases such as systemic lupus erythematosus, polyarteritis nodosa and other vasculitides.
- #14 Uthoffs Symptoms: Tranisent obscuration of vision with exertion or exposure too heat Pulfrich Phenomenon : Impaired depth perception of moving object ie object moving in a straight line likely to have curved tracejctory The most common justification for both the phenomenon is assymetrical conduction of nerve impulses
- #15 Signs of optic nerve dysfunction 1 Reduced visual acuity for distance and near is common but may also occur with a great variety of other disorders. 2 Afferent pupillary defect (see below). 3 Dyschromatopsia (impairment of colour vision), which mainly affects red and green. A simple way of detecting a uniocular colour vision defect is to ask the patient to compare the colour of a red object. 4 Diminished light brightness sensitivity, often persisting after visual acuity returns to normal, as for instance following an attack of optic neuritis. 5 Diminished contrast sensitivity (see Ch. 14). 6 Visual field defects, which vary with the underlying pathology, include diffuse depression of the central visual field, central scotomas, centrocaecal scotomas, nerve fibre bundle and altitudinal (
- #16 The light reflex is mediated by the retinal photoreceptors and subserved by four neurones (Fig. 19.33). 1 First (sensory) connects each retina with both pretectal nuclei in the midbrain at the level of the superior colliculi. Impulses originating from the nasal retina are conducted by fibres which decussate in the chiasm and pass up the opposite optic tract to terminate in the contralateral pretectal nucleus. Impulses originating in the temporal retina are conducted by uncrossed fibres (ipsilateral optic tract) which terminate in the ipsilateral pretectal nucleus. 2 Second (internuncial) connects each pretectal nucleus to both Edinger–Westphal nuclei. Thus a uniocular light stimulus evokes bilateral and symmetrical pupillary constriction. Damage to internuncial neurones is responsible for light-near dissociation in neurosyphilis and pinealomas. 3 Third (pre-ganglionic motor) connects the Edinger–Westphal nucleus to the ciliary ganglion. The parasympathetic fibres pass through the oculomotor nerve, enter its inferior division and reach the ciliary ganglion via the nerve to the inferior oblique muscle. 4 Fourth (post-ganglionic motor) leaves the ciliary ganglion and passes in the short ciliary nerves to innervate the sphincter pupillae. The ciliary ganglion is located within the muscle cone, just behind the globe. It should be noted that, although the ciliary ganglion serves as a conduit for other nerve fibres, only the parasympathetic fibres synapse there.
- #23 The findings of the ONTT, reported in more than 50 publications during the past 20 years, have numerous implications. Although the debate continues over the use of intravenous steroids in the management of acute optic neuritis to modify short-term risk of MS in patients with high-risk magnetic resonance imaging (MRI) results, there are other important evidence-based conclusions that make the ONTT legacy indisputable. As a result of the ONTT: Oral steroids (in standard 1 mg/kg doses) are not used to treat isolated optic neuritis. The risk of subsequent MS development can now be reliably estimated and MRI is firmly established as the single most important predictor of risk of developing MS. A low-risk profile (normal MRI results in men with poor vision, severe disc swelling, and no pain) for subsequent MS development was identified. There is an enormous body of data (vision deficits, MRI findings, spinal fluid analysis, neurologic disability, and vision-related quality of life issues) characterizing the clinical profile of optic neuritis obtained from analysis of carefully characterized and studied patients. Computerized threshold perimetry and its analysis were rigorously tested and used to characterize optic nerve dysfunction. Radiologic and laboratory testing of patients with optic neuritis to secure a diagnosis was shown to be unnecessary. Intravenous corticosteroid treatment was shown to be safe and to be associated with minimal adverse effects in this patient group. Novel electronic methods of data sharing and remote monitoring of clinical trials were established. More evidence-based information concerning the relationship of optic neuritis and MS is available for patients and physicians to discuss. Fellow eye abnormalities and the possibility of simultaneous bilateral or occult demyelinating disease involving the prechiasmatic and retrochiasmatic pathways were confirmed. Contrast sensitivity and vision testing in general became commonplace and important outcome measures in many MS treatment trials. Neurologic disability in patients who developed MS after optic neuritis was determined to be mild. An important subset of patients more apt to have permanent visual impairment with more severe initial vision loss was identified as a target group for future clinical trials, perhaps using neuroprotective drugs, myelin restoring compounds, or both.