OPTIC NEURITITS and its management

                  OPTIC NEURITIS AND ITS      

            MANAGEMENT

                           

                  NEURO-OPTHALMOLOGY ESSAY

        RESIDENT: ALIMUL HAQ

              TUTOR: PROFESSOR DR SHEREEN FATHI

         DEPARTMENT OF NEUROLOGY

                                                              KASR AL AINY HOSPITAL

                                                                    WORD COUNT: 4625

                                                                                       

                                       INTRODUCTION

Optic neuritis is an inflammatory, demyelinating condition that causes acute, usually monocular, visual loss. It is highly associated with multiple sclerosis (MS). Optic neuritis is the presenting feature of MS in 15 to 20 percent of patients and occurs in 50 percent at some time during the course of their illness [1].

The term 'optic neuritis' means inflammatory optic neuropathy from any cause, but is sometimes used to refer to acute demyelinating optic neuritis. In this article, 'optic neuritis' (ON) refers to optic neuritis of any type, and 'acute demyelinating optic neuritis' (ADON) will be used for that specific form. Other terms used in the literature are papillitis (if the optic nerve head is affected) and retrobulbar neuritis (if the nerve is affected more posteriorly).[2]

ADON is a common cause of ON in parts of the world where multiple sclerosis (MS) is common. However, there are many other possible causes which must not be overlooked, as they may require different and urgent management. [2]

Neuromyelitis optica (NMO), also known as Devic's disease or Devic's syndrome, is a rare condition in which there are recurrent and simultaneous optic neuritis and myelitis of the spinal cord. Lesions are different from those observed in MS, and the condition requires a different course of treatment[2]

The term optic neuritis is sometimes applied to other inflammatory and infectious conditions affecting the optic nerve. These and other causes of optic neuropathy are discussed separately.[1]

The epidemiology, pathophysiology, clinical features,types, Prognosis and diagnosis and treatment of optic neuritis will be covered here.

EPIDEMIOLOGY —

 Most cases of acute demyelinating optic neuritis occur in women (two-thirds) and typically develop in patients between the ages of 20 and 40 .

The incidence of optic neuritis is highest in populations located at higher latitudes, in the northern United States and western Europe, and is lowest in regions closer to the equator. In the United States, studies have estimated the annual incidence of optic neuritis to be as high as 6.4 per 100,000.In the United States, optic neuritis occurs more frequently in whites than blacks ,In Asia, optic neuritis is proportionately more common relative to the incidence of multiple sclerosis than in the United States or western Europe [1].

PATHOPHYSIOLOGY — 

The most common pathologic basis for optic neuritis is inflammatory demyelination of the optic nerve. The pathology is similar to that of acute multiple sclerosis (MS) plaques in the brain, with perivascular cuffing, edema in the myelinated nerve sheaths, and myelin breakdown. Inflammation of the retinal vascular endothelium can precede demyelination and is sometimes visibly manifest as retinal vein sheathing. Myelin loss exceeds axonal loss.

It is believed that the demyelination in optic neuritis is immune-mediated, but the specific mechanism and target antigen(s) are unknown. Systemic T cell activation is identified at symptom onset and precedes changes in the cerebrospinal fluid. Systemic changes also normalize earlier (within two to four weeks) than central changes. T cell activation leads to the release of cytokines and other inflammatory agents. B cell activation against myelin basic protein is not seen in peripheral blood but can be demonstrated in the cerebrospinal fluid of patients with optic neuritis [1].

As with MS, a genetic susceptibility for optic neuritis is suspected. This is supported by an over-representation of certain human leukocyte antigen (HLA) types among patients with optic neuritis [1].

CLINICAL FEATURES

Acute features — Optic neuritis is usually monocular in its clinical presentation. In about 10 percent of cases, symptoms occur in both eyes, either simultaneously or in rapid succession . Bilateral optic neuritis is more common in children younger than 12 to 15 years old and also in Asian and black South African patients .Because bilateral symptoms are relatively uncommon, they should suggest an alternative cause of optic neuropathy. However, subclinical visual deficits in acuity, contrast sensitivity, color vision, and visual field in the contralateral eye can often be elicited by detailed visual testing in patients with clinically monocular disease . Because these deficits usually resolve along with the clinical deficits in the symptomatic eye, it is unlikely that these findings represent prior episodes of optic neuritis. [1].

Other clinical features of optic neuritis were systematically characterized in the Optic Neuritis Treatment Trial (ONTT), which enrolled 457 patients, aged 18 to 46 years, with acute unilateral optic neuritis. The two most common symptoms of optic neuritis are vision loss and eye pain:

●Vision loss typically develops over a period of hours to days, peaking within one to two weeks. Continued deterioration after that time suggests an alternative diagnosis .Greater than 90 percent of patients in the ONTT had a significant decrease in central visual acuity. In most, the visual acuities ranged from 20/25to 20/190 (median visual acuity 20/60). However, some patients had 20/20 acuity (11 percent), and, at the other extreme, a few had no light perception (3 percent).

●Eye pain occurred in 92 percent of patients in the ONTT and often worsened with eye movement. The onset of pain generally coincided with the visual acuity loss and improved along with it. [1]

Other common visual symptoms and signs include:

●An afferent pupillary defect always occurs in optic neuritis if the other eye is uninvolved and otherwise healthy. This is demonstrated by shining a light alternately in one eye and then the other and finding that the direct response to light is more sluggish in the affected eye. The room should be dark, and the patient should fixate on a distant target to prevent miosis due to accommodation. [1]

●The visual field defect in optic neuritis is typically characterized as a central scotoma. However, in the ONTT, almost all types of visual field defects were seen, including diffuse vision loss and altitudinal, arcuate, hemianopic, and cecocentral defects. Nonetheless, a defect that extends to the periphery should suggest a compressive lesion, while an altitudinal defect, particularly an inferior altitudinal defect, is more common in anterior ischemic optic neuropathy Visual field defects usually resolve; in the ONTT, 56 percent had normalized at one year and 73 percent had normalized at 10 years . [1]

●Papillitis with hyperemia and swelling of the disk, blurring of disk margins, and distended veins is seen in one-third of patients with optic neuritis.  Two-thirds of these patients have retrobulbar neuritis with a normal funduscopic examination .Papillitis is more common in children less than 14 years old and in certain ethnic populations, including black South Africans and Southeast Asians. Peripapillary hemorrhages are rare in optic neuritis, but are a common accompaniment to papillitis due to anterior ischemic optic neuropathy [1].

●Photopsias (flickering or flashes of light) are often precipitated with eye movement and were reported by 30 percent of patients in the ONTT [1].

●Loss of color of vision out of proportion to the loss of visual acuity is specific to optic nerve pathology. Abnormal color vision by Ishihara plates was found in 88 percent of involved eyes in the ONTT; this increased to 94 percent with the more sensitive Farnsworth-Munsell 100 hue test [1].

●Other signs of ocular inflammation may be observed by the ophthalmologist on funduscopic or slit lamp examination. Perivenous sheathing or periphlebitis retinae can be seen in about 12 percent of patients with optic neuritis and implies a high risk for multiple sclerosis (MS) [1]. Uveitis, cells in the anterior chamber,and/or pars planitis are uncommonly seen in optic neuritis and are more typical of infections and other autoimmune diseases. [1]

Chronic features —

 Even after clinical recovery, signs of optic neuritis can persist. These signs in a patient without a history of optic neuritis may suggest a previous, subclinical attack. When a patient presents with a possible first attack of MS elsewhere in the central nervous system, these signs are often sought because evidence of other demyelinating episodes separated in "time and space" can affect prognosis and treatment decisions.

 Chronic signs of optic neuritis can include:

●Persistent visual loss. Most patients with optic neuritis recover functional vision within one year. However, on testing, deficits in color vision, contrast sensitivity, stereo acuity, and light brightness are detectable in most patients at up to two years

●A relative afferent pupillary defect remains in approximately one-fourth of patients two years after presentation .

●Color desaturation refers to a qualitative inter-eye difference in color perception that can be tested by comparing vision of a red object with each eye. A patient with monocular "red desaturation" may report that the red color appears "washed out," pink, or orange when viewed with the affected eye.

●Temporary exacerbations of visual problems in patients can occur with increased body temperature (Uhthoff's phenomenon). Hot showers and exercise are classic precipitants.

●Optic atrophy to at least some degree almost always follows an attack of optic neuritis, despite the return of visual acuity .Normal, 20/20 visual acuity requires less than one-half of normal foveal axons .The disc appears shrunken and pale, particularly in its temporal half (temporal pallor).[1]

The disk pallor extends beyond the margins of the disk into the peripapillary retinal nerve fiber layer.

●The pattern-shift visual evoked response remains delayed in most patients, even with visual recovery. Although latencies continue to shorten (improve) up to two years after presentation, abnormalities are seen in most (80 percent) at two years [1].

Causes of optic neuritis (ON)[3][4]
Type	Conditions/notes
Acute demyelinating ON	The most common cause of ON in regions where MS is relatively common (Caucasian populations and high latitudes).
Ischaemic optic neuropathies	Giant cell arteritis (cranial arteritis), anterior and posterior optic neuropathy, diabetic papillopathy.
Corticosteroid-responsive ON	Autoimmune diseases, including sarcoidosis, systemic lupus erythematosus,[5]Behçet's disease, neuromyelitis optica (Devic's syndrome - affects optic nerves and the spinal cord),[6][7] autoimmune ON, chronic relapsing inflammatory ON.
Other inflammatory causes	Post-infection, post-vaccination, neuroretinitis, acute disseminated encephalomyelitis.
Infections	Tuberculosis, syphilis,[8] mycoplasma and other respiratory tract infections, Lyme disease,[9] toxocariasis,[10] helminthiasis, cryptococcosis, viral ON (a rare complication of chickenpox),[11] Q fever,[12] periorbital infections (orbital cellulitis, severe suppurative sinusitis). Other viral infections which have been known to cause ON include measles, mumps, rubella, herpes zoster, infectious mononucleosis.
Nutritional	Vitamin B12 deficiency.
Drugs and toxins	Amiodarone, ethambutol, isoniazid,[13] methanol intoxication, tobacco-methanol amblyopia.
Inherited	Leber's hereditary ON.
Optic neuritis in children	Viral infection is a common cause.

[2]

Typical Features of Acute demyelinating optic neuritis :

Adult patient age <45.

Symptoms:

Unilateral reduction in vision.

Time course: Acute or subacute onset of visual loss, which progresses for ≤2 weeks.

Spontaneously improves within 3 weeks in nearly all patients.

Pain - periocular, onset preceding or with visual loss, worse on eye movement, does not disturb sleep. [2]

Patients with multiple sclerosis (MS) may have recurrent attacks of ON, which means that a history of previous episodes of decreased vision in the same or fellow eye may be elicited.

Signs:

Visual loss varies from mild to no perception of light.

Ipsilateral relative afferent pupillary defect (RAPD).

Loss of contrast and colour vision out of proportion to loss of acuity.

Normal or swollen optic disc; disc pallor occurs later (4-6 weeks after onset).

Visual field defect - any type.

Normal macula and peripheral retina. [2]

Warning' or atypical features suggesting another cause

Patient aged <12 or >50, black or Asian race.

Symptoms: Bilateral reduction in vision.

Time course:

Vision loss continuing to progress >2 weeks after onset.

No recovery by 5 weeks after onset.

Pain - absent, or severe enough to disturb sleep/restrict eye movements, or pain persisting >2 weeks after onset, or pain following onset of vision loss.

History suggesting another cause - eg, autoimmune or inflammatory conditions, infection, malignancy, immunosuppression, systemic symptoms.

Deterioration after withdrawal of corticosteroids (if given).

Signs:

Severe visual loss - no perception of light.

Lack of RAPD. [2]

Temporal field defect in contralateral eye.

Unusual ocular findings - eg, marked ocular inflammation, markedly swollen optic disc, marked disc haemorrhages, macular star.[2]

NATURAL HISTORY

Natural history of acute ON is to worsen over several days to 2 weeks end then to improve. Improvement intially is rapid and starts approximately 3 weeks after

onset. Recovery of vision is nearly complete by 5 weeks after onset. Improvement continues up to 1 year. Lana--Peixoto and Andrade reported (2001) that the clinical features of childhood ON differ from those observed in adults. In children is a better visual outcome and a lower conversion rate to multiple sclerosis than in adults. [5]

DIFFERENTIAL DIAGNOSIS — 

In a young child, infectious and postinfectious causes of optic nerve impairment should be considered as alternatives to optic neuritis, while in an older patient (>50 years), ischemic optic neuropathy (due, for example, to diabetes mellitus or giant cell arteritis) is a more likely diagnosis than optic neuritis.

Alternative diagnoses should also be considered in patients with a bilateral presentation or those with other neurologic or systemic symptoms.

In cases of recurrent optic neuritis that are not due to neuromyelitis optica or MS, other causes of recurrent optic neuritis should be thoroughly investigated (such as sarcoidosis, lupus, chronic relapsing inflammatory optic neuropathy (CRION), or paraneoplastic optic neuropathy (serum CRMP-5/CV2 antibody)). [1].

EVALUATION AND DIAGNOSIS

Diagnosis —

. In general, optic neuritis is a clinical diagnosis based upon the history and examination findings. Because important findings on funduscopic examination help differentiate typical from atypical cases of optic neuritis, an ophthalmologic examination should be considered an essential feature of the clinical evaluation. Magnetic resonance imaging study of the brain and orbits with gadolinium contrast provides confirmation of the diagnosis in most cases and also provides and assessment of the risk of subsequent multiple sclerosis.

Further diagnostic testing is directed toward excluding other causes of visual loss in atypical cases [1]

Magnetic resonance imaging —

 A magnetic resonance imaging study (MRI) of the brain and orbits with gadolinium contrast provides confirmation of the diagnosis of acute demyelinating optic neuritis and important prognostic information regarding the risk of developing MS. [1]

Innovations in MRI technology (eg, short tau inversion recovery [STIR], fast spin echo [FSE], and fluid-attenuated inversion recovery with fat suppression techniques [FLAIR], diffusion tensor imaging [DTI]) have improved imaging of the optic nerve .Optic nerve inflammation can be demonstrated in about 95 percent of patients with optic neuritis with gadolinium contrast-enhanced MRI of the brain and orbits . The longitudinal extent of nerve involvement as seen on MRI correlates with visual impairment at presentation and with visual prognosis [1]. Gadolinium enhancement persists for a mean of 30 days since onset [1]. The signal abnormality in the nerve can still be seen after recovery of vision, and is also present in as many as 60 percent of patients with MS who do not have a clinical history of optic neuritis [1].

The brain MRI often shows white matter abnormalities characteristic of MS . Typical lesions are ovoid, periventricular, and larger than 3 mm.

 The reported prevalence of white matter abnormalities varies substantially among patients with optic neuritis (23 to 75 percent) .In the ONTT, almost 40 percent of patients had MRI lesions, but this trial represents a selected patient group [7]. Small case series of unselected patients have noted a higher coincidence of MRI brain lesions [1]. Individuals with white matter abnormalities are at a higher risk of developing MS.

The yield of spinal cord imaging is low in unselected patients. Among 115 patients presenting with optic neuritis, MRI abnormalities in the spinal cord were seen in only four patients with a normal brain MRI [1].

Lumbar puncture — 

Lumbar puncture is not an essential diagnostic test in optic neuritis, but should be considered in atypical cases (eg, those with bilateral presentation, <15 years in age, or symptoms suggesting infection) 

 Approximately 60 to 80 percent of patients with acute optic neuritis have nonspecific abnormalities in the cerebrospinal fluid (CSF), including lymphocytes (10 to 100) and elevated protein [1].

Other CSF findings in optic neuritis can include :

●Myelin basic protein in about 20 percent

●IgG synthesis in 20 to 36 percent

●Oligoclonal bands (OCB) in 56 to 69 percent

The presence of OCB implies a higher risk of developing MS. However, since OCB are also associated with white matter lesions on brain MRI, their presence is not clearly of independent prognostic importance [1]

Other testing — 

When there are relevant clues to an alternative diagnosis , measurement of the erythrocyte sedimentation rate, antinuclear antibodies, and angiotensin converting enzyme levels and serologic and CSF tests for Lyme disease and syphilis should be obtained [1]

Fluorescein angiography — 

Fluorescein angiography is not routinely performed in the evaluation of optic neuritis and is often normal. Up to 25 percent demonstrate either dye leakage or perivenous sheathing . These findings may identify patients at somewhat higher risk for developing MS. [1].

Visual evoked response — 

A delay in the P100 of the visual evoked response (VER) is the electrophysiologic manifestation of slowed conduction in the optic nerve as a result of axonal demyelination. This test is not usually helpful in the diagnosis of acute optic neuritis, unless there is a suspicion that the visual loss is functional.

Abnormalities in the VER can persist after recovery of full vision. At one year, 80 to 90 percent will be abnormal; 35 percent will return to normal at two years . The VER is often employed to find evidence of previous, asymptomatic, episodes of optic neuritis, but the sensitivity and specificity are imperfect [1].

The multifocal VER is a technical advance that appears to be more sensitive and specific for identifying optic neuritis, but this technology is not generally available [1].

VISUAL FIELD TEST

Virtually any type of optic nerve visual field loss can occur in optic neuritis, including altitudinal, arcuate, central or cecocentral, diffuse,and even unilateral hemianopic visual field defects or asymmetric upper nasal quadrantanopsia.22,23 Visual field defects are often found in the contralateral eye[5]

Contrast sensitivity impairment is found in virtually all patients with optic

neuritis, usually parallels the severity of visual loss.

OPTHALMOSCOPY

The optic disc appears normal (retrobulbar ON) in about two-thirds of patients. Optic disc swelling will be present in 20 to 40% of cases or, if the patient has experienced a previous clinical or subclinical attack of optic neuritis, pale. Both the swelling and the pallor are nonspecific findings in ON, and neither is useful in distinguishing demyelinating ON from the ON that may accompany other inflammatory or infectious diseases. The degree of swelling does not correlate with the severity of optic nerve disfunction. Optic disc or peripapillary hemorrhages are uncommon[5]

Optical coherence tomography —

 Optical coherence tomography (OCT) measures the thickness in the retinal nerve fiber layer and detects thinning in most (85 percent) of patients with optic neuritis . These abnormalities are also common in patients with MS who do not have a clinical history of optic neuritis . While lower values correlate with impaired visual outcome, the utility of OCT as a prognostic tool is limited in that abnormal values do not show up until early swelling disappears. In one study, OCT was less sensitive than VER in detecting subclinical optic neuritis

A number of studies have found that a greater severity of optic nerve injury seen on OCT suggests neuromyelitis optica rather than optic neuritis associated with multiple sclerosis [1].

Aquaporin-4-specific serum autoantibody —

 Patients with recurrent optic neuritis may be particularly at risk neuromyelitis optica (NMO) or Devic's disease. This is particularly true for patients with a normal brain MRI and those with optic neuritis events in rapid succession or with a presentation of severe vision loss . In one series of 51 patients with either severe or recurrent optic neuritis, six patients were seropositive for the aquaporin-4-specific serum autoantibody, a sensitive biomarker for NMO while 10 patients were seropositive for antibodies to myelin-oligodendrocyte glycoprotein (MOG), which has also been associated with NMO . In other studies, seropositivity for the aquaporin-4-specific serum autoantibody was predictive of subsequent NMO among patients with recurrent optic neuritis. The serum NMO antibody test is suggested for individuals with recurrent ON, particularly if the MRI brain is negative for any abnormal T2/FLAIR lesions outside of the affected optic nerve(s). The role for testing MOG antibodies is investigational. [1].

Management

Consider corticosteroids during the acute phase:

Treatment with methylprednisolone speeds up visual recovery in the acute phase, but has no effect on final visual acuity. Side-effects of corticosteroids can be serious. Therefore, they are usually reserved for patients who need to hasten visual recovery, such as those with poor vision in the fellow eye or bilateral visual loss, or for occupational reasons.

Recommended treatment is methylprednisolone 1 g daily for three days. [2]

Oral prednisolone is not recommended because of (uncertain) evidence that it may increase the recurrence rate.

There is no treatment that can reverse poor visual outcome in the long term.

Information for patients is important (see 'Prognosis', below).

Consider brain MRI, to give information about the risk of developing MS.

Consider referring to a neurologist for assessment of the patient's risk of developing MS, and the value of disease-modifying drugs in this context (see 'Role of disease-modifying drugs', below).

For Pulfrich's phenomenon (disturbed perception of movement), symptoms may be helped by using spectacles with a tinted lens over the unaffected eye, to balance the delay in conduction from the other side.[2]

For Uhthoff's phenomenon symptoms (worsening vision with raised body temperature), avoid hot environments and take cool drinks; reassure patients that this symptom is reversible and does not further damage vision. [2]

Intravenous immunoglobulin has generally been found to be of no benefit. One trial (small and non-randomised, using a different regimen) reported improved vision with immunoglobulin treatment. [2]

Prognosis

Visual prognosis

·         The prognosis for vision in ADON is usually good.^[15]

·         The Optic Neuritis Treatment Trial (ONTT), was a large study of ADON with 15-year follow-up, and found that:

·         93% of patients showed improvement within five weeks of onset of ADON; vision continued to improve for up to one year. One year after onset, 93% had visual acuity better than 6/12 in the affected eye. At 15-year follow-up, 92% had acuity better than 6/12 in the affected eye, and only 1% had vision worse than 6/60 in both eyes.

·         The severity of initial visual loss seems to be related to the final visual outcome; however, even with initial visual acuity of ≤6/60, 85% recover vision to 6/12 or better.

·         Although visual outcome is good in objective tests, many patients experience subjective reductions in vision, colour vision, contrast sensitivity or depth/movement perception after recovery from ADON. [2]

Risk of recurrence

·         ADON can recur in either eye.

·         The risk of recurrence was 35% over 10 years in the ONTT. [2]

Risk of developing MS

·         ADON is associated with MS.

·         In the ONTT, for adults with a single episode of unilateral ADON, the risk of MS was 38% at 10 years after onset, and 50% at 15 years.^[16] Another study found the MS risk was 54% after 30 years. The risk of developing MS is lower for children and for men. [2]

·         MRI of the brain gives information about the risk of developing MS. The presence of white matter abnormalities increases the MS risk and their absence reduces it. In the ONTT, the risk of developing MS at 15-year follow-up was 25% for patients with no lesions on MRI, and 75% for those with white matter lesion(s).[2]

Role of disease-modifying drugs

·         Interferon beta increases the time interval to relapse in MS. Trials suggest that, in a scenario such as a patient with ADON and white matter lesions on brain MRI, where the risk of developing MS is relatively high, interferon beta may similarly delay the onset of MS symptoms.

·         However, bear in mind that:

·         Many patients with a first episode of ADON and an abnormal MRI scan will not develop MS.

·         Treatment is only partly effective - eg, six years of interferon beta treatment prevents one relapse.

·         The visual prognosis is good even if MS develops. [2]

MAJOR STUDY FINDINGS FOR TREATMENT OF OPTIC NEURITIS BY AMERICAN ACADEMY OF OPTHALMOLOGY:

Combination drugs speed recovery. ONTT helped define the role of corticosteroids in the treatment of acute optic neuritis. When the study originated, many doctors were treating the condition with oral corticosteroids. The study looked at oral prednisone vs. high-dose intravenous methylprednisolone vs. placebo and found that the IV methylprednisolone followed by a tapering course of oral prednisone accelerated visual recovery by a few weeks. [4]

Recovery of vision occurs with or without treatment. The investigators found that the choice of regimen has no effect on final visual outcome. Most patients in the placebo group recovered vision, on average, in six to eight weeks. Oral prednisone alone was no better than placebo with respect to visual recovery and, in fact, was associated with twice the risk of recurrent optic neuritis. It is no longer recommended for an initial episode of typical, presumed demyelinative optic neuritis. The therapy should include either high-dose methylprednisolone or nothing, Dr. Beck explained [4].

White matter lesions predict MS. The initial findings, published 16 years ago, in 1992, still apply today, said Dr. Beck. But in addition to determining a therapeutic regimen, the ONTT defined the risk factors for development of MS among patients with optic neuritis. The presence of asymptomatic white matter lesions on the MRI scan is the strongest predictor for MS. Few patients at the start of the study had any history of MS, but over time the numbers grew. [4]

Outcome favorable and stable. For the majority of patients, even those with MS, the visual outcome is good. Those who develop MS are more likely to exhibit abnormal visual function findings, but their vision is normal about 60 percent of the time.

There was little or no change in visual acuity in the affected eye between the 10- and 15-year examinations, in most patients. After 15 years, 72 percent of patients with optic neuritis had visual acuity of 20/20 or better; and 66 percent had acuity of 20/20 or better in both eyes.[4]

Conclusion

Patients with MS may develop disturbances of visual sensory function and disorders of ocular motor system. These disturbances may precede, or occur coincidentally with neurologic manifestations. Sometimes, disturbances

of the visual sensory system are themselves asymptomatic but may be important findings that establish the diagnosis of MS in a patient with a single symptomatic

neurologic deficit. Visual impairment occurs in numerous patients with MS and may be the presenting symptom. MRI scanning of the brain should be undertaken

in all cases of acute ON for diagnostic and prognostic purposes. Disorders of ocular motor system are frequently the initial sign of multiple sclerosis and occur

as its presenting sign weeks, month, or years before other neurologic symptoms and signs develop[5]

Finally The most common presentation is inflammatory, demyelinating, idiopathic, or “typical” ON, which may be associated with multiple sclerosis. This must be differentiated from “atypical” causes of ON, which differ in their clinical presentation, natural history, management, and prognosis. Clinical “red flags” for an atypical cause of ON include absent or persistent pain, exudates and hemorrhages on fundoscopy, very severe, bilateral, or progressive visual loss, and failure to recover. In typical ON, steroids shorten the duration of the attack, but do not influence visual outcome. This is in contrast to atypical ON associated with conditions such as sarcoidosis and neuromyelitis optica, which require aggressive immunosuppression and sometimes plasma exchange. The visual prognosis of typical ON is generally good. The prognosis in atypical ON is more variable. Future therapeutic directions may include enhancing repair processes, such as remyelination or adaptive neuroplasticity, or alternative methods of immunomodulation. Pilot studies investigating the safety and proof-of principle of stem cell treatment are currently underway. [3]

REFERENCE:

1)      http://www.uptodate.com/contents/optic-neuritis-pathophysiology-clinical-features-and-diagnosis

2)      http://patient.info/doctor/acute-optic-neuritis

3)      https://www.dovepress.com/new-developments-in-the-treatment-of-optic-neuritis-peer-reviewed-article-EB

4)      http://www.aao.org/eyenet/article/ontt-long-term-optic-neuritis-study-finished

5)       Cerovski et al.: Multiple Sclerosis and Neuro-Ophthalmologic Manifestations, Coll. Antropol. 29 (2005) Suppl. 1: 153–158