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Table of Contents    
EDITORIAL
Year : 2012  |  Volume : 60  |  Issue : 5  |  Page : 459-460

Optic neuritis: A blurry issue


Department of Neurology, All India Institute of Medical Sciences, New Delhi, India

Date of Submission10-Sep-2012
Date of Decision12-Sep-2012
Date of Acceptance12-Sep-2012
Date of Web Publication3-Nov-2012

Correspondence Address:
Rohit Bhatia
Department of Neurology, All India Institute of Medical Sciences, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.103177

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How to cite this article:
Bhatia R, Singhal A. Optic neuritis: A blurry issue. Neurol India 2012;60:459-60

How to cite this URL:
Bhatia R, Singhal A. Optic neuritis: A blurry issue. Neurol India [serial online] 2012 [cited 2019 Aug 25];60:459-60. Available from: http://www.neurologyindia.com/text.asp?2012/60/5/459/103177


Optic neuritis (ON) is an inflammation of one or both optic nerves, usually resulting in a temporary visual loss. It commonly affects young adults with a male to female ratio of 1:3 and in children can present with bilateral involvement frequently. Although the most common aetiology is demyelination and a strong association exists with multiple sclerosis (MS) and neuromyelitis optica (NMO), [1] yet workup to exclude infectious, granulomatous, nutritional, toxic, ischemic, infiltrative, structural and hereditary causes may be required. The term clinically isolated syndrome (CIS) is used in neurological practice to describe a first clinical episode of symptoms and signs suggestive of an inflammatory demyelinating disorder of the central nervous system (CNS) affecting optic nerve, spinal cord, cerebral hemisphere, cerebellum or brainstem. [2]

Majority of the information about the natural history of demyelinating ON comes from the Optic Neuritis Treatment Trial (ONTT) which enrolled 448 patients. [3] Among these, 389 patients without a diagnosis of either clinically definite MS (CDMS) or probable MS were prospectively followed up for 15 years to determine the rate and risk factors for conversion to CDMS. The probability of developing MS by the end of 15-years was 50% and strongly related to presence of lesions on the baseline cranial magnetic resonance imaging (MRI); 25% for patients with no lesions and 72% for patients with one or more lesions at baseline. The ONTT also observed a reduction for the occurrence of second demyelinating event in the intravenous steroid group as compared to oral steroids or placebo. However, there was no discernible difference between three treatment groups at the end of 15 years. [3] A recently concluded meta-analysis in the pediatric population echoed the same findings but with a significantly different prognostication. [4] It showed a 27 fold increased risk of MS with an abnormal MRI as compared to a 3 fold increase in risk of MS in adult population as observed in ONTT. This huge disparity however, needs to be confirmed in future studies. The authors also concluded that laterality was not predictive of MS risk. One important factor to consider in interpreting these results is the technologic MRI advances that have occurred since the initiation of ONTT. Current imaging techniques are more sensitive in the detection of demyelination and might distinguish risk of MS even better according to the presence or absence of MRI abnormalities. Some of the studies have suggested that ON as a presenting symptom in CIS has a lesser chance of converting into MS as compared to other CIS, However, an abnormal MRI in ON and other topographic CIS presentation found no difference of converting into MS. [5] Visual function in patients with ON is usually assessed by visual acuity, and more sensitive measures of visual impairment, such as contrast sensitivity and low-contrast letter acuity. Emerging evidence strongly supports that retinal nerve fibre layer thickness (RNFL) on optical coherence tomography (OCT) is related to visual impairment although its ability to predict future risk of MS is still not established. A recent meta-analysis showed that the estimated RNFL loss in MSON eyes versus unaffected eyes is larger than that calculated for the comparison of MS without optic neuritis and controls. An important prognostic finding was that above a threshold of about 75 μm loss of RNFL thickness, the chances of recovery of visual function seem to reduce. [6]

The study by Pandit and colleagues [7] in this issue of the journal reflects observations on consecutive Indian patients with ON from a South Indian Demyelinating Disease Registry. The probability of conversion to MS in this cohort was 49% over a period of 5 years which is similar to the ONTT follow up results. This study also highlights ON due to NMO, an important differential in the evaluation of ON since the treatment and prognosis is much different than MS. Quite a few number of patients in this series were diagnosed as chronic relapsing inflammatory optic neuropathy (CRION) a steroid responsive condition with no definitive aetiology but within the continuum of autoimmune diseases and more likely an entity within the NMO spectrum disorders. In this study the authors did not observe any significant difference in mean duration to second attack in those treated with oral versus parenteral steroids, a finding different from the ONTT results, although the period for ascertaining the second relapse is not mentioned. A limitation of this study is the absence of MRI during the first attack of ON in majority of the patients thus precluding prediction to CDMS over a period of time. Another issue which remains unaddressed was the absence of baseline ophthalmoscopy findings such as optic disc oedema, peripapillary hemorrhages and retinal exudates as their presence may suggest a diagnosis other than MS as previously shown in the ONTT. The authors did not categorize ON as retro bulbar or anterior since retro bulbar neuritis predicts MS more often. Authors suggest a cost effective strategy of testing NMO antibody in patients with either a severely affected visual acuity or recurrent optic neuritis. Although this approach is commonly followed in practice, it may be worthwhile testing NMO antibody in patients with sequential or bilateral ON at presentation. [8] ON is a serious condition and in our experience and from the reported literature, the first attack of NMO may not always severely affect the visual acuity. Dilemma therefore remains about testing NMO antibody in each case of ON at first presentation. A close follow up to ascertain the degree of recovery and imaging findings at baseline can help decide for NMO antibody testing. Finally, whether CRION is a separate entity or a seronegative NMO is still unclear, as pointed out by the authors in this study too. The authors make an important point about the need of having a close interaction between neurologists and ophthalmologists for a timely and correct diagnosis of ON.

Another important question then arises is how should patients with demyelinating ON be managed long-term? The trials on CIS [9],[10],[11],[12],[13] suggest that early treatment by a disease modifying therapy (DMT) reduces MRI disease activity and subsequent relapse rates. However, this approach requires the recognition of CIS features that indicate a diagnosis of MS. [13],[14] Considering the high cost of therapy, relative lack of ease of administration of DMT's and commitment for long-term use decision to start DMT after a CIS is difficult and requires many considerations, of which severity of the attack and MRI changes at baseline drive the decision making; the patient being fully involved in the decision making process.

Evaluation of ON thus requires a brilliant clinical detail, appropriate laboratory workup and imaging. Although identifying cases with likelihood of having MS or any other specific disease is possible with the currently available MR imaging, long term follow up as in the present study is essential to ascertain true disease behavior and prognosis.

 
  References Top

1.Wingerchuk DM, Lennon VA, Lucchinetti CF, Pittock SJ, Weinshenker BG. The spectrum of neuromyelitisoptica. Lancet Neurol 2007;6:805-15.  Back to cited text no. 1
    
2.Miller DH, Chard DT, Ciccarelli O. Clinically isolated syndromes. Lancet Neurol 2012;11:157-69.  Back to cited text no. 2
    
3.Optic Neuritis Study Group. Multiple sclerosis risk after optic neuritis: Final optic neuritis treatment trial follow-up. Arch Neurol 2008;65:727-32.  Back to cited text no. 3
    
4.Waldman AT, Stull L, Galetta SL, Balcer LJ, Liu GT. Pediatric optic neuritis and risk of multiple sclerosis: Meta-analysis of observational studies. J AAPOS 2011;15:441-6.  Back to cited text no. 4
    
5.AbouZeid N, Bhatti MT. Acute inflammatory demyelinating optic neuritis evidence-based visual and neurological considerations. Neurologist 2008;14:207-23.  Back to cited text no. 5
    
6.Petzold A, de Boer JF, Schippling S, Vermersch P, Kardon R, Green A, et al. Optical coherence tomography in multiple sclerosis: A systematic review and meta-analysis. Lancet Neurol 2010;9:921-32.  Back to cited text no. 6
    
7.Pandit L, Shetty R, Misri Z, Bhat S, Amin H, Pai V, et al. Optic neuritis: Experience from a south Indian demyelinating disease registry. Neurol India 2012;60:470-75.  Back to cited text no. 7
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8.Giovannoni G. To test or not to test: NMO-IgG and optic neuritis. Neurology 2008;70:2192-3.  Back to cited text no. 8
    
9.Comi G, Filippi M, Barkhof F, Durelli L, Edan G, Fernández O, et al. Effect of early interferon treatment on conversion to definite multiple sclerosis: A randomized study. Lancet 2001;357:1576-82.  Back to cited text no. 9
    
10.Jacobs LD, Beck RW, Simon JH, Kinkel RP, Brownscheidle CM, Murray TJ, et al. Intramuscular interferonbeta-1a therapy initiated during a first demyelinating event in multiple sclerosis. CHAMPS Study Group. N Engl J Med 2000;343:898-904.  Back to cited text no. 10
    
11.Kappos L, Polman CH, Freedman MS, Edan G, Hartung HP, Miller DH, et al. Treatment with interferon beta-1b delays conversion to clinically definite and McDonald MS in patients with clinically isolated syndromes. Neurology 2006;67:1242-9.  Back to cited text no. 11
    
12.Comi G, Martinelli V, Rodegher M, Moiola L, Bajenaru O, Carra A, et al. for the PreCISe study group. Effect of glatiramer acetate on conversion to clinically definite multiple sclerosis in patients with clinically isolated syndrome (PreCISe study): A randomized, double-blind, placebo-controlled trial. Lancet 2009;374:1503-11.  Back to cited text no. 12
    
13.Comi G, de Stefano N, Freedman MS, Barkhof F, Polman CH, Uitdehaag BM, et al. Comparison of two dosing frequencies of subcutaneousinterferon beta-1a in patients with a first clinical demyelinating event suggestive of multiple sclerosis (REFLEX): A phase 3 randomized controlled trial. Lancet Neurol 2012;11:33-41.  Back to cited text no. 13
    
14.Coyle PK. Early treatment of multiple sclerosis to prevent neurologic damage. Neurology 2008;71(24 Suppl 3):S3-7.  Back to cited text no. 14
    




 

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