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Table of Contents    
EDITORIAL
Year : 2015  |  Volume : 63  |  Issue : 6  |  Page : 824-825

Multiple sclerosis-Indian perspective


Department of Neurology, Bombay Hospital Institute of Medical Sciences, Mumbai, Maharashtra, India

Date of Web Publication20-Nov-2015

Correspondence Address:
Bhim Singhal
Department of Neurology, Bombay Hospital Institute of Medical Sciences, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.170065

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How to cite this article:
Singhal B. Multiple sclerosis-Indian perspective. Neurol India 2015;63:824-5

How to cite this URL:
Singhal B. Multiple sclerosis-Indian perspective. Neurol India [serial online] 2015 [cited 2019 Dec 16];63:824-5. Available from: http://www.neurologyindia.com/text.asp?2015/63/6/824/170065


Recent years have seen significant advances in the understanding and treatment of multiple sclerosis (MS). The diagnosis requires dissemination of lesions in the white matter of the central nervous system in time and space and exclusion of any other diagnostic possibility.

In India, MS was recognized only in the late 1950s using the Schumacher clinical criteria. In the absence of a diagnostic test, McDonald criteria (incorporating MRI) have been in use since the 1980s throughout the world, including India. More recently, these have been revised to facilitate an early diagnosis.[1]

The true incidence and prevalence of MS in India are difficult to ascertain owing to the lack of large-scale, well-designed epidemiological studies. The earlier crude estimates of clinically definite MS suggested a low prevalence of 1–3 per 100,000 individuals, with the exception of Parsee population, which had a high prevalence of approximately 20–25 per 100,000 individuals. With the increase in the number of neurologists in India as well as easy and affordable availability of magnetic resonance imaging (MRI), more cases of MS are now being diagnosed throughout India, with a rough estimated prevalence of 5–10 per 100,000 individuals.

The clinical features of MS in India are similar to those seen elsewhere. MS is more prevalent in female subjects, and the average age at onset is approximately 25–30 years (mean, 27 years).[2] It appears to follow a pattern similar to that seen in the West—relapsing remitting MS (RRMS), secondary progressive MS (SPMS), and primary progressive MS (PPMS).[3]

The MRI abnormalities in Indian MS patients closely resemble those seen in the West. A proper MRI protocol should be used for the diagnosis of MS and during the follow-up. The other supportive laboratory tests include evoked potential studies, especially visual evoked potentials. The presence of oligoclonal bands (OCB) in the cerebrospinal fluid (CSF), though not diagnostic, is supportive of the diagnosis. In the series reported by Jena et al., in this issue [4] and in some other reports from India, the yield of positive OCB in the Indian patients has been low. It is important to specify the technique used to detect OCBs. With the use of isoelectric focusing, the yield of positive results is likely to be much higher.

Before the advent of MRI, it was believed that MS in Asia has two clinical patterns, namely the "Western type of MS," with widespread lesions, and the "Asian MS," with lesions restricted to the optic nerves and the spinal cord—"opticospinal MS (OSMS)."[5] The features of OSMS included more frequent involvement of the optic nerves, myelitis with a sensory level, and more frequent occurrence of painful tonic spasms. Besides, it was believed that neuromyelitis optica (NMO) or Devic's disease was a variant of MS with a monophasic course and with severe involvement of the optic nerves and the spinal cord.

With the discovery of the aquaporin-4 immunoglobulin G antibodies (AQP4-IgG) by the Mayo group, it became clear that NMO is a distinct disease with a multiphasic course. The criteria for the diagnosis have been revised under the label NMO spectrum disorders (NMOSD) to include NMOSD with or without AQP4-IgG with characteristic features.[6] In the seronegative cases, some have positivity for anti- myelin oligodendrocyte glycoprotein (MOG) antibodies. Many cases of OSMS are seropositive NMOSD; a small number are anti-MOG-positive NMO cases; and some others fall in an unidentified category.

In the series retrospectively analyzed by Jena et al., 59 of 157 patients had OSMS.[4] As they did not study the AQP4-IgG antibodies, it would be difficult to say how many of these belonged to the NMOSD category.

We do not know the precise cause of MS. Both genetic and environmental factors have been implicated. It is believed to be an autoimmune disorder. In the early phases (CIS and RRMS), CNS inflammation predominates. As the years go by, the inflammatory component decreases, and axonal degeneration predominates (SPMS).

Over the past 20 years, disease-modifying agents (DMA) have been developed to reduce the number of relapses and delay the onset of disability. These include injectables such as β-interferons, glatiramer acetate, and natalizumab and oral agents such as teriflunomide, fingolimod, and tecfidera. Alemtuzumab has recently received approval in the West. The injectable medications and oral tecfidera are available in India.

During an acute attack, intravenous methylprednisolone is used for 3–5 days. To reduce relapses and disability, the DMA are administered. This treatment should be started early. The objective is to attain no disease activity (NEDA). A discussion is required with the patient regarding the efficacy, risk profile, and cost of medications. Many Indian patients are denied this benefit in view of the high cost. Vitamin D has some role in reduction of relapses. Other than this, the treatment is largely supportive and symptomatic, especially for fatigue, gait difficulty, and sphincter disturbance. We have, as yet, no therapy for SPMS and PPMS.

The outcome in MS is unpredictable. We do not have biomarkers to predict the outcome in a given patient with MS. The clinical experience from the small retrospectively analyzed series by Jena et al.,[4] supports the knowledge that the outcome is worse in individuals with polysymptomatic presentation and those with motor weakness, sphincter disturbance, ataxia, and partial recovery.

In the Indian context, there is a great need for increased awareness, large-scale epidemiological studies, dedicated MS clinics, optimum rehabilitation services, and affordable DMA.

 
  References Top

1.
Polman CH, Reingold SC, Banwell B, Clanet M, Cohen JA, Filippi M, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol 2011;69:292-302.  Back to cited text no. 1
    
2.
Singhal BS. Multiple sclerosis—Indian experience. Ann Acad Med Singapore 1985;14:32-6.  Back to cited text no. 2
[PUBMED]    
3.
Singhal A, Bhatia R, Srivastava MV, Prasad K, Singh MB. Multiple sclerosis in India: An institutional study. Mult Scler Relat Disord 2015;4:250-7.  Back to cited text no. 3
    
4.
Jena SS, Alexander M, Aaron S, Mathew V, Maya Thomas K, Patil A, et al. Natural history of multiple sclerosis from the Indian perspective: Experience from a tertiary care hospital. Neurol India 2015;63:867-74.  Back to cited text no. 4
    
5.
Kuroiwa Y, Hung TP, Landsborough D, Park CS, Singhal BS. Multiple sclerosis in Asia. Neurology 1977;27:188-92.  Back to cited text no. 5
[PUBMED]    
6.
Wingerchuk DM, Banwell B, Bennett JL, Cabre P, Carrol W, Chitnis T, et al. International Panel for NMO Diagnosis. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology 2015;85:177-89.  Back to cited text no. 6
    



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[Pubmed] | [DOI]



 

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