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      Epilepsy: Indian perspective

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          Abstract

          There are 50 million people living with epilepsy worldwide, and most of them reside in developing countries. About 10 million persons with epilepsy are there in India. Many people with active epilepsy do not receive appropriate treatment for their condition, leading to large treatment gap. The lack of knowledge of antiepileptic drugs, poverty, cultural beliefs, stigma, poor health infrastructure, and shortage of trained professionals contribute for the treatment gap. Infectious diseases play an important role in seizures and long-term burden causing both new-onset epilepsy and status epilepticus. Proper education and appropriate health care services can make tremendous change in a country like India. There have been many original researches in various aspects of epilepsy across India. Some of the geographically specific epilepsies occur only in certain regions of our country which have been highlighted by authors. Even the pre-surgical evaluation and epilepsy surgery in patients with drug-resistant epilepsy is available in many centers in our country. This article attempts to provide a complete preview of epilepsy in India.

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          Toxoplasmosis of the central nervous system in the acquired immunodeficiency syndrome.

          Stephanie Porter, L M Sande (1992)
          Toxoplasmosis is the most common opportunistic infection of the central nervous system in patients with the acquired immunodeficiency syndrome (AIDS). To investigate its clinical course, we reviewed the records of 115 patients with AIDS and central nervous system toxoplasmosis treated at San Francisco General Hospital between 1981 and 1990. The most common presenting symptoms were headache (in 55 percent), confusion (52 percent), and fever (47 percent). Focal neurologic deficits were present in 79 patients (69 percent). The median CD4 cell count at presentation was 50 per cubic millimeter (50 x 10(6) per liter). Thirteen of 80 patients with clinical toxoplasmosis (16 percent) and 4 of 18 patients with pathologically proved disease (22 percent) had undetectable antitoxoplasma IgG antibodies by indirect immunofluorescence assay. Of 103 patients, 94 (91 percent) had enhancing lesions on CT. Single lesions were seen in 28 of 103 patients (27 percent) on CT, and such lesions were seen in 3 of 21 patients (14 percent) on magnetic resonance imaging. Over 90 percent of patients who eventually had clinical and radiographic improvement had evidence of improvement by day 14 of therapy. Adverse drug reactions occurred in 71 patients (62 percent) and led to a change in therapy in 50 patients (43 percent). Among the patients who survived a first episode of toxoplasmosis, the median survival was 265 days. Toxoplasmosis occurs in advanced stages of human immunodeficiency virus infection, and the absence of antitoxoplasma antibodies on immunofluorescence assay does not exclude the diagnosis. The clinical and radiographic response to therapy is usually rapid, but treatment is frequently limited by adverse drug effects.
          Article 0 comments Cited 109 times – based on 0 reviews     Review now
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            Malformation risks of antiepileptic drugs in pregnancy: a prospective study from the UK Epilepsy and Pregnancy Register.

            J. Morrow, A. Russell, E Guthrie … (2006)
            To assess the relative risk of major congenital malformation (MCM) from in utero exposure to antiepileptic drug (AEDs). Prospective data collected by the UK Epilepsy and Pregnancy Register were analysed. The presence of MCMs recorded within the first three months of life was the main outcome measure. Full outcome data were collected on 3607 cases. The overall MCM rate for all AED exposed cases was 4.2% (95% confidence interval (CI), 3.6% to 5.0%). The MCM rate was higher for polytherapy (6.0%) (n = 770) than for monotherapy (3.7%) (n = 2598) (crude odds ratio (OR) = 1.63 (p = 0.010), adjusted OR = 1.83 (p = 0.002)). The MCM rate for women with epilepsy who had not taken AEDs during pregnancy (n = 239) was 3.5% (1.8% to 6.8%). The MCM rate was greater for pregnancies exposed only to valproate (6.2% (95% CI, 4.6% to 8.2%) than only to carbamazepine (2.2% (1.4% to 3.4%) (OR = 2.78 (p<0.001); adjusted OR = 2.97 (p<0.001)). There were fewer MCMs for pregnancies exposed only to lamotrigine than only to valproate. A positive dose response for MCMs was found for lamotrigine (p = 0.006). Polytherapy combinations containing valproate carried a higher risk of MCM than combinations not containing valproate (OR = 2.49 (1.31 to 4.70)). Only 4.2% of live births to women with epilepsy had an MCM. The MCM rate for polytherapy exposure was greater than for monotherapy exposure. Polytherapy regimens containing valproate had significantly more MCMs than those not containing valproate. For monotherapy exposures, carbamazepine was associated with the lowest risk of MCM.
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              Mutations in a gene encoding a novel protein tyrosine phosphatase cause progressive myoclonus epilepsy.

              Bruce Mungall, J A Herbrick, L Jardim … (1998)
              Lafora's disease (LD; OMIM 254780) is an autosomal recessive form of progressive myoclonus epilepsy characterized by seizures and cumulative neurological deterioration. Onset occurs during late childhood and usually results in death within ten years of the first symptoms. With few exceptions, patients follow a homogeneous clinical course despite the existence of genetic heterogeneity. Biopsy of various tissues, including brain, revealed characteristic polyglucosan inclusions called Lafora bodies, which suggested LD might be a generalized storage disease. Using a positional cloning approach, we have identified at chromosome 6q24 a novel gene, EPM2A, that encodes a protein with consensus amino acid sequence indicative of a protein tyrosine phosphatase (PTP). mRNA transcripts representing alternatively spliced forms of EPM2A were found in every tissue examined, including brain. Six distinct DNA sequence variations in EPM2A in nine families, and one homozygous microdeletion in another family, have been found to cosegregate with LD. These mutations are predicted to cause deleterious effects in the putative protein product, named laforin, resulting in LD.
              Article 0 comments Cited 92 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Indian Acad Neurol
                Journal ID (iso-abbrev): Ann Indian Acad Neurol
                Journal ID (publisher-id): AIAN
                Title: Annals of Indian Academy of Neurology
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 0972-2327
                ISSN (Electronic): 1998-3549
                Publication date (Print): March 2014
                Volume: 17
                Issue: Suppl 1
                Pages: S3-S11
                Affiliations
                [1]Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India
                Author notes
                For correspondence: Dr. P. Satishchandra, Department of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS), Hosur Road, Bangalore - 560 029, Karnataka, India. E-mail: drpsatishchandra@ 123456yahoo.com
                Article
                Publisher ID: AIAN-17-3
                DOI: 10.4103/0972-2327.128643
                PMC ID: 4001222
                PubMed ID: 24791085
                SO-VID: 0369ffa1-fda4-43fe-a59a-12f2d57b6e2d
                Copyright © Copyright: © Annals of Indian Academy of Neurology
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 17 February 2014
                Date revision received : 17 February 2014
                Date accepted : 17 February 2014
                Categories
                Subject: Article

                ScienceOpen disciplines: Neurology
                Keywords: epilepsy in india,epilepsy surgery,hot water epilepsy,progressive myoclonic epilepsy,status epilepticus,treatment gap,women with epilepsy
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: epilepsy in india, epilepsy surgery, hot water epilepsy, progressive myoclonic epilepsy, status epilepticus, treatment gap, women with epilepsy

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