|Year : 2020 | Volume
| Issue : 2 | Page : 105-110
Specific considerations for epilepsy in India
Department of Neurology, Lady Hardinge Medical College, New Delhi, India
|Date of Submission||03-Jan-2020|
|Date of Decision||01-Feb-2020|
|Date of Acceptance||02-Feb-2020|
|Date of Web Publication||17-Apr-2020|
Dr. Divyani Garg
Department of Neurology, Lady Hardinge Medical College, New Delhi
Source of Support: None, Conflict of Interest: None
It is estimated that there are around 50 million people living with epilepsy (PWE) globally. Around one-sixth of this population resides in India. Around 10–12 million people with epilepsy reside in India. A significant proportion of PWE do not receive appropriate treatment, leading to a large treatment gap (TG). Poor awareness of antiepileptic drugs (AEDs), cultural practices, social stigma surrounding epilepsy, lack of accessibility to healthcare, and a severe shortage of medical professionals trained in the management of epilepsy are major contributors to the TG. Infectious diseases, particularly neurocysticercosis, form a major bulk of underlying cause for epilepsy. Certain geographical regions exhibit typical patterns of epilepsy. In this article, we attempt to provide a broad overview of the incidence, prevalence, etiology, types, mortality, and treatment of epilepsy derived from the data from Indian studies. India provides particular challenges in the management of patients with epilepsy, not only in terms of the wide spectrum of epileptic conditions but also in the demand for medical practice based on economic constraints.
Keywords: Epilepsy in India, epilepsy surgery, hot water epilepsy, treatment gap, women with epilepsy
|How to cite this article:|
Garg D. Specific considerations for epilepsy in India. Curr Med Issues 2020;18:105-10
| Introduction|| |
Epilepsy, as per the International League Against Epilepsy (ILAE), is defined by at least two unprovoked seizures occurring more than 24 h apart or a single unprovoked seizure with a recurrence risk of at least 60% over the next 10 years or an identifiable epileptic syndrome. The WHO estimates that there are 50 million people living with epilepsy (PWE) worldwide, making it a universal global neurological problem. Eighty percent of PWE are distributed in low- and middle-income countries (LMICs). Consequently, it is estimated that 10–12 million PWE are living in India, contributing to almost one-sixth of disease load. The WHO estimates that epilepsy is responsible for 0.5% of worldwide disease load and 7,419,000 disability-adjusted life years in 2015. The prevalence estimates in India range from 3.0 to 11.9/1000 population,,,,, and incidence from 0.2 to 0.6/1000/year.,,, There is heterogeneity of distribution of epilepsy cases depending on socioeconomic and geographical variations, with higher occurrence in males, rural areas, and lower socioeconomic status. The burden of epilepsy in India has a high treatment gap (TG). TG is defined as the percentage of PWE who remain untreated. The TG is reported to range from 22% in urban areas to as much as 90% in rural areas in India. Contributors to the TG include lack of knowledge about AEDs, social stigma, cultural beliefs, indigenous treatment methods, and a considerable shortage of professionals trained in managing epilepsy. Epilepsy healthcare requires urgent strengthening in the rural areas, especially considering higher rates of epilepsy in these regions, combined with a wide TG. Epilepsy can result in significant injury as well as death, if untreated. Status epilepticus (SE) can be a potentially fatal complication.
| Epidemiology of Epilepsy in India|| |
In the Bangalore Urban-Rural Neuro-Epidemiological Survey, a population of 102,557 people was covered and a prevalence rate of 8.8/1000 was observed. The prevalence rate in rural communities was estimated to be 11.9, which was almost twice of that observed in urban areas (5.7). There are several prevalence studies on epilepsy published in India. Some recent studies are summarized in [Table 1].,,,
Data on incidence of epilepsy from India is scarce. A study from Kolkata estimated an age-standardized incidence rate of 27.3/100,000 per year. Even the burden of drug-refractory epilepsy (DRE) remains largely unclear.
Treatment gap in epilepsy in India
PWE, especially those residing in LMICs, frequently do not experience suitable treatment for epilepsy. This phenomenon is referred to as “treatment gap.” This is expressed as the proportion of people with active epilepsy who are untreated or are being treated but with inappropriate or insufficient therapy. The TG has two components – the first is the proportion of patients who are not able to access healthcare services and the second is the proportion of patients who do not adhere to appropriate medical therapy despite access to suitable healthcare services. Contributors to TG include poor knowledge of AED therapy, social stigma, insufficient healthcare services, and an inadequacy of healthcare professionals trained in the treatment of epilepsy. Targeting the TG requires removing specific causes contributing to the TG in a particular area by the most cost-effective means.
| Etiology of Epilepsy in India|| |
The ILAE 2017 Classification organizes seizure type by the mode of onset into focal, generalized, and unknown onset. Focal epilepsy may be associated with or without loss of awareness and motor and nonmotor manifestations and may have generalization. Remote symptomatic epilepsy arises from a substrate following a one-time insult, whereas symptomatic progressive epilepsy included progressive disorders such as tumors or neurodegenerative disorders. In a study by Bharucha et al., it was reported that symptomatic epilepsy comprised 23% of the cases, with 21% being remote symptomatic and 2% being progressive symptomatic type. In this study, 56% had focal and 46% had generalized seizures.
Among the risk factors for epilepsy, developmental delay, family history of epilepsy, and head trauma were the additional risk factors in one study. A population-based, case–control study reported the presence of family history of epilepsy, febrile seizures, complicated birth delivery, and presence of neonatal seizures as strong risk factors for subsequent epilepsy. In a study conducted in Calicut district of Kerala, South India, 1403 children aged between 8 and 12 years were studied. This study projected the lifetime incidence of febrile seizures to be 10.1%. Recurrent febrile seizures were dominant and were strongly associated with perinatal insult. Indices of infective illness and the mothers' education were found to be independent risk factors for febrile seizures. Among children who had febrile seizures, epilepsy developed in 2.7%.
In terms of seizure classification, hospital-based studies observed a higher frequency of focal epilepsy accounting for up to 80% of seizure type. However, in community-based studies, generalized epilepsy was the more common type, with generalized tonic–clonic being the most common subtype.,, This may be due to secondary generalization of focal epilepsy being misrepresented as primary generalized in community-based studies.
Neuroinfections are a major etiological category in epilepsy in India.
Acute seizures occur in pyogenic meningitis, central nervous system (CNS) tuberculosis, viral encephalitides (including herpes simplex, Japanese encephalitis, and dengue virus), neurocysticercosis (NCC), and a spate of other infections. Japanese encephalitis has regional propensity in India and can lead to epilepsy due to postviral sequelae. Some parts of India are known epidemic regions of Japanese encephalitis where epilepsy occurs as a result of long-term sequelae. 1978 and 2005 saw major outbreaks of the disease affecting parts of Eastern Uttar Pradesh, India, particularly Gorakhpur district. It has also been reported from Southern India as well as West Bengal. In a study that studied neuropathological correlates in fatal SE, infections (34%) were identified as the most frequent cause of fatal SE.
NCC is among the most common causes of epilepsy in India. It occurs due to the larval form of the cestode tapeworm, Taenia solium. Feco-oral route of transmission occurs in the setting of poor sanitation and lack of hygiene. Although teniasis is due to consumption of pork infected with cysticerci, NCC can occur in vegetarians as well. Solitary cysticercus granuloma (SCG) was the most common presentation and accounted for 60% of NCC in India. Over 90% of patients with SCG presented with seizures. In a large community-based survey in Vellore district in Tamil Nadu in Southern India involving above 50,000 participants, NCC was the etiology of active epilepsy in 30% of individuals. Based on this study, the prevalence of NCC causing active epilepsy was determined to be 1/1000 population, leading to a figure of 1.2 million people with active epilepsy being affected with NCC. The prevalence of active epilepsy caused by it ranges from 1.3 to 4.5/1000 population in Indian studies.,,, In a series of 500 children with NCC, seizures occurred in 94.8%; 83.7% of these were partial type. The cost estimated for the treatment of all prevalent cases of SCG was estimated to be INR 1.184 billion in 2007. In 2011, NCC-associated active epilepsy caused Rs. 12.03 billion in median yearly loss; Rs. 9.78 billion from North India and Rs. 2.22 billion from South India. The results indicate that human NCC causes significant health and economic impact in India.
Traumatic brain injury (TBI) is an important cause of epilepsy, especially in young adults. Seizures can develop following head trauma and are designated as posttraumatic seizures. The diagnosis of epilepsy is made if two or more unprovoked seizures occur. In a cohort of 520 patients with TBI, 11.4% developed seizures during the duration of the study. 6.5% had immediate-onset seizures, 2.1% had early-onset (<1 week) seizures, and 2.7% had late-onset (>1 week of head trauma) seizures.
Epilepsy may arise from a host of metabolic conditions including hypocalcemia/hypercalcemia, hyponatremia/hypernatremia, and hypoglycemia/hyperglycemia. In childhood, inborn errors of metabolism such as aminoaciduria or phenylketonuria may also be a cause of seizures. However, data from India are lacking on these causative factors. In the elderly population, metabolic causes formed the second most common provoking factor of epilepsy following stroke.
Data on mortality in PWE in India are extremely limited. In general, PWE have an increased risk of premature death. Their life expectancy may be reduced by 2–10 years. The common causes of death are injuries, sudden unexpected death in epilepsy (SUDEP), SE, infections such as aspiration, drug intoxication, and suicide. A mortality rate of 29% was reported among 117 patients with SE in India. In another study, a mortality rate of 29.7% was reported among SE patients with CNS infections. Higher mortality was seen to be associated with abnormal neurological examination, elderly patients, drug-refractoriness, and male sex. Additional factors included low socioeconomic status, time since diagnosis, higher frequency of seizures, prolonged duration, delayed onset of treatment, coma at admission, and poor drug compliance. In a longitudinal study in an urban population carried out in Kolkata, a total of 52,377 people were screened. Of these, 66 patients had incident and 309 prevalent epilepsy. During a 5-year follow-up, 20 of the patients with active epilepsy died. The average annual mortality rate was determined to be 7.63 (95% confidence interval 4.45–11.26) per 100,000/year. All-cause standardized mortality ratio for PWE was 2.58. SUDEPs are deaths in PWE that are not due to trauma, drowning, or SE and cannot be explained by any other medical condition. From India, one study reported prolonged duration of seizures as a risk factor for SUDEP.
| Specific Epilepsy Types|| |
Progressive myoclonic epilepsy
Progressive myoclonic epilepsy (PME) is a syndromic condition characterized by myoclonus associated in association with cognitive impairment, ataxia, visual dysfunction, etc. It includes a list of differential diagnosis such as Lafora body disease (LBD), neuronal ceroid lipofuscinosis (NCL), Unverricht–Lundborg disease (ULD), myoclonic epilepsy with ragged red fiber (MERRF) syndrome, sialidoses, dentato-rubro-pallido-luysian atrophy, storage diseases, and some inborn errors of metabolism. In a study from NIMHANS, Bangalore, which assessed 147 patients with PME, 36.7% of the cases were LBD, 44.2% NCL, 5.4% ULD, 6.8% MERRF, and 6.8% Tay-Sachs disease More Details.
Hot water epilepsy
Reflex epilepsy is a condition where seizures are precipitated by a specific sensory stimulus. In hot water epilepsy (HWE), also called water-immersion or bathing epilepsy, the stimulus is bathing with hot water which is poured over the head, leading to seizures. Multiple reports of this unusual reflex epilepsy have originated from South India. The pathogenesis is not clearly elucidated, but putative mechanisms include genetic factors, consanguineous parentage, possible environmental factors, as well as high-temperature water bath. The cohort of patients with HWE chiefly belongs to two adjacent districts, i.e., the Mandya-Mysore belt in Karnataka in South India, where it may account for up to 3.6%–3.9% of all epilepsy. Triggers identified were chiefly high water temperature combined with exposure of the scalp to hot water. A strong family history of epilepsy has also been demonstrated in these patients. Putative mechanisms include a dysregulation of the thermoregulatory system in this patient group, which may be sensitive to the increased temperature of water. Impaired sympathetic and vagal balance occurs in HWE which leads to augmentation of sympathetic activity and attenuation of parasympathetic activity. The hypothalamus has also been implicated through its control over autonomic regulation. Treatment entails intermittent therapy with clobazam, 1–1½ h before hot water head bath. Antiepileptic drugs are indicated if HWE is additionally combined with nonreflex seizures.
This is a complex reflex epilepsy also referred to as “prandic epilepsy.” In this, seizures are either precipitated by eating only, or eating-induced seizures occur twice as frequently as spontaneous seizures. In 1984, 13 patients with eating epilepsy were reported of which 12 had temporal lobe epilepsy, from Southern India. In 1988, 17 cases were reported from Delhi. Six patients were reported from NIMHANS in 2013 and studied in detail using video-electroencephalography (EEG), single photon emission computed tomography (SPECT), and magnetic resonance imaging (MRI). The authors suggested that lesions near the perisylvian area might be responsible for this epilepsy syndrome.
| Epilepsy in India in Special Populations|| |
Epilepsy in women
There are almost 1.5 million women with epilepsy (WWE) in the reproductive age in India constituting one-sixth of WWE worldwide. 52% of them are in the reproductive (15–49 years) age group. Reproductive issues are an important consideration for WWE.
Around 30% WWE report an increased propensity for seizures during menstruation, a phenomenon referred to as catamenial epilepsy. A study observed that the risk of seizure was increased during the ovulatory than the anovulatory phase. Infertility also seems to increase in WWE, especially if they are on multiple drugs. In prospective study with follow-up over 10 years, the risk of infertility was higher with AED exposure versus no exposure and also increased with the number of drugs used. Increased risk was observed with the use of phenobarbital. AEDs may impact the sex hormone profile. Valproate is known to induce polycystic ovarian disease which contributes to infertility. Enzyme-inducing AEDs may increase the metabolism of estrogen and progesterone. Epilepsy may also have adverse outcomes during pregnancy. Reports from the Kerala Registry of Epilepsy and Pregnancy (KREP) indicate that anemia, ovarian cyst, fibroid uterus, and spontaneous abortions are more frequent in WWE.
Teratogenesis is the major concern with the use of AEDs during pregnancy. Predisposing factors may be a genetic predisposition toward congenital malformation in WWE, teratogenic effect of drugs or seizures, injuries, and falls due to seizures, as well as inadequate antenatal care. Data from the KREP had shown that there is no familial tendency for congenital malformations in the first- and second-degree relatives of WWE when compared to their spouses who do not have epilepsy. Seizures may induce placental hypoperfusion and lead to teratogenicity. The most important modifiable factor is the use of AEDs. In a study that observed 1297 pregnancies in WWE, 47.8% were seizure-free during pregnancy. Recurrence of seizures occurred most commonly in the first 3 peripartum days. WWE, who were on multiple drugs, had increased propensity for seizures with an odds ratio of 2.98 as compared to those on monotherapy. The study also determined that the occurrence of seizures in the prepregnancy state was the most important predictor of development of seizures during pregnancy.
AEDs predispose to congenital malformations. The mechanism of the same may be folate deficiency caused by AED usage that predisposes to the development of neural tube defects. Other mechanisms considered are alterations in retinoic acid pathways, homeobox genes, histone deacetylation, and AED transporter polymorphisms., WWE considering conception should be initiated on 5 mg of folic acid daily 2 months before planned conception.
Epilepsy in children
In a long-term study of 123 children with difficult to control epilepsy, etiological factors included an age of onset <2 years (71.5%); male sex (69%); mixed, secondary generalized, or complex partial seizures (77%); mental retardation (64%); and neurological abnormalities (52%). Static neurological disease was seen in 63%. Epileptic syndromes were noted in <50% of children. In 100 patients who had adequate follow-up, 67% showed good response, with 35% having complete and 32% having more than 50% reduction in seizures.
In a study from Chandigarh in Northern India, 3684 children in the age group of 1–18 years were screened of which 45 had epilepsy. Among the children with epilepsy, the most common seizure type was generalized tonic–clonic seizures (69.6%), followed by simple partial seizures (56.5%) and complex partial seizures (4.3%). Febrile seizure was found to be the most common etiology of acute symptomatic seizures in childhood, accounting for 11 (68.7%) cases. Other causes were meningitis, acute meningoencephalitis, and NCC.
Epilepsy in the elderly
In a hospital-based study in rural North India in patients above 60 years, 110 patients were studied. The most frequent etiologies were stroke (46%), focal calcifications (11.8%), neoplasms (9%), trauma (6%), dementias (6%), and unknown (16.6%). The frequency of epilepsy decreased with advancing age. Sridharan and Murthy, in a meta-analysis from India, demonstrated that prevalence was the highest between 10 and 19 years (0.89%) and then progressively receded with age, reaching 0.21% above 50 years.
| Management of Epilepsy|| |
Despite the wide spectrum of etiological categories associated with epilepsy, it has been demonstrated that 70%–80% of epilepsy can be easily managed with single AED as well as inexpensive strategies. The remaining 20%–30% fall into the category of DRE.
Drug-refractory epilepsy in India
Intractable epilepsy or DRE has been defined as occurrence of two or more monthly seizures for >2 years, despite the use of two or more AEDs in appropriate and adequate doses. According to a North Indian study on patients with intractable epilepsy, 83% had focal and 7% had generalized seizures. The significant risk factors for drug refractoriness were structural lesion on neuroimaging, lack of clinical remission to first AED, developmental delay, frequent seizures, focal seizures, younger age of onset (<14 years), as well as febrile seizures. The most common radiological lesions observed in the intractable group were mesial temporal sclerosis, dysembryoplastic neuroepithelial tumor, and perinatal hypoxic ischemic insult.
Surgical management of epilepsy in India
As many as 70%–80% of persons with newly diagnosed epilepsy eventually achieve remission, with majority achieving it within 2 years of onset. Nearly one-third of PWE continue to experience seizures despite optimal therapy with AEDs.
Nearly one-third of epilepsy patients have intractable epilepsy and require surgical management. A comprehensive epilepsy surgery program requires cohesive framework involving neurology, neurosurgery, neuroradiology, and psychiatric services, as well as the medical social worker. In addition, evaluative tools such as MRI, SPECT, positron emission tomography, and magnetoencephalography are valuable assets. Epilepsy surgery was kick-started in India in 1952 at CMC, Vellore. Seizure freedom rates following temporal lobe epilepsy surgeries are 70% and cessation of drug therapy 2 years following epilepsy surgery may occur in up to 30% patients undergoing epilepsy surgery.
| Conclusion|| |
The burden of epilepsy in India can be reduced by alleviating poverty as well as reducing preventable risk factors such as perinatal insult, neuroinfections, and head injuries. Narrowing of the TG is imperative, particularly in rural areas. DRE accounts for 80% of the healthcare cost in epilepsy. Factors have also been determined that predict drug-refractoriness, such as early age of seizure onset, higher seizure frequency before treatment, and cryptogenic epilepsy. These factors can be identified in the pediatric population, enabling early recognition of DRE and early referral to tertiary level epilepsy centers.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
The author of this manuscript declares that this scientific work complies with reporting quality, formatting, and reproducibility guidelines set forth by the EQUATOR Network. The author also attests that this clinical investigation was not determined to require Institutional Review Board/Ethics Committee review. I also certify that I have not plagiarized the contents in this submission and have done a plagiarism check.
| References|| |
Das SK, Biswas A, Roy J, Bose P, Roy T, Banerjee TK, et al
. Prevalence of major neurological disorders among geriatric population in the metropolitan city of Kolkata. J Assoc Physicians India 2008;56:175-81.
Gourie-Devi M. Epidemiology of neurological disorders in India: Review of background, prevalence and incidence of epilepsy, stroke, Parkinson's disease and tremors. Neurol India 2014;62:588-98.
] [Full text]
Gourie-Devi M, Gururaj G, Satishchandra P, Subbakrishna DK. Prevalence of neurological disorders in Bangalore, India: A community-based study with a comparison between urban and rural areas. Neuroepidemiology 2004;23:261-8.
Radhakrishnan K, Pandian JD, Santhoshkumar T, Thomas SV, Deetha TD, Sarma PS, et al
. Prevalence, knowledge, attitude, and practice of epilepsy in Kerala, South India. Epilepsia 2000;41:1027-35.
Sridharan R, Murthy BN. Prevalence and pattern of epilepsy in India. Epilepsia 1999;40:631-6.
Goel D, Agarwal A, Dhanai JS, Semval VD, Mehrotra V, Saxena V, et al
. Comprehensive rural epilepsy surveillance programme in Uttarakhand state of India. Neurol India 2009;57:355-6.
] [Full text]
Saha SP, Bhattachrya S, Roy BK, Basu A, Maity A, Das SK. A prospective incidence study of epilepsy in a rural community of West-Bengal, India. Neurol Asia 2008;13:41-8.
Sawhney IM, Singh A, Kaur P, Suri G, Chopra JS. A case control study and one year follow-up of registered epilepsy cases in a resettlement colony of North India, a developing tropical country. J Neurol Sci 1999;165:31-5.
Mani KS, Rangan G, Srinivas HV, Kalyanasundaram S, Narendran S, Reddy AK. The Yelandur study: A community-based approach to epilepsy in rural South India – epidemiological aspects. Seizure 1998;7:281-8.
Banerjee TK, Ray BK, Das SK, Hazra A, Ghosal MK, Chaudhuri A, et al
. A longitudinal study of epilepsy in Kolkata, India. Epilepsia 2010;51:2384-91.
Bharucha NE. Epidemiology and treatment gap of epilepsy in India. Ann Indian Acad Neurol 2012;15:352-3.
] [Full text]
Meyer AC, Dua T, Ma J, Saxena S, Birbeck G. Global disparities in the epilepsy treatment gap: A systematic review. Bull World Health Organ 2010;88:260-6.
Pandey S, Singhi P, Bharti B. Prevalence and treatment gap in childhood epilepsy in a north Indian city: A community-based study. J Trop Pediatr 2014;60:118-23.
Shah PA, Shapoo SF, Koul RK, Khan MA. Prevalence of epilepsy in school-going children (6-18 years) in Kashmir Valley of North-West India. J Indian Med Assoc 2009;107:216-8.
Rajshekhar V, Raghava MV, Prabhakaran V, Oommen A, Muliyil J. Active epilepsy as an index of burden of neurocysticercosis in Vellore district, India. Neurology 2006;67:2135-9.
Srinath S, Girimaji SC, Gururaj G, Seshadri S, Subbakrishna DK, Bhola P, et al
. Epidemiological study of child adolescent psychiatric disorders in urban rural areas of Bangalore, India. Indian J Med Res 2005;122:67-79.
Scheffer IE, Berkovic S, Capovilla G, Connolly MB, French J, Guilhoto L, et al
. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58:512-21.
Bharucha NE, Bharucha EP, Bharucha AE, Bhise AV, Schoenberg BS. Prevalence of epilepsy in the Parsi community of Bombay. Epilepsia 1988;29:111-5.
Murthy JM, Yangala R. Etiological spectrum of symptomatic localization related epilepsies: A study from South India. J Neurol Sci 1998;158:65-70.
Kannoth S, Unnikrishnan JP, Santhosh Kumar T, Sankara Sarma P, Radhakrishnan K. Risk factors for epilepsy: A population-based case-control study in Kerala, Southern India. Epilepsy Behav 2009;16:58-63.
Hackett R, Hackett L, Bhakta P. Febrile seizures in a south Indian district: Incidence and associations. Dev Med Child Neurol 1997;39:380-4.
Joshi V, Katiyar BC, Mohan PK, Misra S, Shukla GD. Profile of epilepsy in a developing country: A study of 1,000 patients based on the international classification. Epilepsia 1977;18:549-54.
Koul R, Razdan S, Motta A. Prevalence and pattern of epilepsy (Lath/Mirgi/Laran) in rural Kashmir, India. Epilepsia 1988;29:116-22.
Michael BD, Solomon T. Seizures and encephalitis: Clinical features, management, and potential pathophysiologic mechanisms. Epilepsia 2012;53 Suppl 4:63-71.
Tiwari S, Singh RK, Tiwari R, Dhole TN. Japanese encephalitis: A review of the Indian perspective. Braz J Infect Dis 2012;16:564-73.
Rajshekhar V, Haran RP, Prakash GS, Chandy MJ. Differentiating solitary small cysticercus granulomas and tuberculomas in patients with epilepsy. Clinical and computerized tomographic criteria. J Neurosurg 1993;78:402-7.
Singhi P, Ray M, Singhi S, Khandelwal N. Clinical spectrum of 500 children with neurocysticercosis and response to albendazole therapy. J Child Neurol 2000;15:207-13.
Raina SK, Razdan S, Pandita KK, Sharma R, Gupta VP, Razdan S. Active epilepsy as indicator of neurocysticercosis in rural Northwest India. Epilepsy Res Treat 2012;2012:802747.
Jayaraman T, Prabhakaran V, Babu P, Raghava MV, Rajshekhar V, Dorny P, et al
. Relative seroprevalence of cysticercus antigens and antibodies and antibodies to Taenia
ova in a population sample in South India suggests immunity against neurocysticercosis. Trans R Soc Trop Med Hyg 2011;105:153-9.
Goel D, Dhanai JS, Agarwal A, Mehlotra V, Saxena V. Neurocysticercosis and its impact on crude prevalence rate of epilepsy in an Indian community. Neurol India 2011;59:37-40.
] [Full text]
Prasad KN, Verma A, Srivastava S, Gupta RK, Pandey CM, Paliwal VK. An epidemiological study of asymptomatic neurocysticercosis in a pig farming community in Northern India. Trans R Soc Trop Med Hyg 2011;105:531-6.
Singh BB, Khatkar MS, Gill JP, Dhand NK. Estimation of the health and economic burden of neurocysticercosis in India. Acta Trop 2017;165:161-9.
Thapa A, Chandra SP, Sinha S, Sreenivas V, Sharma BS, Tripathi M. Post-traumatic seizures-A prospective study from a tertiary level trauma center in a developing country. Seizure 2010;19:211-6.
Sudhir U, Kumar AT, Srinivasan G, Kumar RV, Punith K. Aetiology of seizures in elderly. J Indian Med Assoc 2013;111:686-8, 691.
Yang R, Zheng X, Tian D, Chen G, Chen S. Comorbidities and group comparisons of epilepsy-caused mental disability in China. Epilepsy Behav 2013;27:77-80.
Kalita J, Nair PP, Misra UK. A clinical, radiological and outcome study of status epilepticus from India. J Neurol 2010;257:224-9.
Misra UK, Kalita J, Nair PP. Status epilepticus in central nervous system infections: An experience from a developing country. Am J Med 2008;121:618-23.
Thomas SV, Reghunath B, Sankara Sarma P. Mortality among epilepsy patients attending a tertiary referral center in a developing country. Seizure 2001;10:370-3.
Dabla S, Puri I, Dash D, Vasantha PM, Tripathi M. Predictors of seizure-related injuries in an epilepsy cohort from North India. J Epilepsy Res 2018;8:27-32.
Sinha S, Satishchandra P, Gayathri N, Yasha TC, Shankar SK. Progressive myoclonic epilepsy: A clinical, electrophysiological and pathological study from South India. J Neurol Sci 2007;252:16-23.
Satishchandra P. Hot-water epilepsy. Epilepsia 2003;44 Suppl 1:29-32.
Meghana A, Sinha S, Sathyaprabha TN, Subbakrishna DK, Satishchandra P. Hot water epilepsy clinical profile and treatment – A prospective study. Epilepsy Res 2012;102:160-6.
Gururaj G, Satishchandra P. Correlates of hot water epilepsy in rural south India: A descriptive study. Neuroepidemiology 1992;11:173-9.
Satishchandra P, Ullal GR, Shankar SK. Hot water epilepsy. Adv Neurol 1998;75:283-93.
Nagaraja D, Chand RP. Eating epilepsy. Clin Neurol Neurosurg 1984;86:95-9.
Patel M, Satishchandra P, Saini J, Bharath RD, Sinha S. Eating epilepsy: Phenotype, MRI, SPECT and video-EEG observations. Epilepsy Res 2013;107:115-20.
Thomas SV. Managing epilepsy in pregnancy. Neurol India 2011;59:59-65.
] [Full text]
Thomas SV, Sarma PS, Nirmala C, Mathai A, Thomas SE, Thomas AC. Women with epilepsy and infertility have different reproductive hormone profile than others. Ann Indian Acad Neurol 2013;16:544-8.
] [Full text]
Thomas SV, Syam U, Devi JS. Predictors of seizures during pregnancy in women with epilepsy. Epilepsia 2012;53:e85-8.
Sahota P, Prabhakar S, Kharbanda PS, Bhansali A, Jain V, Das CP, et al
. Seizure type, antiepileptic drugs, and reproductive endocrine dysfunction in Indian women with epilepsy: A cross-sectional study. Epilepsia 2008;49:2069-77.
Thomas SV, Sindhu K, Ajaykumar B, Sulekha Devi PB, Sujamol J. Maternal and obstetric outcome of women with epilepsy. Seizure 2009;18:163-6.
Dansky LV, Rosenblatt DS, Andermann E. Mechanisms of teratogenesis: Folic acid and antiepileptic therapy. Neurology 1992;42:32-42.
Wells PG, McCallum GP, Chen CS, Henderson JT, Lee CJ, Perstin J, et al
. Oxidative stress in developmental origins of disease: Teratogenesis, neurodevelopmental deficits, and cancer. Toxicol Sci 2009;108:4-18.
Jose M, Thomas SV. Role of multidrug transporters in neurotherapeutics. Ann Indian Acad Neurol 2009;12:89-98.
] [Full text]
Udani VP, Dharnidharka V, Nair A, Oka M. Difficult to control epilepsy in childhood – A long term study of 123 cases. Indian Pediatr 1993;30:1199-206.
Verma A, Kumar A. Clinical and etiological profile of epilepsy in elderly: A hospital-based study from rural India. Acta Neurol Belg 2017;117:139-44.
Tripathi M, Padhy UP, Vibha D, Bhatia R, Padma Srivastava MV, Singh MB, et al
. Predictors of refractory epilepsy in North India: A case-control study. Seizure 2011;20:779-83.