[Downloaded free from http://www.cmijournal.org on Tuesday, May 18, 2021, IP: 251.143.64.164]
Review Article
Specific Considerations for Epilepsy in India
Divyani Garg
Department of Neurology, Lady Hardinge Medical College, New Delhi, India
Abstract
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.
Key words: Epilepsy in India, epilepsy surgery, hot water epilepsy, treatment gap, women with epilepsy
Address for correspondence: Dr. Divyani Garg, Department of Neurology, Lady Hardinge Medical College, New Delhi, India.
E‑Mail: divyanig@gmail.com
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.[1] The WHO estimates that there are 50 million people living with epilepsy (PWE) worldwide, making it a
universal global neurological problem.[2] 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.[2] The prevalence estimates in India range from 3.0 to 11.9/1000 population[3‑8] and incidence from 0.2 to 0.6/1000/year.[9‑12]
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.[13] The TG is reported to range from 22% in urban areas to as
much as 90% in rural areas in India.[14] 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.
Date of Submission: 03‑Jan‑2020
Date of Acceptance: 02-Feb-2020
Date of Review: 01-Feb-2020
Date of Web Publication: 17-Apr-2020
Access this article online
Quick Response Code:
Website:
www.cmijournal.org
This is an open access journal, and articles are distributed under the terms of the Creative
Commons Attribution‑NonCommercial‑ShareAlike 4.0 License, which allows others to
remix, tweak, and build upon the work non‑commercially, as long as appropriate credit
is given and the new creations are licensed under the identical terms.
For reprints contact: reprints@medknow.com
DOI:
10.4103/cmi.cmi_6_20
© 2020 Current Medical Issues | Published by Wolters Kluwer - Medknow
How to cite this article: Garg D. Specific considerations for epilepsy in
India. Curr Med Issues 2020;18:105-10.
105
[Downloaded free from http://www.cmijournal.org on Tuesday, May 18, 2021, IP: 251.143.64.164]
Garg: Epilepsy in India
Epidemiology of Epilepsy in India
Prevalence
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).[5] There are several
prevalence studies on epilepsy published in India. Some recent
studies are summarized in Table 1.[15‑18]
Incidence
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.[12] 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.[19]
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.,[20] 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.[21] 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.[22] In a study conducted in Calicut district of Kerala,
South India, 1403 children aged between 8 and 12 years were
studied.[23] 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.[24] However, in community‑based
studies, generalized epilepsy was the more common type,
with generalized tonic–clonic being the most common
subtype.[11,20,25] This may be due to secondary generalization
of focal epilepsy being misrepresented as primary generalized
in community‑based studies.
Neuroinfections
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.[26] Some parts
of India are known epidemic regions of Japanese encephalitis
where epilepsy occurs as a result of long‑term sequelae.[27]
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.
Neurocysticercosis
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
Table 1: Prevalence of epilepsy in various recent studies in India
Author
Years
Prevalence/100,000
Pandey et al.[15]
Shah et al.[16]
Rajshekhar et al.[17]
Srinath et al.[18]
2014
2009
2006
2005
Gourie‑Devi et al.[5]
2004
6.2
3.2
3.8
10.0 (0-3 years)
7.0 (4-16 years)
8.8
106
Sample
3684 children between 1 and 18 years
15,218 children aged 6-18 years
50,617 subjects
2064 children aged 0-16 years
102,572 subjects
Current Medical Issues ¦ Volume 18 ¦ Issue 2 ¦ April‑June 2020
[Downloaded free from http://www.cmijournal.org on Tuesday, May 18, 2021, IP: 251.143.64.164]
Garg: Epilepsy in India
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.[28] Over 90% of patients with SCG presented
with seizures.[29] 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.[17] 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.[30‑33] In a series of 500 children with NCC,
seizures occurred in 94.8%; 83.7% of these were partial type.[29]
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.[34] The results indicate that
human NCC causes significant health and economic impact
in India.
Head trauma
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.[35]
Metabolic conditions
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.[36]
Mortality
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.[37] 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.[38] In another study, a
mortality rate of 29.7% was reported among SE patients with
CNS infections.[39] 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
Current Medical Issues ¦ Volume 18 ¦ Issue 2 ¦ April‑June 2020
frequency of seizures, prolonged duration, delayed onset of
treatment, coma at admission, and poor drug compliance.[40]
In a longitudinal study in an urban population carried out in
Kolkata, a total of 52,377 people were screened.[12] 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.[41]
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.[42]
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.[43] The cohort of patients
with HWE chiefly belongs to two adjacent districts, i.e., the
Mandya‑Mysore belt in Karnataka in South India,[44] where it
may account for up to 3.6%–3.9% of all epilepsy.[45] 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.[46] 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.
107
[Downloaded free from http://www.cmijournal.org on Tuesday, May 18, 2021, IP: 251.143.64.164]
Garg: Epilepsy in India
Eating epilepsy
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.[47] 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.[48]
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. [49] 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.[50]
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.[51] 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.[52] 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.[53]
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.[53] 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. [51]
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
108
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.[54]
Other mechanisms considered are alterations in retinoic acid
pathways, homeobox genes, histone deacetylation, and AED
transporter polymorphisms.[55,56] 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%).[57]
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,[15] 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,[58] 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,[7] 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
Current Medical Issues ¦ Volume 18 ¦ Issue 2 ¦ April‑June 2020
[Downloaded free from http://www.cmijournal.org on Tuesday, May 18, 2021, IP: 251.143.64.164]
Garg: Epilepsy in India
intractable epilepsy, 83% had focal and 7% had generalized
seizures.[59] 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.
References
Surgical management of epilepsy in India
4.
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.
Epilepsy surgery
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.
1.
2.
3.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Financial support and sponsorship
Nil.
18.
Conflicts of interest
There are no conflicts of interest.
Ethical statement
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.
Current Medical Issues ¦ Volume 18 ¦ Issue 2 ¦ April‑June 2020
19.
20.
21.
22.
Definition of Epilepsy 2014. International League against
Epilepsy.
Available
from:
https://www.ilae.org/guidelines/
definition‑and‑classification/definition‑of‑epilepsy‑2014. [Last accessed
on 2020 Jan 21].
Epilepsy. World Health Organization. Available from: http://www.who.
int/news‑room/fact‑sheets/detail/epilepsy. [Last accessed on 2020 Jan
21].
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.
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.
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.
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,
109
[Downloaded free from http://www.cmijournal.org on Tuesday, May 18, 2021, IP: 251.143.64.164]
Garg: Epilepsy in India
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
110
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.
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.
40. 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.
41. 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.
42. 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.
43. Satishchandra P. Hot‑water epilepsy. Epilepsia 2003;44 Suppl 1:29‑32.
44. 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.
45. Gururaj G, Satishchandra P. Correlates of hot water epilepsy in rural
south India: A descriptive study. Neuroepidemiology 1992;11:173‑9.
46. Satishchandra P, Ullal GR, Shankar SK. Hot water epilepsy. Adv Neurol
1998;75:283‑93.
47. Nagaraja D, Chand RP. Eating epilepsy. Clin Neurol Neurosurg
1984;86:95‑9.
48. 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.
49. Thomas SV. Managing epilepsy in pregnancy. Neurol India
2011;59:59‑65.
50. 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.
51. Thomas SV, Syam U, Devi JS. Predictors of seizures during pregnancy
in women with epilepsy. Epilepsia 2012;53:e85‑8.
52. 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.
53. Thomas SV, Sindhu K, Ajaykumar B, Sulekha Devi PB, Sujamol J.
Maternal and obstetric outcome of women with epilepsy. Seizure
2009;18:163‑6.
54. Dansky LV, Rosenblatt DS, Andermann E. Mechanisms of teratogenesis:
Folic acid and antiepileptic therapy. Neurology 1992;42:32‑42.
55. 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.
56. Jose M, Thomas SV. Role of multidrug transporters in neurotherapeutics.
Ann Indian Acad Neurol 2009;12:89‑98.
57. 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.
58. 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.
59. 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.
Current Medical Issues ¦ Volume 18 ¦ Issue 2 ¦ April‑June 2020