235

Journal of Pediatric Neurology 11 (2013) 235240

DOI 10.3233/JPN-130627
IOS Press

Study of etiological profile of infantile and

childhood focal seizures at a tertiary care
centre in South India
Vykuntaraju K.N. Gowdaa,*, Smitha H. Vasannab, Pragalath Kumarb, Shivanandab,
Ramesh R. Lakskmanc, Govindrajb and Premalatha Ramaswamyb
a

Department of Pediatric Neurology, Indira Gandhi Institute of Child Health, Bangalore, India
Department of Pediatrics, Indira Gandhi Institute of Child Health, Bangalore, India
c
Department of Radiology, Indira Gandhi Institute of Child Health, Bangalore, India
b

Received 18 July 2013

Revised 25 August 2013
Accepted 17 September 2013

Abstract. Objective is to evaluate the etiology of focal seizures at a tertiary care center in Indian children. Design is a cross
sectional study. Setting is outpatient and inpatient of a tertiary care teaching children hospital in South India. A total of 150
consecutive children aged 1 mo to 18 yr presenting with focal seizures defined as per international league against epilepsy
classification, participated in this study. A detailed history was taken and clinical examination was done was along with the
investigation for the etiology of focal seizures with routine and specific tests, computerized tomography (CT) scan and/or
magnetic resonance imaging (MRI) and electroencephalography (EEG). All of the findings were recorded in a pre-designed pro
forma and results were analyzed. The mean age presentation was 6.5 yr. Male preponderance was noticed with a ratio of 1.2 : 1.
Complex partial seizures were the most common (68%) type of focal seizures. Neurologic deficits were noticed in 36 (24%)
patients; most common form was hemiparesis. CT scan abnormalities were noted in 76% of the patients, most common CT
finding was inflammatory granuloma. In four cases, where CT scan was inconclusive of neurocysticercosis (NCC) versus tuberculoma, MRI showed features of tuberculoma. The most common etiology of focal seizures was inflammatory granulomas;
NCC (69%) and tuberculoma (15%), followed by perinatal insult (8%) and stroke (7.3%). EEG was diagnostic in cases of
Rolandic epilepsy in seven (4.6%) cases. CT brain is a valuable tool in identifying the underlying etiology of focal seizures. MRI
is helpful in cases of diagnostic dilemma between NCC and tuberculoma by CT scan. EEG is diagnostic of benign Rolandic
epilepsy.
Keywords: CT, MRI, EEG, focal seizures, infections, India

1. Introduction
Seizure disorders are among the most frequent
neurologic problems that occur in childhood. Child___________________________________________
*Correspondence: Dr. Vykuntaraju K.N. Gowda, Bangalore
Child Neurology and Rehabilitation Center, HANS Complex, 8/A
1st Main 1st Cross, Manuvana, Near Adhichunchanagiri Choultry,
Vijayanagar, Bangalore, 560040, India. Tel.: +80 23301212, +91
9535212556; Fax: +80 26541799; E-mail: drknvraju@hotmail.com.

hood epilepsies are a heterogeneous group of conditions that differ in their diagnostic criteria and management and have dramatically different outcomes.
Focal epileptic seizures are conceptualized as originating within networks limited to one hemisphere.
The international league against epilepsy (1981 seizure document) used the terms simple partial, complex partial, and partial seizures secondarily generalized. The 2010 classification did not group focal sei-

1304-2580/13/$27.50 2013 IOS Press and the authors. All rights reserved

236

V.K.N. Gowda et al. / Etiological profile of focal seizures

zures in to different subcategories, instead it recommended that focal seizure be described according to
features that are the most useful for a given specific
purpose. The category of focal seizures without impairment of consciousness or awareness, with observable motor or autonomic components, roughly
corresponds to the concept of simple partial seizure.
The category of focal seizures with impairment of
consciousness or awareness roughly corresponds to
the concept of complex partial seizure. The third
category of focal seizures evolving to a bilateral,
convulsive seizure (involving tonic, clonic, or tonic
and clonic components), replaces the term secondarily generalized seizure [1].
Focal seizures are not infrequent in children. In fact,
the most frequent childhood epilepsy is probably
benign childhood epilepsy with centrotemporal spikes,
also called as benign Rolandic epilepsy [2]. The
overall incidence of childhood epilepsy from birth to
16 yr is approximately 40 cases in 100,000 children
per year (410%) of which 60% are focal seizures and
more than 50% starts in childhood [3].
Acute-onset focal seizures in an otherwise asymptomatic child may be genetic, structural/metabolic, or
of unknown cause. If no focal structural lesion is
found, the seizures may be either the expression of a
genetic disorder (benign Rolandic epilepsy) or may
have an unknown cause. In developing countries like
India, more than 60% of focal seizures are structural.
The causes of structural focal seizures in children in
India have been found to be somewhat different from
those reported from the West. The common reported
causes of focal epilepsy in children of developed
countries include gliomas, cortical dysplasias, calcifications, and infarcts; those reported in Indian studies
include predominantly infections (neurocysticercosis
[NCC] and tuberculomas) [4]. Wadia et al. [5] reported that at least 26% of Indian patients with focal
epilepsy has single small enhancing computerized
tomography (CT) lesion. The proportion of tuberculomas of the brain among the space occupying lesions
ranges from 1.415.9% [6]. Sufficient information is
available regarding the clinical profile and etiology of
focal seizures in children from developed countries [7,
8]. Surprisingly, similar studies on children from
developing tropical countries are scarce. Therefore,
the present study was undertaken to investigate the
etiology of focal seizures at a tertiary care centre in
Indian children.

2. Materials and methods

This is a cross sectional study done at a tertiary care
teaching hospital in South India, from July 2011 to
June 2012. One hundred and fifty consecutive cases in
the age group between 1 mo and 18 yr of age with
following inclusion criteria were included: a) had one
or more focal seizures, b) had complete historical data
and had undergone relevant investigations. Patients
presenting with focal seizures during acute central
nervous system insult like neuroinfection, stroke were
included. Children with febrile convulsions and seizures other than focal seizure types (generalized tonic
clonic seizures [GTCS], absence, atonic, etc.) were
excluded from the study.
Children presenting to our hospital with focal seizures defined as per international league against epilepsy classification-2010 formed the study group. A
total of 150 children were included, of which 22 cases
were from the outpatient department and 128 children
from the inpatient department. A detailed history was
taken from parents about semiology of seizures, birth
history, developmental history, and significant past
history of neuroinfections and head injury. Clinical
examination was done for assessment of sensorium,
any neurological abnormality, signs of meningeal
irritations, presence of neurocutaneous markers and/or
associated illness by a pediatric neurologist. These
children were investigated for the etiology of focal
seizures with routine and specific investigations including Mantoux test, cerebrospinal fluid analysis,
blood glucose, serum calcium, electroencephalography (EEG) and with neuroimaging, CT scan and/or
1.5 Tesla magnetic resonance imaging (MRI). All the
findings were recorded in a pre designed pro forma
and results were analyzed. MRI was done in cases
where differentiating NCC from tuberculoma by CT
scan was a diagnostic dilemma and also in cases
where CT was inconclusive. EEG was done in all
cases. The standard treatment protocol was followed
for all the children. Ethical committee approval was
obtained from the institutional ethical review board.
Written informed consent was obtained.
The following criteria were employed on CT findings for the diagnosis of tuberculoma and NCC: tuberculoma was considered if the lesion is greater than
20 mm, with an irregular margins, associated with
midline shift, and/or conglomerate lesions with isodense contents, peripheral thick enhancement and
presence of perilesional edema. The diagnosis of NCC

V.K.N. Gowda et al. / Etiological profile of focal seizures

was considered based on size of the lesion (< 20 mm),

regular margins, no midline shift, multiple ring or disc
lesions, eccentric scolex and calcified lesions as described by Rajshekar et al. [9].

3. Results
One hundred and fifty cases comprised the study
group. The age of onset of seizures varied between 2
mo to 17 yr. The mean age of presentation was 6.5 yr.
Eighty-two (55%) were males and 68 (45%) were
females with a ratio of 1.2:1. Regarding the type of
seizures, only three cases (2%) presented with no
impairment of consciousness (simple partial seizures),
103 cases (68%) had an impairment of consciousness
(complex partial seizures) and 44 cases (30%) had
evolved to a bilateral, convulsive seizure (secondary
generalization). Motor symptoms were present in all
cases, sensory symptoms in 6% cases. Right-sided
(58%) focal seizures were more common than left
sided (42%). Seventeen (11%) children presented
with status epilepticus. The causes for status epilepticus included neuroinfection (11), cerebral palsy (2),
intracranial bleed (3), and cortical malformation (1).
Prior history of seizure was present in 25 cases, of
which seven cases had GTCS in the past and 18 cases
had complex partial seizures.
History of tuberculosis was present in two cases of
neurotuberculosis. One child with focal seizures
secondary to tuberous sclerosis had six family members with tuberous sclerosis. In two patients there was
family history of genetic (idiopathic) epilepsy in
second-degree relatives. Among six children with
global developmental delay, one each due to
Sturge-Weber syndrome, tuberous sclerosis, and
neurofibromatosis and the rest three were due to perinatal asphyxia. Twelve children (8%) had microcephaly (< 3 SD). One child with neurofibromatosis
had cafe au lait spot and axillary freckles. Ash leaf
macules were seen in two children with tuberous
sclerosis. Two children with hemorrhagic disease had
severe pallor with bulging anterior fontanelle. One
child with hemiplegia due to septic embolic infarct
had orbital cellulites. Cyanosis and clubbing was
noticed in a child with infarct who had tetralogy of
Fallot. Neurological examination showed that 51% of
children had abnormal neurological findings. Vesicular pleomorphic lesions were noticed in a child with
focal seizures, diagnosed to have varicella meningoen-

237

Table 1
Various etiologies of focal seizures
Etiologies
Inflammatory granulomas and infections
Neurocysticercosis
Tuberculoma
Pyogenic meningitis and ventriculitis
Cytomegalovirus infection
Brain abscess
Perinatal insult
Porencephalic cyst
Gliosis
Stroke
Rolandic epilepsy
Intracranial hemorrhage
Intra parenchymal bleed
Suddural hemorrhage
Subarachanoid hemorrhage
Cortical malformations
Neurocutaneous syndromes
Sturge-Weber syndrome
Neurofibromatosis
Tuberous sclerosis
Oligodendroglioma
Hypocalcemic seizures
No identifiable cause

Ratio
83 (55.3%)
57
12
8
1
5
12 (8%)
4
8
11 (7.3%)
7 (4.6%)
5 (3.3%)
2
2
1
4 (2.6%)
4 (2.6%)
1
1
2
1 (0.6%)
1 (0.6%)
22 (14.6%)

cephalitis. Of the eight cases of meningitis, five had

signs of meningeal irritation. Of total 150 patients, a
vast majority (72%) had normal Glasgow coma scale
score, 36 (24%) patient had neurological deficit at
presentation of which 20 (55%) patients had hemiparesis, quadriparesis was noticed in six (16%) cases
of cerebral palsy, monoparesis and Todds palsy was
observed in five cases each.
Imaging studies were carried out in 143 of the 150
patients. CT scan was done in 134 cases and MRI in
13 cases. Both CT and MRI were done in four cases.
EEG was diagnostic of Rolandic epilepsy in seven
cases; hence, no imaging studies were carried out in
them. The most common CT finding was NCC in 57
(43.8%) cases, tuberculoma in 12 (9.2%) cases, and
infarct was noted in 11 (8.4%) cases, cortical malformation in four, and brain abscess in five cases.
Fifty of total 57 cases of NCC had solitary lesion and
seven cases had multiple lesions. One child had classic
starry sky appearance on CT scan. MRI was done in
13 cases. The CT results of four cases were inconclusive of NCC versus tuberculoma, the results of MRI of
all four cases were more consistent with tuberculoma.
Two cases had cortical malformation, of which one had

238

V.K.N. Gowda et al. / Etiological profile of focal seizures

Table 2
Different etiologies with the age group of subjects presented with focal seizures
Etiologies
Neurocysticercosis
Tuberculoma
Rolandic epilepsy
Unknown Epilepsy
Stroke
Cortical malformation
Pyogenic meningitis
Intracranial hemorrhage
Hypoxic ischemic encephalopathy
Neurocutaneous syndrome
Brain abscess
Tumor

an agenesis of corpus callosum and the other had

subependymal heterotopias. The MRI imaging of one
case was suggestive of Sturge-Weber syndrome, the
remaining six had normal MRI.
Parietal lobe was the most common lobe involved
in NCC, constituting 39 cases (78%), followed by
frontoparietal region in 10 cases (20%). The lesions of
22 (44%) cases were on the right cerebral hemisphere
while 28 cases (56%) had lesions on the left cerebral
hemisphere. Parietal lobe was the common lobe involved in tuberculoma, eight (53%) cases involving
right and four (47%) cases involving left hemisphere.
EEG was abnormal in 60% of cases. The most
common abnormality noted on EEG was focal discharges. EEG was diagnostic of Rolandic epilepsy in
seven cases. The most common etiology of focal
seizures was inflammatory granulomas; NCC (69%)
followed by tuberculoma (15%) and neuroinfections
(Table 1).
NCC was predominantly observed in children of 5
15 yr age group. The youngest age of NCC occurrence
was 2.6 yr. The most common age group of occurrence of tuberculoma was 510 yr. Cortical malformations, pyomeningitis, intracranial hemorrhage were
found more frequently in younger children (Table 2).

4. Discussion
In the present study, a total of 150 children with
focal seizures were evaluated for the etiology of focal
seizures. We included acute symptomatic focal seizures and focal epilepsy. Children aged 1 mo to 18 yr
formed the study group. The mean age of presentation

1 m1 yr

2
5
4
4
2
1

25 yr
13
4
1
7
4
2
2
1
4
1
2
1

610 yr
24
6
2
10
3

4
1
2

1118 yr
24
2
4
2
1

was 6.5 yr and had a male preponderance, which is on

par with Singhi and Singhi [4]. Motor symptoms were
present in all children and sensory symptoms in only
6% of cases. Focal seizures with impairment of consciousness were the commonest form of focal seizure,
followed by focal seizure evolving to a bilateral,
convulsive seizure. Right-sided focal seizures were
more common than left sided. The above observations
well correlated with the study done by Singhi and
Singhi [4]. Past history of seizures was present in 25
(16%) cases, GTCS in seven cases and focal seizures
in 18 cases. Six (4%) cases had global developmental
delay, of which three were neurocutaneous syndromes
and rest three were due to perinatal asphyxia. Microcephaly was present in 12 (8%) cases.
General physical examination gave valuable clue
towards the etiology of focal seizures in cases with
presence of neurocutaneous markers like cafe-au-lait
spots, and axillary freckles and ash leaf macules were
suggestive of neurofibromatosis type 1 and tuberous
sclerosis respectively. Pallor with bulging anterior
fontanelle suggestive of hemorrhagic disease of
newborn and clubbing and cyanosis in a case of tetralogy of Fallot pointing towards infarct as the etiology of focal seizures, all of which were later confirmed by imaging studies. Majority had normal
Glasgow coma scale at the time of presentation.
Hemiparesis was the common abnormal neurological
finding observed in our study correlating with study
done by Singhi and Singhi [4], however majority of
patients had normal neurological examination. Hemiparesis was observed in eight cases of stroke, four
cases of tuberculoma, four cases of meningitis, three
cases of neurocutaneous syndrome, one case each of

V.K.N. Gowda et al. / Etiological profile of focal seizures

brain abscess and cortical malformation. Signs of

meningeal irritation was present in five (3.3%) of
seven cases of meningitis.
In the present study, abnormal neuroimaging finding was observed in 71% of children, which may be a
valuable finding in differentiating a symptomatic
focal seizure from a genetic and unknown cause of
focal seizure. Solitary ring enhancing lesions were the
commonest CT findings. MRI was a helpful imaging
modality in cases of diagnostic dilemma between
NCC and tuberculoma by CT scan. NCC and tuberculomas were the common inflammatory granulomas.
Ring enhancing lesions were the common CT findings
of NCC. Two cases of neurotuberculosis had Mantoux
positivity. Among infections, pyomeningitis and brain
abscess were noticed.
The most common etiology of focal seizures was
inflammatory granulomas and infections. Among
inflammatory granulomas, NCC was the commonest
(69%) followed by tuberculoma (15%). Inflammatory
granulomas and infections formed the major etiological group as per our observation, so also observed by
Singhi and Singhi [4], Jain and Mangal et al. [10] and
Kapoor et al. [11]. In systematic review of studies
reporting the frequency of NCC worldwide, the most
striking finding was that the proportion of NCC
among persons with epilepsy was very consistent and
estimated at 29.6% (95% confidence interval [CI]:
23.536.1%) from 12 studies conducted in Latin
America, Sub-Saharan Africa and Southeast Asia. In
patients less than 20 yr of age, the percentage of NCC
among persons with epilepsy ranged from 11.1%
(95% CI: 2.429.2%) in a community based study in
Burkina Faso (Carabin, unpublished data) to 45.2%
(95% CI: 27.364.0%) in the Eastern cape province of
South Africa, with an overall estimate of 24.8% (95%
CI: 18.232.2%) [12]. In India door-to-door survey
observed 28.4% of active epilepsy is due to NCC [13].
In a study from South India, which included 2531
patients, 1591 patients had localization-related epilepsy, 23% of all epilepsy patients had cerebral solitary cysticercus granuloma [14]. In a large study from
north India, which included 1023 patients with partial
seizures, CT revealed solitary cysticercus granuloma
in 513 (50%) of patients [15].
Wadia et al. [4] studied 150 consecutive cases of
focal seizures and observed following causes; ring or
disc enhancement in 26%, tumors in 9.5%, unknown
in 32%, vascular in 16.2%, atrophic lesions in 6.6%,
tuberculoma (histologically proven) in 1.3%, focal

239

calcifications in 3.3%, and other causes in 6.6% of

cases. Study done by Aggarwal et al. [16] in 131
children with partial epilepsy, 76% patients had
symptomatic epilepsy and 23% were genetic. In
symptomatic epilepsy, various causes noted were
inflammatory granuloma (49%), previous central
nervous system infection (14%), perinatal insult (9%),
trauma (3%), and Sturge-Weber syndrome (0.7%).
Our study is comparable to these studies.
Meningitis and brain abscess accounted for the rest
of the cases. The next common cause noticed was
perinatal insult and stroke. Differentiating the two by
CT scan alone was quite challenging in few cases,
which required further work up with MRI scan.
Neuroinfections like pyomeningitis and brain abscess
together accounted for 21% of infectious etiology.
Our observation clearly shows that infectious etiology
still predominates in the developing country like ours
unlike western population where the predominance of
Rolandic epilepsy and cortical dysplasias has been
observed.
Among the non-infectious causes, the common
etiology was perinatal insult in 12 (8%) cases of
whom four had CT diagnosis of porencephalic cyst.
Stroke accounted for 7.3% cases, 4% children had
clinical and EEG diagnosis of Rolandic epilepsy.
Neurocutaneous syndrome accounted for 2.6% cases
and presence of neurocutaneous markers were valuable in arriving at a cause for the seizure. Cortical
malformation was seen in four cases (2.6%), however,
no clinical clue for malformation on examination,
suggested the need for imaging (especially MRI), in
establishing the etiology of focal seizures. There were
two cases of agenesis of corpus callosum, two cases of
subependymal heterotopias. There was one case of
oligodendroglioma. Hypocalcemia was observed in a
3-month-old child with severe vitamin D deficiency.
Even after thorough investigation, no identifiable
etiology was observed in 22 (14%) cases. EEG was
diagnostic in cases of benign Rolandic epilepsy,
which showed characteristic centrotemporal spikes.
The limitation of this study was etiology not representative of community, because study was conducted
in tertiary care teaching hospital and small sample
size.
In conclusion, inflammatory granulomas like NCC
and tuberculoma were the most common etiology of
focal seizures. CT brain is a valuable tool in identifying the underlying etiology of focal seizures. MRI is
helpful in cases of diagnostic dilemma between NCC

240

V.K.N. Gowda et al. / Etiological profile of focal seizures

and tuberculoma by CT scan and also to diagnose

cortical malformation. EEG is useful in diagnosis of
benign Rolandic epilepsy. Identification of exact etiology of focal seizure with appropriate investigation
gives valuable information for the treatment and
prognostication.

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