Classification of Epilepsy Syndromes and Role
of Genetic Factors
Roula N. Choueiri, MD, Michel N. Fayad, MD, Antoine Farah, MD, and
Mohamad A. Mikati, MD
In this report the types of epilepsy syndromes seen in
children in a tertiary referral center in Beirut, Lebanon were studied and the importance of consanguinity
and family history in the occurrence of these syndromes was investigated. Records of 230 pediatric
patients evaluated during a 1-year period with the
diagnosis of single seizure, febrile seizure, or epilepsy
were reviewed. Each patient was classified according to
the International League Against Epilepsy classification. The occurrence of consanguinity, of family history of febrile seizures or epilepsy, and of other
variables was noted. Thirty-six percent of patients
were diagnosed with localization-related epilepsy,
21.7% with generalized epilepsy, 11.7% with undetermined generalized or focal, and 24.3% with special
syndromes. Twelve percent of patients were diagnosed
with idiopathic, 15.1% with symptomatic, and 30.3%
with cryptogenic epilepsies. Consanguinity was more
common in patients with symptomatic and cryptogenic
epilepsies than in patients with idiopathic epilepsies or
with incidental seizures (P < 0.05). Family history of
epilepsy was more common in patients with symptomatic, cryptogenic, and idiopathic epilepsies than in
patients with incidental seizures (P < 0.05). Family
history of febrile seizures but not consanguinity was
more common in patients with febrile seizures (P <
0.05). We conclude that genetic factors are important
not only in idiopathic epilepsies and febrile seizures but
also in cryptogenic and symptomatic epilepsies.
© 2001 by Elsevier Science Inc. All rights reserved.
Choueiri RN, Fayad MN, Farah A, Mikati MA. Classification of epilepsy syndromes and role of genetic factors.
Pediatr Neurol 2001;24:37-43.
From the Department of Pediatrics and the Adult and Pediatric
Epilepsy Program; American University of Beirut, Beirut, Lebanon.
© 2001 by Elsevier Science Inc. All rights reserved.
PII S0887-8994(00)00231-9 ● 0887-8994/01/$—see front matter
Introduction
Clinical studies have increased our understanding of
epilepsy syndromes and of their courses. More recently
these studies have become even more important given the
recognition of numerous familial and genetic forms of
epilepsy and given the increasing use of the techniques of
modern genetics in the investigation of epilepsy. The
International Classification of Epileptic Seizures was proposed in 1969 and revised in 1981 by the International
League Against Epilepsy (ILAE). The ILAE also proposed
a classification of epilepsies and of epileptic syndromes in
1985, which was later revised in 1989 [1]. This classification, which grouped epilepsies as syndromes based on
clinical descriptions and electroencephalograms (EEGs),
is more precise for diagnosis and prognosis than previous
classifications [2]. The execution of studies applying
appropriate statistical methods to the problem of epilepsy
is desirable and needed despite obvious difficulties [3].
Various studies have been conducted in different countries
based on this classification [4-9]. Determining the incidence of epilepsy syndromes in different populations,
comparing the results with those of other populations, and
investigating the importance of genetic and environmental
factors in those syndromes can provide further insights
into the problem of epilepsy. This result is particularly true
in view of the ongoing revision of the current ILAE
epilepsy syndrome classification.
The goals of this study were as follows: (1) to determine
the types of epilepsy syndromes, and the usefulness of the
1989 ILAE classification, in patients seen in our tertiary
care center and (2) to investigate the importance of
specific clinical, consanguinity, and family history factors
in the occurrence of these disorders in our patient population.
Communications should be addressed to:
Dr. Mikati; Professor and Chairman, Department of Pediatrics;
Director, Adult and Pediatric Epilepsy Program; American University
of Beirut; 850 Third Avenue, 18th floor, New York, NY 10022.
Received March 8, 2000; accepted August 30, 2000.
Choueiri et al: Genetic Factors in Pediatric Epilepsy 37
Materials and Methods
This study was cross-sectional. The records of all children (0-13 years
of age) seen with the diagnosis of seizures or of epilepsy during a 1-year
period in the Department of Pediatrics at the American University of
Beirut Medical Center were reviewed. Initial and follow-up evaluations
of inpatients (including the neonatal care units) and outpatients were
included. The following variables were determined: age at onset of first
seizure; duration of time between onset and presentation; sex; clinical
presentation; etiology; description of the seizures; precipitating factors (if
any); family history (in first-degree relatives) of seizures, of febrile
seizures, or of epilepsy; consanguinity; extent of seizure control; and
developmental status at the time of the latest follow-up during the above
year. Computed tomography (CT) and/or magnetic resonance imaging
(MRI) results and the results of any metabolic tests or of other
investigations were also documented. All available EEG studies, usually
performed on an 18-channel machine in our hospital, were interpreted by
one of the investigators. In 15 patients was the actual EEG performed
elsewhere, and only the report was available. The decision to perform
brain imaging or metabolic tests on some patients depended on the
physician’s judgment at the time of the evaluation. For the purposes of
the study the following definitions were used: (1) incidental seizures:
single seizures or seizures occurring only in the context of central
nervous system (CNS) infection, head trauma, electrolyte imbalance, or
similar precipitating factors other than fever; (2) febrile seizures: seizures
occurring in children from 3 months to 5 years of age, with a temperature
of 38°C or more and in the absence of CNS infection and of other
significant precipitating events; (3) epilepsy: a condition in which there
is a demonstrated tendency for recurrent unprovoked seizures as evidenced by the occurrence of two or more unprovoked seizures. Consanguinity was empirically defined to be present if the parents were either
first- or second-degree cousins.
Clinical, EEG, and other relevant data were used to confirm the
diagnosis of the seizure disorder or of the epilepsy syndrome and then to
classify each patient’s seizure types and epilepsy syndrome according to
the ILAE classification. Each patient was reviewed by at least two of the
investigators who had to agree, independently, on the classification. If
there was disagreement (which was unusual), then the data were
discussed, and, if necessary, further information or investigations were
obtained to classify the case. If the patient had a history of more than one
seizure type or epilepsy syndrome (e.g., history of febrile seizures in a
patient with subsequent temporal lobe seizures), then the most recent
active seizure type(s) and the most recent data available on the patient
were used for classification, and the history of a prior seizure type was
noted. In addition to first classifying our patients according to the ILAE
criteria, we found it helpful, based on our experience and on that of
previous investigators [4-6], to subsequently add the following subcategories to the ILAE classification. These subcategories (category 1.2 g,
subcategories 1.3 a and 1.3 b, and subcategory 2.2 e) were added, for the
purposes of our study, to better describe many of our patients and to
better classify several other patients (categories 1.2 g, 1.3 b, and 2.2e)
that were not classifiable using the ILAE criteria alone (see below and
Table 1).
1. To the category of ILAE category 1.2, the following subdivision was
added: *Category 1.2 g: “Symptomatic Localization Related Epilepsy, lobe not defined.” Patients were classified in this category
whenever they clearly had a localization-related epilepsy syndrome,
but the EEG and clinical information available did not allow for
definitive localization of the epileptogenic focus.
2. The “Cryptogenic Localization Related Epilepsies” (ILAE category
1.3) were subdivided into two subcategories: *Subcategory 1.3a
“Normal Development Cryptogenic Localization Related Epilepsy”
and *Subcategory 1.3b: “Abnormal Development Cryptogenic Localization Related Epilepsy.” In these patients, development was
documented by the Denver Developmental Scale or by similar
measures, and all tests failed to reveal the cause of the epilepsy.
These patients did not fit in the Symptomatic Epilepsies (category
38
PEDIATRIC NEUROLOGY
Vol. 24 No. 1
1.1.2) because the patients classified under symptomatic epilepsies
should have a known etiology.
3. To the category of “Generalized Epilepsy, Cryptogenic or Symptomatic” (ILAE category 2.2), the following subcategory was added:
*Subcategory 2.2e: “Cryptogenic not defined above.” This addition
was necessary because some patients had generalized cryptogenic
epilepsy clinically and by EEG, but their clinical picture did not
completely fit in any of the specific cryptogenic syndromes described
in the ILAE classification (subcategories 2.2 a-d and 2.3.1 a-b).
The presence of consanguinity and family history of seizures, febrile
seizures, or of epilepsy were compared among the three groups of
incidental seizures, febrile seizures, and epilepsy using the chi-square and
the Fisher Exact Probability tests [3]. The occurrence of these factors in
patients with various epilepsy syndromes was also investigated using the
same statistical methods.
Results
Patient Population
A total of 230 patients (122 males and 108 females)
were seen during the study period because of seizures or
epilepsy (Table 2). There were 31 children with incidental
seizures, 25 with febrile seizures, and 174 with epilepsy.
Primarily generalized tonic-clonic seizures occurred in
32.6% of the patients, complex partial seizures in 30.5%,
secondary generalized seizures in 20.5%, and simple
partial seizures in 6.5%. Many patients (18.7%) had
having more than one seizure type. CT or MRI studies of
the brain were performed on 142 patients. Eighty-nine
patients had normal brain imaging and 53 patients had
abnormalities. The most common abnormal finding was
“atrophy,” which was noted in 20 patients, followed by
brain malformations seen in eight. An underlying etiology
was identified in 107 patients (Table 2). Normal development was noted in 29/31, 24/25, and 106/174 patients with
incidental seizures, febrile seizures, and epilepsy, respectively.
Classification of Epilepsy Syndromes
Using the ILAE classification, we were able to classify
205/230 (89%) of our patients (Tables 1 and 3). By adding
the four subcategories defined in the Materials and Methods section, 11 additional patients (4.7%) could also be
classified. Fourteen (6%) patients were not classifiable
because of lack of data: EEGs were not available in 13,
and one patient had an unwitnessed seizure and was
subsequently lost to follow-up.
The most common epilepsy syndromes we found were
the “localization-related epilepsy syndromes” (36% of our
patients), and in this category, “cryptogenic localizationrelated epilepsy syndromes” were the most common of
those patients. Generalized epilepsy syndromes were
21.7%, and those “undetermined if generalized or localization-related” were 11.7%. Special syndromes (febrile
seizures, isolated seizures, and seizures associated with
Table 1. Classification of patients according to type of epilepsy
syndrome
Epileptic syndrome
1. Localization-related
1.1 Idiopathic
a) Benign childhood epilepsy with centrotemporal spikes
b) Childhood epilepsy with occipital
paroxysms
c) Primary reading epilepsy
1.2 Symptomatic
a) Chronic progressive epilepsia partialis
continua of childhood
b) Seizures with specific modes of
precipitation
c) Temporal lobe
d) Frontal lobe
e) Parietal lobe
f) Occipital lobe
g) Not defined*
1.3 Cryptogenic
a) Normal development*
b) Abnormal development*
2. Generalized epilepsies
2.1 Idiopathic
a) Benign neonatal familial convulsions
b) Benign neonatal convulsions
c) Benign myoclonic epilepsy of infancy
d) Childhood absence
e) Juvenile absence
f) Juvenile myoclonic epilepsy
g) Grand mal on awakening
h) Other generalized not defined
i) Seizures precipitated by specific modes
2.2 Cryptogenic or symptomatic
a) West syndrome
b) Lennox-Gastaut syndrome
c) Epilepsy with myoclonic-astatic seizures
d) Epilepsy with myoclonic absence
e) Cryptogenic not defined above*
2.3 Symptomatic
2.3.1 Nonspecific etiology
a) Early myoclonic encephalopathy
b) Early infantile epileptic encephalopathy
with suppression burst
c) Other symptomatic generalized not defined
2.3.2 Specific syndromes
Table 2.
Etiologies according to patient group
N 5 230
%
Etiology
83
6
6
36
2.6
20
8.6
Intraventricular
hemorrhage
Neurocutaneous
Metabolic
Degenerative
diseases
Brain tumor
Trauma
Stroke
Fever
Congenital infections
Asphyxia
Meningitis
Encephalitis
CNS malformation
Other
Unknown
Total
1
5
4
4
6
57
35
22
50
22
2
24.7
21.7
9.5
Incidental*
n 5 31
Febrile
n 5 25
Epilepsy*
n 5 174
Total
n 5 230
0
0
2
2
0
3
0
0
0
0
2
11
1
2
14
1
0
0
3
0
0
2
2
8
0
0
13
31
0
0
0
25
0
0
0
0
0
0
0
25
1
5
1
0
5
15
5
5
8
3
110
174
1
5
4
25
5
17
7
13
8
3
123
230
* As explained and defined in the text, patients with incidental
seizures are those classified under section 4a and 4b in the ILAE
classification (Table 2), and patients with epilepsy are patients that
fit in ILAE categories 1, 2, and 3. These definitions also apply to
the other tables.
2
3
1
14
13
2
6
5
15
11
5.6
6.5
1
10
4
3. Undetermined if generalized or focal
3.1 With both generalized and focal seizures
a) Neonatal seizures
b) Severe myoclonic epilepsy in infancy
c) Epilepsy with continuous spike-waves
during slow-wave sleep
d) Acquired epileptic aphasia (Landau-Kleffner
syndrome)
e) Other undetermined epilepsies not defined above
3.2 Without unequivocal generalized or focal
seizures
27
18
11
1
11.7
7.8
5
9
3.9
4. Special syndromes
a) Febrile seizures
b) Isolated seizures or status epilepticus
c) Seizures associated with metabolic or toxic
events
Not classifiable
56
25
28
3
24.3
10.9
12.2
1.3
14
6.1
1
* Subdivisions added by us, for the purposes of our study, to the ILAE
classification (see text for details).
metabolic or toxic events) constituted 24.3% of our study
population. Of 174 patients who had epilepsy, 32 (18%)
had a personal history of a prior febrile seizure(s). The
details of the distribution of the different types of epilepsy
syndromes are included in Table 1. Table 3 demonstrates
that a positive personal history of febrile seizures occurred
more commonly in patients with temporal lobe epilepsy
than in those with primary generalized epilepsy, and more
commonly in the latter group than in patients with incidental seizures (P , 0.05).
Role of Genetic Factors
Consanguinity. Patients with epilepsy had a higher
consanguinity rate than those with incidental seizures, who
themselves did not differ from those with febrile seizures
(19.5%, 0%, and 4%, respectively; Table 4). Patients with
cryptogenic and symptomatic epilepsies had higher consanguinity rates than those with idiopathic epilepsies or
with incidental seizures (24.3%, 22.9%, 3.4%, and 0%,
respectively; Table 5).
Family History of Febrile Seizures. Patients with
febrile seizures were more likely to have a family history
of febrile seizures (20%) than patients with epilepsy (1.1%;
P , 0.0001) and, possibly, more than those with incidental
seizures (3.2%, the difference approached, but did not
achieve, statistical significance, P 5 0.079; Table 4).
Family History of Epilepsy. Patients with epilepsy
were more likely to have a family history of epilepsy than
Choueiri et al: Genetic Factors in Pediatric Epilepsy 39
Table 3. Personal history of febrile seizures in patients with incidental seizures, primary generalized
epilepsy, and temporal lobe epilepsy
Personal history of fibrile
seizures present
Total
Paired
Comparison (P)
INC*
PIGE*
TLE*†
0 (0%)
3 (6%)
5 (35.7%)
31
50
14
INC vs PIGE and INC vs TLE
both P , 0.05 PIGE vs
TLE 5 0.0097
* Patients included in this table were older than 3 months of age.
†
These 14 patients included the five patients with 1.2c (symptomatic localization-related) and nine patients
with either 1.3a or 1.3b (cryptogenic temporal lobe epilepsy).
Abbreviations:
INC 5 Incidental seizures
PIGE 5 Primary idiopathic generalized epilepsy
TLE 5 Temporal lobe epilepsy, includes patients from categories 1.2c and 1.3 in Table 2
patients with incidental seizures, who themselves did not
differ from those with febrile seizures (20.1%, 3.2%, and
8% respectively; Table 4). Family history of epilepsy was
equally present in symptomatic, cryptogenic and idiopathic epilepsies and was more commonly found in those
epilepsies than in patients with incidental seizures (28.6%,
21.4%, 25.0%, and 3.1% respectively; Table 5).
Concordance. In families with multiple epileptic
patients, we investigated the concordance in epilepsy
syndrome types in different patients within the same
family. In six families, at least two members of the family
could be fully studied by one of the investigators to
definitively determine their specific epilepsy syndromes.
We found that in three of the six families, there was a lack
of concordance in the epilepsy syndromes occurring in
different family members.
Table 4.
groups
Discussion
ILAE Classification
We found that the ILAE system was useful in classifying our patient population. We were able to classify most,
but not all, of our patients by using that system alone. A
difficulty we encountered in using the ILAE classification
was that many of our patients clearly had cryptogenic
epilepsy but could not fit in one of the clinically described
cryptogenic epilepsies. These patients had developmental
delay and multiple seizure types but had not yet developed
all the clinical criteria of the known cryptogenic epilepsies, such as Lennox-Gastaut syndrome. Neuroradiologic
examinations often demonstrated nonspecific findings
such as atrophy, which did not help much in the classification of the epilepsy syndrome. However, at other times
Consanguinity and family history in the incidental seizures, febrile seizures, and epilepsy
INC
FEB
EP
Consanguinity present
0 (0%)
1 (4%)
34 (19.5%)
Family history of febrile
seizures present
1 (3.2%)
5 (20%)
2 (1.1%)
Family history of epilepsy
present
1 (3.2%)
2 (8%)
35 (20.1%)
31*
25
174
Total
Paired Comparisons
(P value)
INC vs. EP 5 0.007
FEB vs. EP 5 0.104
INC vs. FEB 5 0.446
INC vs. FEB 5 0.079
FEB vs. EP 5 0.000
INC vs. EP 5 0.940
INC vs. EP 5 0.043
INC vs. FEB 5 0.848
FEB vs. EP 5 0.238
* Patients included are older than 3 months of age, and the patients with febrile seizures were all older than
3 months of age.
Abbreviations:
EP 5 Epilepsy
FEB 5 Febrile seizures
INC 5 Incidental seizures
40
PEDIATRIC NEUROLOGY
Vol. 24 No. 1
Table 5. Consanguinity and family history of epilepsy in the incidental seizure group and in different
epilepsy syndromes
INC
CRY
IDI
SYM
Consanguinity present
0 (0%)
17 (24.3%)
1 (3.6%)
8 (22.9%)
Family history of epilepsy
present
1 (3.1%)
15 (21.4%)
7 (25%)
10 (28.6%)
31
70
28
35
Total
Paired Comparison
(P values*)
CRY vs. INC 5 0.0026
CRY vs. IDI 5 0.0100
SYM vs. IDI 5 0.0273
SYM vs. INC 5 0.0041
SYM vs. INC 5 0.0057
CRY vs. INC 5 0.0209
IDI vs. INC 5 0.0206
* All other comparisons were not significant (P . 0.05)
Abbreviations:
CRY 5 Cryptogenic
IDI 5 Idiopathic
INC 5 Incidental seizures
SYM 5 Symptomatic
the changes were specific and quite helpful (such as the
presence of medial temporal sclerosis on MRI). The other
difficulty was that the ILAE classification was easier to
apply to patients who were more extensively studied. It
was more difficult to use for ambulatory patients with less
extensive investigations. For example, most patients in the
category “localization-related epilepsy, lobe not defined”
that we added could probably have been classified under
the appropriate lobe if video EEG monitoring had been
used on them. However, because this technique, even
when readily available, is not routinely used on all
patients, the exact lobe may not necessarily be identified.
It will be helpful to have, as part of the ILAE classification
and in addition to its current electroclinical system, a
classification system that is exclusively based on the
clinical description of the seizures. This recommendation
is supported not only by our experience but also by the
experience of several other investigators [5-9].
Types of Epilepsy Syndromes
We found that the most common epilepsies in our
population were localization-related epilepsies. In both
localization-related and generalized epilepsies, the symptomatic and cryptogenic syndromes were more frequent
than the idiopathic syndromes. These findings are consistent with previous reports that have generally demonstrated higher frequencies of localization-related and
symptomatic syndromes in developing countries than in
developed countries. In fact, our results are intermediate
between those two categories of countries. Our study, like
many previous studies, reflects the patient population seen
in a tertiary referral center rather than one seen in the
general population. However, it does have the advantage
of having used both EEG and clinical criteria in classification of the patients, which was not the case in many, but
not all, of the previous studies [5-11]. The differences
between developing and developed countries have been
attributed to the importance of perinatal insults, to CNS
infections, and to other environmental factors in the
former countries. In addition, in developed countries the
lower rates of cryptogenic epilepsies, relative to symptomatic epilepsies, could be the result of the more detailed
monitoring and investigations that patients receive in those
countries.
Role of Genetic Factors
We found that genetic factors are important not only in
idiopathic epilepsies and febrile seizures, as one may have
expected, but also, perhaps even more so, in symptomatic
and cryptogenic epilepsies. Parental consanguinity was
more common in symptomatic and cryptogenic epilepsies
than in patients with idiopathic epilepsies and in patients
with incidental seizures. This finding, to our knowledge, is
a new one. In a recent study reported by Ottman et al. [12],
genetic factors were important in cryptogenic but not in
symptomatic epilepsies. However, those authors were
studying a different patient population in the United
States, which, presumably, also had lower consanguinity
rates. Our findings strongly favor the hypothesis that, at
least in our patient population, symptomatic epilepsies are
not necessarily because of prior exogenous, usually environmental, insults to the brain, but that such insults are
more likely to result in epilepsy (cryptogenic or symptomatic) if they occur on a genetic background favoring the
development of epilepsy. Some of these genetic factors are
probably inherited as autosomal-recessive or multifactorial traits (as evidenced by the increased rates of parental
consanguinity in patients with cryptogenic and symptomatic epilepsies) or as dominant traits (as suggested by the
increased family history of epilepsy in those patients).
Exposure to the same or similar environmental factors by
members of the same family is another factor that could
Choueiri et al: Genetic Factors in Pediatric Epilepsy 41
have contributed to those findings. We hypothesize that
“epilepsy predisposing genes” may increase the risk for
the development of symptomatic and cryptogenic epilepsies, and the interaction of those genes with environmental
factors may determine further the development of epilepsy
and its types. This hypothesis is supported by the following evidence: (1) in many of our patients, there was lack of
concordance in the type of epilepsy syndromes manifested
in different members of the same family; (2) Berkovic et
al. [13] found occasional, although not frequent, lack of
concordance in the types of epilepsy in twins; and (3) the
Italian League Against Epilepsy found concordance for
the same clinical form of epilepsy in only 38.9% of the
studied families with $ three cases of idiopathic epilepsy
[14].
It is known that several idiopathic epilepsies, such as
benign familial neonatal epilepsy and benign epilepsy with
centrotemporal spikes, are thought to be transmitted as
autosomal-dominant traits. This factor may explain our
observations of an increased rate of family history of
epilepsy and the lack of an increase in parental consanguinity in idiopathic epilepsies (as compared with the
comparison group). Consanguinity contributes to the occurrence of multifactorial and autosomal-recessive traits,
whereas dominant traits are more likely to demonstrate a
positive family history. The inclusion of various cryptogenic epilepsies in one group and similarly of the various
idiopathic epilepsies and of the various symptomatic
epilepsies each in a separate independent group is justified
by the fact that epilepsy syndromes within each of these
groups share common clinical and susceptibility factors
despite differences that do occur in their pathophysiology
and outcome [12].
We found a significantly increased rate of positive
family history of febrile seizures in our febrile seizure
patients. However, rates of consanguinity and of family
history of epilepsy were not different from those of the
comparison group of incidental seizures. This is consistent
with the single major-locus model of inheritance with a
dominantly inherited susceptibility to febrile seizures proposed previously [15-17]. Our data also demonstrated a
high rate of occurrence (18.4%) of prior febrile seizures in
children with epilepsy. Sofijanov [17] found a rate of
20.3% and Camfield [18] a rate of 14.9%.
The limitations of our study must be emphasized. This
study was retrospective, and was thus prone to bias in data
collection and to referral bias. In addition, the analyses we
performed did not correct for variations that may have
existed in family size or in other confounding variables in
the different subgroups we studied. We did not make
corrections for the multiple statistical comparisons that
were performed, and our comparison group (patients with
incidental seizures) was not a completely homogenous
group itself. Also, the rate of consanguinity found in this
group probably represents an underestimate of the real
consanguinity rate of our general population because it
was based on a retrospective review of data collected at
42
PEDIATRIC NEUROLOGY
Vol. 24 No. 1
the time of the clinical encounter. The possibility should
also be raised that some of the differences we found in the
family history and consanguinity rates between different
groups may also be secondary to the methodology we used
rather than real differences. However, because the same
method was used in all of our groups (incidental seizures,
febrile seizures, and epilepsy including idiopathic epilepsy, cryptogenic epilepsy, and symptomatic epilepsy
groups) the comparisons we made and the conclusions we
derived are justifiable at least as initial hypotheses about
the importance of genetic factors in epilepsy. Future
studies should investigate these hypotheses prospectively
[19].
We conclude that the ILAE is useful in classifying our
patient population. Modifications of the current ILAE
system are, however, probably needed. The relatively high
frequency of localization-related epilepsies suggests that
environmental factors are important indicators of epilepsy
in our patients. However, genetic factors are also important and contribute not only to the occurrence of febrile
seizures and idiopathic epilepsy syndromes, as one may
expect, but also to the occurrence of cryptogenic and
symptomatic epilepsies. We believe that further prospective investigations into the above clinical and genetic
factors are bound to improve our understanding of the
biology and of the clinical phenomenology of epilepsy.
Acknowledgments
The authors thank Dr. Iman Nuwayhed for his helpful comments and review
of the manuscript. Supported in part by a grant from Sanofi-Sadco.
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