Epilepsia, 52(6):1052–1057, 2011
doi: 10.1111/j.1528-1167.2011.03041.x
CRITICAL REVIEW AND INVITED COMMENTARY
The etiologic classification of epilepsy
Simon D. Shorvon
UCL Institute of Neurology, University College London, Queen Square, London, United Kingdom
SUMMARY
The etiology of epilepsy is a major determinant of clinical
course and prognosis, yet the current classifications of
epilepsy do not list etiology in any detail. In this article, a
classification (database) of the etiologies of epilepsy is
proposed. In this scheme, the etiology of epilepsy is
divided into four categories: idiopathic, symptomatic,
provoked, and cryptogenic. These are defined and subcat-
egories are proposed. A commentary addressing the
It is remarkable how few attempts have been made to
develop a synoptical listing of causes of epilepsy, or
indeed how little the etiology of epilepsy has been consid-
ered in the official classifications of epilepsy, which have
largely focused on seizure semiology and electroencepha-
lography. This is despite the oft-repeated mantra that
‘‘epilepsy is a symptom of underlying neurologic dis-
ease.’’ A major purpose of any classification scheme is to
provide a framework for clinical practice, and an empha-
sis on etiology is one central aspect of this. The diagnostic
process in clinical practice comprises two stages: (1) the
classification of the seizure type/syndrome and (2) the
assignment of cause. The classifications of epilepsy have
focused largely on the former and not the latter, but etiol-
ogy is as important and is a major determinant of treat-
ment, prognosis, and clinical course. Etiology was
mentioned only in passing in the 1969, 1981, and 1989
International League Against Epilepsy (ILAE) classifica-
tions of seizures and syndromes and later schemes (Gas-
taut, 1969, Commission on Classification and
Terminology of the International League Against Epilepsy
1981, 1989, Engel, 2001; Luders et al., 2003). In their
recent report, the ILAE Commission for Classification of
the Epilepsies has addressed etiology and divided epilep-
Accepted January 24, 2011; Early View publication March 30, 2011.
Address correspondence to Simon Shorvon, UCL Institute of Neurol-
ogy, National Hospital for Neurology and Neurosurgery, PO Box 5, Queen
Square, London WC1N 3BG, United Kingdom. E-mail: s.shorvon@
ion.ucl.ac.uk
Wiley Periodicals, Inc.
ª 2011 International League Against Epilepsy
1052
following points is included: problems associated with
assigning causation, symptomatic versus idiopathic epi-
lepsy, focal versus generalized epilepsy, acquired epilepsy,
acute symptomatic epilepsy, risk factor analysis, pro-
voked epilepsy genetic and developmental epilepsy, and
epilepsy as a disease not a symptom.
KEY WORDS: Epilepsy, Cause, Classification, Etiology,
Idiopathic epilepsy, Symptomatic epilepsy, Provoked
epilepsy.
sies into three categories (genetic, structural/metabolic,
unknown cause), but they do not list etiologic categories
any further (Berg et al., 2010). The Commission recom-
mended that a future classification will be flexible and
multidimensional, in essence a ‘‘database forming the
basis of a diagnostic manual.’’ It is in response to this
aspiration that the etiologic scheme presented herein is
conceived, as a database of etiologies. The purpose of this
commentary is to propose a framework for such a data-
base of etiology, and also to suggest that a detailed con-
sideration of etiology should be an important axis or
dimension of a classification scheme. It is hoped that this
will be prove a useful synoptical overview of all the etiol-
ogies underpinning epilepsy. It should be added, however,
that this etiologic dimension is only one of the multidi-
mensional aspects of a classification, and as a ‘‘database’’
does not replace other aspects of the ILAE classification
systems.
Any consideration of cause should also pay attention
to the historical development of the concept, and a brief
historical survey is attempted in the accompanying
article (Shorvon, 2011). In relation to classification, it
can be noted that in the earlier ILAE classification
schemes the emphasis on seizure semiology and
electroencephalographic features was perhaps largely
because electroencephalography (EEG) was the major
investigatory modality available. With advances in imag-
ing and molecular chemistry, it is now possible to iden-
tify an etiologic basis for many types of epilepsies, and
one can muse on how different the ILAE classifications
of epilepsy might have been for instance if magnetic

resonance imaging (MRI) had been invented before
EEG.
Suggested Scheme for a
Classification of Epilepsy
by Etiology
The classification (database) of etiologies of the epilep-
sies is divided into four main categories (Table 1).
Definitionsa
1. Idiopathic epilepsy—defined here as an epilepsy of pre-
dominately genetic or presumed genetic origin and in
which there is no gross neuroanatomic or neuropatholog-
ic abnormality. Included here are epilepsies of presumed
multigenic or complex inheritance, but for which cur-
rently the genetic basis has not been elucidated.
2. Symptomatic epilepsy—defined here as an epilepsy of
an acquired or genetic cause, associated with gross ana-
tomic or pathologic abnormalities, and/or clinical fea-
tures, indicative of underlying disease or condition. We
thus include in this category developmental and congeni-
tal disorders where these are associated with cerebral
pathologic changes, whether genetic or acquired (or
indeed cryptogenic) in origin. Also included are single
gene and other genetic disorders in which epilepsy is
only one feature of a broader phenotype with other cere-
bral or systemic effects.
3. Provoked epilepsy—defined here as an epilepsy in which
a specific systemic or environmental factor is the pre-
dominant cause of the seizures and in which there are
no gross causative neuroanatomic or neuropathologic
changes. Some ‘‘provoked epilepsies’’ will have a
genetic basis and some an acquired basis, but in many no
inherent cause can be identified. The reflex epilepsies are
included in this category (which are usually genetic) as
well as the epilepsies with a marked seizure precipitant.
4. Cryptogenic epilepsy—defined here as an epilepsy of
presumed symptomatic nature in which the cause has not
been identified. The number of such cases is diminishing,
but currently this is still an important category, account-
ing for at least 40% of adult-onset cases of epilepsy.
It must be emphasized that there are obviously cases for
which categorization is difficult and to a significant extent
arbitrary. Such difficulties are encountered particularly in
relation to: (1) The differentiation of ‘‘presumed genetic’’
(i.e., idiopathic) and ‘‘cryptogenic,’’ for instance in relation
to the benign focal epilepsies or even the idiopathic general-
ized epilepsies. This distinction is arbitrary, but the idio-
pathic category is kept separated here because of the general
a
Note: The definition of ‘‘gross anatomic or pathologic abnormality,’’ in
the above paragraphs, is any identifiable pathologic or anatomic abnormal-
ity that can be detected in normal clinical investigation, including clinical,
microscopy, histology, and neurochemistry.
1053
Etiologic Classification of Epilepsy
clinical features and/or age specificity of these conditions,
which point strongly to a presumed genetic (including epi-
genetic and epistatic) etiology. (2) The categorization of
some of the childhood syndromes. Some of these are
included under the ‘‘idiopathic grouping,’’ but evidence of a
genetic basis is only presumptive, for instance, the benign
rolandic epilepsy. Others are included in the symptomatic
epilepsy despite the fact that there is a presumption of a
genetic cause in at least a proportion of cases, for instance in
the West or Lennox-Gastaut syndromes. (3) The categoriza-
tion as ‘‘symptomatic’’ those single gene disorders without
clear neuropathologic abnormalities but which have sys-
temic metabolic features and which cause a wide range of
symptoms of which epilepsy is only one (e.g., Rett syn-
drome, Angelman syndrome, progressive myoclonic epilep-
sies). There are arguments for including these conditions
within the category of idiopathic epilepsy.
Commentary
Problems with assigning causation
There are a number of factors that complicate the assign-
ment of cause, and these are often overlooked. These will
have an impact on any attempt to classify epilepsies accord-
ing to cause:
1. Multifactorial cause of epilepsy: As has been frequently
reiterated, epilepsy is in the great majority of cases multi-
factorial. In any individual case, the epilepsy is often
(perhaps almost always) the result of both genetic and
acquired influences and also influenced by provoking
factors (and many epilepsies clearly have both exciting
and predisposing causes, to reintroduce an old concept).
Assignment of such cases to any single etiology is, there-
fore, to an extent arbitrary. However, in most cases, there
is a predominant cause to which the case is assigned. In
clinical practice there are many obvious reasons why
such assignment of predominant cause is necessary and
valuable.
2. Cause versus mechanism: Hughlings Jackson urged that
the cause of epilepsy be considered to be mechanism of
ictogenesis or epileptogenesis, and not the more down-
stream underlying condition leading to the epilepsy (see
Taylor, 1930). He viewed most seizures to have a similar
final common pathway, regardless of causative lesion. In
the genetic epilepsies, we are currently closer to defining
cause by molecular mechanism, but in most symptomatic
epilepsies, the mechanisms of ictogenesis are largely
obscure. If knowledge was more complete, categoriza-
tion of cause according to mechanism would be the opti-
mal approach, and indeed should be at the heart of any
classification scheme. This issue should be a major focus
of future research but currently a list of downstream
causes remains necessary.
3. Cause depends on degree of investigation: The identifi-
cation of cause is of course highly dependent on investi-
Epilepsia, 52(6):1052–1057, 2011
doi: 10.1111/j.1528-1167.2011.03041.x
1054
S. D. Shorvon

Table 1. Suggested scheme for an etiological classification of epilepsy

Main category
Idiopathic epilepsy
Symptomatic epilepsy
Predominately genetic or
developmental causation
Predominately acquired
causation
Provoked epilepsy
Cryptogenic epilepsiesb
DNET, dysembryoplastic neuroepithelial tumor.
a
These examples are not comprehensive, and in every category there are other causes.
b
By definition, the causes of the cryptogenic epilepsies are ‘‘unknown.’’ However, these are an important category, accounting for at least 40% of epilepsies
encountered in adult practice and a lesser proportion in pediatric practice.
This list is derived from the book Causes of Epilepsy (Shorvon et al., 2011b).
Subcategory
Pure epilepsies due to single
gene disorders
Pure epilepsies with complex
inheritance
Childhood epilepsy syndromes
Progressive myoclonic epilepsies
Neurocutaneous syndromes
Other neurologic single gene disorders
Disorders of chromosome function
Developmental anomalies of cerebral
structure
Hippocampal sclerosis
Perinatal and infantile causes
Cerebral trauma
Cerebral tumor
Cerebral infection
Cerebrovascular disorders
Cerebral immunologic disorders
Degenerative and other neurologic
conditions
Provoking factors
Reflex epilepsies
Examplesa
Benign familial neonatal convulsions; autosomal dominant nocturnal
frontal lobe epilepsy; generalized epilepsy with febrile seizures plus;
severe myoclonic epilepsy of childhood; benign adult familial
myoclonic epilepsy
Idiopathic generalized epilepsy (and its subtypes); benign partial
epilepsies of childhood
West syndrome; Lennox-Gastaut syndrome
Unverricht-Lundborg disease; Dentato-rubro-pallido-luysian atrophy;
Lafora body disease; mitochondrial cytopathy; sialidosis; neuronal
ceroid lipofuscinosis; myoclonus renal failure syndrome
Tuberous sclerosis; neurofibromatosis; Sturge-Weber syndrome
Angelman syndrome; lysosomal disorders; neuroacanthocytosis;
organic acidurias and peroxisomal disorders; prophyria; pyridoxine-
dependent epilepsy; Rett syndrome; Urea cycle disorders; Wilson
disease; disorders of cobalamin and folate metabolism
Down syndrome; Fragile X syndrome; 4p-syndrome; isodicentric
chromosome 15; ring chromosome 20
Hemimegalencephaly; focal cortical dysplasia; agyria-pachygyria-band
spectrum; agenesis of corpus callosum; polymicrogyria;
schizencephaly; periventricular nodular heterotopia; microcephaly;
arachnoid cyst
Hippocampal sclerosis
Neonatal seizures; postneonatal seizures; cerebral palsy; vaccination
and immunization
Open head injury; closed head injury; neurosurgery; epilepsy after
epilepsy surgery; nonaccidental head injury in infants
Glioma; ganglioglioma and hamartoma; DNET; hypothalamic
hamartoma; meningioma; secondary tumors
Viral meningitis and encephalitis; bacterial meningitis and abscess;
malaria; neurocysticercosis, tuberculosis; HIV
Cerebral hemorrhage; cerebral infarction; degenerative vascular
disease; arteriovenous malformation; cavernous hemangioma
Rasmussen encephalitis; SLE and collagen vascular disorders;
inflammatory and immunologic disorders
Alzheimer disease and other dementing disorders; multiple sclerosis
and demyelinating disorders; hydrocephalus and porencephaly
Fever; menstrual cycle and catamenial epilepsy; sleep-wake cycle;
metabolic and endocrine-induced seizures; drug-induced seizures;
alcohol and toxin-induced seizures
Photosensitive epilepsies; startle-induced epilepsies; reading epilepsy;
auditory-induced epilepsy; eating epilepsy; hot-water epilepsy

gatory technology. Prior to the advent of MRI for
instance, most cases of cortical dysplasia and of hippo-
campal sclerosis could not be identified definitively.
Similarly, prior to the advances in genomics, most
genetic causes of epilepsy (both idiopathic and symp-
tomatic) could not be diagnosed.
Symptomatic and idiopathic epilepsy
The concept of ‘‘symptomatic epilepsy’’ might, at first
glance, seem fairly straightforward, but in fact this is not the
case. For most of the 19th century, symptomatic epilepsy
(often previously known as organic epilepsy) was not con-
sidered to be a ‘‘genuine epilepsy’’ at all, and was rather
ignored. The pendulum swung, and by the middle of the
20th century, it had become axiomatic that all or almost all
epilepsies were in fact symptomatic—in the sense that the
epilepsy was a symptom of an underlying cause, even if the
cause could not be identified. In more recent times, a new
meaning has been assigned to the term, largely because the
meaning of its opposite, idiopathic epilepsy, has changed.

Epilepsia, 52(6):1052–1057, 2011

doi: 10.1111/j.1528-1167.2011.03041.x

This latter term was previously used to denote any epilepsy
in which there was no demonstrable cause, but now is used
only for those epilepsies that are primarily genetic in origin
and in which there is no gross neuroanatomic or neuropatho-
logic abnormality.
In the framework proposed in this article, genetic condi-
tions that result in either pathologic or anatomic change (for
instance, the epilepsy due to tuberous sclerosis or neurofi-
bromatosis), or more subtle changes at the molecular patho-
logic level (for examples the epilepsies due to Rett
syndrome, CDKL5, Angelman syndrome) are included in
the symptomatic category. Also included are epilepsies due
to developmental abnormalities where there are neuropatho-
logic changes, despite the fact that these are due to aberrant
development (and are sometimes largely genetic) rather
than to an external acquired cause. These developmental/
congenital disorders are a gray area between core ‘‘idio-
pathic’’ and core ‘‘acquired’’ epilepsies.
Of course this definition is open to criticisms on a number
of fronts. The idiopathic epilepsies may have subtle ana-
tomic abnormalities, or synaptic, membrane, neurotransmit-
ter, or network changes. The distinction from symptomatic
epilepsy, based as it is on the absence of a ‘‘gross lesion’’
(defined above as any identifiable pathologic or anatomic
abnormality that can be detected in normal clinical investi-
gation, including clinical microscopy, histology, and neuro-
chemistry) is to an extent, therefore, arbitrary.
In the most recent ILAE Classification Commission
report, it was suggested that the terms idiopathic, symptom-
atic, and cryptogenic are replaced by the terms genetic,
structural/metabolic, and unknown. This suggestion has not
been followed here, for a number of reasons. Firstly, the
term idiopathic has been honored in history and should be
replaced only if there are major advantages to doing so, and
there is widespread disagreement about the need for this
change (see for instance Ferrie, 2010; Guerrini, 2010; Wolf,
2010). Furthermore, the idiopathic epilepsies are due in all
likelihood to a combination of genetic and environmental
influences (epistatic and epigenetic influences, particularly
in development), and although genetic influences probably
predominate, these have proved largely conjectural. There
are also many genetic causes of ‘‘symptomatic epilepsy.’’
For these reasons, the term idiopathic seems worthy of
retention. Similarly, replacing the term ‘‘symptomatic’’ by
‘‘structural/metabolic’’ also seems largely unnecessary, not
the least because many of the symptomatic conditions are
neither structural nor metabolic, in the normal sense of these
words. Replacing the term ‘‘cryptogenic epilepsy’’ with
‘‘epilepsy of unknown cause’’ seems also simply to anglicize
and remove the venerable Greek origin to the word, rather
than to change the conceptual basis in any meaningful way.
Provoked epilepsy
This category is included in this ‘‘database,’’ and it is
not found in the recent commission report. In any etiologic
1055
Etiologic Classification of Epilepsy
listing, however, this category is, in the author’s opinion,
valuable and important. In the 19th century, it was fully
recognized that most cases of epilepsy had ‘‘exciting’’ as
well as ‘‘predisposing’’ causes (the spark and the gunpow-
der; see accompanying article, Shorvon, 2011a). Both are
‘‘causes,’’ and it is surely ingenuous to somehow claim
that the provoking factor (including ‘‘stress,’’ lack of sleep,
and so on) is in some way not a ‘‘cause.’’ The exciting
causes were environmental or systemic, and in recent
years have been largely ignored. This has occurred despite
the fact that one estimate found a provoking factor to be
the predominant cause of epilepsy in 17% of 500 drug-
resistant cases, and that manipulating these factors in these
cases could greatly improve seizure control in such
patients (Aird, 1983). It is clear that seizure provocation
can influence genetic and acquired epilepsies and focal or
generalized epilepsies, and does not map easily across
conventional seizure-type or syndromic classifications, but
how such precipitants produce seizures is largely obscure.
It is for this reason that the category has been included
here, to incorporate the causes of reflex epilepsies (those
epilepsies in which the predominant cause is a highly
specific provocation) and also the more common seizure
precipitants (stress, lack of sleep, and so on).
Focal versus generalized epilepsy
It should be emphasized that an etiologic categorization
often does not divide the epilepsies into clear-cut focal or
generalized subdivisions, and this distinction (problematic
as it is) does not map across the idiopathic versus symp-
tomatic categorization. Some symptomatic epilepsies are
generalized and some idiopathic epilepsies are focal.
Furthermore, both generalized and focal seizures may be
‘‘provoked,’’ and provoked seizures can be either genetic or
acquired. This dichotomy really has little utility when it
comes to etiologic classification.
Acquired epilepsy
The term ‘‘acquired’’ is used to refer to ‘‘symptomatic’’
epilepsies excluding the predominately genetic or develop-
mental causes. The term includes those epilepsies due exter-
nal or environmental causes as well as internal pathologic
processes, which have no known major environmental
component (e.g., tumor, neurodegenerative disorders, auto-
immune disorders). Excluded also are the epilepsies due to
systemic nonneurologic diseases (e.g., fever, metabolic
change, reflex epilepsy) without neuropathologic findings,
and these are categorised under the term ‘‘provoked epi-
lepsy’’ (a distinction based on the 19th century dichotomy
of exciting/predisposing causes).
Acute symptomatic epilepsy
One term that should probably be dropped is ‘‘acute symp-
tomatic epilepsy.’’ Currently this is used to include: (1)
‘‘causes’’ that are better included as ‘‘provoking factors’’ such
Epilepsia, 52(6):1052–1057, 2011
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1056
S. D. Shorvon
as fever, metabolic disturbance, alcohol, and (2) acute brain
injury, which are best included as ‘‘symptomatic’’ causes. It
is senseless to include both types of ‘‘causes’’ within one cate-
gory, as they are wholly different in terms of physiology and
clinical features. If the term is to survive it should be
restricted to the ‘‘early seizures’’ in acute brain injury
(trauma, stroke, etc.), which clearly have a different patho-
physiology and prognosis compared to the later seizures
induced by these conditions (Shorvon & Guerrini, 2010).
Risk factor analysis
The most precise approach to the assignment of etiology
is to take a statistical route and to compare the frequency of
an etiologic factor in the epilepsy population (preferably at
the time of diagnosis) with that in a control population (of
the same demographic and geographic constitution). This
has seldom been attempted, although the reverse study—a
case control study to define the frequency of epilepsy within
a defined etiology—has been more commonly performed,
for instance in head injury, stroke, and some infections. In a
case control study, the following conditions should be met
(as noted by Beghi, 2004): (1) temporal association—expo-
sure to the risk factor should precede epilepsy; (2) strength
of the association—the greater the difference in incidence
between exposed and unexposed populations, the more
likely is this to be a true association; (3) consistency—the
association should be reproducible; (4) biologic gradi-
ent—evidence of a ‘‘dose–response’’ effect; and (5) biologic
plausibility.
Genetic and developmental mechanisms
The recent advances in genetics have made limited
inroads into understanding the genetic basis of epilepsy. The
most impressive findings have been made in relation to the
symptomatic epilepsies of metabolic origin, and the defec-
tive gene causing almost all of the single-gene metabolic–
neurologic disorders has now been identified. Fifteen genes
have also been identified coding for ‘‘pure’’ epilepsies, but
despite intensive efforts, the genetic bases of the great
majority of idiopathic epilepsies remain largely obscure.
The reason is likely to be that idiopathic epilepsy is caused
by more complex genetic or developmental processes, and
large epistatic and epigenetic influences will be present. The
current emphasis on finding causal single nucleotide poly-
morphisms (SNPs) seems naive, and untangling the epige-
netic and epistatic mechanisms will pose a formidable
challenge, yet these mechanisms probably hold the key to
the ‘‘missing heritability’’ of epilepsy. Other genetic
approaches may also help, and these include studies of such
mechanisms as copy number variation, genomic imprinting,
chromosomal imbalance, X inactivation, and mitochondrial
mechanisms. How the category of ‘‘idiopathic’’ epilepsy will
appear in the future after these further research efforts have
come to fruition is unclear. It should also be noted that many
genetic influences are not ‘‘all or none’’ but confer
Epilepsia, 52(6):1052–1057, 2011
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susceptibility. Where the line is drawn in these cases
between a genetic or cryptogenic categorisation is arbitrary.
Epilepsy as a disease not a symptom
As mentioned earlier, epilepsy is, like headache or ane-
mia, often considered a ‘‘symptom’’ of a neurologic condi-
tion and not a condition per se, and the main reason for
considering it thus is because there are so many different
potential causes. This of course raises a question about the
definition of disease in general, a topic beyond the scope of
this article (and as mentioned earlier, in the 19th century
epilepsy was often considered only to apply to the idiopathic
condition). Despite this, and perhaps rather contradictorily,
there is also an increasing tendency to define ‘‘syndromes’’
of epilepsy, and to consider these entities in their own right.
In relation to etiology, there is a danger of mixing up ‘‘dis-
ease’’ with ‘‘cause of disease’’ and this is at its most difficult
in consideration of some syndromes. Some syndromes are
genetic (e.g., Severe Myoclonic Epilepsy of Infancy) or pre-
sumed genetic (e.g., the Idiopathic Generalized Epilepsies),
and others have mixed etiologies (e.g., West syndrome).
The definition of syndrome is frequently sufficiently vague
to allow inclusion of many different groups and subgroups,
and there is a continuing debate among the splitters and
lumpers of the epilepsy world about what to include.
Furthermore, some conditions are so well defined from the
etiologic point of view (severe myoclonic epilepsy of
infancy is an example) that it is not really a ‘‘syndrome’’ but
an epilepsy etiologic type, in the same sense that posttrau-
matic epilepsy is not considered a syndrome but a specific
etiologic type of epilepsy. Therefore, whether epilepsy is
considered a symptom or a disease, and to what extent epi-
lepsies are grouped into syndromes or not, will depend to an
extent on the importance placed on etiology. Certainly a
definition and classification of epilepsy on etiologic
grounds has very different results from those using semio-
logic or electrographic criteria.
Acknowledgment
The classification scheme proposed here is based on the framework pro-
posed in the Causes of Epilepsy (Shorvon et al., 2011b), and the commen-
tary on several chapters from this book (Shorvon, 2011b,c; Shorvon et al.,
2011a).
Disclosure
I have no conflicts of interest to declare. This work was undertaken at
UCL and received a proportion of funding from the Department of Health’s
NIHR Biomedical Research Centre’s funding scheme. I confirm that I have
read the Journal’s position on issues involved in ethical publication and
affirm that this report is consistent with those guidelines.
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