Epilepsia, 49(Suppl.
1):19–25, 2008
doi: 10.1111/j.1528-1167.2008.01445.x
SUPPLEMENT - MANAGEMENT OF A FIRST SEIZURE
First seizure: EEG and neuroimaging following
an epileptic seizure
∗
Bernd Pohlmann-Eden and †Mark Newton
∗
Bethel Epilepsy Center, Bielefeld, Germany; and †Comprehensive Epilepsy Program, Austin Health,
Heidelberg, Australia
SUMMARY
An early EEG (within 48 h) and high-resolution
magnetic resonance imaging (hr_MRI) are the
methods of choice for an accurate diagnosis after a
first seizure presentation. Together with a careful
history and examination, they will allow definition
of the epilepsy syndrome in two-thirds of patients
and help assess the individual risk for seizure re-
currence, which is determined by the specific syn-
drome and is highest with focal epileptiform ac-
tivity on EEG. Despite the heterogeneity of first
seizure studies, EEG and etiology are consistently
found to be the best predictors for seizure recur-
rence and prognosis. The additional yield of sleep-
A first seizure is a very common condition and also
a very frightening event, which raises urgent health and
lifestyle issues and makes counseling rather complex. Par-
ticularly important is the question whether the seizure is
a symptom of a transient encephalopathy or an under-
lying epileptogenic brain pathology as these conditions
will determine the prognosis with regard to seizure re-
currence. Numerous studies have been performed in the
last 3 decades to identify predictors of seizure recurrence.
Berg and Shinnar’s (1991) careful meta-analysis identi-
fied an abnormal EEG and an underlying documented
cause as the most consistent findings. While the early
studies based their etiological assessment and diagnosis
of a symptomatic seizure or epilepsy mainly on clinical
findings (seizure semiology, physical examination, history)
aided sometimes by imaging with computerized tomog-
raphy (CT) and EEG, there are now advanced EEG and
neuroimaging procedures that not only confirm these data
Address correspondence to Bernd Pohlmann-Eden, M.D., Ph.D.,
Professor of Neurology and Public Health, Head and Chair, Bethel
Epilepsy Center, Maraweg 21, D-33617 Bielefeld, Germany. E-mail:
pohleden@gmx.net
Blackwell Publishing, Inc.

C International League Against Epilepsy
19
deprived EEG and sleep EEG is uncertain; yet MRI
is essential for detecting brain tumors and other
structural bases for new epilepsy. The rate occur-
rence of remote symptomatic seizures increases
significantly with age and the most common eti-
ology in the elderly with a first seizure is stroke;
however, its exact relevance to epileptogenicity is
yet to be defined. There is a striking lack of system-
atic studies using early EEG and hr_MRI in order to
better characterize epileptogenic areas and eluci-
date the mechanisms of seizure provocation.
KEY WORDS: First seizure, Diagnosis, EEG,
Computerized tomography, Magnetic resonance
imaging.
but also allow early determination of a possible underlying
epilepsy syndrome (King et al., 1998; Jallon et al., 2001).
This review will address the following: (1) What novel
information can be derived from first seizure (FS) stud-
ies using functional and structural diagnostic procedures?
(2) What are the potential interpretations and limitations
of EEG and neuroimaging in current FS studies? (3) How
much obligatory are EEG and neuroimaging to define an
epilepsy syndrome? (4) What are the principal consid-
erations for prognosis and the future challenges of FS
research?
W HAT N OVEL I NFORMATION C AN BE
D ERIVED FROM FS S TUDIES U SING
F UNCTIONAL AND S TRUCTURAL
D IAGNOSTIC P ROCEDURES ?
Seizure selection bias: An FS only comes to medical at-
tention if the individual (or witness) becomes aware of it
and feels threatened so to seek help. Thus, the entire dis-
cussion and evaluation of data is biased by the fact that
most of the FS studies deal with patients after their first
tonic-clonic seizure. Clinical experience and systematic
investigations tell, however, that many of these patients
20
B. Pohlmann-Eden and M. Newton
already had previous minor epilepsy symptoms. Aware-
ness of the event or aftermath is crucial for presentation
and events during sleep will pass unnoticed. Thus, the “first
seizure” is a concept (or sometimes the tip of an iceberg)
rather than a clearly defined event. We have no clear idea
of the individual considerations making a brain epileptic or
of the complex interplay between genetic, structural, bio-
chemical, and functional factors. We do not know if an ac-
cumulation of provoking factors over time will lower the
seizure threshold. Nor do we know why a significant pro-
voking factor only sometimes leads to a seizure in one
individual, but not in another. This raises the question of
what exactly is provocation. Is every seizure somehow pro-
voked?
According to the International League Against Epilepsy
(ILAE) definition, a seizure or repeated seizures occur-
ring in close temporal association with an acute systemic,
metabolic, or toxic cerebral insult are considered to be
“provoked,” as compared to seizures occurring in relation
to a well-demonstrated antecedent condition, substantially
increasing the risk for epileptic seizures, which are consid-
ered to be “unprovoked” (Commission on Epidemiology
and Prognosis and International League Against Epilepsy,
1993). Hauser & Beghi (2007) review these widely ac-
cepted definitions in this volume, which have operationally
helped to organize and understand study findings. How-
ever, they leave us with the question if “provoked” and “un-
provoked” are distinct points rather than transitional states
within a spectrum of provoking and inhibiting factors.
According to the most recent ILAE definition, epilepsy
is a disorder of the brain characterized by an enduring pre-
disposition to generate epileptic seizures. In that sense, the
definition of epilepsy requires the occurrence of at least
one epileptic seizure (Fisher et al., 2005).
We certainly want to get subtle information with regard
to this enduring predisposition, by collecting detailed in-
formation of the functional state and structural condition of
the brain close to the time of the FS and in clearly defined
homogenous study groups. Unfortunately, we are currently
far from this ideal situation. Data have therefore to be in-
terpreted with all caution and qualification.
EEG F INDINGS IN C URRENT FS
S TUDIES : P OTENTIAL
I NTERPRETATIONS AND
L IMITATIONS
Whether an EEG should be obtained routinely in pa-
tients after an FS is still under debate. There are pragmatic
implications (Fountain & Freeman, 2006) and some au-
thors would not treat after an FS, even if the EEG is abnor-
mal. Yet EEG remains an essential tool for understanding
the underlying process and providing the best counseling.
Epilepsia, 49(Suppl. 1):19–25, 2008
doi: 10.1111/j.1528-1167.2008.01445.x
There are surprisingly few data on the significance and
prognosis of EEG recordings in the early course of epilepsy
for long-term prognosis. A community-based study al-
most 20 years ago identified three variables highly pre-
dictive of achieving 5-year seizure-freedom: (1) no early-
life damage, (2) never having had a generalized tonic–
clonic seizure, and (3) no generalized epileptiform activ-
ity (Shafer et al., 1988). However, several studies have ad-
dressed the role of EEG for early prognosis in patients pre-
senting with an FS. This will be the focus of this brief re-
view, which is not intended to be exhaustive, addressing
only the most relevant findings in well-controlled clini-
cal trials and acknowledging the heterogeneous nature of
the study populations. The importance of these studies for
practical counseling was recently emphasized (Pohlmann-
Eden et al., 2006). The value of the EEG lies in (1) sug-
gesting the presence of focal lesions (with localized slow
waves), (2) allowing individual prediction of SR, and (3)
indicating a specific epilepsy syndrome (e.g., 3-Hz spike-
wave pattern).
In a prospective FS study in 157 adult patients present-
ing mostly with generalized tonic clonic seizures, standard
EEG was more sensitive in detecting abnormalities com-
pared to the clinical and neuroradiological data (Schreiner
& Pohlmann-Eden, 2003); the neurological status was ab-
solutely normal in 10 out of 20 patients (50%) with cere-
bral neoplasms, while the EEG was abnormal in 91.7%. In
patients with underlying cerebrovascular disease, the EEG
showed abnormalities in 88.6% when only one-third had
obvious focal clinical findings.
According to the careful meta-analysis of 16 FS stud-
ies in children and adults by Berg and Shinnar in 1996,
in all reports except one (Hopkins et al., 1988), the pres-
ence of any EEG abnormality was associated with a
significantly higher risk for seizure recurrence. To appro-
priately interpret these data, however, it is necessary to
carefully look at the study population, design, and method-
ology, yet this information is often lacking or incomplete
(see Table 1).
Till the mid nineties, the available studies (Cleland et
al., 1981; Elwes et al., 1985; Annegers et al., 1986; Hop-
kins et al., 1988; Hauser et al., 1990) provided very lit-
tle information on the study populations. Since 1995 very
few additional studies have been performed using MRI in
a high percentage (Forsgren et al., 1996; King et al., 1998;
Pohlmann-Eden & Schreiner 1998a; Lindsten et al., 2001;
Schreiner & Pohlmann-Eden, 2003), and only one specif-
ically aimed at identifying the underlying epilepsy syn-
drome by means of clinical, EEG, and neuroimaging data
(King et al., 1998).
The importance of the study design was emphasized
in Berg and Shinnar’s meta-analysis, explaining the wide
range of reported seizure recurrence rates (from 30% to
80% within 3–4 years). The most relevant sources of
heterogeneity are the selection of patients (age, site of
 21
EEG and Neuroimaging after a First Seizure

Table 1. Age groups, study design and study population, ancillary methods in first seizure studies
Early EEG
Authors n Age groups Study design Setting EEG-classes (<48 h) CT MRI
Blom et al., 1978 74 Children Prospective Hospital 3 classes No NA NA
Cleland et al., 1981 70 Adults Retrospective Hospital NA No NA NA
Camfield et al., 1985 168 Children Retrospective Hospital 4 classes No NA NA
Elwes et al., 1985 133 All age groups Retrospective Hospital NA No NA NA
and prospective
Annegers et al., 1986 424 All age groups Retrospective Outpatients 4 classes No NA NA
Hopkins et al., 1988 408 Adults Prospective Hospital 4 classes No NA NA
Hart et al., 1990 564 Adults Retrospective Outpatients NA No NA NA
and prospective
Hauser et al., 1990 208 Adults Prospective Hospital 5 classes No NA NA
van Donselaar et al., 1992 157 Adults Prospective Hospital 3 classes No NA NA
FIR.S.T. 1993 397 Adults Prospective Hospital 2 classes No NA NA
Bora et al., 1995 147 Adults Prospective Hospital 4 classes No NA NA
Forsgren et al., 1996 563 Adults Prospective Population-based NA No 80% 58%
King et al., 1998 300 All age groups Prospective Hospital 3 classes YES NA 89%
Ramos Lizana et al., 2000 217 Children Prospective Hospital
Neufeld et al., 2000 91 Adults Retrospective Hospital 5 classes No 69% Few cases
Jallon et al., 2001 926 All age groups Prospective Practice hospital NA No 58% 7%
Hui et al., 2001 132 All age groups Retrospective Hospital 3 classes No 64% NA
Lindsten et al., 2001 107 Adults Prospective Population-based NA No 98% 45%
Schreiner & 166 Adults Prospective Hospital 4 classes YES 94% 60%
Pohlmann-Eden, 2003a

CT, computerized tomography; MRI, magnetic resonance imaging; NA, not available.
a
The classification of the EEG findings varied across studies (most frequently classified as normal, diffuse slowing, focal slowing,
focal epileptiform, or generalized epileptiform).

recruitment, exclusion criteria, definition of “provoked”
seizure, inclusion of patients with uncertain seizures) the
time point of study entry, and the retrospective versus
prospective design. According to Berg & Shinnar (1991),
the seizure recurrence was 40% in prospective and 52% in
retrospective studies that employed first seizure methods
and 67% in non-FS studies (i.e., new-onset epilepsy).
With regard to the EEG methodology, the time point of
the EEG (tpEEG) recording seems to be of paramount sig-
nificance. The average time from FS to the first EEG was 3
years in a community-based study as compared to 1 month
if the diagnosis of epilepsy was already established (Shafer
et al., 1988). This surprising observation may reflect the
above-mentioned and still current controversy about the
pragmatic (decision-influencing) value of an EEG after an
FS (Fountain & Freeman, 2006).
In the study by King et al. (1998), an EEG performed
within 24 h after an FS detected epileptiform abnormali-
ties in 51%, compared with only 34% of the patients with
a later EEG. The only two other studies with EEG record-
ings within 48 h reported EEG abnormalities in up to 70%
(Neufeld et al., 2000; Schreiner & Pohlmann-Eden, 2003).
In the remaining studies (with no information available but
perhaps later tpEEG; Table 1), the EEG abnormality rates
were significantly lower, between 9% and 51%.
Most of the studies included hyperventilation and photic
stimulation in their routine EEG recordings, but did not de-
fine the exact methodology for a correct interpretation of
potential value and findings of these activations.
The additional yield of sleep-deprived and sleep EEG
is still uncertain. Most patients underwent sleep-deprived
EEG, if they had no epileptiform abnormalities on
their first routine EEG (King et al., 1998; Schreiner &
Pohlmann-Eden, 2003). Most of the studies (Table 1) dis-
tinguished and stratified 3 to 5 classes of EEG findings
(normal, diffuse abnormal [slowing], focal slowing, focal
epileptiform, generalized epileptiform).
The rate of any abnormality ranged from 41% to 80% in
nonselected and from 9% to 63% in selected populations,
and were predictive of seizure recurrence in all but two
studies (Hopkins et al., 1988; Bora et al., 1995). Schreiner
and Pohlmann-Eden reported only 10% normal EEGs in
their FS patients with seizure recurrence compared to 38%
who remained seizure-free.
The reported yield of epileptiform activity in routine
EEG ranged from 12% to 27% (Hopkins et al., 1988; van
Donselaar et al., 1992; Neufeld et al., 2000; Schreiner &
Pohlmann-Eden, 2003) and increased to 23–50% if sleep
recordings could be obtained (van Donselaar et al., 1992;
King et al., 1998; Schreiner & Pohlmann-Eden, 2003).
The proportion with epileptiform activity on the first EEG
was found to be significantly greater in children com-
pared to patients older than 16 years both in a prospec-
tive series (59% versus 39%, King et al., 1998) and in

Epilepsia, 49(Suppl. 1):19–25, 2008

doi: 10.1111/j.1528-1167.2008.01445.x
22
B. Pohlmann-Eden and M. Newton
a retrospective investigation (Neufeld et al., 2000). In a
Dutch prospective study of children, the seizure recur-
rence rate was 71% when an epileptiform EEG was present
(Stroink et al., 1998), while the overall recurrence rate was
54%.
In King et al.’s 300 patients, additional sleep deprived
EEG showed epileptiform activity in another 55 patients
(35%). The much lower additional yield of epileptiform
activity in the series of Schreiner and Pohlmann-Eden (9
out of 166; 8 with generalized epileptiform activity) could
be explained by a longer time interval between first routine
EEG and the sleep deprived study.
The high predictive value of generalized epileptiform
activity for seizure recurrence was only reported in se-
lected patient populations most likely representing idio-
pathic epilepsy (Hauser et al., 1990; van Donselaar et al.,
1992). However, in van Donselaar’s cohort the risk for
seizure recurrence was up to 83% as compared to pa-
tients with nonepileptiform abnormalities (41%) and nor-
mal EEGs (12%).
Focal epileptiform activity especially when associated
with focal slowing carried a significantly higher risk for
seizure recurrence in an FS patient population containing
a substantial proportion of cases with cerebrovascular dis-
ease: focal epileptiform activity was found in 26.5% of
the seizure recurrence group as compared to 13.0% of the
seizure-free patients. These data are also in agreement with
few previous reports in which information was provided on
recurrence risk as a function of etiology and EEG; the risk
was lowest in the idiopathic group and highest in the re-
mote symptomatic group with abnormal EEG (Camfield
et al., 1985, Annegers et al., 1986).
In conclusion, an early abnormal EEG, especially when
showing focal epileptiform activity, seems to be an excel-
lent predictor for seizure recurrence. The yield of subse-
quent sleep-deprived EEG and sleep EEG remains uncer-
tain; however, the few data available support the view that
they provide valuable additional information with regard to
syndrome classification and seizure recurrence rates.
N EUROIMAGING F INDINGS IN
C URRENT FS S TUDIES : P OTENTIAL
I NTERPRETATIONS AND
L IMITATIONS
Compared to the EEG studies, information on structural
findings in FS patients is much poorer and only recently it
has become of interest for the availability of MRI.
It cannot be emphasized enough that these “subclinical
structural” findings have to be interpreted with all caution
in regard to their potential epileptogenicity. They might be
coincidental and have always to be considered in the light
of the epileptogenic mechanisms, encompassing all clini-
cal, functional, and structural information.
Epilepsia, 49(Suppl. 1):19–25, 2008
doi: 10.1111/j.1528-1167.2008.01445.x
Until 1995, etiology and subsequent classification as ei-
ther remote symptomatic or cryptogenic according to the
ILAE criteria was mainly based on clinical data and CT.
However, in those studies there was a striking lack of
detailed information on the CT methodology (e.g., slice
thickness, use of contrast media) and even on the exact
number of patients undergoing CT (classified as “not avail-
able” = “NA” in Table 1). Often CT (and MRI) was only
performed in patients with abnormal clinical findings. Not
too surprisingly, the number of pathological findings in-
creases significantly with MRI, which is more sensitive
than CT in detecting subtle lesions. The abnormality rate
is also dependent on the study population; a higher rate of
acquired brain pathologies will be expected in older pa-
tients.
In a retrospective Hong Kong study (Hui et al., 2001) us-
ing CT in 64% of their 132 adult patients, very few (6.8%,
9 out of 85) showed abnormalities such as cerebral atrophy,
arachnoid cysts, and cerebrovascular disease. It is specula-
tive whether these findings had any causal relationship to
the FS event.
In the population-based study by Forsgren et al. (1996)
done almost 5 years earlier, 563 patients presenting with
an “unprovoked seizure” received CT (80%) and/or MRI
(54%) investigations. In this study, the rate of imaging find-
ings was much higher: stroke was the most common etiol-
ogy, detected in 30% (increasing to 45% at age >60 years).
Tumors were detected in 11%, and changes consistent with
Alzheimer’s dementia in 7%. Unfortunately, the additional
yield of MRI above CT is not documented in this study.
A Swedish prospective study examining remission rates
of newly diagnosed unprovoked epileptic seizures, CT
(performed in 99%) and MRI (41%) revealed a remote
symptomatic etiology in 61% of cases (Lindsten et al.,
2001). However, data on the spectrum of radiological ab-
normalities are scant, with only a high percentage of brain
tumors mentioned (5 meningiomas and 4 gliomas).
The superiority of MRI in the detection of tumors is
stressed by the Australian study (King et al., 1998) and
confirmed by Pohlmann-Eden & Schreiner (1998a). MRI
was done in the majority of King et al’s 300 patients (89%),
showing epileptogenic lesions in 38 patients, 17 being tu-
mors. CT with contrast, however, missed 8 tumors out of
17 (45%), including four astrocytomas—all surgical reme-
diable lesions. In our series without MRI, we would have
missed 3 out of 20 patients with brain tumor diagnosis
(12% of all 166 FS patients) all of them with no focal clin-
ical signs (Pohlmann-Eden & Schreiner, 1998a).
When children were included in the analysis of the Aus-
tralian study (mean age 31.2 years, median 25.6 year),
MRI detected 22 more subtle epileptogenic lesions (dis-
orders of cortical development, trauma, hippocampal scle-
rosis and atrophy, cavernous angioma) and most of these
did not show on CT. In a prospective observational study
in children presenting with their first unprovoked seizure,

45 (21%) out of 218 imaging studies (159 underwent
CT, 59 had MRI) revealed abnormalities, most of them
showing focal ischemic lesions (16 out of 45) or cerebral
dysgenesis (11 out of 45) (Shinnar et al., 2001). Clini-
cally significant neuroimaging abnormalities occurred in
only 8% of a large, retrospective review of children pre-
senting with emergent new-onset afebrile seizures; how-
ever, this percentage increased up to 26%, if the subgroup
of children who met risk factors such as focal seizures
or predisposing conditions were analyzed (Sharma et al.,
2003).
The German study which included a significantly older
study population (mean age 47.8 years, only adults),
showed a high percentage of cerebrovascular lesions (26%
of their 166 patients), followed by brain tumors (12%),
traumatic scars (5%), and other lesions (4%).
Neuroimaging of an FS in the elderly has become a very
important topic. There is no doubt that cerebrovascular dis-
ease is the most frequent underlying pathology associated
with both single seizures and new-onset epilepsy in the
elderly, accounting for almost one-third of these patients,
despite the fact that many studies are flawed by fundamen-
tal design problems (e.g., grouping together different sub-
types of stroke, no distinction between single seizures and
epilepsy). However, in these cases the causal relationship
is not always clear (Pohlmann-Eden et al., 1996). While
it has been repeatedly emphasized that cortical involve-
ment is a strong predictor for SR in poststroke seizures,
our own rigorous analysis of the topography of stroke
lesions in FS patients clearly favored the concept that a dis-
turbed interaction (and/or lesion) of both cortical and sub-
cortical functions may increase the risk of SR: 67.8% had
a combined cortical-subcortical lesion, 19.9% a subcorti-
cal lesion, and 12.3% a cortical lesion (Pohlmann-Eden
et al., 1996). There is some evidence that patients with the
PCI sign (“preserved cortical islands”) and undercut cor-
tex may also be at particular risk for seizure recurrence
after stroke (Pohlmann-Eden et al., 2001). However, this
has yet to be demonstrated by a prospective trial. Subcor-
tical vascular encephalopathy was also found to be asso-
ciated with an increased risk for seizures (Schreiner et al.,
1995).
The potential relevance of occult cerebrovascular dis-
ease in FS in the elderly was recently emphasized by an
epidemiological study. According to the large U.K. Gen-
eral Practice Research Database, 4,709 patients older than
60 years presenting with their FS “of unknown etiology”
were at significantly higher risk to develop stroke com-
pared to 4,709 randomly selected controls without seizures
(Cleary et al., 2004). However, as cerebrovascular lesions
are very frequent, their actual “epileptogenicity” has to be
carefully assessed in each individual.
We agree with the conclusion of the Australian group
that the final diagnostic yield of MRI in FS cases is not
yet known as there are too few data reported so far. MRI
23
EEG and Neuroimaging after a First Seizure
is therefore the method of choice for neuroimaging in the
FS of unknown etiology, with very few exceptions such as
children with 3 s/ spike-wave on EEG and no focal clinical
or EEG findings (Pohlmann-Eden et al., 2006). The role
of MRI in adults presenting with electroclinical features of
IGE is not yet clear, although it is unlikely to be of value.
CT should be only performed when MRI is either not avail-
able or contraindicated.
EEG AND N EUROIMAGING AS
O BLIGATORY D IAGNOSTIC
P ROCEDURES TO D EFINE THE
E PILEPSY S YNDROME
Two studies specifically addressed the question to what
extent EEG and neuroimaging (together with clinical data)
were able to identify an epilepsy syndrome already at
the stage of a probable FS or new-onset epilepsy (King
et al., 1998; Jallon et al., 2001). In the French CAR-
OLE study (Jallon et al., 2001), all but 17 patients had
EEG, 57.9% had CT, and 6.5% had MRI, although half
of the patients who presented with the “first” unprovoked
seizure actually met epidemiological criteria for epilepsy
(926 out of 1,942 patients). There were substantial dif-
ferences in the distribution of epilepsy syndromes in the
FS group compared with the newly diagnosed epilepsy
group. IGE with absence and myoclonic seizures were
not represented in the FS group (except those present-
ing as status epilepticus with ongoing behavioral and
motor disturbances), as they did not come to attention
with their very first symptoms. A specific epilepsy syn-
drome could be assigned to nearly half the FS patients:
8.6% idiopathic localization-related, 16.1% symptomatic
localization-related, 10% cryptogenic localization-related,
16% idiopathic generalized, 1.4% symptomatic general-
ized, and 0.2% undetermined (2 out of 926 patients). The
remaining 441 cases were classified as “isolated seizures.”
A most rigorous approach to determine an epilepsy syn-
drome in an FS presentation (including also new-onset
epilepsy) was adopted by King et al. (1998) using MRI
in up to 90% of their patients and early EEG plus sleep-
deprived EEG, if routine EEG was normal. The authors
were able to classify localization-related or generalized
syndromes in only 47% of cases with clinical information
versus 77% of those with EEG findings, and 81% of those
with MRI.
Their findings emphasize the outstanding role of EEG
for syndrome classification and the comparably low addi-
tional impact of MRI at this time point. These results con-
firm the previous pre-MRI studies in which EEG and clini-
cal data allowed syndrome classification in the majority of
their cases.
In summary, we strongly suggest that both early EEG
and MRI should be part of a systematic comprehensive
Epilepsia, 49(Suppl. 1):19–25, 2008
doi: 10.1111/j.1528-1167.2008.01445.x
24
B. Pohlmann-Eden and M. Newton
diagnostic approach in FS patients including all appropri-
ate clinical information.
P RINCIPAL C ONSIDERATIONS
AND F UTURE C HALLENGES
In general, current studies have no rigorous design and
basically confirm the results of the old studies with EEG
and etiology as the most significant risk factors. To un-
derstand the ephemeral hyperexcitability state of the brain
after an FS and its epileptogenic potential, more sophisti-
cated data, prospectively acquired, are needed in both func-
tional and structural domains in well defined populations.
The additional yield of an early EEG recording is already
a clear directive for future research. It is speculative that
a prolonged EEG recording with standardized inclusion of
both sleep and sleep-deprivation (short-term EEG moni-
toring) could provide more insight into the ictogenic and
epileptogenic processes. It could be anticipated that MRI
with its increasing sensitivity will contribute to a much
larger extent to the understanding of epileptogenic struc-
tural changes, and the potential of functional MRI in this
context has yet to be explored.
A methodological paradigm shift and new perspec-
tives on the “FS scenario” might bring new understand-
ing to both isolated and early epilepsy seizures. For ex-
ample, there are very few data on EEG-monitored func-
tional brain disturbances in patients considered to be at
risk for an FS. We ourselves started a pilot project and
prospectively investigated 30 “seizure-free” consecutive
stroke patients with standardized early EEG-monitoring:
almost one-third presented with subclinical epileptiform
activity such as period lateralized epileptiform activity,
spikes, sharp waves, most of them within the very first
hours after the stroke, and significantly more were ob-
served in combined cortical-subcortical extended lesions
(Pohlmann-Eden et al., 1998b); this was confirmed in an
extended series by Strittmatter et al. (2002), in which 6 of
26 poststroke patients developed clinical and subclinical
seizures, some of them simultaneously in topographically
distant areas.
We speculate that future FS studies will carry a high po-
tential for a better understanding of both ictogeneses and
epileptogenesis and the pathophysiological circumstances
of “provocation.”
Disclosure of Conflicts of Interest: The authors have declared no
conflicts of interest.
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