Epilepsia, 44(Suppl.
10):11–17, 2003
Blackwell Publishing, Inc.

C International League Against Epilepsy
Epidemiology of Posttraumatic Epilepsy: A Critical Review
Lauren C. Frey
Department of Neurology, University of Colorado Health Science Center, Denver, Colorado, U.S.A.
Summary: Problem: Traumatic brain injury (TBI) is a major
cause of epilepsy. We need to understand its frequency and its
contribution to the total spectrum of the convulsive disorders.
Methods: A review of selected articles dealing with epilepsy
after brain trauma was undertaken.
Results: The number of epidemiologic studies of post-
traumatic seizures has increased substantially over the past
40–50 years, offering steadily increasing knowledge of the fre-
quency, natural history, and risk factors of this well-recognized
complication of TBI. In general, the incidence of posttraumatic
seizures varies with the time period after injury and population
age range under study, as well as the spectrum of severity of the
inciting injuries, and has been reported to be anywhere from 4
to 53%. As high as 86% of patients with one seizure after TBI
will have a second in the next 2 years. Longer-term remission
“Through trauma, the brain may be injured by contu-
sion, laceration, compression, and it is well known that
these insults may result in epilepsy after a ‘silent period
of strange ripening.’ That period lasts for months or years,
but these insults produce epilepsy in the case of one in-
dividual and not in the case of another. . . . Our attention
should therefore be directed toward the discovery of this
mysterious difference” (1).
The average incidence of traumatic brain injury (TBI)
in the United States is estimated to be between 180 and
220 per 100,000 population per year (2). With recent im-
provements in prehospital care and emergency diagnosis
and care of TBI, mortality rates have decreased from 50%
∼30 years ago to ∼30% currently. However, TBI sur-
vivors still carry a tremendous burden of disability as a
result of their injuries. Of mild head injuries, 10% are
thought to result in permanent disability, as well as 66%
of moderate head injuries and 100% of severe head in-
juries (3). The occurrence of seizures after head injury is
a recognized complication of TBI and has recently been
shown to worsen functional outcome significantly after
TBI (4). Much work has been done in hopes of preventing
the development of, or, at least, minimizing the impact of
Address correspondence and reprint requests to Dr. L. Frey at Univer-
sity of Colorado Health Science Center, B150, 4200 E 9th Ave., Denver,
CO 80262, U.S.A. Email: laurencfrey@hotmail.com
11
rates of 25–40% have been reported. Significant risk factors for
the development of seizures in the first week after injury include
acute intracerebral hematoma (especially subdural hematoma),
younger age, increased injury severity, and chronic alcoholism.
Significant risk factors for the development of seizures >1 week
after TBI include seizures within the first week, acute intra-
cerebral hematoma (especially subdural hematoma), brain con-
tusion, increased injury severity, and age >65 years at the time of
injury.
Conclusions: Epilepsy is a frequent consequence of brain
injury in both civilian and military populations. We un-
derstand some factors associated with its development, but
there remain many unanswered questions. Key Words:
Brain trauma—Posttraumatic epilepsy—Acute symptomatic
seizures—Epidemiology.
posttraumatic epilepsy. Understanding the risk factors and
natural course of the disease is one step toward controlling
this costly sequela of TBI.
DEFINITIONS
The number of published epidemiologic studies on
posttraumatic epilepsy has increased substantially in the
past 40–50 years. Despite differences in study features,
many of the same conclusions are drawn by different
groups of authors. In general, epidemiologic studies on
topics like posttraumatic epilepsy offer two basic cate-
gories of information: information about the frequency
and natural history of the disease within a certain popu-
lation, and information about the associated risk factors.
Before discussing these any further, however, it is more
than worthwhile to formulate working definitions of both
posttraumatic epilepsy and traumatic head injury.
Posttraumatic epilepsy
Throughout the body of literature on the subject, the
terms posttraumatic epilepsy and posttraumatic seizures
(PTSs) are both used to describe the same entity: seizures
occurring after head trauma that are thought to be causally
related to the trauma itself. Most of the articles published
to date define posttraumatic epilepsy as one or more un-
provoked seizures after head trauma. Only recently has
12 L. C. FREY
the diagnosis of epilepsy (of any kind) been reserved for
patients who have had two or more unprovoked seizures.
Distinct advantages and disadvantages exist to adopting
this newer definition. Defining epilepsy as two or more
unprovoked seizures is more in keeping with the current
usage of the term, but it also defines a pattern of sus-
ceptibility to seizures and excludes those patients who
would ever have had only one seizure. Although the ex-
act percentage of head-injury patients in whom this ul-
timately would be true is not known, we do know that,
in one population-based study, 86% of patients with one
late posttraumatic seizure had a second seizure within
2 years (5).
At least two major methodologic disadvantages of wait-
ing for a second unprovoked seizure exist, however (6).
The first disadvantage lies in the fact that some patients,
regardless of how long they are followed up, will have
their first seizure at the end of their follow-up period. Be-
cause the risk of a first seizure continues to be elevated
for >10 years after a severe head injury (7), establishing
a recurrent pattern of events in these patients may take an
unreasonably long time. The second disadvantage is the
increasingly predominant practice of starting antiepilep-
tic drugs (AEDs) after just one seizure, a practice that
may change the natural history of posttraumatic seizures.
Two recent studies have attempted to minimize the im-
pact of AED use on their incidence data. Angeleri et al.
(8) dropped patients from their study if they were started
on AEDs. The study protocol used by Vespa et al. (9) pro-
vided for uniform use of prophylactic phenytoin (PHT) in
their patients, while ensuring that the serum levels for the
drug were not statistically different between the patients
who seized and the patients who did not seize.
The term posttraumatic seizure (PTS) will be used
throughout the rest of this review, even if the original au-
thors used posttraumatic epilepsy, in an attempt to min-
imize any confusion that would result from using both
terms. If it is relevant to the discussion, studies whose pa-
tients were included only after two or more seizures will
be identified as such.
An association between new-onset seizures and an an-
tecedent head trauma has been found with various de-
grees of certainty. Only recently have efforts been made
to search for, identify, and then eliminate other factors
that would independently increase the risk of seizures in
any population, such as a history of epilepsy, a history
of previous head injury, previous brain damage of any
type, severe alcoholism (8), fluid/electrolyte imbalance,
or other causes of acute symptomatic seizures, like hy-
poxia or known brain ischemia (10).
Posttraumatic seizures are usually divided into three
categories: “immediate” seizures, early seizures, and
late seizures. Early seizures are those occurring while
the patient is “still suffering from the direct effects of the
head injury” (6), a period commonly defined as 1 week
Epilepsia, Vol. 44, Suppl. 10, 2003
after head injury. Approximately 90% of seizures occur-
ring within the first 4 weeks after head injury will happen
during this first week (11). In general, seizures that hap-
pen at or minutes after impact—“immediate,” “contact,”
or “concussive” seizures—are not included in studies of
early PTSs. The exact pathophysiology behind immedi-
ate seizures and their exact clinical significance there-
fore remains unclear. Although these seizures are often
thought not to increase susceptibility to later, unprovoked,
seizures, data presented by Kollevold (12) suggest other-
wise. In his study, both immediate and early seizures were
associated with an increased risk of late seizures. No sta-
tistically significant difference was found between the two
as risk factors for late PTSs. Late PTSs are usually defined
as seizures occurring >1 week after injury.
Traumatic head injury
According to Jennett (11), “what matters in head injury
is damage to the brain, either on impact or subsequently
due to processes initiated by that impact.” The best means
of accurately assessing whether damage to the brain has
actually occurred, however, is controversial. At this time,
no unequivocal clinical markers of brain damage are used
consistently in studies of PTSs. In most of the studies done
to date, head trauma to the degree that a patient needed
some level of medical attention was taken as presumptive
evidence of additional underlying brain injury. However,
the level of medical attention required was often variable
and incompletely defined, making it difficult ultimately to
compare the results from different studies. For example,
some study participants were identified simply because
they sought medical care after head injury (6). Other pop-
ulations were drawn from a pool of patients requiring ei-
ther hospital admission (8,10,11,13), or, more specifically,
admission to an intensive care unit (ICU) (9) after head
trauma. Still other populations were defined by their even-
tual need for rehabilitation services (4).
Statistical comparisons within these groups also are dif-
ficult because of variability in the type of injury sustained.
Many studies were done at a time when hospital admis-
sion criteria were very different and patients were admitted
who, today, may be treated in an emergency department
and then discharged home. Current hospital-based series,
therefore, are biased in favor of more serious head injuries.
Advances in medical technology also have improved sur-
vival after head injury, especially after more severe injury,
thus further increasing the proportion of severely injured
patients in the hospital. In addition, patients in series of
wartime injuries (13–18) presumably had a higher per-
centage of missile wounds compared with those in civilian
populations (4–11,19). These missile wounds, with their
increased likelihood of dural penetration, are more likely
to cause severe brain injury.
Specific clinical features have often been used to strat-
ify head injury severity. In some cases, this was as simple
 POSTTRAUMATIC EPILEPSY EPIDEMIOLOGY 13

as dividing patients into groups based on length of their TABLE 2. Frequency of posttraumatic seizures (PTSs)
posttraumatic amnesia (<24 h or >24 h) (11). Annegers stratified by injury severity from select military series
et al. (6) developed a three-tier classification for head- Series Injury severity
injury severity: mild, moderate, and severe. Mild injuries
were those in which no skull fracture was found and the Dura mater intact Dura penetrated
World War I (29) 26.1% 47%
period of posttraumatic amnesia or loss of consciousness World War II (29) — 43.4%
was ≤30 min. The moderately injured group of patients Korea (29) 23.8% 42%
included those with skull fractures or other injuries with Scalp or skull Single lobar Multilobar injury
>30 min of posttraumatic amnesia or loss of conscious- only injury or worse
ness who did not otherwise meet the criteria for a severe Early Late Early Late Early Late
injury. Severe injuries were those with a documented brain Vietnam (15) 3.3% 18.5% 3.5% 25.7% 4.6% 41%
contusion, an intracerebral hematoma (ICH), or >24 h of
posttraumatic amnesia or loss of consciousness. A later
group of authors, however, thought that loss of conscious- sector, a consistently higher proportion of severe head in-
ness or duration of posttraumatic amnesia may not be im- juries was seen in series of wartime injuries. This dis-
portant independent risk factors for PTSs. To support their proportionate severity of wartime injuries is in large part
argument, they point to the fact that loss of consciousness due to a higher proportion of injuries that involve dural
is not necessarily always associated with cortical (and, penetration and widespread brain damage in military pa-
thus, potentially epileptogenic) injuries (4). A universally tients, as mentioned earlier. For example, 40.9% of the
accepted classification for head-injury severity has yet veterans involved in the Vietnam Head Injury Study (15)
to be developed, although a number of alternate strate- had head injuries with damage to multiple lobes of the
gies have been used. Hahn et al. (10), for example, pro- brain, whereas only 7.1% of the civilian patients studied
posed a severity scale for pediatric injuries based on the by Annegers et al. (6) qualified for a diagnosis of severe
Glasgow Coma Scale (GCS) score or, in children brain injury. It only makes sense, then, that these series
younger than 3 years, on the Children’s Coma Score of wartime injuries, with their higher proportion of se-
(CCS). For these patients, mild injury meant a GCS or vere head injuries, would show greater PTS frequencies
CCS ≥13. Moderate injuries had a GCS or CCS be- than would civilian series (Tables 3 and 4). However, even
tween 9 and 12. Severe injuries had a GCS or CCS among the civilian series, the populations of patients who
of ≤8. one would expect to have had more serious injuries, such
as those requiring hospitalization or an ICU admission or
FREQUENCY OF POSTTRAUMATIC SEIZURES those with prominent posttraumatic neurologic deficits re-
quiring rehabilitation, should, and do, have higher seizure
In general, the incidence of PTSs correlates with the frequencies.
severity of the inciting injury (Tables 1 and 2). This corre-
lation between the incidence of PTSs and injury sever- Early seizures
ity explains most of the variability in the overall inci- The incidence of early seizures (usually within 1 week
dence of PTSs, a value that ranges from a low of ∼4% of injury) ranges from 2.1 to 16.9% and, in general, is cor-
to a high of 53%. Compared with series done in the civil related with the distribution of head-injury severity within
the specific group being studied. Of the patients in one se-
ries, 10% were in status epilepticus, a presentation more
TABLE 1. Frequency of posttraumatic seizures (PTSs) common in children (11).
stratified by injury severity in civilian populations
Series Injury severity Late seizures
Adults or mixed series Depending on the series, the incidence of late seizures
PTA <24 h PTA >24 h ranges from 1.9% to >30%. Like the incidence of early
(28) Early Late Early Late PTSs, the variability in this finding is likely due to vari-
2.7% 6.7% 12% 14.2% ability within the patient populations being studied, es-
Mild Moderate Severe pecially with respect to injury severity. In general, most
(7) 1.5 (SIR) 2.9 (SIR) 17.0 (SIR)
(19) 2.8% (Early) 1.7% (Early) 21.6% (Early) late PTSs occur during the first year after injury (7,11),
Pediatric series although they can also occur for many years afterward.
Mild Moderate Severe Exactly how long the increased risk of seizures per-
Early Late Early Late Early Late sists after head injury is unclear. Investigators for the
(6) 1.0% 0.2% 1.1% 1.6% 30.5% 7.4% Vietnam Head Injury Study concluded that, in their popu-
(10) 5.9% 26.9% 35.3%
lation, “. . .posttraumatic seizure incidence does not reach
SIR, standardized incidence ratio; PTA, posttraumatic amnesia. that of the general uninjured population until well after

Epilepsia, Vol. 44, Suppl. 10, 2003

14 L. C. FREY

TABLE 3. The frequencies of posttraumatic seizures (PTSs) in civilian populations

Length of Overall frequency Frequency of Frequency of Population
Reference study of PTSs early PTS late PTS characteristics
Adults or mixed series
(7) 10+ yr 4.4% 2.6% 2.1% Population based
(n = 4,541)
(19) 7+ days – 4.1% – Hospital admissions
(n = 702)
(11) 1–4 yr – 4.6% 5% Hospital admissions
(n = 1,000)
(4) 5+ yr – 16.9% 24.5% Required intensive
(n = 490) rehabilitation
Pediatric series
(20) 4–12 yr 7.03% 6.5% 1.3% Pediatric hospital
(n = 4,465) admissions
(10) 7+ mo 9.8% 9.6% – Pediatric hospital
(n = 937) admissions

15 years after injury” (17). In an initial study of the
civilian population in Olmsted County, Minnesota, PTS
risk overall did not differ significantly from baseline
risk after 5 years (6). However, with extended follow-
up of the same population of head-injured patients, the
authors concluded that, “. . .even unprovoked seizures
occurring more than 10 years after a severe traumatic
brain injury can be attributed in large part to the injury”
(7).
The exclusion of other causes of seizures is an important
factor in the accurate determination of the risk of seizures
strictly attributable to a head injury. Looking back over
the data from the Vietnam Head Injury Study, investiga-
tors thought that “neither subsequent head injury, other
encephalopathy, nor alcohol abuse played an important
role” in the occurrence of late PTSs, particularly in those
patients whose seizures began >10 years after their index
injury (18). More often, however, investigators formally
incorporated these factors into their study exclusion cri-
teria. Other important exclusions included a history of
seizures before head injury (4–7,11), known prior head in-
jury or brain damage (6–8), fatal injuries (7,8), evidence
of hypoxia, and fluid or electrolyte imbalances (10), as
mentioned earlier.
THE PEDIATRIC EXPERIENCE
The overall incidence of PTSs in children ranges from
0.2 to 9.8%. Overall, early seizures were more common
than late ones in the pediatric population: 9.3% of children
with head injuries in one series had early PTSs, whereas
only 0.2% had late PTSs (9). Early seizures in children
tended to occur earlier within the first week after injury
than they did in the adult population. In the study by Hahn
et al. (10), 94% of their patients with PTSs seized during
the first 24 h after injury.
Younger children are at proportionally increased risk
of both early and late seizures after head injury; 30.8%
of children younger than 7 years in one civilian series
had early PTSs, compared with 20% of children aged
8–16 years and 8.4% of children 16 years or older

TABLE 4. The frequencies of posttraumatic seizures (PTSs) in military series

Length of Overall frequency Frequency of Frequency of Population
Reference study of PTSs early PTSs late PTSs characteristics

World War I (29) 7–20 yr 34% – – Gunshot wounds

(n = 317)
World War II (29) 5 yr 43% – – Gunshot wounds
(n = 820)
World War II (29) 7–8 yr 28% – – Unselected
(n = 739)
Korean War (14) 8–11 yr 30% 10% within first month – Unselected
(n = 356)
Vietnam War (15) 4+ yr 33.4% 4.4% 27.9% Required neurosurgical
(n = 1,030) attention
Vietnam War (16) 4+ yr 35% 3.9% 31% Required neurosurgical
(n = 1,221) attention
Vietnam War (18) 15+ yr 53% – – Penetrating missile
(n = 421) injuries

Epilepsia, Vol. 44, Suppl. 10, 2003

 POSTTRAUMATIC EPILEPSY EPIDEMIOLOGY 15

(p < 0.0001) (4), findings similar to those of Jennett (11) TABLE 5. Independent risk factors for posttraumatic seizures
and Hendrick and Harris (20). The correlation between age
at injury and risk of PTSs is less clear in the very youngest Risk factors for early Risk factors for late
age group. In one series, early seizures were even more posttraumatic seizures posttraumatic seizures
common in patients younger than 5 years at time of in- Acute intracerebral hematoma Early posttraumatic seizures
Acute subdural hematoma, in Acute intracerebral hematoma,
jury (11). However, two other studies found no significant children especially subdural hematoma
difference in the risk of seizures in the very young (up to (in all patients)
3–5 years) (10,19). Younger age Brain contusion
Increased injury severity, Increased injury severity,
Younger children are more likely to have status epilep- including loss of consciousness including loss of consciousness
ticus as the presenting feature of their PTSs. In one or posttraumatic amnesia or posttraumatic amnesia
study, status was more than twice as common in children lasting >30 min lasting >24 h
Chronic alcoholism Age older than 65 yr at time of
younger than 5 years than in all other age groups combined injury
(p < 0.001) (11).
Higher incidences of PTSs are seen in more severely
injured children (Table 1). In general, this is true re- trials, a pooled estimate of 13.3% seized despite aggres-
gardless of the age of the child. Uniquely, however, in sive treatment regimens (22). Very little is specifically
one study, 17% of children younger than 5 years with known about the chance of remission of PTSs that begin
“trivial” injuries (no loss of consciousness, no posttrau- in childhood.
matic amnesia, no depressed skull fracture, and no ICH)
had an early seizure, compared with only 2% of all pa- RISK FACTORS FOR
tients older than 5 years (adults and children) (11), find- POSTTRAUMATIC SEIZURES
ings similar to those of Kollevold (21). Epilepsy “rarely
Early seizures
followed a trivial injury except in children under 5” (11),
The risk factors that have been found to be significant
a phenomenon that is of unclear clinical significance.
for the development of early PTSs are listed in Table 5.
The most consistent risk factor is the presence of an intrac-
NATURAL HISTORY OF erebral blood collection, which confers a ≤30% increase
POSTTRAUMATIC SEIZURES in the risk of early PTSs, regardless of the patient’s age
or other features of their injury (11,19). This increased
The lifetime total number of seizures in patients with
risk is especially true for subdural hematomas in children
PTSs is not associated with any identifiable variables such
(10). In this same age group, intraparenchymal and epidu-
as age or severity of injury, and often varies widely even
ral hematomas do not confer the same risk of early seizure
within generally homogeneous populations. For example,
development, presumably because of the lesser degree of
39% of patients in the Korean conflict veteran series had
direct cortical irritation from blood products (10).
a total of between one and three seizures during a 10-year
The second most predominant risk factor for the occur-
period of follow-up. Of the same group, however, 38%
rence of early PTSs is higher injury severity, although there
had >30 seizures (15).
is considerable lack of consistency in the use of different
Remission rates among patients with PTSs range from
markers to define subgroups of injury severity (Table 6).
25 to 40%, with higher overall remission rates reported in
This is important because many of these markers of injury
studies done after the development of effective AEDs. One
likely represent differing aspects of actual brain damage.
early study found that seizure remission was less likely in
For example, patients who respond only to pain at presen-
patients whose seizures began later after injury, especially
tation after head injury are assumed to have sustained a
if the latency to seizure onset was >4 years (11). However,
more severe injury than have those patients who are less
the burden of the other evidence suggests that no signifi-
encephalopathic (can follow commands). Patients who re-
cant relation exists between the latency to first seizure and
spond only to pain have a statistically significant increase
seizure duration or persistence (15,18), although patients
in the risk of early PTSs. However, if the severity of injury
with frequent seizures in the first year will often continue
to have frequent seizures and have a smaller chance of
seizure remission (18). TABLE 6. Commonly used clinical markers of head-injury
Most patients who will have a second unprovoked late severity
PTS do so during the first 2 years after their first late
Extent of brain damage: multilobar vs. Level of alertness
PTS. Haltiner et al. reported that up to 86% of TBI sur- single-lobe involvement on presentation
vivors with a first PTS will also have a second within the Brain-volume loss on CT scan Glasgow Coma Score
following 2 years (5). A certain percentage of PTS pa- Length of posttraumatic amnesia Depth of wound
Length of loss of consciousness Size of cranial defect
tients remain refractory to AED therapy. For example, in
the treatment arms of various anticonvulsant prophylactic CT, computed tomography.

Epilepsia, Vol. 44, Suppl. 10, 2003

16 L. C. FREY
is measured by the extent of actual brain involvement in
the same group of patients (i.e., single vs. multilobar in-
volvement), the significantly increased risk of early PTSs
no longer exists (although those patients remain at a sig-
nificantly higher risk for late seizures) (15).
In many studies, early seizures occurred 50–100% more
frequently in children than they did in adults with compa-
rable injuries (7,21). In a population study of head injury
in the Bronx, this conclusion held at all levels of injury
severity (W.A. Hauser, personal communication, 2002). In
a population study of inhabitants of Rochester, Minnesota,
however, it was true for only severe and mild injuries (6).
Younger age is not an independent risk factor for the oc-
currence of early PTSs if the incidence is adjusted for the
increased risk of seizures that exists for this population,
regardless of antecedent head injury (7).
Other risk factors that likely influence the occurrence
of early PTSs include diffuse cerebral edema (in chil-
dren), intracranial metal-fragment retention, residual focal
neurologic deficits, and depressed or linear skull fractures
(adults only).
Late seizures
The risk factors that have been found to be significant
for the development of late PTSs are listed in Table 5. In
this case, the presence of early PTSs was the most con-
sistently significant risk factor for the development of late
PTSs, although, in one study (7), the occurrence of early
seizures was not an independent risk factor in multivariate
analysis. If it is significant, the presence of early PTSs will
increase the risk of late seizures regardless of how many
seizures actually occurred during the first week after injury
(11). The relation between early PTSs and the develop-
ment of late PTSs varies based on age. Jennett (11) found
that the risk of late PTSs is not significantly increased in
children younger than 16 years who only have focal early
seizures. In another study, no children with early PTSs
were at increased risk of developing late seizures, regard-
less of their early seizure type (6).
ICH also is a risk factor for the occurrence of late PTSs
and may confer a ≤10-fold increase in risk (7). Subdu-
ral hematomas are likely responsible for most of this in-
creased risk in both children and adults. The presence of a
brain contusion was as strong of a predictor of late seizure
occurrence as was the presence of a subdural hematoma.
Markers of increased injury severity have been shown to
increase significantly the risk of late PTSs, although this
relation is inconsistent. When severe brain injury is de-
fined as multilobar injury (or worse) or loss of conscious-
ness or posttraumatic amnesia lasting >24 h, it is a signif-
icant risk factor for the occurrence of late PTSs. However,
when injury severity is measured by brain-volume loss on
computed tomography (CT) scan or by GCS, the signifi-
cance of the relation disappears, although it is likely that
these parameters will prove useful once they are used in
Epilepsia, Vol. 44, Suppl. 10, 2003
a more standardized fashion (especially a uniform period
between injury and scanning/GCS calculation).
Age older than 65 years at the time of injury is a sig-
nificant risk factor for the development of late PTSs. This
relation is especially important because elderly survivors
of TBI, even without seizures, recover more slowly and
are more likely to be permanently disabled as a result of
their injuries than are younger head injury survivors (D.A.
Arciniegas, personal communication, 2001).
Premorbid chronic alcoholism likely increases the risk
of the development of late PTSs. In one study (21), a higher
percentage of patients with chronic alcohol use had late
PTSs than did comparable patients who did not drink.
In addition, the same study suggested that chronic alco-
hol use may decrease the chance of seizure remission,
although the data were not necessarily tested for signifi-
cance. Conversely, patients with seizures after head injury
have been shown to be at higher risk for both drug and
alcohol abuse (23). The relation between alcohol use and
seizures (of any type) was studied more specifically by
Ng et al. (24), who concluded that “heavy alcohol use is
an independent, dose-related risk factor for seizures.”
Other risk factors for the development of late PTSs
include metal-fragment retention, skull fracture, residual
cortical neurologic deficits, a single CT lesion in the tem-
poral or frontal regions, and persistent focal abnormalities
on EEG >1 month after injury.
Is genetic propensity for seizures a risk factor
for posttraumatic seizures?
The role of genetic susceptibility in posttraumatic
epilepsy is far from being clearly understood. A wide
range of variability is found in individuals’ responses to
similar injuries. Some patients seize frequently after a
head injury, whereas others may seize once or not at all,
despite an almost identical injury severity. Empirically,
Caveness (15) thought that much of this variability was
likely due to “constitutional” or genetic factors regulating
response to cerebral injury. Since then, multiple authors
have attempted more formally to characterize the influ-
ence of an individual’s genes by including the presence or
absence of a family history of epilepsy in their risk-factor
analyses. The majority of these studies have found that a
family history of epilepsy is not a significant risk factor
for the development of seizures after head injury. For ex-
ample, Jennett (11) found that a family history was more
common in patients with late PTSs, but the difference was
significant only in patients younger than 16 years. In the
Vietnam Head Injury Study cohort, family history was not
a significant risk factor for either early or late PTSs (18).
Schaumann et al. (25) found no increased risk of seizures
among the parents, siblings, or offspring of patients with
PTSs. Ottman et al. (26), in their study of clinical markers
of genetic susceptibility to epilepsy, also found that the risk
of seizures among relatives of patients with posttraumatic
 POSTTRAUMATIC EPILEPSY EPIDEMIOLOGY
seizures was no higher than that of the general popula-
tion, suggesting that, ultimately, the prominent variability
in individual response to head injury is not genetically
determined.
Using risk factors to predict the occurrence
of posttraumatic seizures
Attempts have been made to use risk factors, in varying
combinations, to develop a mathematical method for pre-
dicting likelihood of seizures during various periods after
head injury (16,17,27). Although the predictions gener-
ated from these formulas do seem to match the observed
occurrences of PTSs in selected series, they have not yet
found widespread clinical use.
CONCLUSIONS
The occurrence of PTSs is a medically and function-
ally costly complication of TBI. The incidence of PTSs
ranges from 4.4 to 53%, depending on the population
being studied. Risk factors can be identified for the oc-
currence of both early and late PTSs. The presence of an
acute ICH (especially a subdural hematoma), younger age,
and higher injury severity are all risk factors for seizures
occurring early after TBI. The presence of early PTSs, an
acute ICH, a brain contusion, age older than 65 years at
the time of injury, and higher injury severity all increase
the risk of seizures occurring later after TBI.
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Epilepsia, Vol. 44, Suppl. 10, 2003