PRIMARY CARE
Primary Care
E PILEPSY
THOMAS R. BROWNE, M.D.,
AND GREGORY L. HOLMES, M.D.
A
PPROXIMATELY 2 million persons in the
United States have epilepsy,1,2 making the
prevalence of this disorder similar to that of
type 1 diabetes mellitus.3 Each year, 100,000 new
cases of epilepsy are diagnosed in the United States.1,4
Both the prevalence and the incidence of epilepsy
are dramatically higher among elderly persons than
among those who are younger.1 Thus, many primary
care physicians care for a substantial number of pa-
tients with epilepsy.
EVALUATION
Diagnosis of a Seizure Disorder
The first step in the evaluation of a patient with pos-
sible epilepsy is to determine whether the patient does
or does not have seizures. An incorrect diagnosis of a
seizure disorder can have many negative consequenc-
es for the patient, including expensive and potentially
toxic medication regimens, loss of driving privileges,
and loss of work. Disorders that must be differenti-
ated from epilepsy include migraine, syncope, transient
ischemic attack, nonepileptic seizure (psychogenic sei-
zure), the episodic dyscontrol syndrome (rage attacks),
Meniere’s disease, and movement disorders.5 In chil-
dren one must also consider breath-holding spells, pal-
lid infantile syncope, tics, night terrors, somnambu-
lism, and the long-QT syndrome.5 Once it has been
established that the patient has seizures, one must
identify the type (or types) of seizures, since therapy
differs according to the type.
Seizures are classified as partial or generalized (Table
1).5-8 Partial seizures involve only a portion of the
brain at their onset. The most common types of partial
seizures are simple partial seizures, complex partial sei-
zures, and partial seizures that are secondarily gener-
alized. The most common types of generalized sei-
zures are absence seizures and primarily generalized
tonic–clonic seizures.
Two common problems in diagnosing a seizure dis-
order are distinguishing tonic–clonic seizure from syn-
cope and distinguishing absence seizures from com-
plex partial seizures. Tonic–clonic seizure and syncope
From the Department of Neurology, Boston University School of Med-
icine, and the Neurology Service, Department of Veterans Affairs Boston
Healthcare System (T.R.B.); and the Department of Neurology, Harvard
Medical School and Children’s Hospital (G.L.H.) — all in Boston. Address
reprint requests to Dr. Browne at the Department of Neurology, Boston
University School of Medicine, 315 Albany St., C-314, Boston, MA 02118,
or at tbrowne@bu.edu.
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can both be characterized by loss of consciousness and
a fall.9 Syncope is suggested by an onset while the pa-
tient is erect and by a brief duration (10 seconds),
flaccid muscle tone during the event, pale color, cold
and clammy skin, or electrocardiographic abnormal-
ities. Tonic–clonic seizure is suggested by an onset
while the patient is asleep or awake and in any pos-
ture, a duration of one minute or longer, increased
muscle tone during the event, incontinence, biting of
the tongue, flushed color, hot and sweaty skin, ster-
torous respiration, electroencephalographic abnormal-
ities, or a family history of seizures.
Both absence and complex partial seizures may be
characterized by loss of consciousness, with or with-
out automatic behavior.10 It is often assumed that such
clinical findings indicate absence seizures in children
and complex partial seizures in adults. However, ei-
ther type of seizure can occur both in children and
in adults. Absence seizure is suggested by a short du-
ration (10 seconds), a rapid onset without warning,
very rapid recovery, or precipitation of the event by
hyperventilation; a pattern of a spike and a wave at
a frequency of 3 Hz on the electroencephalogram
provides confirmation. Complex partial seizure is sug-
gested by a duration of one minute or more, an aura,
and confusion after the event; temporal slowing or
sharp waves on the electroencephalogram provide con-
firmation.
Seizures often occur as part of an epileptic syn-
drome.5,7,8,11 An epileptic syndrome is a group of signs
and symptoms that customarily occur together.11 Iden-
tification of the syndrome helps determine the appro-
priate therapy and the prognosis. For example, juve-
nile myoclonic epilepsy is a syndrome of myoclonic
and tonic–clonic seizures that usually develop at 12
to 18 years of age.12 Patients typically have a specific
pattern of electroencephalographic abnormalities, with
no abnormalities observed on neurologic examination.
Although the prognosis for seizure control is favor-
able, lifelong treatment with antiepileptic drugs is usu-
ally necessary. Juvenile myoclonic epilepsy is a genet-
ically heterogeneous syndrome involving a molecular
defect that remains unknown. Many of the epileptic
syndromes have a genetic basis, and the genes and
gene products responsible for these syndromes are be-
ing identified at a rapid rate.13
Diagnosis of the Underlying Cause
Seizures are a symptom of an underlying disorder,
which may be genetic, traumatic, metabolic, infectious,
malignant, or pharmacologic (i.e., drug intoxication
or withdrawal). In many cases, the underlying disorder
must be identified and treated in order to control the
seizures and prevent further brain dysfunction.
History
The history obtained from the patient and witness-
es is often the most important information in estab-
 The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne

TABLE 1. PRINCIPAL TYPES OF SEIZURES.

ELECTROENCEPHALOGRAPHIC
TYPE OF SEIZURE CLINICAL FEATURES FEATURES*

Partial
Simple partial seizures (focal)
Complex partial seizures (temporal
lobe or psychomotor)
Secondarily generalized partial sei- Seizures may begin with motor, sensory, au- Focal slowing or sharp-wave ac-
zures (tonic–clonic, or grand mal)
Generalized
Absence seizures (petit mal)
Primarily generalized tonic–clonic
seizures (grand mal)
Signs and symptoms may be motor, sensory, Focal slowing or sharp-wave ac-
autonomic, or psychic, depending on the tivity, or both
location of the electrical discharge; con-
sciousness is not impaired
Seizure may begin with no warning or with Focal slowing or sharp-wave ac-
motor, sensory, autonomic, or psychic tivity, or both
signs or symptoms; consciousness is im-
paired; automatisms (automatic acts of
which the patient has no recollection) may
occur; seizure is often followed by a peri-
od of confusion
tonomic, or psychic signs or symptoms; tivity, or both
consciousness is lost, with tonic increase in
muscle tone; subsequent rhythmic (clonic)
jerks subside slowly; patient is comatose
after seizure and recovers slowly; tongue
biting or incontinence, or both, may occur
Seizure begins rapidly, with a brief period of Spike–wave pattern (3 Hz)
unresponsiveness (average, 10 seconds)
and rapid recovery; there may be increased
or decreased muscle tone, automatisms, or
mild clonic movements. Seizure can be
precipitated by hyperventilation; age at
first seizure, 3–20 yr
Loss of consciousness occurs without warn- Spike–wave pattern (3–5 Hz)
ing or is preceded by myoclonic jerks; clin-
ical features are similar to those of a sec-
ondarily generalized partial seizure

*The electroencephalographic features listed are those observed on routine electroencephalography during which a sei-
zure does not occur.

lishing the diagnosis of a seizure disorder. One should
begin by asking the patient and observers to describe
in detail the events before, during, and after the sei-
zure. Partial seizures may begin with motor, sensory,
autonomic, or psychic symptoms.6 Generalized sei-
zures may begin with bilateral myoclonic jerks. Once
started, a seizure may cause an alteration of conscious-
ness; tonic or clonic movements, or both; tongue bit-
ing; incontinence; automatic behavior; and postictal
behavior. A history of minor types of seizures (e.g.,
myoclonic or absence seizures) in a person presenting
with a possible tonic–clonic seizure helps establish the
diagnosis of a seizure disorder. This information may
not be obtained from the history unless specific ques-
tions are asked.
To determine the cause of a seizure, the clinician
should determine whether there is a family history of
epilepsy or a personal history of head trauma, birth
complications, febrile convulsions, middle-ear or si-
nus infections, alcohol or drug abuse, or symptoms
of cancer.5
Physical Examination
A physical examination is performed to look for
signs of disorders associated with epilepsy, including
signs of head trauma, infections of the ears or sinuses
(which may spread to the brain), congenital abnormal-
ities (e.g., tuberous sclerosis), focal or diffuse neuro-
logic abnormalities, alcohol or drug abuse, and cancer.
Hyperventilation for three minutes will trigger a sei-
zure in most patients with untreated absence seizures.
Electroencephalographic Studies
The electroencephalogram provides three types of
information: confirmation of the presence of abnormal
electrical activity, information about the type of sei-
zure disorder, and the location of the seizure focus.14-18
It is customary to perform electroencephalographic
studies 48 hours or more after a suspected seizure, be-
cause obtaining an electroencephalogram shortly af-
ter a seizure may yield misleading findings. The elec-
troencephalogram should include recordings during
sleep, photic stimulation, and hyperventilation, be-
cause certain types of paroxysmal activity are most like-
ly to occur under these conditions.
In approximately 50 percent of patients who have
epilepsy, a single electroencephalogram shows no ab-
normalities. If the electroencephalographic findings
are normal and the suspicion of epilepsy is high, an-
other electroencephalogram should be obtained, this

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 PRIMARY CARE
time with the use of special (temporal and sphenoidal)
electrodes, after the patient has been deprived of sleep.
This approach may reveal abnormalities. If no abnor-
malities are detected on these two electroencephalo-
grams, prolonged electroencephalography and video
monitoring may reveal evidence of a clinical event or
paroxysmal activity that establishes the diagnosis of a
seizure disorder.15-18 In approximately 10 percent of
persons with true seizures, multiple electroencephalo-
graphic studies show no abnormalities.
Laboratory Tests and Neuroimaging
The studies performed to determine the cause of
a newly diagnosed seizure disorder include electrolyte
and liver-function tests in adults (such screening is not
routinely performed in children14), electroencephalog-
raphy in the waking and sleeping states, and magnetic
resonance imaging (MRI) or computed tomography
(CT). MRI scanning is preferable to CT because it is
more likely to reveal small lesions such as tumors or
mesial temporal sclerosis.14,19,20 A screening test for
toxic substances is performed if alcohol or drug abuse
or withdrawal is suspected, and a lumbar puncture is
performed if infection or cancer is suspected.
The American Academy of Neurology has published
practice guidelines for neuroimaging studies (MRI and
CT) in patients who have had a first seizure.14,19,20 Neu-
roimaging should be performed immediately in pa-
tients who may have a serious structural lesion. These
include patients who have new focal deficits, a persist-
ently altered mental status (with or without intoxica-
tion), fever, recent trauma, persistent headache, or a
history of cancer or anticoagulant therapy and those
who may have the acquired immunodeficiency syn-
drome.19,20 Emergency neuroimaging should also be
performed in children with a postictal focal deficit or
altered mental status that does not resolve rapidly.14 In
addition, neuroimaging on an emergency basis should
be considered if the patient is over 40 years old or has
had a partial seizure.
Nonemergency neuroimaging studies should be
considered for an adult or child in whom no cause
of the seizure has been determined, in a child with a
seizure of focal onset, in a child under the age of one
year who has had a nonfebrile seizure, and in a child
with unexplained cognitive or motor dysfunction or
abnormalities on neurologic examination.14,19,20
Diagnostic Formulation and Treatment Plan
It is usually possible to diagnose a seizure disorder
by using a combination of information from the his-
tory, physical examination, and electroencephalogram.
If the presence of a seizure disorder or its type can-
not be established, one should attempt to obtain fur-
ther information about the event (e.g., from additional
witnesses), perform repeated electroencephalographic
studies under the conditions noted above, or both.
Once the type of seizure disorder has been estab-
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lished, an antiepileptic drug appropriate for that type
is administered if the patient has had two or more sei-
zures. A patient who has had a single seizure is treated
with medication if there are one or more risk factors
for recurrent seizures, such as evidence of a structur-
al lesion, electroencephalographic abnormalities (Ta-
ble 1), a seizure of the partial type, or a family his-
tory of seizures.21 Otherwise, a patient who has had
a single seizure is usually monitored but not given
medication.21
If the diagnosis is uncertain after all the above steps
have been taken, one must act on the basis of the avail-
able information. A trial of an antiepileptic drug is be-
gun if the information strongly suggests that more
than one seizure has occurred. Otherwise, follow-up
without medication is the plan.
In most states, licensed drivers are required to re-
port a seizure condition to the Department of Mo-
tor Vehicles at the time of the diagnosis, and physi-
cians may not report a patient’s condition without
written permission from the patient. However, there
are exceptions. A summary of the requirements in
each state is available from the Epilepsy Foundation
(http://www.efa.org/).
SELECTION AND ADJUSTMENT
OF MEDICATIONS
Treatment is started with an average dose of a first-
line antiepileptic drug. First-line drugs are those that
are most effective and least toxic. For partial seizures,
first-line drugs include carbamazepine, divalproex so-
dium, oxcarbazepine, and phenytoin.22-25 On the basis
of comparative trials, carbamazepine, oxcarbazepine,
and phenytoin appear to be the most effective and least
toxic drugs for the initial treatment of partial sei-
zures.22-25 All three drugs have similar efficacy. Oxcar-
bazepine may have less initial toxicity than carbamaz-
epine or phenytoin.25
Ethosuximide and divalproex sodium are the usual
first-line drugs for absence (petit mal) seizures.26 Both
drugs are effective in controlling absence seizures,27
but ethosuximide has fewer side effects. However, only
divalproex sodium is effective against tonic–clonic sei-
zures, which often accompany absence seizures. The
usual first-line drugs for primarily generalized tonic–
clonic seizures are divalproex sodium and phenyto-
in.24,26 The dosages for these drugs are summarized
in Table 2.
If the average dose of a first-line drug controls the
seizures and does not have side effects, no adjustment
is needed. However, it is often necessary to adjust the
dose of an antiepileptic drug because of toxicity or in-
adequate control of seizures, or both.
The therapeutic range of plasma drug concentra-
tions, which is only a rough guide for determining the
appropriate dose, has been established for some anti-
epileptic drugs.28,29 It is important, however, to treat
the patient, not the plasma drug concentration. If the
 The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne

TABLE 2. USUAL DOSAGES OF ANTIEPILEPTIC DRUGS IN PATIENTS 16 YEARS OF AGE OR OLDER.*

THERAPEUTIC
RANGE OF
STARTING MAINTENANCE PLASMA
DRUG DOSE DOSE FREQUENCY DOSE INCREASE DOSE CONCENTRATIONS

mg/day mg/day µg/ml

Carbamazepine (Carbatrol, Te- 400 Carbatrol or Tegretol- 200 mg/day at 1-wk intervals 600–1200 4–12
gretol, Tegretol-XR) XR, twice a day;
Tegretol or generic,
three times a day
Divalproex sodium (Depakote) 500–1000 Twice a day 250 mg/day at 1-wk intervals 1000–3000 50–150
Ethosuximide (Zarontin) 500 Twice a day 250 mg/day at 1-wk intervals 1000–2000 40–120
Gabapentin (Neurontin) 900 Three times a day 300 mg/day at 24-hr intervals 900–3600 Not established
Lamotrigine† (Lamictal) 50 Twice a day 50 mg/day at 2-wk intervals‡ 300–500 Not established
Levetiracetam (Keppra) 1000 Twice a day 1000 mg/day at 2-wk intervals 1000–3000 Not established
Oxcarbazepine (Trileptal) 600 Twice a day 600 mg/day at 1-wk intervals 600–2400 Not established
Phenobarbital 90 Daily 30 mg/day at 4-wk intervals 90–120 10–40
Phenytoin (Dilantin) 300 Daily 100 mg/day at 4-wk intervals§ 300–500 10–20
Primidone (Mysoline, 100–125 Three times a day Days 1–3, 100–150 mg daily at 750–1000 5–12
Neurosyn) bedtime; days 4–6, 100–125
mg twice a day; days 7–9,
100–125 mg three times a day;
day 10, 250 mg three times a
day
Tiagabine (Gabitril) 4 Twice a day to four 4–8 mg/day at 1-wk intervals 32–56 Not established
times a day
Topiramate (Topamax) 25–50 Twice a day 25–50 mg/day at 1-wk intervals 200–400 Not established
Zonisamide (Zonegran) 100 Twice a day 100 mg/day at 2-wk intervals 400–600 Not established

*Data are from Browne and Holmes.5 Information on dosages for younger patients is also available from this source.
†The information shown is for persons who are taking lamotrigine in combination with an enzyme-inducing antiepileptic drug (carbamaz-
epine, phenobarbital, phenytoin, or primidone) and who are not taking valproic acid. For persons who are not taking an enzyme-inducing
antiepileptic drug or who are taking valproic acid, the dose schedule is different. Consult the package insert.
‡After four weeks, the daily dose can be increased by 100 mg every two weeks.
§The dose should be increased at a rate of 30 to 50 mg per day at four-week intervals when the phenytoin plasma concentration is higher
than 10 µg per milliliter.

concentration is at the upper end of the therapeutic Initial Toxicity

range, the patient is still having seizures, and the drug
has no side effects, the dose should be increased. Plas-
ma drug concentrations within the therapeutic range
may have toxic effects. In some patients, seizures are
controlled with plasma drug concentrations that are
below the therapeutic range.
Titration of the dose of phenytoin deserves special
attention because phenytoin has nonlinear pharma-
cokinetics.30 When the plasma phenytoin concentra-
tion is higher than 10 µg per milliliter, an increase
in the dose results in a disproportionate increase in
the plasma concentration, which can lead to toxic ef-
fects; conversely, a decrease in the dose results in a
disproportionate decrease in the plasma concentra-
tion, which can lead to breakthrough seizures. The
practical solution to this problem is to increase or
decrease the dose of phenytoin by only 30 to 50 mg
per day when the plasma concentration is higher than
10 µg per milliliter.
Sedation, dizziness, ataxia, headache, and nausea
are common during the initiation of treatment with
antiepileptic drugs.22,23,31 The toxic effects can be man-
aged by reducing the dose by 25 to 50 percent and
waiting two weeks for tolerance to develop. Treatment
with the initial dose or a regimen of gradually in-
creased doses can then be resumed.
Most antiepileptic drugs can cause a rash during the
first weeks of therapy.31,32 Although the rash usually
resolves without sequelae, in some cases it progresses
to the Stevens–Johnson syndrome or other serious
conditions. Rashes caused by antiepileptic drugs are
erythematous maculopapular or morbilliform erup-
tions, often beginning on the trunk, face, or upper
arms. Danger signs — indicating the risk of a severe
reaction — include a temperature that exceeds 40°C,
exfoliation, mucosal lesions, facial edema, confluent
erythema, skin pain, palpable purpura, skin necrosis,
lymph-node enlargement, and asthmatic symptoms.

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 PRIMARY CARE
If possible, a patient with a rash should be seen im-
mediately by a physician in order to rule out a cause
that is unrelated to the antiepileptic drug (e.g., tinea
infection or heat rash) and to check for signs that the
patient is at risk for a severe reaction. If the rash ap-
pears to be associated with the antiepileptic drug or if
the rash cannot be observed by a physician because
of logistic problems, the dose should be rapidly ta-
pered, in the absence of signs that a severe reaction
may occur. If such signs are present, the drug should
be stopped. Gabapentin,33 divalproex sodium,34 and
levetiracetam,35 which rarely cause rashes, can be pre-
scribed to control seizures while the drug that has
caused the rash is being withdrawn.
Toxic Effects during Long-Term Therapy
Neurotoxic effects are common during long-term
treatment with antiepileptic drugs.22,23,31 If the seizures
are fully controlled and neurotoxic effects are present,
the dose of the antiepileptic drug can be reduced. If
the seizures are not fully controlled and neurotoxic
effects are present, the patient should be given anoth-
er antiepileptic drug.
Inadequate Seizure Control
If the seizures are not controlled with the initial
dose of a first-line drug and if there is no evidence of
serious toxicity, the dose of the drug should be sys-
tematically increased until the seizures are controlled
or until side effects preclude further increases in the
dose. If the maximal tolerated dose of the first-line
antiepileptic drug has been used and the seizures are
still not controlled, another first-line antiepileptic drug
or a second-line antiepileptic drug should be added.
A number of drugs can be used as second-line thera-
py for the most common types of seizure, which are
partial seizures (Tables 2 and 3).25,33-39 One practical
way to deal with the large number of available drugs
is to select one for maximal safety and one for max-
imal efficacy.
When starting a second antiepileptic drug, we usu-
ally continue to administer the first antiepileptic drug
to provide protection until a full dose of the second
drug is being administered. Once the second drug is
being given at a full dose, there are strong arguments
for gradually withdrawing the first drug (according
to the guidelines discussed in the next section). The
advantages of this approach include reduced risks of
idiosyncratic reactions, drug interactions, teratogenic-
ity, and other adverse events.40 However, if two-drug
therapy completely controls seizures, caution is re-
quired in removing the first drug because of the risk
of recurrent seizures, which can lead to loss of driv-
ing privileges or employment.
In recent years, regimens of two or more antiepi-
leptic drugs were generally used for the treatment of
partial seizures only after two or more first-line drugs
given as monotherapy had been ineffective. Since most
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of the newer antiepileptic drugs for partial seizures
(Table 3) are approved by the Food and Drug Admin-
istration only as adjunctive therapy, however, there has
been increased use of two-drug regimens that consist
of one first-line drug and one of the newer second-
line drugs. These two-drug regimens have been fairly
effective and reasonably safe.25,33-39,41
DISCONTINUING THERAPY
Once antiepileptic-drug therapy has been initiated,
it is maintained for two or more years, even if the pa-
tient is free of seizures. If after two years of therapy the
patient remains free of seizures, withdrawal of the an-
tiepileptic drug should be considered. The disadvan-
tages of continuing treatment indefinitely include the
risks of side effects, drug interactions, and teratogen-
icity, as well as the costs of the therapy.
The risk of recurrent seizures is approximately 25
percent among patients without risk factors and more
than 50 percent among those with risk factors.42,43
Approximately 80 percent of recurrences occur with-
in four months after a regimen of tapered doses has
been initiated, and 90 percent occur within the first
year.42,43 Driving and other potentially dangerous ac-
tivities should be prohibited for at least the first four
months after the start of drug withdrawal.43
Factors associated with a high risk of recurrent sei-
zures include a known structural lesion, electroenceph-
alographic abnormalities, the onset of the seizure dis-
order during adolescence, neurologic abnormalities,
and severe epilepsy (i.e., a history of frequent seizures
or seizures that have been difficult to control, requir-
ing more than one antiepileptic drug).42,43 Factors as-
sociated with a low risk of recurrent seizures include
idiopathic seizures, normal findings on the electroen-
cephalogram, the onset of the disorder in childhood,
the absence of neurologic abnormalities, and seizures
that have been easily controlled with one antiepileptic
drug.42,43
The decision about whether to stop treatment must
be individualized. The following factors should be
weighed: the probability of recurrent seizures, the con-
sequences of a recurrence (e.g., loss of the patient’s
driver’s license), and the advantages of discontinuing
medication. If the decision is made to discontinue an-
tiepileptic therapy, the drug (or drugs) should be with-
drawn slowly in order to reduce the risk of withdrawal-
associated seizures.42-44 One approach is to reduce the
daily dose by 25 percent every two to four weeks.44
Rapid withdrawal of a benzodiazepine or a barbiturate
is particularly likely to precipitate seizures.
WHEN TO SEEK NEUROLOGIC
CONSULTATION
Refractory Status Epilepticus
Status epilepticus is a condition in which the patient
has more than one seizure and does not fully recover
 The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne

TABLE 3. ADJUNCTIVE MEDICATIONS FOR PARTIAL SEIZURES.*

INTERACTIONS
RESPONSE WITH OTHER FREQUENCY
DRUG RATE† TOXICITY DRUGS OF ADMINISTRATION
SERIOUS MINOR

Divalproex sodium (Depakote) 30–40 Yes Yes Yes Twice a day

Gabapentin (Neurontin) 25–30 No Occasional No Three times a day
Lamotrigine (Lamictal) 30–40 Yes Occasional Occasional Twice a day
Levetiracetam (Keppra) 35–40 No Occasional No Twice a day
Oxcarbazepine (Trileptal) 30–50 Yes Yes Yes Twice a day
Phenobarbital NA Occasional Yes Yes Daily
Primidone (Mysoline, Neurosyn) NA Yes Yes Yes Three times a day
Tiagabine (Gabitril) 20–30 Yes Yes Yes Twice a day or three
times a day
Zonisamide (Zonegran) 25–30 Yes Yes Yes Twice a day

*Data are from Browne and Holmes.5

†The response rate denotes the percentage of patients with at least a 50 percent reduction in the frequency of partial
seizures. The data are from separate studies that involved only adults and that differed in the methods used. The results
may therefore not be strictly comparable and may not apply to children. NA denotes not available from recent, controlled
studies.

between seizures.45,46 The most common form of this
disorder is tonic–clonic status epilepticus, which be-
gins as a series of tonic–clonic seizures (phase I).46
Tonic–clonic status epilepticus is usually managed
by a regimen of intravenous diazepam or lorazepam
plus intravenous phenytoin or fosphenytoin.45,47 If this
regimen fails to control the seizures, the patient is at
risk for prolonged seizures and brain damage, often in
the form of phase II, or subtle, status epilepticus.46
Patients with phase II status epilepticus are unrespon-
sive and sometimes have myoclonus or focal motor ac-
tivity. A characteristic series of electroencephalographic
changes accompanies phase II status epilepticus, and
an electroencephalogram must be obtained to confirm
the diagnosis. Phase II status epilepticus is a dangerous
condition that is difficult to treat.45-47
Other Conditions
Persons with prolonged confusion, agitation, or dis-
orientation after a seizure may have absence or com-
plex partial status epilepticus. Patients who have had
more than one seizure within a period of hours are
at risk for status epilepticus. A change in the type of
seizure may indicate that the patient has a progressive
or new brain lesion. Recent changes in medications
may precipitate seizures through drug interactions or
other mechanisms.
Routine Consultations
Neurologic consultation may also be useful if the
diagnosis is uncertain, if two or more antiepileptic
drugs have failed to control seizures, if the patient is
considering becoming pregnant, or if the patient has
a form of epilepsy that is particularly difficult to treat,
such as the Lennox–Gastaut syndrome or infantile
spasms.
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of epilepsy: principles and practice. 2nd ed. Baltimore: Williams & Wilkins,
1997:165-72.
2. Hauser WA, Hesdorffer DC. Epilepsy: frequency, causes and conse-
quences. New York: Demos, 1990.
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