INVITED REVIEW ARTICLE
Frontal Lobe Seizures
Ritu Bagla, MD and Christopher T. Skidmore, MD
Background and Objective: Frontal lobe epilepsy is the second most
common localization-related or focal epilepsy. Frontal lobe seizures
are challenging to diagnose as the clinical manifestations are diverse
due to the complexity and variability of the patterns of epileptic
discharges, and the scalp electroencephalograph (EEG) can often be
normal or misleading. This review focuses on the clinical and EEG
features of seizures arising from the frontal lobe.
Review Summary: The clinical manifestations in patients with frontal
lobe epilepsy are varied. Frontal lobe seizures can be divided into
perirolandic, supplementary sensorimotor area, dorsolateral, orbito-
frontal, anterior frontopolar, opercular, and cingulate types. Seizures
originating from the perirolandic and supplementary sensorimotor
areas are clinically distinct, characterized by motor activity or
asymmetric tonic posturing with preserved awareness. Seizures arising
from dorsolateral, orbitofrontal, frontopolar, and cingulate areas are
not as well characterized and have more variable clinical manifesta-
tions. Scalp EEG recording is sometimes helpful in localization but is
usually normal or misleading in frontal lobe epilepsy. The treatment is
similar to other localization-related or focal epilepsies. Medications are
the first line of therapy, and surgery is considered for patients who fail
to respond to medications. The surgical outcome in frontal lobe
resections is less favorable than in anterior temporal lobectomies due
to the challenge in locating the epileptogenic zone and the presence of
functional areas (eloquent cortex) that can limit the resection.
Conclusions: Frontal lobe seizures are characterized by diverse
behavioral manifestations. Only a few well-described frontal lobe
syndromes exist. The variety of clinical manifestations reflects both the
varying sites of seizure origin and propagation routes that seizures may
take. Although this review provides a framework for the understanding
of these seizures, one should remain cautious in diagnosing seizure
localization based on clinical or EEG description. Only a few patients
have well-described syndromes and can be diagnosed with confidence.
For most patients, new diagnostic methods and genetic testing may
help improve our ability to diagnose and treat the conditions discussed
in this study.
Key Words: frontal lobe, epilepsy, seizures, extratemporal
(The Neurologist 2011;17:125–135)
T here has been a lot of interest in frontal lobe epilepsy over
the past decade. The interest is due to the complex nature
of its associated behavioral manifestations. It is useful to
divide frontal lobe epilepsy into syndromes to characterize the
epileptogenic zone and potentially determine if surgery can be
done to eliminate seizures in medically refractory patients. The
prevalence of frontal lobe seizures is not known due to limited
From the Jefferson Comprehensive Epilepsy Center, Thomas Jefferson
University, Philadelphia, PA.
Reprints: Christopher T. Skidmore, MD, Jefferson Comprehensive
Epilepsy Center, Thomas Jefferson University, 900 Walnut Street,
Suite 200, Philadelphia, PA 19107. E-mail: christopher.skidmore@
jefferson.edu.
Copyright r 2011 by Lippincott Williams & Wilkins
ISSN: 1074-7931/11/1703-0125
DOI: 10.1097/NRL.0b013e31821733db
The Neurologist  Volume 17, Number 3, May 2011
epidemiologic data. In a prospective community-based study
of 160 patients with localization-related epilepsy, 36 or 22.5%
were frontal, 43 or 27% were temporal, 9 or 5.6% were
frontotemporal, 10 or 6.3% were parietal, 52 or 32.5% were
central, and 10 or 6.3% were occipital.1 In the Montreal
surgical series, temporal lobe epilepsy represented 56%,
frontal lobe 18%, central or sensorimotor 7%, parietal 6%,
and occipital 1% of 2177 patients,2 but this does not reflect
prevalence. Seizures arising from frontal lobe may start at any
age, with both sexes equally affected.
FRONTAL EPILEPTIC SYNDROMES
The most common idiopathic benign epilepsy in child-
hood is benign childhood epilepsy with centrotemporal spikes
or Rolandic epilepsy, first described by Loiseau and Beaussant
in 1958.3 The prevalence of this condition is 15% of all
childhood epilepsy. It is among the epilepsies in the 1 to 15
years age group and has a male predominance (B60% male).
The defining features are clinical manifestations emanating
from the lower part of the precentral or postcentral gyri, onset
between 3 and 13 years of age, normal neurologic examina-
tion, development and cognitive skills, and centrotemporal
spikes. The ictal behavior consists of simple partial seizures
with hemifacial or oropharyngeal sensorimotor symptoms or
speech arrest; nighttime seizures may secondarily generalize.
The interictal electroencephalograph (EEG) shows centrotem-
poral spikes, which are high amplitude sharp and slow wave
complexes which have a maximum negative potential at C3/T3
and C4/T4. They are commonly bilateral, occur independently,
and increase in rate of occurrence during sleep (Fig. 1). The
spikes have a horizontal dipole with maximum electronega-
tivity in centrotemporal regions, and positivity in the frontal
regions.4 Video-EEG monitoring is rarely indicated in these
children. Benign childhood epilepsy with centrotemporal
spikes is genetically determined but heterogeneous in its
manifestations. There is evidence for linkage to a region on
chromosome 15q14.5 The prognosis is excellent with remis-
sion within 2 to 4 years of onset and before the age of 16 years.
The risk of having recurrent seizures after remission is 1% to
3%, similar to that of the normal population.
Autosomal dominant nocturnal frontal lobe epilepsy, with
a penetrance of 69%, was recently described in 5 families with
47 affected individuals.6 Seizures occur in clusters, are brief,
nocturnal, and have predominantly motor manifestations of
hyperkinetic or tonic activity. Age of onset is in the first or
second decade in the majority of cases; however unlike benign
childhood epilepsy with centrotemporal spikes, the seizures
persist through adult life. The interictal EEG is usually normal,
and the ictal EEG can show frontally predominant sharp and
slow wave discharges. Video-EEG monitoring remains invalu-
able in differentiating this syndrome from parasomnias,
psychogenic disorders, nocturnal paroxysmal dystonia, dyski-
nesias, and other medical conditions. Autosomal dominant
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Bagla and Skidmore
FIGURE 1. A and B, Centrotemporal spikes in a patient with benign Rolandic epilepsy. The spikes have a horizontal dipole with
maximum electronegativity in centrotemporal regions, and positivity in the frontal regions.
nocturnal frontal lobe epilepsy is not “benign” as seizures
persist through adult life.
In 1895, Kozhevnikov7 described epilepsia partialis
continua (EPC) as a disorder of persistent localized motor
seizures that result from focal cortical encephalitis. Rasmus-
sen’s encephalitis and malformations of cortical development
are the main causes in children; however, there are many other
causes, including vascular, demyelinating, neoplastic lesions,
infections (such as human immunodeficiency virus), Creutz-
feldt-Jakob disease, mitochondrial disorders (ie, myoclonic
epilepsy with ragged red fibers), and metabolic disorders such
as nonketotic hyperglycemia. EPC is thought to have a cortical
origin and is defined by the occurrence of rhythmic or
semirhythmic muscular contractions that remain localized to 1
part of the body and persist for hours, days, or even years.
Onset occurs at any age, with both sexes equally affected. The
ictal EEG can be normal. In a study of 32 cases, the most
common EEG finding was regional spiking.8 Jerk-locked back
averaging, somatosensory-evoked potentials and sequential
EMG can help differentiate EPC from noncortical disorders
such as hemifacial spasm. The prognosis depends on the cause,
but is usually poor. All patients with EPC should be carefully
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The Neurologist  Volume 17, Number 3, May 2011
evaluated for an underlying cause as the treatment may be
correction of a metabolic defect or curative resective surgery in
refractory cases.
Other inherited forms of benign partial epilepsies have
been described but are less well characterized.9 Benign focal
epilepsy in infants with central and vertex spikes and waves
during sleep is characterized by behavioral arrest or focal tonic
seizures, and central and vertex spikes which are not specific to
this syndrome.10 Patients with benign childhood focal seizures
associated with frontal or midline spikes have onset of
complex partial seizures with automatisms or tonic seizures
by the age of 10 years, midline spikes and focal abnormalities
in the frontal lobe.11 So far these partial epilepsies have been
associated with a benign course, but need to be better
characterized. Ictal recording data are limited as well.
PATHOLOGY
The causes of symptomatic extratemporal lobe epilepsies
are diverse and include neoplasm, trauma, vascular insults,
malformations of cortical development (dysplasia, neurofibro-
matosis, tuberous sclerosis), infections, inflammatory disease,
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inborn errors of metabolism, and systemic causes (eg, celiac cingulate cortex, as well as the depths of sulci in the frontal
disease). Cortical malformations often require high-resolution lobe are inaccessible to surface electrodes. In many cases, the
magnetic resonance imaging (MRI) scan to be visualized12; seizure generator may be too small to be detected on the
some nonpopulation-based studies report these as the most surface. Epileptiform discharges recorded on the scalp EEG
common cause of uncontrolled seizures of extratemporal can be falsely localized and represent spread to another region
origin.13–15 A recent surgical series of 70 patients with frontal or lobe, or even falsely lateralized if an obliquely oriented
lobe epilepsy reported dysplasias in 41% of patients with dipole projects activity to the opposite hemisphere. The
abnormal MRI and in 17% of patients with normal MRI; in presence of epileptiform discharges in multiple lobes or
this series, 19% of patients had tumors, 3% had vascular bilateral discharges could be misleading and imply a large
malformations, and 10% were cryptogenic based on MRI and epileptogenic network. Unlike temporal lobe complex partial
surgical pathology.14 In another surgical series of 25 patients seizures, the scalp ictal recording may not be associated with a
who underwent frontal lobe surgery, 32% of patients had dys- clear EEG correlate in 30% of patients.16,21,22
plasias, and 20% had low-grade neoplasms, with 4 gang- Interictal epileptiform abnormalities are present in most
liogliomas and 1 dysembryonic neuroepithelial tumor.13 patients with frontal lobe epilepsy; however, they are usually
not restricted to the frontal lobe. Generalized spike and wave,
bilaterally synchronous frontal spikes or secondary bilateral
SEIZURE SEMIOLOGY AND synchrony, and ipsilateral and contralateral temporal lobe
ELECTROENCEPHALOGRAPHIC spikes can be present in addition to frontal epileptiform
CHARACTERISTICS IN FRONTAL LOBE EPILEPSY discharges. Lateralized discharges usually indicate which
Frontal lobe seizures are challenging to diagnose and can hemisphere is abnormal.16,21 Secondary bilateral synchrony
be mistaken for nonepileptic events, such as psychogenic is more likely to occur with mesial parasagittal, orbitofrontal,
seizures, parasomnias, and movement disorders. The clinical or cingulate foci,22–24 and is rare in refractory temporal lobe
manifestations are diverse and none are absolutely specific for epilepsy.16 The ictal scalp recording may be less useful in
1 region in the frontal lobe with the possible exception of focal localizing frontal lobe seizures than the interictal recording.
clonic jerking. Moreover, the first behavioral change from The onset is not infrequently obscured by muscle artifact, or
seizures that arise in clinically silent regions occurs only after may show general attenuation of amplitude and no definite
spread of the ictal discharge to an eloquent cerebral area (ie, ictal discharge.16,22 Seizure onset can be localized in about
motor cortex or Broca’s area). 30% of patients, but like interictal discharges, sometimes to the
Many types of frontal lobe seizures have features that opposite hemisphere or temporal lobe. The most common ictal
distinguish them from temporal lobe seizures. Frontal lobe pattern is nonlocalized with widespread, sometimes bilateral,
seizures often occur during sleep, can cluster and produce early changes with rapid spread to other regions.18,21,25–27
motor manifestations with vocalizations (Table 1).16 Approxi-
mately 50% of patients who had surgical evaluations had an
aura and typically brief seizures (10 to 30 s) with minimal or
TABLE 2. Clinical Manifestations of Frontal Lobe Syndromes
no postictal confusion. Kotagal et al17 compared the behavior
in patients with mesial temporal lobe epilepsy to patients with Location Ictal Behavior
frontal lobe epilepsy, and found that repetitive, proximal upper Perirolandic or primary Focal motor seizures with or without
extremity movements, complete loss of consciousness, com- motor Jacksonian march
plex motor, and hypermotor (large repetitive movements of the Speech arrest or dysphasia
proximal musculature, ie, bicycling movements) activity were Vocalization
more common in frontal lobe seizures. Supplementary Focal tonic or asymmetric tonic
Scalp EEG recording is sometimes helpful in localization sensorimotor posturing
but can be misleading in frontal lobe epilepsy. Studies in Versive movements of head and eyes
patients with refractory frontal lobe epilepsy have shown few Speech arrest
Vocalization
patients have localized interictal epileptiform discharges, and Dorsolateral Focal tonic or clonic activity
only 30% to 40% of patients evaluated with intracranial EEG Versive movements of head and eyes
have localized ictal onsets.18–20 The orbitofrontal, mesial and Speech arrest or dysphasia
Orbitofrontal Complex motor automatisms
Olfactory hallucinations and illusions
TABLE 1. Ictal Behavior of Frontal Lobe Seizures Autonomic features
Percentage Anterior frontopolar Versive movements of head and eyes
Forced thinking
Behavior (No. Patients) Initial loss of contact or “absence like”
Early motor 94 (15/16) Speech or motor arrest
Vocalization 63 (10/16) Opercular Mastication, salivation, swallowing,
Aura 56 (9/16) laryngeal symptoms
Nocturnal tendency 38 (6/16) Speech arrest or dysphasia
Tonic posturing 38 (6/16) Epigastric aura, fear
Tendency to cluster 50 (8/16) Autonomic features
Secondary generalization 63 (10/16) Facial clonic activity
Complex bilateral motor automatisms 44 (7/16) Gustatory hallucinations
Catamenial exacerbation 6 (1/16) Cingulate Fear
Oroalimentary automatisms 0 (0/16) Vocalization
Prolonged ictal state (excluding convulsions) 0 (0/16) Emotional or mood changes
Complex motor automatisms
Reproduced with permission from Neurology. 1995;45:780–787. Autonomic features

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Bagla and Skidmore The Neurologist  Volume 17, Number 3, May 2011

Frontal lobe seizures can be divided into perirolandic,
supplementary sensorimotor area, dorsolateral, orbitofrontal,
anterior frontopolar, opercular, and cingulate types (Table 2).28
Perirolandic seizures are characterized by motor activity which
typically starts unilaterally in the face, then spreads to the arm,
followed by speech arrest and eye blinking, with preservation
of consciousness.29 The behavior is a result of activation of the
primary motor cortex or Brodman area 4.30 Figure 2 shows an
example of a focal motor seizure in a 31-year-old, left-handed
man with refractory perirolandic seizures for 2 years. He
awakens from sleep with a choking sensation and no impair-
ment in consciousness. MRI and interictal EEG are normal.
The ictal scalp EEG shows only muscle artifact with no seizure
discharge apparent. With intracranial recording, the seizures
localized to the throat motor area in the right frontal opercular
cortex.
Supplementary motor seizures are clinically distinct
because of tonic posturing of 1 or more extremities on both
sides (mainly proximal muscles affected) and preserved
awareness. They are brief (<30 s), frequent, may occur only
during sleep, and can be preceded by a sensory aura.
Supplementary motor seizures can produce ipsilateral or
contralateral head turning or limb posturing, so lateralization
of the focus is often uncertain. Contralateral tonic extension is
not a reliable finding. In contrast, seizures arising from
premotor nonsupplementary motor cortex produce contra-
lateral tonic posturing, which is a reliable lateralizing sign.31 It
can be associated with speech arrest or vocalization, and
followed by clonic movements.25 The head usually turns
contralaterally, but without secondary generalization, head
turning is an unreliable lateralizing sign,32,33 and versive
movements are rare.30 Kotagal et al34 in 2000 studied the

FIGURE 2. A–E, Electroencephalograph (EEG) of a 31-year-old man with refractory focal motor seizures for 2 years. He awakens from
sleep with a choking sensation and no impairment in consciousness. A and B, The ictal scalp EEG shows only muscle artifact with no
seizure discharge apparent. C, A map shows subdural electrodes sampling the right frontal lobe. D and E, Intracranial EEG recording
shows seizures arising from the throat motor area in the right frontal opercular cortex at contact RPFG 18. The seizure begins with b
activity (D) that attenuates and then evolves to rhythmic spikes (E). RPFG indicates right posterior frontal grid; RSYL, right sylvian.

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The Neurologist  Volume 17, Number 3, May 2011 Frontal Lobe Seizures

lateralizing value of asymmetric tonic posturing or “figure of 4
sign,” defined as a striking asymmetry of limb posture during
the tonic phase of a generalized tonic-clonic seizure in 31
patients with focal epilepsy. The extended arm was found to be
contralateral to the seizure focus in 10 of 12 temporal lobe
cases and 7 of 8 extratemporal lobe cases. The figure of 4 sign
may have lateralizing value in the early phase of secondary
generalization in patients with supplementary motor seizures.
The majority of patients with mesial frontal seizures have
normal interictal and ictal surface recordings.19,25,27 If present,
interictal sharp waves are at or near the vertex; however, it
becomes difficult to differentiate this activity from normal
sleep, and the lateralization may be misleading.25 Closely
placed scalp electrodes may help determine whether midline
spikes project asymmetrically,35 but are of uncertain value.
Figure 3 shows an example of a focal tonic seizure in a 31-
year-old, right-handed woman with refractory supplementary
sensorimotor seizures starting at the age of 5 years. Seizures
consist of frequent episodes of left leg stiffening, at times,
followed by clonic activity without impairment of conscious-
ness. MRI and interictal EEG were normal. The ictal surface
EEG shows rhythmic vertex and parietal midline sharp waves.
With intracranial recording, the seizures arose in the right
supplementary motor cortex with spread to the primary motor

FIGURE 3. A–G, Electroencephalograph (EEG) of a 31-year-old woman with refractory supplementary motor seizures starting at the age
of 5 years. Seizures consist of frequent episodes left leg stiffening, at times, followed by clonic activity without impairment of
consciousness. A and B, The ictal EEG shows rhythmic vertex and parietal midline sharp waves (arrows). C, A map shows subdural
electrodes sampling the right supplementary and primary sensorimotor cortex. D, Intracranial EEG recording shows seizures arising from
the supplementary motor cortex at contacts RSFG 4 and RSFG 5. D and E, The seizure begins with rhythmic spikes that are preceded by
an increase in the spike bursts seen interictally (big arrows). The ictal discharge spreads to the primary motor cortex at contact RSFG 10
(small arrow). F, As the spikes at RSFG 4 and RSFG 5 slow down in frequency, rhythmic d is seen at RSFG 10. G, The spike bursts slow
down in frequency before seizure end. RSFG indicates right subfrontal grid.

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Bagla and Skidmore The Neurologist  Volume 17, Number 3, May 2011

cortex or symptomatic zone. In published studies, intracranial
electrodes have shown rapid spread from the supplementary to
primary motor cortex.36 Mesial frontal foci adjacent to the
corpus callosum can generate widespread epileptiform dis-
charges37 that may become lateralized after an anterior corpus
callosotomy.
Dorsolateral, orbitofrontal, frontopolar, and cingulate
seizures have more variable clinical manifestations. Seizures
originating from these regions are not as well characterized as
primary and supplementary motor cortex probably because
significant overlap among these areas makes seizures difficult
to localize. Seizures arising from these regions do not always
produce loss of awareness, but often remain complex partial
(without generalization) when awareness is lost.
Focal tonic or clonic movements, versive movements of
the head or eyes, and speech arrest characterize dorsolateral
seizures. Version is characterized by clonic or tonic head and
eye deviation that is forced, sustained, and unnatural. It is
activated by discharges in a frontal eye field or Brodman areas
6 and 8, located in the posterior part of the middle frontal
gyrus, with lateralizing significance to the hemisphere
contralateral to the field of movements.32 However, ipsilateral
head turning can occur before version. Auras of nonvertiginous
dizziness, fear, or epigastric sensations have been reported in
half of the patients with dorsolateral seizures,38 and this
probably reflects propagation. Dorsolateral seizures have been
associated with multiple seizure types depending on pattern of
spread.13 Localized interictal epileptiform discharges and ictal
onsets to the frontal lobe are more common in dorsolateral
frontal foci due to the proximity of the epileptogenic zone to
the scalp electrodes.19 Figure 4 shows an example of a
dorsolateral seizure in an 18-year-old, right-handed woman
with refractory seizures starting at the age of 14 years and a
right dorsolateral frontal cortical dysplasia. Seizures consist of
immediate loss of awareness, staring and blinking, followed by
versive movement of the head to the left and facial clonic
activity. The seizure begins with brief diffuse attenuation
followed by rhythmic sharply contoured a discharge in the
right frontotemporal region, and postictal right frontotemporal
sharp waves. Interictal EEG showed right frontotemporal sharp
waves (F8) in sleep. Figure 5 shows another example of a
dorsolateral frontal seizure in a 28-year-old, right-handed
woman with refractory seizures starting at the age of 20 years.
Seizures consist of an aura of fear followed by left gaze and

FIGURE 4. A–E, Electroencephalograph (EEG) of an 18-year-old woman with refractory seizures starting at the age of 14 years from a right
dorsolateral frontal cortical dysplasia. Seizures consist of immediate loss of awareness, staring and blinking, followed by versive movement
of the head to the left and facial clonic activity. A, Interictal EEG showed rare right frontotemporal sharp waves (F8) in sleep. B and C, The
seizure begins with diffuse attenuation for 2 seconds followed by rhythmic sharply contoured a discharge in the right frontotemporal
region that evolves into high amplitude d intermixed with spikes (arrows). D and E, The EEG is then obscured by muscle artifact from the
clonic activity, ends with attenuation, and postictal right frontotemporal periodic lateralized epileptiform discharges (arrow). F, Magnetic
resonance imaging scan of the brain shows a cortical dysplasia in the right middle frontal gyrus.

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The Neurologist  Volume 17, Number 3, May 2011 Frontal Lobe Seizures

head turning to the left, facial clonic movements, and inability

FIGURE 5. A and B, Electroencephalograph (EEG) of a
28-year-old woman with history of refractory dorsolateral frontal
seizures starting at the age of 20 years. Seizures consist of an
aura of fear followed by left gaze and head turning to the left,
facial clonic movements, and inability to speak with preserved
awareness. A, The seizure begins with left frontocentral b activity
with some right-sided spread. B, The discharge increases in
amplitude after she presses the button, and decreases in
frequency.
to speak with preserved awareness. MRI and interictal EEG
were normal. The seizure begins with left frontocentral b
activity with some right-sided spread.
Epileptic involvement of the frontal operculum can
produce chewing, salivation, swallowing and gustatory hallu-
cinations, or autonomic manifestations such as flushing, pallor,
tachycardia, pupillary dilation, or apnea. Activation of Broca’s
area can produce difficulty with speech output, including
speech arrest, dysphasia, or comprehension difficulty. Akinetic
seizures can cause speech arrest or an inability to initiate or
sustain movement, and are associated with activation of the
negative motor areas anterior to the primary motor face area.
In a few patients, the paretic limb was found to be contralateral
to the seizure focus.39–42
Seizures originating in the anterior cingulate gyrus have
variable semiology depending on the ictal spread pattern. They
are usually brief and rapidly propagate to other lobes of the
brain.43 The anterior cingulate cortex is part of an inter-
connected system to assess the motivational content of internal
and external stimuli and regulate goal-directed behavior,44 and
seizures are characterized by complex motor behavior,
screaming, fear, emotional, or autonomic symptoms.
Complex partial seizures arising from the orbitofrontal
region are characterized by unresponsiveness or behavioral
arrest, sometimes with vigorous motor automatisms,45–48 but the
behavior can vary depending on the spread pattern. In contrast to
typical complex partial seizures of temporal lobe origin, the
typical motor automatisms during frontal lobe complex partial
seizures are bilateral and complex, and can be quite bizarre.49
Alimentary automatisms can occur, but are more common in

FIGURE 6. A–D, Electroencephalograph (EEG) of a 27-year-old man with refractory orbitofrontal seizures starting at the age of 2 years.
Seizures consist of an aura of anxiety and palpitations, followed by complex bilateral motor activity, chewing, and unresponsiveness.
A and B, The seizure begins with attenuation of amplitude bilaterally with muscle artifact from chewing. C, The EEG evolves to a
rhythmic bilateral a frequency discharge that is not localized. D, The seizure ends with diffuse attenuation.

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Bagla and Skidmore The Neurologist  Volume 17, Number 3, May 2011

temporal lobe epilepsy.17 The behavior may be preceded by a
nonspecific, cephalic sensation. The motor activity frequently
involves both legs, as in thrashing, rocking, thrusting, bicycling,
or running. When the automatisms involve the arms, the move-
ments involve the proximal muscles. Vocalizations, including
laughing, crying, and screaming can be associated with the
behavior, and have no lateralizing value. They often occur
during sleep, and last less than 1 minute. These bilateral,
complex motor seizures have classically been thought to arise
from the orbitofrontal, anterior cingulate, and mesial frontal
regions,50 but can arise from any area in the frontal lobe.
Patients with orbitofrontal and anterior cingulate epilepsy
can have bilaterally synchronous frontal spikes or secondary
bilateral synchrony, or falsely localized spikes to the ipsilateral
or contralateral temporal or frontal lobes. The ictal EEG can
also be falsely localizing to the temporal lobe from propaga-
tion. Figure 6 shows an example of an orbitofrontal seizure in a
27-year-old, right-handed man with refractory seizures starting
at the age of 2 years. Seizures consist of an aura of anxiety and
palpitations, followed by complex bilateral motor activity,
chewing, and unresponsiveness. MRI of his brain shows a prior
left anterior temporal lobectomy. Interictal EEG showed left
midtemporal d and spikes (T3) in wakefulness and sleep. The
seizure begins with bilateral attenuation of amplitudes,
evolving to a rhythmic bilateral a frequency discharge that is
not localized. Figure 7 shows an example of a frontal lobe

FIGURE 7. A–F, Electroencephalograph (EEG) of a 14-year-old man with refractory frontal lobe seizures starting at the age of 4 years.
Seizures consist of nocturnal episodes of cracking his knuckles, staring, rocking and bouncing with unresponsiveness, and brief postictal
confusion. A, Interictal EEG shows independent left and right sphenoidal sharp waves in sleep. B, The seizure starts with mild diffuse
background attenuation. C and D, The patient opens his eyes and blinks 25 seconds after onset. D, Rocking and bouncing movements
begin with unresponsiveness 44 seconds after onset. EEG is obscured by movement artifact. E and F, As the seizure continues, the EEG
shows a late left sphenoidal (E) and then right sphenoidal (F) amplitude maxima. These shifting amplitude asymmetries are not
uncommon, and should not be taken as localizing seizure since they represent late propagation of ictal discharge.

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The Neurologist  Volume 17, Number 3, May 2011 Frontal Lobe Seizures

seizure with falsely localized interictal epileptiform discharges
to the right and left sphenoidal electrodes in a 14-year-old,
right-handed man with refractory seizures starting at the age of
4 years. Seizures consist of nocturnal episodes of cracking his
knuckles, staring, rocking and bouncing with unresponsive-
ness, and brief postictal confusion. MRI was normal. The ictal
EEG is obscured by movement artifact, but shows a late left
sphenoidal and then right sphenoidal amplitude maxima. These
shifting amplitude asymmetries are not uncommon, and should
not be taken as localizing seizure as they represent late
propagation of ictal discharge. With intracranial recording, the
patients shown in Figures 6 and 7 had seizures arising from the
orbitofrontal region. Intracranial electrodes can help differ-
entiate temporal from frontal foci.
Seizures arising from the anterior frontopolar region are
absence-like with a brief lapse of consciousness, version,
forced thinking, or autonomic signs. Frontal pseudoabsence
seizures or “disturbances of contact,”51 and are thought to arise
from the anterior frontal or frontopolar regions by the
involvement of pathways from the corpus callosum to the
thalamus, but are not specific to these regions.46
Insular seizures are typically characterized by laryngeal
discomfort, dyspnea, unpleasant parasthesias or warmth, or
dysphonic or dysarthric speech with preservation of conscious-
ness.52 The insular cortex is richly connected to the temporal
lobe. When the ictal discharge spreads through the limbic
connections to the mesial temporal lobe, behavioral manifesta-
tions indistinguishable to seizures arising from mesial temporal
lobe with visceral auras and oroalimentary automatisms can
occur. In a stereoelectroencephalographic study of 50 patients
suspected of having insular seizures based on clinical
manifestations, scalp EEG discharges were picked up at the
temporal electrodes. In 6 patients, intracranial electrodes found
that onset was in the insular region and there was early spread
to the either the suprasylvian or infrasylvian opercular
cortex.52 Figure 8 shows an insular seizure in a 25-year-old,
left-handed man with refractory seizures starting at the age of 1
year and a left insular cortical dysplasia. He describes a brief
feeling “like hair standing on the back of his neck” and
inability to speak, sometimes followed by jaw clonus. MRI
shows a left opercular and insular cortical dysplasia. Interictal
EEG was normal. The ictal EEG shows muscle artifact with no
seizure discharge apparent. His clinical manifestations suggest
that seizures arise from left frontoparietal opercular cortex.
TREATMENT AND OUTCOME
The treatment for frontal lobe epilepsy is similar to other
localization-related or focal epilepsies. Medications are the
first line of therapy, and surgery is considered for patients who
fail to respond to medication. To our knowledge, there is no
convincing data showing that the location of the epileptogenic
zone influences the probability of medication response.
Antiepileptic drug therapy has little effect on either the rate
of occurrence or appearance of focal interictal spikes in most
patients with extratemporal seizures, though focal discharges
may show slight temporal dispersion after the initiation of
therapy at times.53 The effect of medication on the EEG
manifestations of seizures mainly relates to how medication
affects seizure propagation. As therapy may reduce seizure
severity and lessen the likelihood of secondary generalization
at times, this effect is apparent in the EEG.54

FIGURE 8. A and B, EEG of a 25-year-old man with refractory seizures starting at the age of 1 year from a left insular cortical dysplasia.
He describes a brief feeling “like hair standing on the back of his neck” and inability to speak, sometimes followed by jaw clonus.
Interictal electroencephalograph (EEG) was normal. A, The ictal EEG shows muscle artifact with no seizure discharge apparent. B,
Magnetic resonance imaging scan of the brain with sagittal T1W, coronal fluid attenuated inversion recovery and T2W images showed a
left opercular cortical dysplasia extending into the insula.

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Bagla and Skidmore
The surgical outcome in frontal lobe resections is less
favorable than anterior temporal lobe resections for mesial
temporal lobe epilepsy. In recent series, the seizure-free rates
after a frontal resection vary considerably, though most reports
suggest a 30% to 50% seizure-free rate.55–60 The reasons for
discrepancy between studies are probably related to demo-
graphic differences, patient selection, use of differing diag-
nostic methods, and limited ability to resect the epileptogenic
zone if it is near eloquent cortex. Patients with frontal lobe
lesions tend to fare better than patients without structural
abnormalities, which highlights the importance of modern,
high-resolution neuroimaging techniques. The extent of lesion
resection also influences outcome. In a recent series reporting
outcome in 70 patients after frontal resection for refractory
epilepsy,14 if the resections were felt to be incomplete, the
seizure-free rate was 40%. When complete removal was
possible, in the presence of a lesion on MRI and an EEG
abnormality restricted to an area in the frontal lobe, 80% of
patients were seizure free at 1 year, 66% at 3 years, and high as
40% at 5 or more years.14 Seizures caused by tumors and other
well-circumscribed pathologic lesions had the best outcome.
The suboptimal surgical outcome after frontal resections
may have several explanations. In the absence of clinical
manifestations with specific localizing value, a well-localized
EEG, or focal lesion seen with MRI, localization of the
epileptogenic zone is quite difficult. The epileptogenic zone may
overlap important functional areas (eg, motor or language
cortex) so a complete resection might not be possible. In patients
with refractory frontal lobe epilepsy, an anterior corpus
callosotomy may afford relief,61 or callosotomy combined with
a frontal resection might improve seizure outcome.16
REFERENCES
1. Manford M, Hart YM, Sander JW, et al. National General Practice
Study of Epilepsy (NGPSE): partial seizure patterns in a general
population. Neurology. 1992;42:1911–1917.
2. Rasmussen T. Surgery for central, parietal and occipital epilepsy.
Can J Neurol Sci. 1991;11:611–616.
3. Loiseau P, Beaussart M. The seizures of benign childhood epilepsy
with rolandic paroxysmal discharges. Epilepsia. 1973;14:381–389.
4. Gregory DL, Wong PK. Topographic analysis of the centrotem-
poral discharges in benign rolandic epilepsy of childhood.
Epilepsia. 1984;25:705–711.
5. Neubauer BA, Fiedler B, Himmelein B, et al. Centrotemporal
spikes in families with rolandic epilepsy: linkage to chromosome
15q14. Neurology. 1998;51:1608–1612.
6. Scheffer IE, Bhatia KP, Lopes-Cendes I, et al. Autosomal
dominant nocturnal frontal lobe epilepsy. A distinctive clinical
disorder. Brain. 1995;118:61–73.
7. Koshewnikow. Eine besondere Form von corticaler Epilepsie.
Neurol Zentralbl. 1895;14:47–48.
8. Thomas JE, Reagan TJ, Klass DW. Epilepsia partialis continua.
Arch Neurol. 1977;34:266–275.
9. Panayiotopoulos CP. Benign childhood partial seizures and related
epileptic syndromes. In: Panayiotopoulos CP, ed. The Epilepsies:
Seizures, Syndromes and Management. Oxford: Bladon Medical
Publishing; 2005:223–269.
10. Capovilla G, Beccaria F. Benign partial epilepsy in infancy and
early childhood with vertex spikes and waves during sleep: a new
epileptic form. Brain Dev. 2000;22:93–98.
11. Kutluay E, Passaro EA, Gomez-Hassan D, et al. Seizure semiology
and neuroimaging findings in patients with midline spikes.
Epilepsia. 2001;42:1563–1568.
12. Barkovich AJ, Chuang SH, Norman D. MR of neuronal migration
anomalies. AJR. 1988;150:179–187.
134 | www.theneurologist.org
The Neurologist  Volume 17, Number 3, May 2011
13. Jobst BC, Siegel AM, Thadani VM, et al. Intractable seizures of
frontal lobe origin: seizure characteristics, localizing signs, and
results of surgery. Epilepsia. 2000;41:1139–1152.
14. Jeha LE, Najm I, Bingaman W, et al. Surgical outcome and
prognostic factors of frontal lobe epilepsy surgery. Brain. 2007;
130:574–584.
15. Janszky J, Jokeit H, Schulz R, et al. EEG predicts surgical outcome
in lesional frontal lobe epilepsy. Neurology. 2000;4:1470–1476.
16. Laskowitz DT, Sperling MR, French JA, et al. The syndrome of
frontal lobe epilepsy: characteristics and surgical management.
Neurology. 1995;45:780–787.
17. Kotagal P, Arunkumar G, Hammel J, et al. Complex partial
seizures of frontal lobe onset statistical analysis of ictal semiology.
Seizure. 2003;12:268–281.
18. Salanova V, Morris HH, Van Ness PC, et al. Comparison of scalp
electroencephalogram with subdural recordings and functional
mapping in frontal lobe epilepsy. Arch Neurol. 1993;50:294–299.
19. Bautista RED, Spencer DD, Spencer SS. EEG findings in frontal
lobe epilepsies. Neurology. 1998;50:1765–1771.
20. Swartz BE, Walsh GO, Delgado-Escueta AV, et al. Surface ictal
electroencephalographic patterns in frontal versus temporal lobe
epilepsy. Can J Neurol Sci. 1991;18:649–662.
21. Quesney LF. Preoperative electroencephalography investigation in
frontal lobe epilepsy: electroencephalographic and electrocortico-
graphic recordings. Can J Neurol Sci. 1991;18:559–563.
22. Williamson PD, Spencer DD, Spencer SS, et al. Complex partial
seizures of frontal lobe origin. Ann Neurol. 1985;18:497–504.
23. Ralston BL. Cingulate epilepsy and secondary bilateral synchrony.
Electrenceph Clin Neurophysiol. 1961;13:591–598.
24. Tharp BR. Orbitofrontal seizures. A unique electroencephalo-
graphic and clinical syndrome. Epilepsia. 1972;13:627–642.
25. Morris HH, Dinner DS, Lüders H, et al. Supplementary motor
seizures: clinical and electroencephalographic findings. Neuro-
logy. 1988;38:1075–1082.
26. Foldvary N. Ictal electroencephalography in neocortical epilepsy.
In: Lüders HO, Comair YG. Epilepsy Surgery. 2nd ed.
Philadelphia: Lippincott Williams & Wilkins; 2000:431.
27. Pedley TA, Tharp BR, Herman K. Clinical and electroencephalo-
graphic characteristics of midline parasagittal foci. Ann. Neurol.
1981;9:142–149.
28. Commission on Classification and Terminology of the International
League Against Epilepsy. Proposal for revised classification of
epilepsies and epileptic syndromes. Epilepsia. 1989;30:389–399.
29. Salanova V, Morris HH, Van Ness P, et al. Frontal lobe seizures:
electroclinical syndromes. Epilepsia. 1995;36:16–24.
30. Hamer HM, Lüders HO, Knake S, et al. Electrophysiology of focal
clonic seizures in humans: a study using subdural and depth
electrodes. Brain. 2003;126:547–555.
31. Janszky J, Fogarasi A, Jokeit H, et al. Lateralizing value of
unilateral motor and somatosensory manifestations in frontal lobe
seizures. Epilepsy Res. 2001;43:125–133.
32. Wyllie E, Lüders H, Morris HH, et al. The lateralizing significance
of versive head and eye movements during epileptic seizures.
Neurology. 1986;36:606–611.
33. Kernan JC, Devinsky O, Luciano DJ, et al. Lateralizing
significance of head and eye deviation in secondary generalized
tonic-clonic seizures. Neurology. 1993;43:1308–1310.
34. Kotagal P, Bleasel A, Geller E, et al. Lateralizing value of
asymmetric tonic limb posturing observed in secondarily general-
ized tonic-clonic seizures. Epilepsia. 2000;41:457–462.
35. Morris HH, Lüders H, Lesser RP, et al. The value of closely
spaced scalp electrodes in the localization of epileptic foci: a study
of 26 patients with complex partial seizures. Electrenceph Clin
Neurophysiol. 1986;63:107–111.
36. Baumgartner C, Flint R, Tuxhorn I, et al. Supplementary motor
area seizures: propagation pathways as studies with invasive
recordings. Neurology. 1996;46:508–514.
37. Tukel K, Jasper H. The electroencephalogram in parasagittal
lesions. Electrenceph Clin Neurophysiol. 1952;4:481–494.
38. Quesney LF, Constain M, Fish DR, et al. The clinical differentia-
tion of seizures arising in the parasagittal and anterolaterodorsal
frontal convexities. Arch Neurol. 1990;47:677–679.
r 2011 Lippincott Williams & Wilkins
The Neurologist  Volume 17, Number 3, May 2011
39. Bleasel A, Kotagal P, Kankirawatana P, et al. Lateralizing value
and semiology of ictal limb posturing and version in temporal lobe
and extratemporal epilepsy. Epilepsia. 1997;38:168–174.
40. Noachtar S, Lüders HO. Focal akinetic seizures as documented by
electroencephalography and video recordings. Neurology. 1999;
53:427–429.
41. Gallmetzer P, Leutmezer F, Serles W, et al. Postictal paresis in
focal epilepsies: incidence, duration and causes: a video-EEG
monitoring study. Neurology. 2004;62:2160–2164.
42. Oestreich LJ, Berg MJ, Bachmann DL, et al. Ictal contralateral
paresis in complex partial seizures. Epilepsia. 1995;36:671–675.
43. Mazars G. Criteria for identifying cingulate epilepsies. Epilepsia.
1970;11:41–47.
44. Devinsky O, Morrell MJ, Vogt BA. Contributions of anterior
cingulate cortex to behaviour. Brain. 1995;118:279–306.
45. Ludwig B, Ajmone Marsan C, Van Buren J. Cerebral seizures of
probable orbitofrontal origin. Epilepsia. 1975;16:141–158.
46. So NK. Mesial frontal epilepsy. Epilepsia. 1998;39(suppl. 4):
S49–S61.
47. Roper SN, Gilmore RL. Orbitofrontal resections for intractable
partial seizures. J Epil. 1995;8:146–152.
48. Smith JR, Sillay K, Winkler P, et al. Orbitofrontal epilepsy:
electroclinical analysis of surgical cases and literature review.
Stereotact Funct Neurosurg. 2004;82:20–25.
49. Geier S, Bancaud J, Talairach J, et al. Automatisms during frontal
lobe epileptic seizures. Brain. 1976;99:447–458.
50. Bancaud J, Talairach J. Clinical semiology of frontal lobe seizures.
Adv Neurol. 1992;57:3–58.
r 2011 Lippincott Williams & Wilkins
Frontal Lobe Seizures
51. Geier S, Bancaud J, Talairach J, et al. The seizures of frontal lobe
epilepsy: a study of clinical manifestations. Neurology. 1977;27:
951–958.
52. Isnard J, Guénot M, Sindou M, et al. Clinical manifestations of
insular lobe seizures: a stereo-electroencephalographic study.
Epilepsia. 2004;45:1079–1090.
53. Frost JD Jr, Kellaway P, Hrachovy RA, et al. Changes in epileptic
spike configuration associated with attainment of seizure control.
Ann Neurol. 1986;20:723–726.
54. So N, Gotman J. Changes in seizure activity following antic-
onvulsant drug withdrawal. Neurology. 1990;40:407–413.
55. Mosewich RK, So EL, O’Brien TJ, et al. Factors predictive of the
outcome of frontal lobe epilepsy surgery. Epilepsia. 2000;41:843–849.
56. Zaatreh MM, Spencer DD, Thompson JL, et al. Frontal lobe
tumoral epilepsy: clinical, neurophysiologic features and predic-
tors of seizure outcome. Epilepsia. 2002;43:727–733.
57. Chung CK, Lee SK, Kim KJ. Surgical outcome of epilepsy caused
by cortical dysplasia. Epilepsia. 2005;46(suppl 1):25–29.
58. Lee SK, Lee SY, Kim KK, et al. Surgical outcome and prognostic
factors of cryptogenic neocortical epilepsy. Ann Neurol.
2005;58:525–532.
59. Yun CH, Lee SK, Lee SY, et al. Prognostic factors in neocortical
epilepsy surgery: multivariate analysis. Epilepsia. 2006;47:574–579.
60. Schramm J, Kral T, Kurthen M, et al. Surgery to treat focal frontal
lobe epilepsy in adults. Neurosurgery. 2002;51:644–655.
61. Purves SJ, Wada JA, Woodhurst WB, et al. Results of anterior
corpus callosum section in 24 patients with medically intractable
seizures. Neurology. 1988;38:1194–1201.
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