Review Article

Adult Focal Epilepsies

Address correspondence to
Dr Christopher T. Skidmore,
Thomas Jefferson University,
901 Walnut Street, 4th Floor,
Philadelphia, PA 19107,
christopher.skidmore@
jefferson.edu.
Relationship Disclosure:
Dr Skidmore serves as a
consultant for Upsher-Smith
Laboratories, Inc, and has
received research support from
NeuroPace, Inc.
Unlabeled Use of
Products/Investigational
Use Disclosure:
Dr Skidmore reports
no disclosure.
* 2016 American Academy
of Neurology.
Christopher T. Skidmore, MD
ABSTRACT
Purpose of Review: Focal epilepsy is the most common type of epilepsy in
adulthood. This article discusses the seizure symptomatology, EEG findings, and
imaging findings of the various forms of focal epilepsy. The majority of the article
focuses on temporal and frontal lobe epilepsy as these represent the majority of
focal epilepsies.
Recent Findings: While significant overlap exists in the clinical symptomatology of
the focal epilepsies, detailed seizure descriptions can often provide useful clinical
evidence to help establish an accurate diagnosis. EEG and MRI continue to serve as
the main diagnostic tools for the diagnosis of focal epilepsy.
Summary: The various forms of focal epilepsy generate seizure presentations that
are dependent on the anatomic structures that are involved in the seizure. By
understanding the symptoms typically generated in each region of the brain, a
better understanding of the possible seizure localizations can be made. Most forms
of epilepsy have clear changes on EEG that permit accurate localization, but several
pitfalls exist, which are discussed in this article. Imaging has revolutionized our
ability to accurately identify lesions associated with epilepsy and increased our
ability to localize seizures in the brain.

Continuum (Minneap Minn) 2016;22(1):94–115.

INTRODUCTION Other acquired causes, such as in-

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This article focuses on focal (partial-
onset) epilepsy since it is the most
common form of epilepsy to be
diagnosed during adulthood. Certainly
patients with idiopathic generalized
epilepsy, especially juvenile myoclonic
epilepsy, can have onset in early
adulthood, but the clinical history
and diagnostic workup are the same
as for childhood-onset epilepsy and
are discussed in the article “Infantile,
Childhood, and Adolescent Epilep-
sies” by Elaine Wirrell, MD,1 in this
issue of Continuum.
Focal epilepsy can develop at any
point in life, and the etiologies associ-
ated with it vary by age. In general
terms, congenital abnormalities or
genetic triggers are often associated
with earlier onset, while stroke and
neurodegenerative disorders are asso-
ciated with an older age of onset.
fections or trauma, can be associated
with acute or remote onset of epilepsy.
Obtaining a detailed epilepsy risk
factor history from patients, including
a history of pregnancy complica-
tions, learning or physical disabilities/
milestone delay, febrile seizures, sig-
nificant head trauma, central nervous
system infections, and a family history
of epilepsy, is important to help guide
the clinical workup.
This article outlines the typical
presentation of various forms of focal
epilepsy and highlights the typical
seizure symptomatology, interictal and
ictal scalp EEG, and potential etiologies.
TEMPORAL LOBE EPILEPSY
The temporal lobe is one of the most
common localizations for focal epilepsy,
and it is important to recognize the
common presentations to ensure that
February 2016

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an accurate diagnosis is established. The
features of temporal lobe epilepsy can be
broken down into two broad categories:
mesial and lateral (neocortical) onset.
Mesial Temporal Lobe Epilepsy
Mesial temporal lobe epilepsy is one of
the most well-defined forms of epilepsy
in the literature. It often begins during
late adolescence or early adulthood.
Clinical features. Prolonged febrile
seizures are believed to be a risk
KEY POINT
factor for the development of hippo- h Mesial temporal lobe
campal sclerosis,2 which is a common epilepsy is the most
cause of mesial temporal lobe epi- common form of
lepsy. Hippocampal sclerosis is char- temporal lobe epilepsy,
acterized by atrophy and gliosis of and the most common
the hippocampus, which may be pathology associated
unilateral or bilateral (Figure 5-1 with mesial temporal
and Figure 5-2). Other etiologies that lobe epilepsy is
may be seen in the mesial temporal hippocampal sclerosis.
lobe include cavernous hemangiomas,
gliosis/encephalomalacia secondary to
prior injury, and tumors such as

FIGURE 5-1 Right mesial temporal sclerosis. A, B, Coronal T1-weighted MRIs demonstrate a
smaller right hippocampus. C, D, Coronal fluid-attenuated inversion recovery
(FLAIR) MRIs demonstrate increased signal in the right hippocampus consistent
with gliosis.

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 Adult Focal Epilepsies

FIGURE 5-2 Bilateral mesial temporal sclerosis. Coronal

fluid-attenuated inversion recovery (FLAIR)
MRI demonstrates bilateral increased signal
in the hippocampus consistent with gliosis.

dysembryoplastic neuroepithelial tumors with nondominant temporal lobe sei-

(Case 5-1).
Many patients with mesial temporal
lobe epilepsy experience auras, which
can include psychic sensations (déjà vu
and jamais vu), a gastric rising sensa-
tion, a sensation of “butterflies” in their
stomach, fear, or olfactory symptoms
(usually an unpleasant chemical or
burning smell). The aura is typically
followed by loss of consciousness/
awareness with prominent oral and
manual automatisms in patients with
dominant temporal lobe seizures, while
nondominant temporal lobe seizures
may have preserved awareness with
oral and manual automatisms (Case 5-1).5
Dystonic limb posturing during the ictus
has been described and is very predic-
tive of seizure onset starting in the
mesial temporal lobe contralateral to
the dystonic limb. It is not uncommon
for the patient to have manual autom-
atisms in the hand ipsilateral to the
seizure focus. Symptoms associated
zures include ictal spitting, vomiting,
and urinary urge.6
The seizures typically last 60 to
90 seconds and are often followed by
a period of confusion/disorientation,
more prominent in patients with dom-
inant temporal lobe seizures. After
dominant temporal lobe seizures,
prominent postictal symptoms may be
attributed to involvement of the lan-
guage centers in the ictal discharge.
Seizures from the mesial temporal
region rarely secondarily generalize, but
when they do, it is typically very late
into the seizure in contrast to neo-
cortical temporal lobe or extratemporal
lobe epilepsy, which frequently second-
arily generalizes earlier in the seizure.
Several clinical features help to lateral-
ize the seizure focus to the ipsilateral
temporal lobe regardless of dominance.
These include postictal nose wiping,
ictal unilateral eye blinking (Case 5-2),
and ictal piloerection.6 The hand that

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wipes the nose first after a seizure is
typically ipsilateral to the seizure focus.
A delay often exists in diagnosing
nondominant temporal lobe seizures
because of preserved awareness and
minimal postictal symptoms. Often the
patient is unaware of the ictal automa-
tisms, and until an observer witnesses a
seizure, the symptoms are often mini-
mized or ignored by the patient. How-
ever, once patients are made aware of
the symptoms, they typically can reli-
ably report their seizures.
EEG findings. In mesial temporal
lobe epilepsy, the interictal EEG is
associated with anterior temporal
spikes/sharp waves that are maximum
in electrodes T1/F7 or T2/F8 (FT9/FT10
in the 10/10 system) (Supplemental
Digital Content 5-1, links.lww.com/
CONT/A157). Often the spikes can have
KEY POINT
very focal fields, and, without the h Anterior temporal
addition of extra anterior temporal discharges may often
electrodes (T1, T2), an interictal spike have a limited field, and
may be missed (Supplemental Digital additional electrodes
Content 5-2, links.lww.com/CONT/ (T1 and T2) may aid
A158). The interictal epileptiform activ- in the detection of
ity is typically bilateral,5 even in pa- epileptiform activity.
tients with unilateral seizures, but
typically one side has a preponderance
(Supplemental Digital Content 5-3,
links.lww.com/CONT/A159). Sleep
deprivation can often activate focal
epileptiform discharges; therefore,
an EEG with sleep recording is
recommended during the diagnostic
workup. The presence of mid or
posterior temporal spikes may suggest
a more widespread epileptogenic net-
work even in the presence of clear mesial
temporal pathology. The ictal EEG is
typically characterized by rhythmic

Case 5-1
A 35-year-old woman presented for evaluation after having a seizure associated with loss of
consciousness that resulted in a minor car accident. She did not sustain any injuries during the accident.
Upon questioning, she stated that she first developed a sense of fear and then a butterfly sensation in
her stomach. Ten seconds later, she lost awareness. She reported that she had experienced the aura
sporadically over the last 5 years, and it had increased in frequency over the last 6 months. She denied
prior spells with loss of awareness. According to her partner, when she reported this sensation she
often had oral automatisms; she was able to converse during the events, but her responses were slightly
delayed. Typically, these spells were 45 seconds in duration.
Based on the history of a single complex partial seizure and multiple simple partial seizures
associated with a fear/abdominal aura and oral automatisms with preserved awareness, a diagnosis
of epilepsy was made. To try to define an etiology, an MRI of the brain with and without contrast was
obtained, which demonstrated findings most consistent with a right temporal dysembryoplastic
neuroepithelial tumor (DNET) (Figure 5-3). A routine EEG was obtained, which revealed right anterior
temporal sharp waves (Figure 5-4A). The patient was treated with lamotrigine 150 mg 2 times a day.
Despite maintaining therapeutic blood levels, she continued to experience seizures and was
transitioned to levetiracetam 500 mg 2 times a day and weaned off lamotrigine. She had an initial
seizure-free period of 3 months on levetiracetam monotherapy, but her seizures recurred and she
continued to have four seizures per month.
She was admitted to an epilepsy monitoring unit and underwent continuous video-EEG
monitoring. Her habitual seizures were recorded, and the EEG revealed a right temporal ictal
discharge (Figure 5-4B, 5-4C, and 5-4D). Based on the concordance of her clinical symptomatology,
interictal and ictal EEG, and imaging, a right anterior temporal lobe resection was recommended and
performed. Pathology of the resected lesion showed a DNET. She remained seizure free after the
surgery and was eventually taken off her antiepileptic drugs.
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 Adult Focal Epilepsies

Continued from page 97

FIGURE 5-3 Imaging of the patient in Case 5-1 showing characteristics consistent with right temporal dysembryoplastic
neuroepithelial tumor (DNET). Coronal T1 (A) and fluid-attenuated inversion recovery (FLAIR) (B) and axial
FLAIR (C) MRIs demonstrate a mass lesion in the region of the right amygdala.

FIGURE 5-4 EEGs of the patient in Case 5-1 demonstrating right temporal lobe epilepsy. A, EEG
demonstrates right anterior to midtemporal spikes. Panels BYD reveal a typical right
temporal ictal EEG discharge. The ictal discharge starts with low-amplitude rhythmic
delta activity that evolves on panel C to high-amplitude rhythmic theta before stopping around
the fourth second of panel D.

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 Continued from page 98

FIGURE 5-4 EEGs of the patient in Case 5-1 demonstrating right temporal lobe epilepsy. A, EEG
demonstrates right anterior to midtemporal spikes. Panels BYD reveal a typical
right temporal ictal EEG discharge. The ictal discharge starts with low-amplitude
rhythmic delta activity that evolves on panel C to high-amplitude rhythmic theta before stopping
around the fourth second of panel D.

Continued on page 100

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 Adult Focal Epilepsies

Continued from page 99

FIGURE 5-4 EEGs of the patient in Case 5-1 demonstrating right temporal lobe epilepsy. A, EEG
demonstrates right anterior to midtemporal spikes. Panels BYD reveal a typical
right temporal ictal EEG discharge. The ictal discharge starts with low-amplitude
rhythmic delta activity that evolves on panel C to high-amplitude rhythmic theta before stopping
around the fourth second of panel D.

Comment. The clinical symptomatology in this patient was consistent with seizures emanating
from the mesial temporal region, and, based on the clinical history alone, a diagnosis of focal
epilepsy could be established. EEG and MRI confirmed the clinical diagnosis and better defined the
location and potential cause of her epilepsy. In this case, the patient had the typical mesial temporal
EEG patterns and imaging consistent with a common benign tumor associated with temporal lobe
epilepsy. In this patient, trials of two therapeutic antiepileptic drugs had failed, therefore fulfilling the
definition of drug-resistant epilepsy.3 The likelihood of long-term seizure freedom with medical
therapy was low at that point (less than 5%), and she was referred for consideration of epilepsy
surgery, which led to successful seizure control.3,4

alpha or theta activity that evolves into
higher-amplitude rhythmic delta or
theta activity that may be sharply
contoured or contain discrete spikes
(Supplemental Digital Content 5-4,
links.lww.com/CONT/A160). Often,
the initial ictal discharge may be pre-
ceded by an initial sharp wave or
suppression of the normal EEG
patterns or epileptiform activity that
was occurring immediately before the
ictus. Other patterns at onset include
rhythmic delta with or without spikes
(Supplemental Digital Content 5-5,

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 Case 5-2
A 40-year-old man presented for evaluation of persistent seizures. The patient began to have seizures
at age 22. He stated that his seizures always started with a burning sensation in his stomach that often
rose up through his chest. This occurred over 10 to 15 seconds, after which he lost awareness.
Observers had noted that he stared blankly, was unresponsive to questions, and had oral and manual
automatisms and unilateral left eyelid blinking during the seizure. The seizures typically lasted for
60 to 90 seconds and were followed by postictal fatigue and confusion that lasted for up to 1 hour.
He had three seizures per month. He was being treated with zonisamide 300 mg/d, and previous
treatments with levetiracetam, carbamazepine, lamotrigine, phenytoin, and topiramate had failed.
He continued to work as a math teacher in a junior high school, but needed rides to and from work
because of his inability to drive. He admitted to mild depression in the past that had not required
treatment, but he denied ever considering suicide. He wished to consider alternative treatment
options since medical therapy had failed.
An MRI of the brain was obtained (Figure 5-5A and 5-5B) and was consistent with left mesial
temporal sclerosis. The patient was admitted to the epilepsy monitoring unit for video-EEG
monitoring (Figure 5-6). The interictal EEG revealed frequent left anterior temporal delta slowing
(Figure 5-6A) and left anterior temporal sharp waves (Figure 5-6B) that were maximal at the T1
electrode in the transverse chain and F7 in the anterior-posterior chain of electrodes. The ictal EEG
revealed a left temporal seizure pattern (Figure 5-6C, 5-6D, 5-6E, and 5-6F). Neuropsychological
evaluation revealed normal visual memory and reduced, but still average, verbal memory.

FIGURE 5-5 Imaging of the patient in Case 5-2 showing left mesial temporal lobe sclerosis. Coronal fluid-attenuated inversion
recovery (FLAIR) (A) and T1 (B) MRIs demonstrate increased signal on T2-weighted imaging and atrophy on
T1-weighted imaging of the hippocampus. Coronal T2 MRI demonstrates postoperative encephalomalacia in the
mesial temporal lobe that was created using a minimally invasive laser thermal ablation technique (C).

Comment. Based on the patient’s seizure symptomatology, interictal and ictal EEG, and imaging, he
was diagnosed with mesial temporal lobe epilepsy secondary to hippocampal sclerosis. He was felt to be a
very good candidate for a left anterior temporal lobectomy, but his reduced verbal memory and need to
function as a math teacher were concerns. The patient underwent a new minimally invasive approach
utilizing stereotactic thermal ablation for the treatment of mesial temporal sclerosis7,8 and has remained
seizure free for 2 years since the operation (Figure 5-5C). He remained on zonisamide 300 mg/d and was
back working as a math teacher 2 weeks after the surgery. Follow-up neuropsychological testing
demonstrated no decline when compared to his preoperative data, and he reported no subjective
cognitive concerns.
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 Adult Focal Epilepsies

Continued from page 101

FIGURE 5-6 EEGs of the patient in Case 5-2 demonstrating left mesial temporal lobe
epilepsy. A, Interictal focal slowing in the left anterior temporal region. B,
Frequent left anterior temporal spikes. Panels CYF reveal a left temporal lobe
seizure that begins with moderate-amplitude rhythmic delta and evolves to higher-amplitude
delta rhythmic spiking, which ceases 12 seconds into panel F.

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 Continued from page 102

FIGURE 5-6 EEGs of the patient in Case 5-2 demonstrating left mesial temporal lobe epilepsy.
A, Interictal focal slowing in the left anterior temporal region. B, Frequent left
anterior temporal spikes. Panels CYF reveal a left temporal lobe seizure that
begins with moderate-amplitude rhythmic delta and evolves to higher-amplitude delta rhythmic
spiking, which ceases 12 seconds into panel F.

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 Adult Focal Epilepsies

Continued from page 103

FIGURE 5-6 EEGs of the patient in Case 5-2 demonstrating left mesial temporal lobe epilepsy.
A, Interictal focal slowing in the left anterior temporal region. B, Frequent left
anterior temporal spikes. Panels CYF reveal a left temporal lobe seizure that begins
with moderate-amplitude rhythmic delta and evolves to higher-amplitude delta rhythmic spiking,
which ceases 12 seconds into panel F.

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links.lww.com/CONT/A161 and Supple-
mental Digital Content 5-6, links.lww.
com/CONT/A162).
The seizure discharge may remain
limited to the mesial temporal struc-
tures, but often spreads to the remain-
der of the ipsilateral hemisphere and
contralateral temporal lobe. During
the postictal state, unilateral temporal
lobe slowing that is typically ipsilateral
to the seizure onset may be seen.
Imaging. An MRI of the brain with-
out contrast is recommended in the
evaluation of a patient with suspected
mesial temporal lobe epilepsy. An
enhanced MRI may be used dependent
on local imaging protocols and
suspected etiologies. It is preferable
to include coronal T1- and T2-weighted
images with thin cuts (less than 3 mm)
through the temporal lobes to properly
evaluate the hippocampus. Key imag-
ing characteristics to evaluate for hip-
pocampal sclerosis are asymmetric size
(smaller on the affected side) and
increased T2 signal in the hippocam-
pus consistent with gliosis. Inclusion of
gradient echo imaging may assist in the
identification of vascular etiologies.
Fluorodeoxyglucose positron emission
tomography (FDG-PET) scan imaging
has been extensively studied in pa-
tients undergoing presurgical evalua-
tion, and unilateral temporal lobe
hypometabolism ipsilateral to the sei-
zure focus is a positive predictor of a
good outcome after epilepsy surgery.9
FDG-PET scanning is reserved only
for patients who are being consi-
dered for epilepsy surgery since the
presence or absence of temporal lobe
hypometabolism does not impact
medical treatment.
Genetic considerations. Familial
forms of mesial temporal lobe epi-
lepsy have been described. The ma-
jority of reports describe families with
psychic auras and simple or complex
partial seizures. The imaging studies
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KEY POINTS
are normal, and the disease course is h Imaging of the mesial
benign for most patients. The exact temporal lobe requires
genetic mutation is not known.10 thin-cut coronal
imaging with T1- and
Lateral/Neocortical Temporal T2-weighted images to
Lobe Epilepsy properly visualize the
Lateral/neocortical temporal lobe epi- key structures.
lepsy is less common than mesial tem- h The symptomatology
poral lobe epilepsy and less well-defined. associated with
Because of the rich connections to other neocortical temporal
regions of the brain and the larger total lobe epilepsy is quite
cortical area available to generate seizures, varied and dependent
the symptomatology, EEG findings, and on the location of the
associated pathologies are varied. seizure onset.
Clinical features. Seizures originat- h Auditory auras and
ing from the temporal pole or anterior aphasic seizures are
basal temporal surface often display very suggestive of
auras and other clinical features that neocortical temporal
lobe epilepsy.
are similar to mesial temporal lobe
epilepsy as described earlier. This is
most likely secondary to early spread
of the ictal electrographic discharge to
the mesial temporal lobe structures.
Lateral and perisylvian seizure foci
often have features that involve the
eloquent cortex in that region, such as
aphasic seizures in the dominant tem-
poral lobe and auditory auras due to
involvement of the primary and second-
ary auditory cortex.6 Seizure onsets near
the temporooccipital junction may be
associated with vertiginous symptoms
or visual auras at the onset of the sei-
zures. The auras often evolve to bland
staring and unresponsiveness followed
by rapid secondary generalization. As
the seizures begin to generalize and
activate the motor cortex, it is not
uncommon to have unilateral (contra-
lateral to the seizure focus) clonic
jerking of the face or upper extremity.11
EEG findings. The interictal and
ictal EEG patterns in lateral/neocortical
lobe epilepsy can be similar to those
seen in mesial temporal lobe epilepsy;
however, patients with lateral or
perisylvian foci may have more mid to
posterior temporal foci involving elec-
trodes T4/T3 and T6/T5. The activity
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 Adult Focal Epilepsies

the same MRI techniques described

FIGURE 5-7
in the left mesial temporal region (black arrow) and a
periventricular nodular heterotopia in the right mesial
temporal region (white arrow).
KEY POINT
h Two genetic forms of
lateral temporal lobe
epilepsy have been
identified: autosomal
dominant partial
epilepsy with auditory
features and idiopathic
partial epilepsy with
auditory features.
Temporal malformation of cortical
development. Coronal T1-weighted MRI
demonstrating a transmantle cortical dysplasia
often rapidly propagates to other
lobes, and spread to the contralateral
hemisphere typically occurs earlier
when compared to mesial temporal
lobe epilepsy.11 Foldvary and col-
leagues12 described a lateralized poly-
morphic delta pattern in patients with
neocortical temporal lobe epilepsy,
and paroxysmal fast/beta onset activity
has also been reported (Supplemental
Digital Content 5-7, links.lww.com/
CONT/A163 and Supplemental Digital
Content 5-8, links.lww.com/CONT/
A164). Occasionally the onset is poorly
defined but eventually evolves into a
lateralized temporal lobe ictal dis-
charge (Supplemental Digital Content
5-9, links.lww.com/CONT/A165).
Imaging. Imaging in lateral/neocortical
epilepsy should be obtained with
for mesial temporal lobe epilepsy. The
pathologies associated with this form
of epilepsy can include, but are not
limited to, malformations of cor-
tical development, vascular malfor-
mations, encephalomalacia secondary
to trauma, and tumors (Figure 5-7,
Figure 5-8, and Figure 5-9).11 FDG-PET
scans may show hypometabolism
in the lateral temporal neocortex,
but again, this imaging technique is
reserved for patients undergoing a
presurgical evaluation.
Genetic considerations. Two forms
of genetic lateral temporal lobe epilepsy
have been identified. The familial
form is referred to as autosomal dom-
inant lateral temporal lobe epilepsy or
autosomal dominant partial epilepsy
with auditory features. The sporadic
form is referred to as idiopathic partial
epilepsy with auditory features. Both
forms are associated with partial-onset
seizures, often with auditory auras, but
they may also have other sensory auras,
as described earlier, and frequent sec-
ondary generalization. Imaging is typi-
cally negative, and the EEG findings are
supportive of a lateral temporal neo-
cortical focus. The most common
mutation found in patients with the
familial form of the disorder is in
the leucine-rich, glioma inactivated
1 (LGI1) gene. The familial form has a
penetrance of approximately 70% to
80%. How this mutation causes
epilepsy remains unclear at this time.
The medical treatment of these pa-
tients is no different than that of
patients with other forms of tem-
poral lobe epilepsy, but they typi-
cally have a more benign prognosis
and their seizures can be controlled
with medication.13
FRONTAL LOBE EPILEPSY
Frontal lobe epilepsy is the second most
common type of focal epilepsy. The

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 KEY POINT
h Frontal lobe seizures are
typically brief and
associated with various
motor symptoms.

FIGURE 5-8 Posttraumatic encephalomalacia. Coronal fluid-attenuated inversion recovery

(FLAIR) (A) and T1-weighted (B) MRIs demonstrating extensive areas of
encephalomalacia within the right frontal and temporal lobe (blue arrows).
A smaller region of encephalomalacia and gliosis is also noted in the left lateral temporal
lobe (red arrows).

seizure symptomatology associated with volve motor symptomatology, and oc-

frontal lobe epilepsy varies depending
on the location of the seizure onset zone
within the frontal lobe.14 Compared to
temporal lobe seizures, frontal lobe
seizures are often shorter, usually in-
cur more often from sleep. The
postictal period is often characterized
by a quick return to normal cognition
but is occasionally associated with sub-
tle paresis or frank paralysis of the

FIGURE 5-9 Right temporal cavernous hemangioma. Coronal fluid-attenuated inversion

recovery (FLAIR) (A) and T1-weighted (B) MRIs demonstrate a mass lesion in the
anterior temporal pole, consistent with a cavernous hemangioma.

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 Adult Focal Epilepsies

involved motor region that resolves
over time. Frontal lobe seizures can
often appear unusual or bizarre to the
untrained observer, and many patients
are misdiagnosed with psychogenic
nonepileptic seizures or parasomnias.
Clinical Features
With respect to seizures, the frontal
lobe can be divided into primary
motor, supplementary sensorimotor,
orbitofrontal, dorsolateral, frontopolar,
and opercular regions. Most frontal
regions are associated with prominent
motor phenomena because of the
presence of premotor and motor cor-
tices within the frontal lobe. However,
frontopolar and orbitofrontal seizures
can have bland symptomatology, with
staring, unresponsiveness, and late
motor manifestations (complex autom-
atisms or versive head or eye move-
ment) that can be confused with
temporal lobe epilepsy. Table 5-1 out-
lines the clinical features that can be
seen with seizures from the various
frontal lobe regions. Several of the
more common presentations are
discussed later in the article.
Focal clonic or tonic seizures affecting
a limb or region of the trunk without loss
of consciousness or awareness are highly
suggestive of a seizure focus within the
perirolandic cortex or dorsolateral cor-
tex. Seizures of the perirolandic cortex
are typically clonic movements limited
to one region of the motor homunculus
(eg, face or hand) but can spread to
adjacent regions; this spreading is re-
ferred to as the jacksonian march.
Bilateral asymmetric tonic seizures,
which are described as tonic flexion of
one arm and extension of the other with
or without tonic leg involvement, are
associated with activation of the supple-
mentary sensorimotor area located in
Brodmann area 6 on the mesial or dorsal
aspect of the frontal lobe. These seizures
are also referred to as “fencing seizures”
because of the position of the arms.
They are considered simple partial sei-
zures since patients retain awareness

a
TABLE 5-1 Clinical Manifestations of Frontal Lobe Syndromes

Location Ictal Behavior

Perirolandic or Focal motor seizures with or without jacksonian march,
primary motor speech arrest or dysphasia, vocalization
Supplementary Focal asymmetric tonic posturing, versive movements of head
sensorimotor and eyes, speech arrest, vocalization
Dorsolateral Focal tonic or clonic activity, versive movements of head and
eyes, speech arrest or dysphasia
Orbitofrontal Complex motor automatisms, olfactory hallucinations
and illusions, autonomic features
Anterior Versive movements of head and eyes, forced thinking, initial
frontopolar loss of contact or “absencelike,” speech or motor arrest
Opercular Mastication, salivation, swallowing, laryngeal symptoms;
speech arrest or dysphasia; epigastric aura, fear; autonomic
features; facial clonic activity; gustatory hallucinations
Cingulate Fear, vocalization, emotional or mood changes, complex
motor automatisms, autonomic features
a
Reprinted with permission from Bagla R, Skidmore CT, Neurologist.14 journals.lww.com/
theneurologist/Abstract/2011/05000/Frontal_Lobe_Seizures.1.aspx. B 2011 Lippincott Williams
& Wilkins, Inc.

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despite the bilateral motor manifesta-
tions (Case 5-3). The presence of this
seizure type is often associated with a
mesial frontal or dorsolateral seizure
focus that preferentially spreads to
activate the supplementary sensorimo-
tor area. Seizures associated with large
vigorous proximal muscle movements,
such as bicycling movements of the legs
or windmilling of the arms, are often
associated with activation of the
frontopolar or orbitofrontal region. These
seizures have also been described in
the literature as hypermotor or hyper-
kinetic seizures. Activation of other
specific structures in the frontal lobe
can produce very specific seizure symp-
toms. For example, activation of the
frontal eye field located in the premotor
cortex results in forced head and eye
version, unnatural upward and lateral
KEY POINT
movement, contralateral to the sei- h The supplementary
zure focus. Occasionally, the entire sensorimotor area has
body will turn with the head and eyes, bilateral sensory and
and the patient may spin around the motor representation,
long axis of his or her body several and seizures generated
times. Involvement of the Broca re- from this region have
gion can result in an aphasic seizure, bilateral motor
and activation of the negative motor symptoms with
cortex, located on the posterior aspect preserved awareness.
of the inferior frontal gyrus or near the
supplementary sensorimotor area, can
produce seizures during which the
patient is unable to move a limb or
body part.14,15
EEG Findings
The interictal EEG associated with fron-
tal lobe epilepsy can vary depending
on the location of the seizure focus.
Overall, in a large surgical series, in-
terictal epileptiform activity was within

Case 5-3
A 25-year-old man presented for evaluation after having a generalized tonic-clonic seizure at home. He was
previously diagnosed with psychogenic nonepileptic seizures (PNES) at age 23. When asked to describe his
events, he stated that he often woke up from sleep and had tonic posturing of his arms and legs. He
specifically stated that his right arm was extended and his left arm was flexed toward his chest. At the end of
the seizure, he had several clonic jerks of his entire body. He stated that he is fully aware throughout the
events but cannot speak because he cannot control his mouth. A typical seizure lasted for approximately
20 seconds, and he often had clusters with 5 to 10 seizures per cluster. Immediately following the event, he
felt weak, but within 30 to 60 seconds, he felt normal. He had been evaluated at a local hospital and had a
normal EEG during one of these events. Based on the fact that he recalled the events despite having
bilateral motor manifestations and a negative EEG during one of the events, a diagnosis of PNES had been
made, and he was treated by a behavioral psychologist after that diagnosis, without relief.
Comment. The symptomatology described in the case is consistent with a bilateral asymmetric tonic
(fencing) seizure. These seizures are common for mesial frontal lobe epilepsy with activation of the
supplementary motor cortex. The supplementary motor cortex has bilateral motor and sensory
representation that has somatotopic organization. Therefore, a unilateral ictal discharge could cause
bilateral motor manifestations without impairing consciousness. Because of the limitations of scalp EEG, it is
not uncommon for patients, such as this patient, with mesial frontal lobe epilepsy to have normal EEGs.
A montage that included electrodes Fz, Cz, and Pz could have increased the diagnostic yield of the EEG. Even
in the face of a normal EEG, the stereotyped brief events are not typical of PNES, and PNES should
always remain a diagnosis of exclusion.
This patient was admitted to an epilepsy monitoring unit for continuous EEG monitoring, and
had an MRI of the brain that revealed a small cortical dysplasia in the left mesial frontal region
(Figure 5-10). During his admission, 15 stereotyped seizures were captured as described earlier. The
EEG revealed the onset of rhythmic beta in the central region, maximum at electrode Cz (Figure 5-11).
The patient was started on carbamazepine and was seizure free at last follow-up.
Continued on page 110

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 Adult Focal Epilepsies

Continued from page 109

FIGURE 5-10 Imaging of the patient in Case 5-3 showing left frontal cortical dysplasia.
Coronal fluid-attenuated inversion recovery (FLAIR) MRIs demonstrate an area
of increased cortical thickness in the mesial aspect of the superior frontal gyrus
(A, red arrow) and an associated tail of abnormality that extends toward the ventricle (B, blue
arrow). These findings are consistent with a cortical migrational abnormality.

FIGURE 5-11 EEG of the patient in Case 5-3 demonstrating mesial frontal seizure. During the third second of the EEG, a
paroxysmal fast discharge develops at electrode Cz (arrow). This finding was reproducible with all seizures
and always preceded clinical onset.

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the frontal lobe in 65% of patients,
outside the frontal lobe in 37%, contra-
lateral to the seizure focus in 17%, and
generalized in 24%.16 Dorsolateral and
frontopolar epilepsies are most likely to
show focal epileptiform activity since the
typical scalp EEG electrodes are imme-
diately over these locations. However,
even in these regions, epileptiform
activity may not be recorded with scalp
electrodes because of the size of the
cortical region involved. Based on
simultaneous scalp and intracranial re-
cordings, an area of at least 6 cm2 must
fire simultaneously to generate a depo-
larization that can be recorded reliably
with scalp electrodes.17 This technical
limitation is further exacerbated when
the distance between the generator and
the recording electrode is increased,
such as with foci involving the inter-
hemispheric region, orbitofrontal cortex,
or frontal opercular cortex. The addi-
tion of extra 10-10 electrodes, in partic-
ular over the midline region, may
increase the likelihood of recording
interictal epileptiform discharges and
ictal EEG changes. Because of the rich
connections to and location near the
temporal lobe, orbitofrontal epilepsy
can be associated with epileptiform
activity in the anterior temporal elec-
trodes. The overlap between the clinical
symptomatology and interictal EEG
between orbitofrontal lobe epilepsy
and temporal lobe epilepsy must be
considered, especially in patients with
nonlesional epilepsy.
Bilateral secondary hypersynchrony
has been described in patients with
frontal lobe epilepsy and is character-
ized by the rapid spread of the interictal
spike between the two hemispheres.
These epileptiform discharges often
appear as generalized spikes, poly-
spikes, or spike and wave, and it is
important not to misdiagnose a patient
with generalized epilepsy. Often an
initial spike/sharp wave can be seen
Continuum (Minneap Minn) 2016;22(1):94–115
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
KEY POINT
unilaterally before the “generalized” h The interictal and ictal
discharge, which, if stereotyped, pro- EEG associated with
vides a clue to the lateralization of the frontal lobe epilepsy can
epileptiform activity. Paroxysmal fast be challenging from a
(beta frequency) activity is also a technical perspective
feature of the interictal EEG that has because of movement
been associated with frontal lobe epi- artifact and the limited
lepsy (Supplemental Digital Content ability of scalp
5-10, links.lww.com/CONT/A166).18 electrodes to record
The ictal EEG is also challenging from seizure locations
(basal frontal,
in frontal lobe epilepsy. In the sur-
interhemispheric, and
gical series published by Jeha and
opercular regions) and
colleagues, 16 the ictal discharge in cases with limited
was localized to the frontal lobe in cortical involvement.
51% of cases, unilateral in 14%, and
generalized in 21%. Because of the
prominent motor manifestations asso-
ciated with frontal lobe seizures, ictal
recordings are often obscured by
muscle artifact (EMG). This makes it
difficult to see the initial ictal onset
and spread even after the digital EEG
is filtered. Other challenges include
the technical limitations mentioned
earlier with respect to recording
ictal epileptiform activity from deeper
foci and simple partial seizures that
may involve a limited amount of
cortex. These limitations are not
unique to frontal lobe epilepsy and
apply to all forms of focal epilepsy.
Despite these technical limitations,
several patterns have been associated
with frontal lobe epilepsy, includ-
ing diffuse electrodecrement, focal
rhythmic fast activity, and bilateral
hypersynchrony.18 An example of a
frontal ictal discharge can be seen in
Supplemental Digital Content 5-11,
links.lww.com/CONT/A167.
Imaging
MRI of the brain without contrast
should be obtained in the coronal and
axial plane and should include thin
slices (less than 3 mm). As described
for mesial temporal lobe epilepsy, the
MRI should include T1- and T2-
weighted images, and the use of
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 Adult Focal Epilepsies

KEY POINTS
h MRI scans should
include thin-cut T1- and
T2-weighted images
in the axial and
coronal planes.
h Malformations of
cortical development
are the most common
etiology associated with
frontal lobe seizures in
large surgical series.
h Autosomal dominant
nocturnal frontal lobe
epilepsy is associated
with a genetic mutation
in the neuronal nicotinic
acetylcholine receptor.
contrast will vary depending on poten-
tial etiology and local protocols. In two
surgical series, malformations of corti-
cal development were the most com-
mon etiology associated with frontal lobe
epilepsy (40% to 58%) (Figure 5-12),
compared to tumor (10% to 19%),
vascular (3% to 7%), and encephalo-
malacia (10% to 12%) (Figure 5-8).
Based on imaging or pathology, 10%
to 31% of patients had no identifiable
etiology. MRI scans were nonlesional in
26% to 45% of patients.16,19 Use of
FDG-PET imaging for presurgical plan-
ning is less likely to reveal a deficit in
patients with frontal lobe epilepsy com-
pared to patients with temporal lobe
epilepsy. However, in a 2012 series of
194 patients (34% with frontal lobe
epilepsy), 51% of patients with frontal
lobe epilepsy had regions of hypo-
metabolism identified. This compared
to 67% for temporal lobe epilepsy and
61% for nontemporal and nonfrontal
epilepsies. In the frontal lobe cases with
hypometabolism, the findings were on-
ly helpful in making a surgical decision
in 38% of cases.20 In the frontal lobe
surgical series mentioned earlier, when
PET was performed, the results were
abnormal in 25% of the patients in the
Lazow and colleagues series19 and in
76% of the patients in the Jeha and
colleagues series.16
Genetic Considerations
Autosomal dominant nocturnal frontal
lobe epilepsy is a well-described genetic
frontal lobe epilepsy syndrome. It is
characterized by brief motor seizures that
are stereotyped and occur multiple times
per night and is associated with normal
intelligence and a normal neurologic
examination between attacks. A family
history of similar seizures often exists,
although patients are often misdiagnosed
as having parasomnias, and a detailed
history regarding family members is
needed. The most commonly associated
abnormality with this disorder is in the
neuronal nicotinic acetylcholine recep-
tor, and the penetrance is variable, 29%
to 100% in the literature.21

PARIETAL AND OCCIPITAL

FIGURE 5-12 Left frontal malformation of cortical
development. Coronal T1-weighted MRI
demonstrates a large malformation of
cortical development in the left frontal region
(arrow). Associated enlargement of the left lateral
horn is seen.
LOBE EPILEPSY
Epilepsy associated with the parietal and
occipital lobes is much less common
than temporal or frontal lobe epilepsy.
Due to the rich connections between
the parietal and occipital lobes and the
frontal and temporal lobes, it can often
be challenging to reliably identify these
patients without the use of invasive
techniques. Visual auras are more com-
mon in occipital lobe epilepsy and are
typically elemental auras. Other symp-
toms may include ictal blindness,
blinking, and ocular movement.22 More

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complex visual scenes or objects may
be seen in occipital lobe epilepsy and
suggest spread of the seizure discharge
to the temporooccipital region. Sei-
zure foci below the calcarine sulcus will
preferentially spread to the temporal
region and may generate complex
partial seizures with symptomatology
and ictal EEG typical for temporal lobe
epilepsy.23 Foci above the calcarine
sulcus preferentially spread to the
parietal and frontal lobes.
Parietal lobe epilepsy is often associ-
ated with somatosensory auras that are
typically contralateral to the seizure
focus but can be bilateral.24 Often
patients with parietal lobe epilepsy will
display symptoms associated with
spread to the motor cortex, premotor
regions, or temporooccipital region.
Because of the rapid spread of the ictal
discharge to distant regions, it is very
important to take a detailed history to
try to identify if the first symptom is a
somatosensory aura.
The EEG findings in occipital and
parietal lobe epilepsy can be challeng-
ing. It is possible to see focal interictal
spikes and ictal onsets, but it is also
common to see interictal and ictal
patterns localizing to the temporal
and frontal regions because of the rich
synaptic connections. With midline
parietal or occipital foci, the possibility
exists for false localization to the
wrong hemisphere because of the
orientation of the electrical dipole
pointing to the contralateral hemi-
sphere. In addition, the possibility of
bilateral hypersynchrony, described
earlier for frontal lobe epilepsy, also
exists. An example of the onset of a
left parietal seizure that was associated
with a cortical dysplasia is shown in
Supplemental Digital Content 5-12,
links.lww.com/CONT/A168.
The causes of parietal and occipital
lobe epilepsies are similar to those
mentioned earlier for frontal lobe epi-
Continuum (Minneap Minn) 2016;22(1):94–115
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
KEY POINTS
lepsy. In studies that reviewed occipital h Occipital lobe epilepsy is
and parietal lobe epilepsy, malforma- often associated with a
tions of cortical development and tu- visual aura as the first
mors were more common in occipital clinical sign.
lobe epilepsy,25 while tumors were the h Parietal and occipital
most common etiology for parietal lobe epilepsies
lobe epilepsy.24,26 frequently spread to
adjacent cortical regions
INSULAR AND CINGULATE and may have features
LOBE EPILEPSY of seizures commonly
Focal epilepsy involving the insular associated with temporal
cortex and cingulate is uncommon. or frontal seizures.
Insular seizures should be suspected h Parietal lobe epilepsy is
in patients who present with seizure often associated with a
symptoms involving contraction or a somatosensory aura as
choking sensation of the oropharynx/ the first clinical sign.
larynx or a painful somatosensory h Insular and cingulate
aura.27,28 Cingulate epilepsy is very lobe epilepsy are rare
difficult to differentiate clinically from and should be carefully
the other focal epilepsies. Because of considered in patients
the rich anatomic connections to the with nonlesional
frontal and temporal regions, cingulate epilepsy since the
symptomatology often
seizures often mimic seizures originat-
overlaps with other
ing from these structures.13 In the
types of focal epilepsy.
absence of a clear lesion on MRI, these
cases often require invasive EEG mon-
itoring to confirm an ictal onset in the
cingulate or insular region.
CONCLUSION
The focal epilepsies are very common
in adulthood, and, while overlap in
clinical presentations often exists, each
region of the cortex often has several
distinct clinical presentations, EEG
findings, or imaging findings that may
aid in establishing an accurate diagno-
sis. The clinical history of the seizure
event either as reported by the patient
or observers, or through watching a
video of the event, is extremely impor-
tant. The terms complex partial and
simple partial are certainly helpful in
defining whether a patient has lost
awareness or consciousness or not,
but do not reflect the details that
permit a more accurate diagnosis.
Imaging and EEG are critical in
evaluating patients with focal epilepsy,
www.ContinuumJournal.com 113
 Adult Focal Epilepsies
but one must be cautious to ensure
that the study is properly designed to
ensure that common pathologies or
EEG findings are not missed inadver-
tently. This includes properly imaging
the temporal lobes with coronal views
and obtaining a thin-cut MRI for all
patients with focal epilepsy. The stan-
dard MRI used for stroke imaging is
not sufficient since epileptogenic le-
sions may often be subtle and missed
on an MRI with thicker cuts. The
addition of key midline or temporal
electrodes in the proper clinical con-
text will also assist in making an
accurate diagnosis.
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