RESEARCH—HUMAN—CLINICAL STUDIES

RESEARCH—HUMAN—CLINICAL STUDIES

Tailored Unilobar and Multilobar Resections for

Orbitofrontal-Plus Epilepsy
Demitre Serletis, MD, PhD*
Juan Bulacio, MD‡
Andreas Alexopoulos, MD,
MPH‡
Imad Najm, MD‡
William Bingaman, MD‡
Jorge González-Mart
ınez, MD,
PhD‡
*Department of Neurosurgery, Univer-
sity of Arkansas for Medical Sciences,
Little Rock, Arkansas; ‡Epilepsy Center,
Neurological Institute, Cleveland Clinic,
Cleveland, Ohio
Correspondence:
Jorge González-Martínez, MD, PhD,
9500 Euclid Ave, S60,
Cleveland, OH 44195.
E-mail: gonzalj1@ccf.org
Received, November 18, 2013.
Accepted, May 22, 2014.
Published Online, July 3, 2014.
Copyright © 2014 by the
Congress of Neurological Surgeons.
BACKGROUND: Surgery for frontal lobe epilepsy often has poor results, likely because
of incomplete resection of the epileptogenic zone.
OBJECTIVE: To present our experience with a series of patients manifesting 2 different
anatomo-electro-clinical patterns of refractory orbitofrontal epilepsy, necessitating dif-
ferent surgical approaches for resection in each group.
METHODS: Eleven patients with refractory epilepsy involving the orbitofrontal region
were consecutively identified over 3 years in whom stereoelectroencephalography
identified the epileptogenic zone. All patients underwent preoperative evaluation,
stereoelectroencephalography, and postoperative magnetic resonance imaging.
Demographic features, seizure semiology, imaging characteristics, location of the epi-
leptogenic zone, surgical resection site, and pathological diagnosis were analyzed.
Surgical outcome was correlated with type of resection.
RESULTS: Five patients exhibited orbitofrontal plus frontal epilepsy with the epilep-
togenic zone consistently residing in the frontal lobe; after surgery, 4 patients were free
of disabling seizures (Engel I) and 1 patient improved (Engel II). The remaining 6 pa-
tients had multilobar epilepsy with the epileptogenic zone located in the orbitofrontal
cortex associated with the temporal polar region (orbitofrontal plus temporal polar
epilepsy). After surgery, all 6 patients were free of disabling seizures (Engel I). Pathology
confirmed focal cortical dysplasia in all patients. We report no complications or mor-
talities in this series.
CONCLUSION: Our findings highlight the importance of differentiating between
orbitofrontal plus frontal and orbitofrontal plus temporal polar epilepsy in patients
afflicted with seizures involving the orbitofrontal cortex. For identified cases of
orbitofrontal plus temporal polar epilepsy, a multilobar resection including the
temporal pole may lead to improved postoperative outcomes with minimal morbidity
or mortality.
KEY WORDS: Epilepsy, Focal cortical dysplasia, Multilobar resection, Orbitofrontal, Stereo-
electroencephalography

Neurosurgery 75:388–397, 2014 DOI: 10.1227/NEU.0000000000000481 www.neurosurgery-online.com

I
n longitudinal long-term studies, resective
surgery for frontal lobe epilepsy generally has
poor seizure outcomes.1 This is in stark contrast
to the improved rates of seizure control after
surgery for isolated temporal lobe epilepsy.
ABBREVIATIONS: EZ, epileptogenic zone; FCD,
focal cortical dysplasia; OF, orbitofrontal; OFF,
orbitofrontal plus frontal; OFTP, orbitofrontal plus
temporal polar; SEEG, stereoelectroencephalogra-
phy; SPECT, single-photon emission computed
tomography
Although reasons for this discrepancy remain
unclear, the difference may be due to the challenge
of identifying an epileptogenic zone (EZ) within
the cytoarchitectonic heterogeneity of the frontal
lobe, specifically the orbitofrontal (OF) region,
which has been divided by Brodmann (in 1905
and 1909) into as many as 3 distinct subregions
and by von Economo and Koskinas (in 1925) into
12 parcellated subregions.2-5 Moreover, the expan-
sive size of the frontal lobe and its related networks
of propagation, combined with the problem of
reaching frontobasal and mesial frontal regions
with subdural grid/strip electrodes that may

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themselves fail to sample deeper cortical regions, are other reasons
for the difficulties in localizing an EZ in the frontal lobe. Thus, in
addition to the intrinsic complexity of the OF region and its
extensive interconnectivity to the temporal lobe, it is these factors
that likely contribute to the difficulty of completely localizing the
anatomic boundaries of the EZ and consequently achieving better
seizure outcomes.
Here, we present a retrospective, cross-sectional analysis of
a consecutive cohort of patients with refractory OF epilepsy,
identified by chronic extraoperative invasive recordings using
stereoelectroencephalography (SEEG) methodology. This tech-
nique, as discussed below, is better suited to sampling extensive
epileptogenic networks (including deep cortical structures) using
3-dimensional intracerebral electrodes implanted in strategic foci of
the hypothetical EZ. In particular, the placement of SEEG
electrodes is conventionally guided by the results of a standardized
workup to delineate the hypothetical onset and spread of seizure
activity on the basis of video-EEG, imaging, and other clinical
studies.6,7 Ultimately, the goal of invasive SEEG monitoring is to
establish the topography of the EZ. Thus, in strict adherence to
this fundamental concept and on the basis of clinical and SEEG
features, we present evidence for 2 pathological and electro-clinical
patterns indicating different surgical approaches for each, and we
correlate these strategies with long-term seizure outcome.
METHODS
This study is a retrospective, cross-sectional analysis of a consecutive
cohort of 139 patients with intractable focal epilepsy who were
consecutively implanted with SEEG electrodes between March 2009
and January 2012. Specifically, all patients underwent standard
preoperative evaluation, including video-EEG, magnetic resonance
imaging (MRI), positron emission tomography, ictal single-photon
emission computed tomography (SPECT), and neuropsychological
studies. Of note, SPECT images were acquired by interictal image
subtraction from the ictal image, processed according to conventional
SISCOM (subtraction ictal SPECT coregistered to MRI) methodology.8
As a result of incongruent noninvasive data or the absence of a visible
lesion on the MRI, chronic, tailored frontotemporal implantations with
SEEG electrodes were indicated. Procedures pertaining to the SEEG
methodology, including implantation and removal of electrodes and
SEEG-guided resections, were performed by a single surgeon. The
recommendations for SEEG implantation were made and the general
planning of electrode sites was done during a weekly Epilepsy Center
multidisciplinary patient management conference after detailed review
and discussion of results of the noninvasive localization methods. In
addition to the general selection criteria for invasive extraoperative
monitoring,9-13 indications for SEEG implantation included (1)
improved access to deep-seated cortical regions of the EZ in areas such
as the mesial structures of the temporal lobe, cingulate gyrus, and other
interhemispheric regions, posterior OF area, insula, and depths of sulci;
(2) a failure of a previous subdural invasive study to clearly outline the
exact location of the seizure onset zone; and (3) the need for extensive
bihemispheric explorations in the context of failed lateralization of the
EZ. After an anatomo-functional localizing hypothesis was formulated,
a tailored frontotemporal implantation strategy was planned with the
goal of confirming or rejecting this preimplantation hypothesis.
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RESECTIONS FOR ORBITOFRONTAL-PLUS EPILEPSY
The SEEG implantation map was tailored specifically to each
patient’s type of epilepsy, in keeping with formal SEEG methodology.
The SEEG exploration was focused to sample an anatomic lesion (if
present), the structure(s) most likely to participate in ictal onset, or
possible pathway(s) of seizure propagation within a functional network
(such as the frontal-temporal, temporal-parietal, and limbic networks)
by sampling foci within the hypothetical EZ to capture the spread of
epileptic activity therein. The desired targets were reached with the use
of commercially available depth electrodes (AdTech, Racine, Wisconsin;
Integra, Plainsboro, New Jersey) implanted using conventional stereotactic
technique through 2.5-mm drill holes. From 9 and 14 electrodes were
implanted for each patient (mean, 11 electrodes per patient). Each SEEG
electrode measured 410 mm in total length, with 10 contacts spaced 5 mm
apart across 47 mm of recording length. Of note, within the total group of
139 patients, a total of 87 patients (62.6%) had an electrode targeted to the
OF region as part of their tailored implantation strategy. The decision to
include an OF electrode was based on noninvasive testing supportive of
a hypothetical EZ encompassing the frontal, temporal, or insular regions,
either solely or in combination. In this context, criteria for patient
inclusion in the current study included placement of an OF electrode using
SEEG methodology based on noninvasive, clinical criteria (including the
patient’s seizure semiology) and confirmed epileptic activity originating
from the OF electrode site. Exclusion from the study was limited to those
patients with an OF electrode from which initial seizure onset did not
appear to arise. From the total group of 87 patients with implanted OF
electrodes, we consecutively identified a subset of 11 patients (12.6%) with
seizures specifically originating in the OF cortical region who were thus
included in the present study.
After SEEG implantation, patients were subjected to clinical
monitoring and electrographic recording of all seizure events, as per
the standard protocol at our institution, in addition to functional
mapping with electric stimulation of all implanted SEEG electrodes.
A second patient management conference was held for each patient,
approximately 1 week after implantation, to discuss the results and
implications of the SEEG study and to collectively decide on a plan for
surgical resection. Subsequent to this meeting and approximately 6
weeks after removal of the SEEG electrodes, patients underwent
a standard craniotomy for tailored resection of the hypothetical EZ to
include the ictal onset zone and adjacent regions showing early or fast
spread of epileptic (ie, ictal) activity, in accordance with the scientific
literature defining the EZ.14-16 In addition to guidance from the
preceding SEEG electrode placements (which were visible on the
scalp, in the skull, and even on the cortical surface), surgical resections
were guided by anatomic landmarks and intraoperative Brainlab
neuronavigation. After recovery and discharge from hospital, all
patients were followed up with regular visits to document their seizure
outcomes over time.
Data pertaining to demographic features, seizure semiology,17 MRI
findings, SEEG electrophysiological recordings, location of seizure onset
zone, surgical resection site, and pathological diagnosis were recorded and
analyzed. To confirm the final placement of each electrode contact,
postoperative (ie, postsurgical resection) MRIs were coregistered to
computed tomography scans obtained immediately after the implantation
procedure with the use of voxel-based SPM software (Wellcome Trust
Centre for Neuroimaging, London, United Kingdom) in MATLAB 2008a
(MathWorks, Natick, Massachusetts); this also allowed visual confirmation
that the hypothetical EZ was adequately resected. Postoperative follow-up
appointments were arranged with a neurosurgeon and neurologist
at 3-, 6-, 9-, 12-, 18-, and 24-month intervals, and seizure
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SERLETIS ET AL
outcomes were assessed by the neurologist according to the Engel
classification.18
Of note, this study was approved by our local Institutional Review
Board. All surgical procedures were part of standard patient care, and no
procedures were performed solely for research purposes.
RESULTS
Participants and Descriptive Data
Of our complete series of 139 medically intractable epilepsy
patients, 87 patients (62.6%) had OF electrodes implanted as part
of their invasive SEEG study. Of this group of 87 patients, 11
patients (12.6%) had SEEG-confirmed onset of seizure activity
originating in the OF region. Demographics for this latter study
cohort, including individual clinical features, seizure semiology,
type of epileptic syndrome, and MRI findings, are depicted in
Table 1. Of note, 4 patients (36.4%) with recurrent seizures after
a previous attempted surgical resection were included in the
study; these individuals underwent SEEG electrode implantation
to better localize the EZ. In total, 54 electrographic seizures were
recorded, including 11 subclinical ictal events, across all 11
SEEG-implanted patients. Of note, functional mapping with
electric stimulation of each implanted electrode was attempted
for all 11 patients. Motor mapping (supplementary motor cortex
and primary motor cortex manifestations) was obtained in 5
patients (45.5%). Language mapping (motor speech) was
obtained in 2 patients (18.2%). No functional mapping
responses were obtained in 4 patients (36.4%) who had
electrodes located in noneloquent cortical areas or who were
unable to cooperate during the test. No provoked seizures or
adverse effects were observed during the functional mapping
acquisition procedure. After SEEG investigation, all 11 patients
underwent subsequent tailored resection of the hypothetical EZ
(as per the SEEG data). Patients were continuously followed up
for a mean period of 26.6 months, with a minimal follow-up of
21 months and the longest follow-up of 38 months.
Seizure Outcomes After SEEG and Tailored
Surgical Resection
SEEG evaluation identified the hypothetical EZ in all 11
patients. Each patient was then treated via tailored surgical
resection as guided by the SEEG intracranial recordings. Five
patients (45.5%) underwent left-sided craniotomies, and 6
patients (54.5%) underwent craniotomies on the right side.
Postoperative seizure control was improved for all 11 patients
(100%), as assessed by a neurologist according to the Engel
classification,18 with no complications (including no transient or
permanent postoperative motor deficits) or mortalities observed
in the group. Specifically, 10 patients (90.9%) remained free of
disabling seizures (Engel I) at last follow-up, with no seizures
reported from the time of surgery to the last follow-up
appointment. The remaining patient (9.1%) was clinically
improved but continued to experience rare, occasional seizures
(Engel II). In all patients, pathological analysis from the surgically
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resected specimens was abnormal, revealing focal cortical
dysplasia (FCD) type I in 10 patients and FCD type II in 1
patient. Table 2 summarizes the location of the ictal onset zone,
site of surgical resection, clinical outcomes, and pathological
diagnosis for each patient. From our results, we identified 2
distinct clinical-electrophysiological-pathological patterns associ-
ated with OF seizures that we categorized either as OF plus
frontal (OFF) pattern or as OF plus temporal polar (OFTP)
pattern (Table 3).
Main Results
OFF Epilepsy
Within our group of 11 patients, 5 (45.5%) were identified with
OFF patterns, presenting with seizures characterized by frontal
lobe–type semiology (such as hypermotor or asymmetric tonic
seizures) and abnormal ictal SEEG recordings confined to the
frontal lobe, particularly in the OF cortex, frontal polar, and/or
prefrontal regions. Tailored frontal surgical resection to also
include the hypothetical EZ within the OF and involved frontal
lobe structures resulted in sustained freedom from disabling
seizures in 4 patients (Engel I) and improvement in seizure
severity and frequency in 1 patient (Engel II). It should be noted
that the extent of the frontal lobe resection in each case was
planned to encompass all SEEG electrodes capturing the ictal
onset zone and adjacent regions showing early or fast spread of
epileptic (ie, ictal) activity, in accordance with the scientific
literature defining the EZ.14-16 In all 5 patients within this
subgroup, ictal epileptic signals were recorded from contacts
located in the most anterior and lateral aspect of the OF region,
with rapid spread to frontal polar or prefrontal electrodes.
Surgical pathology revealed FCD types I and II in all resected
specimens from both the OF and related frontal regions in these
patients.
Representative Case. Patient 9, who is right-handed, presented
with a 10-year history of medically refractory epilepsy. The patient
was otherwise healthy, with a normal neurological examination.
The patient’s seizures were classified as complex motor events
with infrequent secondary generalization without any preceding
auras. Seizures typically occurred in nocturnal clusters between 1
and 2 times per week and were considered medically refractory
after multiple medication trials. Extensive workup with scalp
EEG and video-EEG monitoring localized interictal and ictal
epileptic activity to the right frontal region. Ictal SPECT (Figure 1A)
and positron emission tomography (Figure 1B) confirmed hyper-
perfusion and hypometabolism in the ventral and dorsal aspects
of the right anterior frontal region, respectively. MRI (3T)
imaging was normal, suggesting nonlesional epilepsy. Further
investigation with magnetoencephalography confirmed spike
sources in the deep right frontal area. Neuropsychological
testing confirmed frontal lobe dysfunction, with borderline
(ie, low-average) language and memory scores. On review at the
epilepsy conference, the decision was made to proceed with
invasive SEEG implantation to better localize the EZ, with
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TABLE 1. Clinical Features of Orbitofrontal Epilepsy Patients Undergoing Stereoelectroencephalography Evaluationa

Age, Age of Epilepsy Semiological Seizure Previous Resective Surgery Time to Seizure
Patient y/Sex Handedness Onset, y Classification Epileptic Syndrome MRI (Before SEEG) Recurrence, wk
1 20/M L 11 Aura (auditory) / automotor / Focal epilepsy (R FT) R T LGWI ... ...
GTC
Dialeptic
2 29/M R 15 Dialeptic / automotor Focal epilepsy (R FT) Normal ... ...
3 49/Fe R 10 Clonic (R face) / automotor Focal epilepsy (L T) L T LGWI/HS L ATL (39 y) 60
4 55/Fe R 16 Aura (L somatosensory / visual) Focal epilepsy (R FP) Normal R FP CR (49 y) 1
Aura (abdominal) / automotor
5 48/M R 6 Aura (abdominal) / complex Focal epilepsy (L F) L F FCD ... ...
motor
6 49/M R 20 Aura (unclassified) / dialeptic Focal epilepsy (L F) Bilateral ... ...
FEM
GTC
7 50/M R 3 Aura (olfactory) / GTC Focal epilepsy (L FT) L T HS ... ...
Dialeptic / R arm tonic
8 33/Fe L 23 Aura (abdominal/gustatory) / Focal epilepsy (R FT) R T IHS ... ...
complex motor
9 22/M R 9 Complex motor / GTC Focal epilepsy (R F) Normal ... ...
10 56/Fe R 18 Complex motor / GTC Focal epilepsy (R FT) Normal R T CR (53 y) 2
11 55/Fe R 37 Aura (olfactory/gustatory) / Focal epilepsy (L FT) Normal L ATL (40 y) 48
automotor
GTC

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a
ATL, anterior temporal lobectomy; CR, cortical resection; EM, encephalomalacia; Fe, Female; F, frontal; FCD, focal cortical dysplasia; FP, frontoparietal; FT, frontotemporal; GTC, generalized tonic-clonic seizure;
HS, hippocampal sclerosis; IHS, increased hippocampal signal; L, left; LGWI, loss of gray-white interface; M, male; R, right; T, temporal.

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SERLETIS ET AL

TABLE 2. Surgical Planning and Patient Outcomesa

Patient Age at SEEG, y Side of Seizure Origin Ictal Onset Zone Site of Surgical Resection Follow-up, mo Outcome Pathology
1 17 R OF OF 1 TPo 38 Engel I FCD I
2 27 R OF 1 I OF 1 I 29 Engel II FCD IIa
3 47 L OF 1 I OF 1 TPo 1 I 29 Engel I FCD I
4 53 R OF OF 1 I 27 Engel I FCD I
5 46 L FPo OF 1 FPo 27 Engel I FCD I
6 47 L FPo OF 1 FPo 26 Engel I FCD I
7 48 L OF OF 1 TPo 25 Engel I FCD I
8 31 R OF OF 1 TPo 25 Engel I FCD I
9 20 R FPo OF 1 FPo 1 PF 24 Engel I FCD I
10 55 R OF 1 I OF 1 TPo 1 I 22 Engel I FCD I
11 53 L OF OF 1 FPo 1 posterior T 21 Engel I FCD I
a
FCD, focal cortical dysplasia; FPo, frontal polar; I, insula; L, left; OF, orbitofrontal; PF, prefrontal; R, right; SEEG, stereoelectroencephalography; T, temporal; TPo, temporal polar.

15 electrodes placed in the right anterior/posterior cingulate, OFTP Epilepsy

parietal, precentral gyrus (hand area), precentral gyrus (face
area), postcentral gyrus, pars triangularis, anterior/posterior
supplementary motor area, anterior/posterior OF, frontal polar,
posterior frontal polar, and insular and temporal polar regions.
SEEG monitoring while the patient’s antiepileptic medications
were tapered confirmed focal, extratemporal epileptic activity in
the right frontal lobe, with maximal activity recorded in the OF,
frontal polar, and prefrontal regions (Figure 1C). In total, 4
clinical seizures were recorded; functional motor mapping was also
performed and confirmed positive motor responses after stimula-
tion of the mesial contacts of an SEEG electrode in the superior
frontal gyrus (ie, supplementary motor area). On the basis of this
information, the patient underwent subsequent craniotomy for
a right-sided frontal lobe resection extending up to the anterior
limit of the supplementary motor area (ie, anterior to the precentral
gyrus; Figure 1D). Pathological analysis of resected tissue was
consistent with FCD type I (Figure 1E). Postoperatively, the
patient experienced no further seizures or auras (ie, Engel I
outcome) at the 24-month follow-up.
Six patients (54.5%) were classified with multilobar epilepsy
involving the OF and temporal polar regions. In this group, it is
interesting to note that the EZ consistently resided within the OF
cortex associated with the temporal polar region. Seizure semiol-
ogy was characterized by temporal lobe–like semiology (eg,
olfactory or psychic auras associated with dialeptic seizures, in
addition to possible gustatory auras).19-21 After tailored surgical
resection of the OF cortex and temporal pole, all 6 patients
(100%) achieved sustained freedom from disabling seizures at the
end of the follow-up period. In all patients in this subgroup, ictal
epileptic activity was recorded from contacts located in the most
mesial and posterior aspect of the OF region, with rapid spread to
the temporal polar region. Surgical pathology confirmed FCD
type I in all specimens resected from both the OF and temporal
polar regions.
Representative Case. Patient 8, who is left-handed, presented
with a 7-year history of refractory epilepsy. The patient was
otherwise healthy, with a normal neurological examination. The

TABLE 3. Summary and Consolidated Epileptic Pattern Classificationa

Patient Epileptic Syndrome Ictal Onset Zone Site of Surgical Resection Epileptic Pattern
2 R FT OF 1 I OF 1 I OF plus frontal
4 R FP OF OF 1 I OF plus frontal
5 LF FPo OF 1 FPo OF plus frontal
6 LF FPo OF 1 FPo OF plus frontal
9 RF FPo OF 1 FPo 1 PF OF plus frontal
1 R FT OF OF 1 TPo OF plus temporal polar
3 LT OF 1 I OF 1 TPo 1 I OF plus temporal polar
7 L FT OF OF 1 TPo OF plus temporal polar
8 R FT OF OF 1 TPo OF plus temporal polar
10 R FT OF 1 I OF 1 TPo 1 I OF plus temporal polar
11 L FT OF OF 1 FPo 1 posterior T OF plus temporal polar
a
F, frontal; FP, frontoparietal; FPo, frontal polar; FT, frontotemporal; I, insula; L, left; OF, orbitofrontal; PF, prefrontal; R, right; T, temporal; TPo, temporal polar.

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FIGURE 1. Clinical investigations for a representative case of orbitofrontal (OF) plus frontal (OFF) epilepsy. A, ictal single-photon emission computed tomography study
revealing hyperperfusion in the posterior basal aspect of the right frontal lobe and insula, with a 5-second injection time after clinical ictal onset. B, positron emission tomography
imaging suggestive of moderate hypometabolism in the right hemisphere (ie, frontal, parietal, and temporal regions) compared with the left side. C, stereoelectroencephalography
recordings confirming extratemporal epileptic activity in the right frontal region, maximal in the OF and frontal polar (FPo) regions. PFPo, posterior FPo; TPo, temporal polar.
D, T1-weighted magnetic resonance image (sagittal view) showing postoperative changes after resection of the right frontal lobe extending up to the anterior limit of the
supplementary motor area (ie, the anterior prefrontal region). E, histological pathology slide revealing a focal absence of cortical layer 2, consistent with focal cortical dysplasia
type I (hematoxylin and eosin stain, magnification ·200).

patient’s seizures were classified semiologically as focal epilepsy,
preceded by abdominal or gustatory auras followed by complex
motor seizures. Seizures were considered medically refractory
after multiple unsuccessful medication trials. Scalp EEG and
video-EEG analyses identified interictal and ictal epileptic activity
in the right frontotemporal region. MRI (3T) revealed increased
T2/fluid-attenuated inversion-recovery signal in the right amyg-
dala and hippocampal head, with mild enlargement of these
structures compared with the left side. Ictal SPECT showed
hyperperfusion in the right anterior temporal and basal frontal
regions (Figure 2A), and positron emission tomography imaging
detected regional hypometabolism in the right anterior and
mesial temporal lobe. Neuropsychological testing confirmed
average scores for language and memory function. On review
at the patient management conference, recommendations were
made for further assessment via invasive SEEG electrode
implantation and invasive monitoring (while tapering off the
patient’s antiepileptic medications). Specifically, 12 electrodes
were placed in the right planum temporale, planum polare,
anterior/posterior basal temporal, hippocampal head/tail, amyg-
dala, precentral gyrus (face area), pars triangularis, pars oper-
cularis, posterior OF, and frontal polar regions. In total, 6 clinical
seizures were recorded. Electric stimulation was also attempted in
each implanted electrode; however, no clinical manifestations or
afterdischarges were recorded. A decision was subsequently made
to proceed with craniotomy for resection of the right OF gyrus
and anterior temporal lobe (including the mesial structures;
Figure 2B) after SEEG confirmation of focal ictal epileptic
activity arising from the mesial and posterior OF gyrus with
spread to the temporal polar and mesial temporal structures
(Figure 2C). Pathology was consistent with FCD type I in both
the OF (Figure 2D) and temporal polar (Figure 2E) specimens.

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SERLETIS ET AL

FIGURE 2. Clinical investigations for a representative case of orbitofrontal (OF) plus temporal polar (OFTP) epilepsy. A, ictal single-photon emission computed tomography
showing hyperperfusion in the right anterior temporal and basal frontal regions, with an 8-second injection time after clinical ictal onset. B, T1-weighted magnetic resonance
image (sagittal view) confirming postoperative resection of the right OF gyrus and anterior temporal lobe (including the mesial structures). C, preceding stereo-
electroencephalography recordings revealing focal epileptic activity in the mesial and posterior OF gyrus, with spread to the temporal polar and mesial temporal structures. TPo,
temporal polar. D, histological pathology slide from the resected OF specimen illustrating loss of cortical organization, consistent with focal cortical dysplasia (FCD) type I
(hematoxylin and eosin stain, magnification ·200). E, similar features of FCD type I in a slide from the resected temporal polar specimen (hematoxylin and eosin stain,
magnification ·200).

Postoperatively, the patient experienced no further seizures or
auras (ie, Engel I outcome) at the 25-month follow-up.
DISCUSSION
Key Results
We present here a retrospective, cross-sectional analysis of
a consecutive case series of 11 patients with medically refractory
OF epilepsy in whom SEEG was used to identify the EZ. From
clinical and SEEG features, it was possible to stratify these patients
into 2 distinct electro-clinical patterns. Our findings support the
notion that the OF cortex plays a role in primary seizure
generation, either by contributing to epileptic activity solely
confined to the frontal lobe (OFF epilepsy) or by extension to
the temporal lobe (ie, the temporal pole or entorhinal cortex) via
the insula (OFTP epilepsy). The latter pattern is consistent with
similar concepts regarding multilobar seizures involving the
temporal lobe, which have previously been reported in the
literature.22-26 Nevertheless, to the best of our knowledge,
multilobar EZs originating in the OF region and requiring
multilobar resection have not been described to date.
Interpretation of Results
Frontal lobe resections, including lobectomies and lesionecto-
mies, are relatively common procedures for medically refractory
epilepsy, accounting for up to 30% of all epilepsy surgeries.27

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Reported success rates for frontal lobe resections, however, are
generally poor compared with temporal lobe resections (ranging
anywhere between 13% and 47%).1,28-33 With respect to
epileptogenic OF resections, the literature remains sparse,
however. Kriegel et al34 recently identified a small cohort of
10 patients with OF epilepsy confirmed electrophysiologically via
intracranial subdural grids and depth electrodes.34 In their
review, they describe 1 illustrative case wherein focal resection
of the OF region resulted in postoperative seizure freedom. In
general, sustained seizure freedom remains even less likely in
patients with nonlesional MRI.35,36 These lower success rates are
likely due to mislocalization or incomplete resection of the EZ,
especially in the context of a comparatively more limited
resection. In our study, we identified a subgroup of patients
with frontal lobe epilepsy (with seizure onsets in the OF region)
in whom the anatomic boundaries of the EZ extended beyond
the limits of the frontal lobe and into the temporal region
(classified as OFTP epilepsy). For these patients, multilobar
resection, including the anterior superior temporal gyrus and
temporal polar regions, resulted in sustained freedom from
disabling seizures. On the basis of our results, this could
potentially account for previously reported failures in frontal
lobe surgeries resulting from incomplete resection of the EZ,
which could be partly located in extrafrontal cortex (such as the
temporal pole) and thus left behind during resective procedures.
Our results also underscore the fact that the intrinsic organi-
zation and connectivity of the OF region and its contribution to
prefrontal epilepsies remain to be fully understood. According to
extensive work by von Economo and Koskinas,2 the cytoarchitec-
tonic structure of the anterior part of the OF region (ie, areas FF
[the granular orbital area], FFa [the agranular orbital area], and
FFF [the pretriangular orbital area]) more closely resembles that
seen in the frontal polar regions, with a higher degree of
connectivity identified between these areas. Anatomic and
diffusion tensor imaging studies confirm these pathways, with
projection tracts (eg, internal capsule, corona radiata) and
association tracts (short U-shaped intralobar and interlobar
fibers, arcuate fasciculus, cingulum, and inferior fronto-occipital
fasciculus, among others) comprising the white matter connec-
tivity in this region.37 These findings support our results in the
group of OFF epilepsy patients (with seizure onsets in the most
anterior and lateral areas of the OF cortex), with the EZ confined
to the OF, frontal polar, or prefrontal regions. In these patients,
resection of the OF cortex in association with the prefrontal areas
resulted in sustained seizure control.
Conversely, cytoarchitectural similarities have been identified
in the posterior aspect of the OF cortex (ie, areas FJ [the
frontoinsular region] and FK [the frontal piriform area]) and the
temporal polar region, with inherent functional connections
reported between these locations.2 It is now generally accepted
that destruction of the medial inferior (ie, orbital) part of the
frontal lobe is likely to result in emotional changes, likely because
of its function in relation to extrafrontal temporal lobe structures,
including the temporal pole (Brodmann area 38) and entorhinal
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region (Brodmann area 28).38-40 Studying rhesus monkeys, Van
Hoesen et al41 successfully mapped projections from the OF
gyrus to the entorhinal region (Brodmann area 28) and adjoining
cortex (these findings were also confirmed by Leichnetz and
Astruc42,43), lending further evidence to support the intrinsic
connectivity between the posterior OF region and temporal
limbic structures. In contrast, lesions on the dorsal and lateral
convexity of the premotor cortex (Brodmann area 47) have been
reported to produce intellectual deficits and worsened perfor-
mance in delayed-response tasks,44,45 in accordance with
cognitive and executive-type functions arising from the frontal
lobe networks.
From a cytoarchitectonic perspective, the prefrontal cortex is
heterogeneous and contains multiple different subregions.2 At one
extreme, the posterior OF cortex comprises agranular/dysgranular
cortices and prominent deep neuronal layers (V-VI), with
a relatively lower neuronal density and a high cellular ratio of
glia to neurons. These features are similar to the cytoarchitectonic
features of the limbic areas and temporal lobe. At the other
extreme, the eulaminated cortex located in the dorsal-lateral
surface of the premotor cortex is characterized by a higher density
of neurons and a prominent granular layer (IV),46 similar to other
cortical areas in the dorsal surface of the frontal lobe. These
findings are also supported by white matter connectivity
comprising projection tracts (eg, fornix) and association pathways
(eg, uncinate fasciculus, arcuate fasciculus, and cingulum)
between the OF region and the anterior temporal lobe.37
Consequently, our results for a group of 6 patients with OFTP
epilepsy in whom posterior OF-onset seizures involved the
anterior temporal lobe support the idea that pathological epileptic
networks obey the normal neuronal connectivity between the
posterior OF and anterior temporal areas. This hypothesis is
further supported by the fact that a multilobar resection of these
structures led to sustained freedom from disabling seizures (Engel
I status) in all 6 patients.
Limitations and Generalizability
There is undoubtedly a component of selection bias in our study
resulting from its inherent focus solely on patients with OF-onset
epilepsy and their clinical outcomes after surgical resection. We
acknowledge that a comprehensive study is needed to capture the
efficacy of SEEG for its diagnostic capabilities across all brain sites.
This is the subject of a wholly separate report, which we have just
recently completed and submitted for publication. Of relevance to
the present study, we report an overall seizure-free rate (ie, Engel I
outcome) of 67.8% over an average of 2.4 years for patients
undergoing SEEG followed by a tailored surgical resection.47
In addition, within the overall group of 87 patients in our
present study undergoing OF electrode implantation, we were
unable to identify any clinical differences between the patient
cohort with OF-onset epilepsy (ie, the 11 patients included in this
study) and the remaining 76 patients who had seizure onset at
some other site apart from the OF region. Thus, we are unable to
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SERLETIS ET AL
comment further on a specific indication to include an OF
electrode other than noninvasive testing supportive of a hypothet-
ical EZ encompassing, either solely or in combination, the frontal,
temporal, and insular regions (as was done in this study).
It is also possible that a smaller resection may have been
sufficiently appropriate to capture the EZ in the OFTP patients.
However, it is interesting to note that 3 of these patients had
actually undergone prior surgical treatment for presumed temporal
lobe epilepsy via isolated temporal resections (2 with temporal
lobectomy, and 1 with a temporal neocortical resection, as in Table
1), with subsequent postoperative seizure recurrence. It was only
after SEEG implantation and additional resection of the OF-
onset seizure zone, however, that these 3 patients finally achieved
sustained freedom from disabling seizures (Engel I outcomes).
Despite the limitation of a small sample size in our study, this
observation lends more credence to the utility of multilobar
resection in the treatment of OFTP epilepsy. It also suggests that
patients with failed temporal lobe epilepsy should be considered
not only for further extension of the temporal resection but also
for possible multilobar resection to include the OF region as well.
Ultimately, a future randomized controlled trial incorporating
a large cohort of patients would be useful in more definitively
demonstrating the effect of different resections, or possibly
staging these resections, on postoperative seizure outcomes for
patients afflicted with OF epilepsy.
CONCLUSION
It is important to differentiate between OFF and OFTP
epilepsy in patients afflicted with seizures involving the OF cortex
on the basis of clinical and electrophysiological (SEEG) features.
For identified cases of OFTP epilepsy, a multilobar resection
including the OF region and temporal pole may lead to improved
postoperative outcomes with minimal morbidity or mortality.
Disclosure
The authors have no personal, financial, or institutional interest in any of the
drugs, materials, or devices described in this article.
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COMMENTS
I
n the late 1950s, Bancaud, Talairach, and their colleagues were the first
to record the onset of seizure in human beings using intracerebral
electrodes.1 A number of multilead electrodes were stereotactically im-
planted to verify a coherent hypothesis on the anatomo-electro-clinical
correlations. The complex spatial arrangement of the recording devices,
specifically tailored for each patient, allowed defining tridimensionally
the epileptogenic zone (EZ). A few years later, the term stereo-
electroencephalography (SEEG) was coined, and the methodology was
ultimately described in a milestone textbook by the 2 French re-
searchers.2 Despite its efficiency and safety, SEEG methodology re-
mained underused in the United States and in many other countries for
decades, but now it is progressively spreading all over the world. The
authors started with their SEEG program in 2009, studying .130
patients in .3 years. These data clearly show the authors’ enthusiasm for
this rediscovered methodology.
In this study, the authors reported a group of 11 subjects with seizures
originating in the orbitofrontal (OF) cortex. Thanks to SEEG electrodes, it
was possible not only to reveal the ictal onset zone but also to define the EZ,
extending up to the anterior frontal cortex (orbitofrontal plus frontal) or up
to the temporal pole (orbitofrontal plus temporal polar). The authors
therefore identified 2 distinct clinical-electrophysiological-pathological
patterns associated with OF seizures and resected the EZ in all subjects,
achieving excellent results on seizures. This evidence largely overlaps pre-
vious published data.3 In fact, after an accurate analysis of 66 seizures
involving the orbital cortex, the latter authors concluded:
1) . . .ictal discharges can start in the orbital cortex, but, in our
experience, they never remain localized only in the orbital frontal cortex.
2) The symptoms related to the initial orbital discharges are very difficult
to identify, because the most frequent symptom is the lack of evident
symptoms. . . 3) Discharges starting in the orbital cortex may spread at
least to: (a) deep temporal lobe structures without preference for the
amygdala or the anterior Amman’s horn; (b) other frontal structures,
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mainly the cingulate gyrus of the anterior mesial cortex . . .; (c) the lateral
temporal neocortex, without any involvement of the deep structures; and
(d) the opercular region.
Nonetheless, despite the previous reports, the present study is most
likely the first peer-reviewed article reporting on multilobar EZs origi-
nating in the OF region and requiring multilobar resection.
As clearly mentioned by the authors, SEEG methodology let them
record brain activity directly from the OF cortex, a region difficult to be
adequately sampled by means of subdural grids of electrodes. It should be
noted that the implantation of SEEG electrodes was safe in all 11 patients,
with no complications despite previous craniotomies in 4 of them. The
sample size is certainly small, but this study proves once more that SEEG is
a methodology offering high effectiveness and very low morbidity. SEEG
electrodes record electric activity directly from the cortical surface, the
bottom of the sulci, and the white matter, giving also the possibility of brain
mapping by means of electric stimulations. The authors announced that
their experience with SEEG for seizure localization across all brain sites in
a larger cohort of subjects is going to be published soon, and I am sure that
this new study will provide major evidence in the field of epilepsy surgery.
Francesco Cardinale
Milano, Italy
1. Bancaud J. Apport de l’exploration fonctionnelle par voie stéréotaxique à la chirurgie
de l’épilepsie [in French]. Neurochirurgie. 1959;5(1):55-112.
2. Bancaud J, Talairach J. La Stéréo-électroencéphalographie Dans L’épilepsie. Paris,
France: Masson & Cie; 1965:231-310.
3. Munari C, Bancaud J. Electroclinical symptomatology of partial seizures of orbital
frontal origin. In: Chauvel P, Halgren E, Delgado Escueta AV, Bancaud J, eds.
Advances in Neurology. Vol 57. New York, NY: Raven Press; 1992:257-265.
T
his report from an epilepsy center experienced in the use of stereo-
electroencephalography (SEEG) presents 2 groups of patients who
were found to have seizures originating from orbital frontal electrodes:
those whose seizures spread frontally and those whose seizures spread
temporally. Excellent results with reasonable follow-up established that
the localization technique led to a “curative” site of resection.
The report is important in that it is a demonstration of the value of
SEEG as a low-morbidity, useful procedure in the localization of intrac-
table focal epilepsy. As an epileptologist, though, perhaps an equally
important question is not how but where.
Whether the area is best accessed with the SEEG technique as in the
current report, with subdural grids or strips, or with a hybrid technique of
subdural and selected depth electrodes is just as important as the seizure
semiology, neuroimaging, neuropsychological, and scalp EEG findings
that led the team to implantation within the orbital frontal region in the
first place. For example, of their case series, 87 patients had electrodes
implanted in that region. Of the 87, 11 had seizures arising from the
orbital frontal region. What is not clear in this report is the difference in
symptoms between the 11 orbital frontal and 76 nonorbital frontal
subjects.
Both the technique of SEEG and the rationale for implantation in
specific brain regions require equal emphasis in guiding other physicians
in the challenging field of invasive electrocortigraphy. This excellent group
appears capable of enriching the field with both.
Mark Quigg
Charlottesville, Virginia
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