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Complex partial seizures of frontal lobe origin.

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Complex Partial
Seizures of Frontal Lobe Origm
Peter D. Williamson, MD," Dennis D. Spencer, MD,? Susan S. Spencer, MD," Robert A. Novelly, PhD,*$
and Richard H. Mattson, MD"
Complex partial seizures of medial or orbital frontal origin were documented in 10 of 90 patients with intractable
epilepsy who were studied with depth electrodes. The clinical features that, in part, served to distinguish these seizures
from complex partial seizures originating elsewhere included brief, frequent attacks, complex motor automatisms with
kicking and thrashing, sexual automatisms, vocalization, and frequent development of complex partial status epilepticus. The constellation of clinical characteristics was often bizarre, leading to the erroneous diagnosis of hysteria.
Stereotyped attack patterns helped establish the diagnosis of epilepsy. Interictal and ictal scalp electroencephalograms
were often not helpful and were sometimes misleading.
Williamson PD, Spencer DD, Spencer SS, Novelly RA, Mattson RH: Complex partial seizures
of frontal lobe origin. Ann Neurol 18:497-504, 1985
Although uncommon, frontal lobe seizures with complex symptomatology have been recognized for more
than 30 years 126,271. Some reports suggest that frontal lobe complex partial seizures (FLCPS) can be clinically differentiated from complex partial seizures originating elsewhere E2, 13, 14, 21, 24, 34, 417, but a
syndrome of E C P S s has not been consistently defined. We describe the clinical seizure characteristics
and interictal and ictal electroencephalogram (EEG)
findings in 10 patients with FLCPSs diagnosed by
depth electrode studies.
Methods
Specific criteria for selection of patients in this series with
intractable epilepsy have been described previously 13 1, 32).
Initial evaluation included extensive neurological, medical,
psychological, and psychiatric examinations. Monitoring using a conventional scalp EEG with or without nasopharyngeal
andor sphenoidal electrodes and closed-circuit television
(CCTV/EEG) was continued until at least three habitual seizures were recorded. All patients who did not have obvious
structural lesiom as a probable cause of epilepsy had depth
electrode investigations. Linear composite electrodes with 18
contacts distributed equally along their length were used
[29]. Placement was designed to sample medial temporal
structures and the medial and orbital frontal cortex bilaterally
(Fig 1). The exact number and placement of electrodes was
dictated by clinical considerations. Additional recording over
cerebral convexities was obtained in some patients using insulated stainless steel pins inserted through the outer table
into the inner table of the skull 157. The day after electrode
placement, CCTVlEEG monitoring was begun and con~~
Results
General Clinical Features
FLCPs occurred in 10 of 90 patients with complex
partial seizures w h o were evaluated for epilepsy
surgery with depth electrodes during the past 12 years.
There were 9 men and 1 woman. Age when evaluated
with depth electrodes was 18 to 47 years (mean, 28.6
years). Age when seizures began was 5 to 2 1 years
~~
From the Departments of "Neurology, ?Surgery (Neurosurgery),
and $Psychiatry, Yale University School of Medicine, New Haven,
CT 06510*and
Haven
Center' West
CT
06516.
tinued until at least three seizures were recorded. The EEG
was recorded on split-screen video and on 16- or 20-channel
chart recorders. Selected channels were recorded on FM
tape in patients whose seizures spread rapidly. Recent patients were monitored using a 64-channel computer-based
system @}.
Data for this study were derived from patient and family
interviews, medical records, videotapes, and scalp and depth
EEGs. Seizure duration was determined by calculating the
time between clinical onset and mental clearing as recorded
on videotape. Therefore, seizure duration included ictal and
postictal states. Seizures were not included in the duration
calculation if they secondarily generalized into tonic-clonic
convulsions or if complex partial status epilepticus occurred.
Whenever possible, physicians andor nurses examined the
patients during seizures. Clinical seizure characteristics were
determined by repeatedly viewing videotaped attacks. Subjective sensations before seizures were determined by history review, patient interview, and reviewing videotapes in
which patients described their sensations. Ictal and interictal
scalp and depth EEGs were examined by three or more
electroencephalographers for consistent paroxysmal foci, location of seizure onset, and seizure spread.
Received Jan 3 , 1985, and in revised form Mar 6. Accepted for
publication Mar 7, 1985.
Address reprint requests to Dr Williamson, Epilepsy Center, West
Haven VA Medical Center, West Haven, CT 06516.
497
'
c--/
/
/
Fig I . Depth electrode placement. LS, RS = medialfrontal and
supplementav motor region; LF,RF = medial and orbitalfrontal region; LMT, RMT = intermediatefrontal, insular egion
and anterior temporal region; LPT, RPT = acc$ital-parietal,
hippocampus, amygdzla. Lateral phcement was a4usted to the
area sampled.
(mean, 12 years). General intelligence was normal to
high normal in all but 1 patient who had an I Q of 73.
Two patients had subtle frontal non-contrast enhancing radiolucent lesions on computed tomography (CT).
Both lesions initially escaped recognition but were
later interpreted as small areas of encephalomalacia
secondary to trauma or infarct. Findings of neurological examinations were normal except in 1 patient who
had sensory neural hearing loss. The presumed cause
of epilepsy was unknown in 6 patients, head trauma in
2 patients, birth injury in 1 patient, and frequent febrile seizures in 1 patient.
Clinical Seizure Characteristics
Clinical seizure characteristics of the 10 patients with
FLCPSs are described in detail in Table 1. By history,
seizures were frequent, often occurring in flurries of
many per day (mean, 10 per day), but there were
sometimes periods of days or weeks without seizures.
During evaluation, 154 seizures were recorded, 69
during scalp monitoring and 85 during depth recording. Seizures were brief in 8 patients (14 to 70 seconds; mean, 32 seconds) with minimal postictal confusion. Seizures lasting several minutes occurred only in
the 2 patients with consistent secondary spread to medial temporal structures (as will be discussed later).
Complex motor automatisms, often appearing semipurposeful, occurred in all patients either suddenly
at the beginning of seizures or after a change in facial
expression. Bilateral coordinated leg movements were
a prominent feature of motor automatisms.
Initial tonic or clonic activity was rare and never a
consistent feature of any patient's seizures. Vocaltza498 Annals of Neurology
Vol 18 No 4
October 1985
tion, often bizarre, occurred during seizures in 8 patients. Six patients had histories of prolonged confusion in addition to isolated seizures. Complex partial
status epilepticus was documented in 4 of them during
monitoring. The frenetic, often bizarre, behavior during seizures with rapid return of contact frequently
resulted in the erroneous diagnosis of hysteria. We
considered 4 of the patients hysterical after viewing
initial seizures during scalp monitoring. The stereotyped patterns of attacks, the lack of hysterical characteristics in neuropsychological assessment, scalp EEG
abnormalities, when present, and history of rare tonicclonic attacks helped to establish the correct diagnosis
prior to electrode placement. Eight patients claimed to
be aware during seizures, but this could never be documented. Test objects and phrases were not remembered, and partial responsiveness was only occasionally
seen, usually toward the end of seizures. Prominent
changes in autonomic functions (flushing, pallor, and
piloerection) were not observed.
Scalp and Depth EEG
The results of scalp EEG monitoring between and during seizures were seldom helpful for localization and
were misleading in 5 patients who had temporal foci.
Only 2 patients had interictal records with bilateral foci
suggesting secondary bilateral synchrony { 361. Seven
patients had no appreciable scalp EEG change other
than artifact during some of their seizures. The EEG
in 1 patient was abnormal only during a prolonged
episode of complex partial status epilepticus. Ictal
changes, when present, were usually generalized, slowing after seizure onset.
Interictal depth recordings are notoriously complex
and sometimes misleading {l, 6, 7, 15, 22, 40). All
patients had medial or orbital frontal paroxysmal foci
in the region of seizure onset. Nine patients also had
unilateral or bilateral independent medial temporal
foci. Seizures began in medial or orbital frontal regions
and were usually obvious with depth recording. Interictal abnormalities were replaced by high-frequency activity. Initial EEG suppression or flattening prior to
seizure discharges occurred in some seizures. Seizure
discharges were confined to the frontal lobes in the 8
patients who had short clinical attacks (Fig 2). The 2
patients with more prolonged attacks exhibited clear
delayed secondary spread of sustained seizures to medial temporal structures (Fig 3). Rapid spread to contralateral frontal areas occurred commonly. Rapid
spread precluded consistent lateralization in 4 patients,
even after computer-assisted and time-expansion analyses. Seizures began consistently in one medial frontal
lobe in 2 patients, but onset was not localized to a
specific region. Well-localized and laterahzed seizure
onset was established in 4 patients. Recording over
frontal convexities with stainless steel pins demon-
Table I , Clinical Seizure Characteristics
Patient
.T
Frequency
Average
Duration
1
l-4O/day
I5 sec
2
10-15/mo
3
0-4Olday
4
1-3lday
9.
Warning
Seizure
Onset
Buzzing noise,
visceral sensation
Stare
Claims aware;
not documented
Tightness in
chest
Stare
No; amnesic
70 sec
No
Stare
Claims aware;
not documented
14 sec
T&tness in
Frightened
expression
Claims aware;
not documented
Startled
expression
Claims aware;
not documented
Complex
Claims aware;
not documented
3.5 sec
arms
5
5-50/day
21 sec
6
0-40/day
20 sec
Tghtness in
chest, generaiized tinding
Complex psychosensory
motor
automatis m
7
2-3/day
Consciousnessl
Memory
during
Seizure
36 sec
Breathless
feeling
Complex
motor
automatisms
Claims aware;
IIIiIIiilldy
responsive
Motor
Automatisms
Vocalization
Complex
Partial Status
Epilepticus
Seizures
Recorded
Considered
Hysterical
Kicking, thrashing, rubbing,
scratching,
pelvic thrusting, genital
manipulation
Kicking, thrashing, rolling,
chewing, lip
smacking,
genital manipulation
Kicking, complex arm
movements
with posturing, groping,
picking,
genital manipulation
Abduction posturing of
arms, then
kicking,
thrashing,
genital manipulation
Thrashing, rocking, arms flailing
None
History of prolonged confusion; not
documented
13 seizures:
3 scalp,
10 depth
Yes
Shouted
obscenities
No
7 seizures:
3 scalp, 4
depth
Yes
None
Documented
9 seizures:
3 scalp, 6
depth
No
Prolonged
musical
hum,
snort
Documented
12 seizures:
3 scalp, 9
depth
No
Shouted
obscenities
No
15 seizures:
7 scalp, 8
depth
Yes
Kicking, s t e p
ping, thrashing, rocking,
bouncing,
groping, picking, pelvic
thrusting,
genital manipulation
Legs slapping
together,
stepping,
bouncing,
waving, patting, clawing,
clutching
hand movements, head
nodding and
shaking,
bizarre facial
expressions,
tongue protrusion and
whimpers,
squeals
No
30 seizures:
20 scalp,
10 depth
Yes
Repetitive
vowel
sounds
and
squeals
No
20 seizures:
7 scalp,
13 depth
Yes
Monotonous hum
Documented
15 seizures:
5 scalp,
10 depth
Yes
Gibberish.
moans,
whimpers
Documented
14 seizures:
7 scalp, 7
depth
Yes
Hum,
screams,
shouts
History of prolonged confusion; not
documented
19 seizures:
11 scalp,
5 depth
Yes
Wagging
8
O-4day
20 sec
Tightness in
throat, smell
Stare
Claims aware;
not documented
9
O-lO/day
52 sec
Visual illusion
Stare
Claims aware;
minimally
responsive
10
0-15/day
Lightheaded
Complex
motor
automatisms
No; amnesic
6.2 min
Restless leg
movements,
thrashing,
writhing
Thrashing,
writhing, kicking, bizarre
facial expressions, genital
manipulation
Kicking, thrashing, abduction
posturing of
arms
L = left; R = right.
Williamson et al: Frontal Lobe Complex Partial Seizures 499
strated lack of seizure onset from these areas but was
otherwise not helpful.
Surgery
The surgical methods and results are summarized in
Table 2. Although surgical decisions were heavily influenced by ictal depth EEG findings, other factors,
including overall clinical evaluations, consistent interictal data, speech dominance, and CT abnormalities, also
were considered. Two patients with seizures inconsistently lateralized to the left language dominant side
had division of the anterior two-thirds of the corpus
callosum. Three patients did not have surgery. Of the
5 patients who had frontal lobectomies, all had good to
excellent seizure control. However, one of these patients developed an incapacitating frontal lobe syndrome.
Discussion
The clinical characteristics of FLCPS we have described help distinguish them from complex partial sei500
Annals of Neurology
Vol 18 No 4 October 1985
Fig 2. Patient 9. Electroencephalographicrecording during seizure. (A) Onset can be seen as high-amplitude,slow complex
followed by low-amplitude, high-freqwency seizure discharge restricted to the left orbitalfrontal region (LF 16). There was
either no change orjattening at other recording sites. (B) Thirty
seconds afer onset, the seizure discharge remained confined t o LF
16. (Abbreviationsas in Figure 1 legend.)
zures originating elsewhere. These features are listed
in Table 3 with the citations referring to other reports
on FLCPS that mention the characteristics. Although
all of the features have been noted previously, they are
usually found in case descriptions without further comment. No prior reports compile all of the characteristics into a clinical syndrome of FLCPS.
Most, if not all, of the characteristics have been related to complex partial seizures in general and to temporal lobe seizures in particular. Some of the characteristics, such as change in facial expression at seizure
onset and complex illusionary warnings, have been included to indicate that they do occur in patients with
A
LF
I
B
I
2-8
10-18
I
LMT 1-15
14-18
RPT 1-11$,/**
L'
11-12
l2-I4
14-18
1
'
Fig 3. Patient 2.Electroencephalographicrecording during seizure. (A)Repetitive sharp activity can be seen, followed b./ lmamplitude, high-frequency seizure discharge in the right medial
frontal region (RPT 2-6). There was alerting response elsewhere. (B) Twenty seconds after right frontal onset, the seizure
developed in the right hippocampus (RPT 14). (Abbreviationsas
in Figure 1 legend.)
FLCPS. Others may be more specific for FLCPS. Several authors emphasize the prominence of complex,
semipurposeful motor automatisms in FLCPS 12, 13,
14, 34). We have observed sexual automatisms only
with FLCPS 1323. In our experience, complex partial
status epilepticus has occurred only with extratemporal, usually frontal, seizure onset 1421. Consideration of seizure frequency and duration combined with
the other clinical characteristics serves to clarify the
identity of these seizures.
isnc
I
Examination of seizure frequency and duration in
terms of different complex partial seizure types has not
been reported previously. The authors in the FLCPS
references cited in Table 3 described frequent brief
seizures, but frequency and duration were seldom precisely defined. Recent reports of videotaped complex
partial seizures described average durations of over 2
minutes 19, 351. Even assuming these studies included
some FLCPS, the average durations were at least four
times the mean duration we found in FLCPS. Average
frequency determinations for complex partial seizures
are not available. For comparison purposes, we calculated seizure frequency and duration for the last 20
patients with temporal lobe complex partial seizures
from our series. Mean seizure frequency was 4.7 per
month (range, 3 to 9), and mean duration was 3.8
minutes (range, 1 to 20 minutes). The mean frequency
for FLCPS was 10 per day (range, 0 to SO), and duration was 32 seconds (range, 15 to 70 seconds not in-
Williamson et al: Frontal Lobe Complex Partial Seizures
501
Table 2. Surgery and Results
Patient
No.
Depth
Lateralization
Depth
Localization
Operation Performed
Pathologic Findings
ResuldFollow-up
1
R frontal
Orbital frontal
R frontal lobectomy
Dense orbital frontal gliosis
2
R frontal
Medial frontal
R frontal lobectomy
Mild diffuse gliosis
3
L frontal
Surgery refused
None
4
Bilateral
frontal L
>R
Diffuse medialintermediate
frontal
Diffuse medialintermediate
frontal
1 year seizure
free, then recurrence at reduced frequencyl8 yr,
employed
N o seizures14
yrs, employed
Unchanged4 yr,
college student
Anterior *h callosal
section
Normal (L medial
frontal biopsy)
5
R frontal
Diffuse medial
frontal
R frontal lobectomy
Mild diffuse gliosis
6
Diffuse medialintermediate
frontal
Diffuse medialintermediate
frontal
Supplementary
motor area
Surgery refused
None
R frontal lobectomy
8
Bilateral
frontal L
>R
Bilateral
frontal R
>L
R frontal
Oligodendroglioma, R medial frontal
Mild diffuse gliosis
9
L frontal
L orbital frontal
Diffuse medial
frontal
Not recommended
None
Anterior 2 h callosal
section
None
7
10
L
=
Bilateral
frontal L
>R
R medial frontal resection
Brief nocturnal
seizures every
10-14 days13
yr, employed
Three isolated
generalized
seizures
when noncompliant/3
yr, employed
Unchanged3 yr,
unemployed
N o seizures13 yr,
employed
No seizures12 yr,
postoperative
frontal lobe
syndrome, unemployed
Unchanged2 yr,
unemployed
Reduced seizure
frequency and
severity12 mo
left; R = right
cluding the 2 patients with secondary temporal lobe
involvement).
Some of the characteristics of FLCPS have been produced by stimulating medial and orbital frontal regions
of the human brain. Complex ipsilateral, contralateral,
and bilateral motor activity followed medial frontal and
supplementary motor area stimulation 13, 26, 33, 381.
Bilateral motor activity in the legs was emphasized in
one report 131. Genital manipulation was described in
1 patient 1337. Vague sensory symptoms (tightness,
numbness, and dizziness) and reality distortions also
were reported 126, 381. Supplementary motor area
stimulation resulted in both vocalization and speech
arrest [26, 381. Vocalization was rhythmic, continuous,
or repetitive 1261. Orbital frontal stimulation is usually
associated with autonomic changes only 120, 377.
502 Annals of Neurology
Vol 18 No 4
October 1985
However, Heath 116, 171 reported pleasurable, sexually related responses following stimulation of the septal region. One patient described a “compulsion to
masturbate” 1.177.
The insufficient accuracy of scalp EEGs in FLCPS
observed by us and others C12-14, 19, 21, 341. emphasizes the need for depth electrode studies in these
patients if surgery is planned. However, the use of
depth electrodes or other intracranial recording techniques does not always accurately localize seizure onset
1227. Precise localization of seizure onset was accomplished in only 4 of our patients, and consistent lateralization was observed in another 2. Rapid seizure
spread has been described in frontal lobe seizures 14,
231 and could explain the inability to lateralize the side
of onset. Insufficient sampling, inherent in all depth
Table 3 . Snmmury of Characteristics
of Frontal Lobe Complex Partial Seizures
Characteristic
References
Frequent seizures, often in clusters, with many per day
Brief seizures, under 1 minute
Short postictal period with rapid
clearing
Prominent motor automatisms,
usually complex, often beginning suddenly
Aggressive sexual automatisms as
part of motor automatisms
Vocalization, with variable complexity from simple hum to
shouted obscenities
Frequent warnings, usually
nonspecific but sometimes
complex with psychic and illusional qualities
Complex partial status epilepticus
Bizarre attacks that appear hysterical
Stereotyped pattern
4 , 6 , 11-14, 18, 21,
34
4, 6, 13, 18, 21, 34
21, 34
2, 4, 6, 11-14, 18,
21, 27, 34, 41
12, 13, 18
2, 6, 12, 13, 34
13, 18, 2 , 34
4, 14, 42
11, 18, 2
. 27
11-14, 18, 21,27, 34
electrode investigations C7, 15, 25, 401, could account
for both inconsistent lateralization and imprecise localization. This is particularly so in the large frontal
lobes in which sampling all potential epileptogenic regions would require an uhacceptable number of electrodes.
Comparison of our intracranial recording results
with other studies reveals several common findings.
Complex partial seizures originating in the frontal
lobes usually begin in medial or orbital structures [4,
11, 12, 18, 21, 26, 343. Furthermore, these seizures
may not spread beyond the frontal lobes C12, 13, 21,
28, 341. In our series, secondary spread to medial temporal structures occurred in only 2 patients, in contrast
to the earlier concept that all complex partial seizures
originating extratemporally spread to involve the temporal lobes l301.
Additional evidence indicates that complex partial
seizures can, in part, be clinically subdivided by region
of seizure onset. Delgado-Escueta and associates {9,
101 respectively analyzed videotaped seizures from
a series of CCTV/EEG-monitored patients. They
defined two basic types of complex partial seizures.
Type 1 seizures, the most common, started with a
motionless stare, progressed to stereotyped automatisms, and ended with a period of partial responsiveness. Type I1 seizures were similar but lacked a
motionless stare at onset and began with stereotyped
motor automatisms. Type I1 seizures were reevaluated
because of poor seizure control following temporal
lobectomy [393. The authors concluded that type I1
seizures originated extratemporally. Many of the type
11 seizures they described resembled FLCPS as defined
in this report. Wieser 1411 reported findings in 51
patients with complex partial seizures studied with
depth electrodes. He defined five different seizure
types based upon depth EEG localization patterns and
correlated them with clinical findings on videotapes.
Clinical features of frontal lobe seizures (frontobasalcingulate seizure type) were very similar to the seizures we describe and included sudden onset with facial expression change, vocalization, and complex
motor automatisms.
Our analysis supports and extends the concept of an
identifiable FLCPS syndrome. It can be argued that
many of these characteristics are seen in complex partial seizures originating in other brain regions. It is the
constellation of these characteristics in patients having
frequent, brief seizures that serves to identify frontal
lobe origin. Although infrequent, delayed spread to
medial temporal structures resulted in more prolonged
seizures. The initial clinical features included those
listed in Table 3, suggesting frontal origin. Recognition
of potentially localizihg seizure patterns is of particular
importance in patients being considered for epilepsy
surgery.
Supported in part by Neurological Research Center (Epilepsy) NIH
Grant NS06208-18.
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