close

Вход

Забыли?

вход по аккаунту

?

Characteristics of medial temporal lobe epilepsy II.

код для вставкиСкачать
Characteristics of Medial Temporal Lobe
Testing, Neuroimagmg, Surgical Results,
and Pathology
P. D. Williamson, MD,” J. A. French, MD,i V. M. Thadani, MD,” J. H. Kim, MD,$ R. A. Novelly, PhD,Wtt
S. S. Spencer, MD,BI-t D. D. Spencer, MD,”*t?-and R. H. Mattson, MD$T+
Sixty-seven patients with temporal lobe epilepsy without circumscribed, potentially epileptogenic lesions, who were
studied with intracranial electrodes and who became seizure free following temporal lobectomy were retrospectively
evaluated with regard to preoperative scalp electroencephalographic (EEG) findings, neuropsychological test results,
neuroimaging findings, results of surgery, and pathology of resected tissue. Interictal scalp EEG showed paroxysmal
abnormalities during prolonged monitoring in 64 patients (96%).These were localized in the anterior temporal region
in 60 (94%) of these 64 patients. Bilateral independent paroxysmal activity occurred in 42% of the patients and was
preponderant over the side of seizure origin in half. Ictal EEG changes were rarely detected at the time of clinical
seizure onset, but lateralized buildup of rhythmic seizure activity during the seizure occurred in 80% of patients. In
1396,the scalp EEG seizure buildup was, however, contralateral to the side of seizure origin as subsequently determined
by depth EEG and curative surgery. Lateralized postictal slowing, when present, was a very reliable lateralizing
finding. Neuropsychological testing provided lateralizing findings concordant with the side of seizure origin in 73%
of patients. When neuropsychological testing produced discordant results or nonlateralizing findings, those patients
were usually found to have right temporal seizure origin. Intracarotid amobarbital (Amytal) testing demonstrated
absent or marginal memory functions on the side of seizure onset in 63% of patients, but 26 patients (37%) had
bilaterally intact memory. In those patients who had magnetic resonance imaging, it was very sensitive in detecting
subtle medial temporal abnormalities. These abnormalities were present in 23 of 28 magnetic resonance images, and
corresponded with mesial temporal sclerosis on pathological examination in all but 2 patients. Eighty-one percent of
the 5 1 patients who had adequate pathological examination of tissue had mesial temporal sclerosis. Forty-one patients
with adequate pathological examination had histories of febrile seizures and of these 38 (93%) had mesial temporal
sclerosis.
Williamson PD, French JA, Thadani VM, I m JH, Novelly KA, Spencer SS, Spencer DD, Mattson RH
Characteristics of medial temporal lobe epilepsy 11. Interictal and ictal scalp electroencephalography,
neuropsychological testing, neuroimaging, surgical results, and pathology Ann Neurol 1993,34 781-787
This is the second in a series of reports designed to
critically examine a group of 67 patients who did not
have mass lesions, in whom medial temporal seizure
origin was documented during intracranial recording,
and who became seizure free following temporal lobectomy. The first report examined those findingsthat
were available following the initial history and Physical
examination
This study evaluates the results of
interictal and ictal scalp electroencephalographic (EEG)
monitoring, neuropsychological testing including intra-
From the ‘Section of Neurology, Dartmouth Hitchcock Medical
Center, Lebanon, NH; +Department of Neurology, Graduate HosPit’,
PA;
Of
(Neuropathology),
§Neurology, TlPsychiatry, and *”Surgery (Neurosurgery), Yale University School of Medicine, New Haven, CT; and ftEpilepsy Center,
Veterans Administration Medical Center, Wesr Haven, CT.
carotid amobarbital (Amytal) testing, neuroimaging,
surgery, and pathological examination of resected tissue.
and Methods
All 67 patients in this study had temporal lobe epilepsy El}
and when retrospectively selected for this study met the criteria for class I surgical outcome as defined by Engel [Z}. Patients in whom a circumscribed mass lesion was detected with
neuroimaging, or with pathological examination of resected
Received Jan 19, 1993, and in revised form Jun 21. Accepted for
publication JuI 1, 1993.
Address correspondence Dr Williamson, Section of Neurology,
Dartmouth-Hitchcock Medical Center, Lebanon, N H 03756.
Copyright 0 1993 by the American Neurological Association
781
tissue, were excluded from this study. Prior to 1987, all patients without detectable mass lesions had intracranial EEG
monitoring. High-resolution magnetic resonance imaging
(MRI) became available to our program in 1986. Between
1987 and 1989, as resolution improved and as we becaine
more familiar with the signal and anatomical changes associated with medial temporal disease, 18 patients with mostly
congruent findings on MRI, scalp EEG, and neuropsychological testing underwent successful temporal lobe surgery without intracranial electrode placements. All the patients in this
series, which was between 1972 and 1990, however, had
intracranial studies. Our current presurgical evaluation procedures were recently described [3].
Scalp EEGs were examined for background abnormalities,
interictal paroxysmal activity, ictal onset changes, lateralization of ictal paroxysmal rhythmic buildup, and lateralized
postictal slowing. Ictal EEG changes were carefully related
to the clinical seizure onset. This was determined by the first
objective evidence of seizure activity on videotape, or by the
patients’ subjective awareness of seizure onset which caused
them to press the alarm button. Scalp EEG localization or
lateralization was done using only standard 10-20 electrode
placements. The paroxysmal abnormality was considered to
be anterior if phase reversal occurred at the F7 or FHelectrode
or between F,/F, and TJT,. Midtemporal localization involved phase reversal at T, or T,, and the abnormality was
considered posterior temporal if phase reversal occurred at
T,/TG o r between T,/TG and T,/T,. While nasopharyngeal
or sphenoidal recording was used in some patients, it provided no additional information arid is not included in this
analysis. Currently, more elaborate computerized spatial resolution methods are being used [4, 51, but those data are
not included.
Intracarotid amobarbital testing of memory and language
function was done in all patients. Memory was considered
adequate if three o r more items out of six were correctly
identified by spontaneous recall or recognition in a multiplechoice format. Two correctly identified items were considered marginal memory, and one or less was scored as a
failure.
Detailed neuropsychological testing was performed on all
patients. This included examination of upper-extremity
strength and dexterity, sensory perceptual examinations in
three major modahties (auditory, visual, and tactile), speech
and language testing, quantification of both immediate and
delayed verbal and nonverbal memory, evaluation of intellectual function (Wechsler Adult Intelligence Scale-Revised
{WAIS-R)), and assessment of personality structure. For purposes of this study only the final impression, in terms of
localization and lateralization, was used.
High-quality MRIs have been available since 1986. MRIs
were obtained using a GE Signa 1.5-Tmachine. Images were
obtained in the sagittal, coronal, and axial planes. Parameters
used for T1-weighted images were repetition time (TR)/echo
time (TE) of 800111 msec; for T2-weighted images, TRiTE
of 2500130180 msec; and SPGR, TR/TE of 2515 msec. Special care was taken to avoid head rotation. MRIs were
interpreted using visual inspection only. The first author
(P. D. W.) was blinded to the identity of the patient. Hippocampal atrophy was identified in accordance with the criteria
of Berkovic and colleagues [GI.
Surgical results were determined by routine clinic followup, and by phone calls to families and patients. Results of
pathological examination of resected tissue were determined
by reviewing pathology reports, or by reviewing specimens
with one of the authors (J. H. K.).
Results
Eiectroencep~ai~~raphic
Datu
Long-term scalp EEG monitoring records were evaluated for interictal paroxysmal activity on daytime and
overnight recordings in all patients (Table 1). Prolonged monitoring failed t o detect interictal paroxysmal activity i n only 3 patients (4%). Scalp EEGs from
64 patients exhibited clear paroxysmal activity consisting of sharp and slow wave complexes. Strictly unilateral temporal paroxysmal activity was present in 35
patients (52$7j), and was anteriorly located in all b u t 3.
I t was concordant with t h e side of seizure origin in 33,
as determined by subsequent d e p t h EEG and surgical
cure, and discordant in 2.
Twenty-eight patients (42%!)had bilateral independ e n t temporal paroxysmal activity as t h e predominant
abnormality. This was all located anteriorly, except
in 1 patient w h o had a midtemporal focus on t h e side
contralateral t o the seizure origin. In 2 1 patients, t h e
abnormalities had a lateralized preponderance with t h e
ratios ranging from 3 :2 t o 30 : 1. The lateralized preponderance was concordant with the side of seizure
onset in 15 patients, with t h e ratios ranging from 2 : 1
t o 30: 1. I n 6 patients, t h e preponderance was discordant, with t h e ratios ranging f r o m 3: 2 to 20: 1.
I n 7 patients, the abnormalities were equal on t h e
two sides. O n l y 1 patient had bilateral synchronous
activity as t h e prominent interictal finding. This patient
also had a less active anterior temporal sharp focus on
the side of seizure origin.
Ictal scalp EEG records were examined for electrographic changes at the time of clinical seizure onset,
and for lateralized buildup of rhythmic seizure dis-
Table I . Scalp Electroencephalogr~ph~c,
Interictal Puroxysmal Activity
Preseni
Absent
Strictly unilateral
Concordant
Discordant
Anterior temporal
Midtemporal
Posterior temporal
Bilateral independendanterior temporal predominant
Equal
Lateralized preponderance
Concordant
Discordant
Bilaterai synchronous predominant
782 Annals of Neurology Vol 34 No 6 December 1993
64
3
35
33
2
32
1
2
28
7
21
15
6
1
Tuble 2. Scab Electroencephalographic, Ictal Cbanges
Total no. of patients
Bilateral ictal changes
Lateralized ictal onset
Concordant
Lateralized buildup (including 4 with lateralized ictal
67
13
4
4
54
onset)
Concordant
Discordant
Alternating bilateral
Lateralized postictal slow
Concordant
47
5
2
45
45
charges (Table 2). Clear EEG changes at or before clinical seizure onset were observed in only 4 patients
(6%). All were concordant with the side of seizure
origin, as determined by subsequent depth EEG and
surgical results. Predominantly lateralized ictal EEG
buildup of rhythmic 5- to 10-Hz sharp activity was
detected in seizures from 54 patients (81%). This appeared within 30 seconds after the first subjective or
objective indication of seizure origin. The ictal EEG
buildup was concordant with the side of seizure onset
in 47 patients and discordant in 5 patients. Two patients exhibited lateralized buildup on different sides
with different seizures. Lateralized postictal slowing
was detected in 45 patients, and was always concordant
with the side of seizure origin.
Neuropsycbologicul Testiug
All patients underwent left and right intracarotid amobarbital injections to determine language dominance
and memory function. Six of 5 1 right-handed patients
had speech dominance on the right side. Fourteen of
16 left-handed patients had left-sided speech dominance. All 6 of the right-handed patients with rightsided speech dominance had left-sided seizure origin,
and all 6 patients had a risk factor or possible etiology
for epilepsy during the first year of life. Memory on
the side of seizure origin was absent in 30 patients,
and was marginally present in 11. Two patients had
marginal memory opposite the side of seizure origin.
Absent memory contralateral to the side of seizure origin would have precluded surgery. Twenty-six patients
had bilateral intact memory.
Detailed neuropsychological testing was conducted
on all patients. Here, only the final impression is used
in terms of lateralization and localization. Neuropsychological test findings were considered normal in only
1 patient. This patient had seizure origin in the left
temporal lobe. Bilateral deficits without lateralized predominance were found in 8 patients, 6 with seizure
origin in the right temporal lobe, and 2 with seizure
origin in the left temporal lobe. The remaining 58 patients (87%) had evidence of lateralization on neuropsychological testing. In 9, this was discordant with the
side of seizure origin. All 9 of these patients had seizures beginning in the right temporal lobe. Therefore, 49 patients (73% ) had concordant laterahation.
Among these, localization of the neuropsychological
deficit was to the temporal lobe in 35 (52%), of whom
27 had left temporal lobe seizure origin and 8 had right
temporal lobe seizure origin.
Newoimuging
Computed tomography (CT) scans were obtained on
all patients, and in all but 1 patient they appeared normal. One patient had a small area of encephalomalacia
in the left frontoparietal region, presumably due to
birth trauma.
MRIs were available for review in 28 patients. Five
scans were read as normal. Of the 5 patients whose
MRIs were read as normal, pathological examination
revealed normal hippocampi and mild white matter gliosis in 3 and mild hippocampal dysplasia in 1; one
specimen contained no hippocampus. Twenty-three
scans were interpreted as showing unilateral hippocampal atrophy (12 left, 11 right). Pathological examination
showed that MRI correctly identified and lateralized
mesial temporal sclerosis (MTS) in 21 (91%) of 23
patients, with one false-positive and one false-negative
result.
Results of Stlrgery
Of the 67 patients, 37 had left temporal surgery and
30 had right temporal surgery. Eight of the earlier patients had standard en bloc temporal lobectomies while
the remaining 59 underwent modified anterior temporal lobectomies and hippocampectomies as described
by Spencer and colleagues [7}. Postoperative follow-up
has been 2 to 14 years (mean, 5.7 years). Table 3 lists
the specific surgical results. Using Engel's classification
scheme { 2 ] , 28 patients (42gl) had a perfect class IA
result. Twelve additional patients had no complex partial seizures (CPSs) but experienced a few brief auras
only during the first postoperative year. If these are
included in the class IA category, then 60% of patients
achieved that level. Auras without impaired consciousness persisted in 6 patients, making the initial class I
rate 69%. Rare postoperative generalized tonic-clonic
seizures (GTCs) or CPSs occurred in 21 patients
(31%), including 4 with persistent auras. Most postoperative seizures were GTCs and were usually associated with noncompliance with medications. They occurred during the first 2 postoperative years in 15 of
the 21 patients. Six patients had isolated seizures beyond 2 years, but to date have been seizure free for 2
or more years. All patients have therefore had effective
class I outcomes.
The ultimate goal following epilepsy surgery is to
have patients seizure free without taking any antiepileptic drugs. This was achieved in 26 patients. Two
Williamson et al: Characteristics of MTLE: I1 783
Table 3. Results of S z r g e y
No auras, no seizures
Transient auras, first year
Persistent auras
Postoperative seizures
28
12
6
21
Convulsive
18
(off medications-13)
(off medications-6)
(off medications-2)
(off medications and
without seizures-7)
(4 also with persistent
auras)
Complex partial
3
Reason for seizures
Noncompliance
Supervised drug
withdrawal
Unknown
15
3
3
additional patients were off all medications but had
auras. This was their choice, as auras did not occur
when they were taking medications. Seven of the patients who had postoperative seizures successfully
stopped taking medications.
Pathology
Tissue was available for review in 64 of the 67 patients.
Five specimens were inadequate (part or all of the hippocampus was missing). Forty-eight (81%) of the remaining 5‘) specimens revealed &ITS on the basis of
routine pathological examination. Tissue from 6 patients showed mild subcortical gliosis only, and three
specimens had ectopic or abnormal neurons, one of
which also had mild gliosis. Tissue was reported as
normal in rwo specimens.
Table 4 compares the possible risk factors with pathology. Forty-one of 59 patients with adequate pathological exarnination had febrile seizures. Thirty-eight
(93%) of these patients had MTS. MTS was also seen
in patients with histories of meningitis (3/4),
head
trauma ( 2 / 5 ) ,encephalitis (ill), toxemia (l/l),and anaphylaxis (Ul). Of the 10 patients with no known risk
factors, 3 had MTS.
Discussion
The results and discussion in this and the companion
article [l] are limited to the 67 patients in our surgical
series who had no evidence of mass lesions, had medial
temporal seizure onset documented with intracranial
EEG, and were cured by temporal lobectomy. In the
same time period, 18 similar patients who did not have
prior intracranial EEG studies were also cured by temporal lobectomy. The latter group had clinical histories,
MRI, and EEG findings very similar to those described
here (Thadani et al, unpublished data, 1993), but owing to a lack of depth EEG data are not included in
this discussion of the medial temporal lobe epilepsy
(MTLE) syndrome. Patients with temporal lobe epilepsy due to mass lesions were described previously
[S}, and often had surgery without prior study with
intracranial electrodes.
Scalp Electroencephalographic Abnormalities
Previous reports relied mainly on scalp EEG abnormalities or clinical seizures of the complex partial type to
identify patients with “temporal lobe epilepsy” 13,
lo]. Extratemporal origin of CPSs has, however, been
documented repeatedly [ 11-18], as has the existence
of temporally located interictal abnormalities in patients with extratemporal seizure origin { 15, 17-20).
This study differs from previous ones in that all patients had documented MTLE. The most important
scalp EEG finding in our study is that, with very few
exceptions, interictal scalp paroxysmal activity was located in the anterior temporal regions (94%). Posterior
temporal scalp foci and elementary visual hallucinations are both common findings in patients with documented occipital lobe epilepsy { 171, and such patients
may previously have been misdiagnosed as having temporal lobe epilepsy 191. While in the past, bilateral independent temporal paroxysmal activity had been considered a relative contraindication to surgery, the
results of this and other studies show that excellent
surgical outcome is possible in this group of patients
{21-231.
Table 4. Risk Factor Verius Pathology
Inadequate
andior
f i s k Factor
Total
MTS
Gliosis
Dy splasia
Febrile seizures
45
4
38
3
1
1
1
-
1
1
1
2
1
1
1
-
2
-
1
-
10
3
2
1
Meningitis
Encephalitis
Head trauma
Toxemia
5
Anaphylaxis
None
~~
MTS
=
mesial temporal sclerosis.
784 Annals of Neurology Vol 34 No 6 December 1993
Normal
Missing
Lateralized seizure buildup was detected in 54
(Sl$6) of the patients from this series. These ictal EEG
changes were detected well after the clinical seizure
had started. Detectable EEG changes at the time of
clinical seizure onset were found in only 4 patients.
Other reports described early ictal EEG changes in the
majority of patients 120, 24, 251, but careful electroclinical correlations were not done since these studies predated video-EEG recording. The authors were
probably describing the earliest EEG changes, rather
than EEG findings at the actual time of seizure onset.
False EEG lateralization in patients with temporal
lobe seizures has been reported as high as 10% [26].
In our study, with the results of depth EEG and surgical success providing proof of lateralization, interictal
findings of lateralized slowing and sharp activity were
misleading in 13% of patients, and lateralized ictal
scalp EEG buildup was misleading in 7%. However, in
all the 45 patients (67%’)whose scalp EEG recordings
revealed lateralized postictal slowing, and in the 4 patients in whom scalp EEG changes could be detected
immediately at the time of clinical seizure onset, depth
EEG was confirmatory.
Nezlropsychological Testing
Most patients in our series had neuropsychological
deficits that correctly lateralized to the side of seizure
origin, and in slightly over half, localization was to the
temporal lobe. However, neuropsychological testing
was much more sensitive in detecting left-sided abnormalities than right-sided ones. Of the 35 patients with
correct neuropsychological lateralization and localization, 27 had left temporal and 8 had right temporal
lobe seizure origin. As an indication of the side of
seizure origin, left-sided neuropsychological deficits
appear to be relatively sensitive but nonspecific, while
the opposite is true for right-sided deficits. This is
probably a reflection of strong verbal (left hemisphere)
influences in most testing situations {27).
lntracarotid amobarbital studies are performed primarily to lateralize language function and to determine
if the side contralateral to anticipated surgery can support memory {28]. This test also can provide adjunctive information regarding lateralization of disease.
Memory deficits on the side of seizure origin were
detected in 61% of the patients from this series. These
results are in close agreement with recent studies examining the lateralization value of the intracarotid amobarbital test C29, 301.
Imaging Studies
CT scans were nonspecific or appeared normal in all
but 1 patient. In the 1 patient with the abnormalappearing CT scan, the abnormality was probably unrelated to seizures, as it was not in the temporal lobe.
MRI, however, proved extremely sensitive and specific
in detecting patients with MTS. Because of the controversy surrounding MRI detection of MTS, we elected
to have one person (P. D. W.) blindly interpret the
MRIs. The overall accuracy for detecting the presence
or absence of MTS was greater than 90%. Berkovic
and colleagues [6] described the hippocampal asymmetries observed on MRI as “striking,” and we would
agree. Why other reports do not describe these findings is unclear [31, 331, but it must relate in part to
technique.
Tissue Pathology
MTS was by far the most common pathological finding.
It was present in 83% of adequately sampled temporal
lobes. While this is a somewhat higher percentage than
previously described (for review, see Babb and Brown
{ 34}), other reports included patients with circumscribed mass lesions and did not consider surgical outcome. Correlation of MTS with risk factors in our
patients [l] showed that 93% of patients with a history
of febrile seizures and adequate pathological examination of resected tissues had MTS. This high association
of MTS and febrile seizures is in agreement with Falconer’s 1351 earlier observations. While this association
is implied by others 121, 22, 36, 377, such a strong
relationship has also been disputed {38, 39}. Only 2
patients with MTS had no identified risk factors. An
earlier theory, which equated MTS or incisural sclerosis with hippocampal injury during birth [40]. has previously been challenged [34]. The lack of any recognized perinatal complicacions in our patients who had
MTS also refutes that theory.
Only 10 patients with adequate tissue specimens did
not have MTS. Seven of these patients had normal
tissue or mild gliosis. Cortical dysplasias have been associated with epileptogenesis 1341, and the 3 remaining
patients had abnormal neurons or heterotopias.
Ogtcome
To be included in this series, patients had to achieve a
class I result as defined by Engel [ 2 ] . Although the
majority of patients (69%) had no seizures following
surgery, 21 had rare seizures that gradually stopped.
The issue of when antiepileptic drugs can be safely
discontinued following surgery has not been resolved.
The results from our study suggest that 2 years following surgery should be a minimum time before antiepileptic drugs are completely withdrawn. Only 2 of our
67 patients were successful taking themselves off all
antiepileptic medication before 2 years had elapsed,
but later 42% were seizure free without medication.
We now attempt to maintain therapy with a single antiepileptic drug for 4 to 5 years.
Persistent auras were described in prior reports 12,
41,423 and 10 of our patients continued to experience
auras. While persistent auras are accepted when calcuWilliamson et al: Characteristics of MTLE: I1
785
lating surgical success, they are not entirely benign in
terms of patients’ perceptions. They serve to remind
patients of their previous condition and can be accompanied by the dread of recurrent seizures with loss of
contact. Why auras persist is not completely understood. Logic would dictate that they originate in residual epileptogenic brain, either ipsilateral or contralateral to the side of resection. While this must be true,
such an explanation is difficult to accept, particularly
when auras are related to discrete hippocampal discharges observed during intracranial recording. One
would expect such auras to be abolished by hippocampal resection.
Conclusions
This second report on our series of 67 patients with
MTLE allows us to make the following conclusions:
1. The predominant interictal scalp EEG spike, sharp,
and slow wave foci are located in the anterior temporal regions in the vast majority of patients (9496)
with MTLE. In about half of the patients the abnormalities are unilateral, while in the other half they
are bilateral but usually with unilateral prominence.
2. Ictal scalp EEG changes are rarely detectable at the
time of clinical seizure onset, but a lateralized sharp
theta o r faster buildup occurs about 30 seconds
later in approximately 80% of patients. That, as
well as lateralized postictal slowing, when detectable, are reliable lateralizing signs for seizure origin.
3. Neuropsychological testing detects lateralized deficits in most patients ( 8 7 % ) , but lateralization is not
concordant with the side of seizure origin in approximately 15%. Incorrect lateralization, or no lateralization, is much more likely to occur when
seizures originate in the right temporal lobe.
Intracarotid amobarbital testing documents absent
or deficient memory on the side of seizure origin
in the majority of patients with MTLE, but about
40% of patients have intact memory bilaterally.
4. MRI is very sensitive in detecting medial temporal
abnormalities, and these are correlated with MTS
on pathological examination of resected tissue. The
majority of patients (86%) with MTLE will have
MTS as the probable cause of their epilepsy. There
is a strong association between MTS and cornplicated febrile seizures.
5 . Noncompliance is the usual cause of postoperative
seizures in patients who ultimately become seizure
free. Most of these patients have seizures during
the first 2 postoperative years, but many can later
be successfully withdrawn from medication. Two
years is the minimum time for which antiepileptic
drugs should be maintained.
786 Annals of Neurology Vol 34 No 6 December 1993
References
1. FrenchJA, Williamson PD, Thadani VM, et al. Characteristics of
medial temporal lobe epilepsy: I. Results of history and physical
examination. Ann Neurol 1993;34:774-780
2. Engel J Jr. Outcome with respect to epileptic seizures. In: Engel
J Jr, ed. Surgical treatment of the epilepsies. New York: Raven,
1987:55 3-5 7 1
3. Williamson PD. Evaluation of patients for epilepsy surgery at
che West Haven VAiYale-New Haven Epilepsy Unit. In: Spencer SS, Spencer DD, eds. Surgery for epilepsy. Boston: Blackwell Scientific, 1991:36-52
4. Ebersole JS, Wade PB. Spike voltage topography and equivalent
dipole localization in complex partial epilepsy. Brain Topogr
1990;3:21-34
5 . Ebersole JS, Wade PB. Spike voltage topography identifies two
types of fronto-temporal epileptic foci. Neurology 1991;41:
1425-1433
6. Berkovic SF, Andermann F, Olivier A, et al. Hippocampal sclerosis in temporal lobe epilepsy demonstrated by magnetic resonance imaging. Ann Neurol 1991;29:175-182
7 . Spencer DD, Spencer SS, Mattson RH, Williamson PD, Novelly RA. Access to the posterior medial temporal lobe structures
in the surgical treatment of temporal lobe epilepsy. Neurosurgery 1984;15:667-67 1
8. Boon PA, Williamson PD. Presurgical evaluation of patients
with partial epilepsy. Indications and evaluation techniques for
resective surgery. Clin Neurol Neurosurg 1989;91:5-13
9. King DW, Ajmone-Marsan C. Clinical features and ictal patterns
in epilepcic patiencs with EEG temporal lobe foci. Ann Neurol
1977;2: 138- 147
10. Theodore WH, Porter RJ, Penry JK. Complex partial seizures:
clinical characteristics and differential diagnosis. Neurology
1983;33:1115-1121
11. Penfield W, Jasper H . Epilepsy and the functional anatomy of
the human brain. London: Churchill, 1954
12. Ajmone-Marsan C, Ralston BL. The epileptic seizure. Its functional morphology and diagnostic significance. Springfield, IL:
Thomas, 1957:211-215
13. Dodge HW. Epileptic seizures associated with mass intracranial
lesions. Proc Staff Meeting Mayo Clin 1958;33:487-496
14. Walker AE. Pre-frontal lobe epilepsy. Int J Neurol 1966;5:422429
15. Williamson PD, Spencer DD, Spencer SS, Novelly RA, Mattson
RH. Complex partial seizures of frontal lobe origin. Ann Neurol
1985;18:497-504
16. Williamson PD. Spencer SS. Clinical and EEG features of complex partial seizures of extratemporal origin. Epilepsia 1986;27
(SUPPI 2):46-63
17 Williamson PD, Thadani VM, Darcey TM, Spencer DD, Spencer SS, Mattson RH. Occipital lobe epilepsy: clinical characteristics, seizure spread patterns, and results of surgery. Ann Neurol
1992;31:3-13
18 Williamson PD, Boon PA, Thadani VM, et al. Parietal lobe
epilepsy: diagnostic considerations and results of surgery. Ann
Neurol 1992;31:193-201
19 Schneicler RC, Crosby EC, Farhat SM. Extratemporal lesions
triggering the temporal-lobe syndrome: the role of association
bundles. J Neurosurg 1964;22:246-263
20 Mass DW. Electroencephalographic manifestations of complex
panial seizures. In: Penry JK, Daly DD, eds. Complex partial
seizures and their treatment. New York: Raven, 1975:113-140
2 1 So N, Gloor P, Quesney LF, Jones-Gotman M, Olivier A, Andermann F. Depth electrode investigations in patients with bitemporal epileptiform abnormalities. Ann Neurol 1989;25:
423-431
22 So N, Olivier A, Andermann F, Gloor P, Quesney LF. Results
of surgical treatment in patients with bitemporal epileptiform
abnormalities. Ann Neurol 1989;25:432-439
23. Gloor P. Electroencephalography and the role of intracerebral
depth electrode recordings in the selection of patients for treatment of epilepsy. New York: Raven, 1984:433-437
24. Gastaut H. So-called “psychomotor” and temporal epilepsy-a
critical study. Epilepsia 1953;7:85-138
25. Mass DW, Espinosa RE, Fischer-Williams M. Analysis of concurrent electroencephalographic and clinical events occurring
sequentially during partial seizures. Electroencephalogr Clin
Neurophysiol 1973 ;34::28 (Abstract)
26. Walter RD. Tactical considerations leading to surgical treatment
of limbic epilepsy. In: Brazier MA, ed. Epilepsy: its phenomena
in man. New York: Academic, 197399-1 19
27. Powell G, Polkey C, McMillan T. The new Maudslcy series of
temporal lobectomy. I . Short term cognitive effects. Br J Clin
Psycho1 198>;24:109-124
28. Rausch R. Psychological evaluation. In: Engel J Jr, ed. Surgical
treatment o f the epilepsies. New York: Raven, 1987:181195
29. Salanova V, Morris HH, Rehm P, et al. Comparison of the
intracarotid amobarbital procedure and interictal cerebral 18fluorodeoxyglucose positron emission tomography scans in refractory temporal lobe epilepsy. Epilepsia I
30. W’yllie E, Naugle R, Chelune G, Luders H,
C. Intracarotid amobarbital procedure: 11. Lateralizing value in
evaluation for temporal lobectomy. Epilepsia 1932;32:865-869
31. Sperling MR, Wilson G, Engel J Jr, Babb TL, Phelps ME, Bradley W. kfagnetic resonance imaging in intractable partial epilepsies: correlative srudies. Ann Neurol 1986;20:57-62
32. Theodore WH, Katz D, Kufts C , et al. Pathology of temporal
lobe foci: correlation of CT, MRI, and PET. Neurology 1990;
40:797-803
33. Engel J Jr. Diagnostic evaluation. In: Seizures and epilepsy. Philadelphia: Davis, 1989:303-3 39
34. Babh TL, Brown WJ. Pathological findings in epilepsy. In: Engel
J Jr, ed. Surgical treatment of the epilepsies. New York: Raven,
1987:511-540
35. Falconer MA. Mesial temporal (Ammon’s horn) sclerosis as a
common causc of epilepsy: etiology, treatment and prevention.
Lancet 1374;2(7883):767-770
36. Glaser GH. Natural history of temporal lobe-limbic epilepsy.
In: Engel J Jr, ed. Surgical treatment of the epilepsies. New
York: Raven, 1987:13-30
37. Duncan JS, Sagar HJ. Seizure characteristics, pathology and outcome after temporal lobectomy. Neurology 1987;37:405-409
38. Sosijanov N, Sadikario A, Dukovski M, Kutubec M. Febrile
seizures and later development of epilepsy. Am J Dis Child
3983;137:123-126
39. Leviron A, Cowan LD. Do febrile seizures predispose to complex partial seizures? An epidemiologic assessment. In: Nelson
KB, Ellenberg JH, eds. Febrile seizures. New York: Raven,
1981: 65-74
40. Earle Uf,
Baldwin M, Penfield W. Incisural sclerosis and temporal lobe seizures produced by hippocampal herniation at birrh.
Arch Neurol Psychiatr 19>3;6‘):27-42
4 1. Rasinussen T. Surgical treatment of patients with complex partial seizures. In: Penry JK, Daly DD, eds. Complex partial seizures and their treatment. New York: Raven, 1975:415-449
42. Primrose DC, Ojemann GA. Outcome of resective surgery for
temporal lobe epilepsy. In: Luders H, ed. Epilepsy surgery. New
York: Raven, 1991:601-61 I
Williamson et al: Characteristics of MTLE: I1 787
Документ
Категория
Без категории
Просмотров
1
Размер файла
699 Кб
Теги
characteristics, media, temporal, epilepsy, lobel
1/--страниц
Пожаловаться на содержимое документа