• Surgery effectiveness;
  • Nonlesional form epilepsy


  1. Top of page
  2. Abstract
  7. Acknowledgments

Summary:  Among 70 patients with intractable focal epilepsy and no specific lesion, as determined by both MRI (magnetic resonance imaging) and histopathology, outcome after resective surgery was polarized: 26 (37%) became seizure free (SF), and 27 (39%) were not helped. Eighteen (42%) of 43 standard temporal resections rendered patients SF, somewhat more than eight (30%) of 27 other procedures. To seek reliable prognostic factors, the subsequent correlative data compared features of the 26 SF patients with those of the 27 not helped. Although ictal semiology guided the site of surgical resection, it and other aspects of seizure and neurologic history failed to predict surgical outcome. However, two aspects of preoperative scalp EEGs correlated with SF outcomes: (a) among 25 patients in whom >50% of clinical seizures arose from the later resected lobe and no other origins, 18 (72%) became SF compared with seven (28%) of 25 with other ictal profiles; (b) 13 (93%) of 14 temporal lobe patients whose interictal and ictal EEGs lacked features indicative of multifocal epileptogenesis became SF compared with five (33%) of 15 with such components. The considered need for subdural (SD) EEG reduced SF outcome from 18 (90%) of 20 patients without SD to eight (24%) of 33 with SD; this likely reflected an insufficient congruity of ictal semiology and interictal and ictal scalp EEG for localizing epileptogenesis. Within this SD group, >50% of clinical seizure origins from a later resected lobe increased SF outcome somewhat: from two (14%) of 14 without this attribute to six (40%) of 15 with it; 100% of such origins increased SF outcome from two (12%) of 16 to six (46%) of 13.

Can resective surgery be considered in the ∼20% of patients with intractable focal epilepsy whose neurologic history, examination, and magnetic resonance imaging (MRI) disclose no potentially epileptogenic lesion (1,2)? Fourteen epilepsy surgery series (3–16) used MRI and/or histopathology to disclose specific lesions. Eight of these (3,4,6,9–12,15) agreed with Penfield (17,18) that the presence of a specific epileptogenic lesion usually augurs a favorable postsurgical outcome (Table 1). Additionally, Bengzon et al. (19), compiling the Montreal experience, found a higher proportion of patients with lesions in the favorable-outcome group than among those in whom resective surgery was unhelpful. However, six of these 14 reports (5,7,8,13,14,16) found no correlation between the presence of a specific, causative lesion and outcome.

Table 1. Focal lesion and surgery outcome: literature review
 No lesionLesion  
 SFNot helpedSFNot helpedTotalp Value
  1. SF, Seizure free includes six adequate series indicating SF and not-helped outcomes and defining lesion, no-lesion groups; Fisher's exact test; NS, not significant.

Complete series
 Spencer (1996)182512629226<0.0001
 Guldvog et al. (1994a)1511 27 9 80NS
Temporal lobe
 Guldvog (1994a)13 8 16 5 53NS
 Duncan & Sagar (1987) 1 4 37 6 58 0.0048
 Berkovic et al. (1995) 7 6 53 7103 0.0088
 Falconer et al. (1964) 8 8 45 9100 0.0164
Extratemporal lobe
 Zentner et al. (1996) 2 4 28 4 56 0.0116
 Guldvog et al. (1994a) 2 3 11 4 27NS

This study assessed the effectiveness of resective surgery among patients in whom both MRI and histopathology failed to disclose a specific lesion and sought clinical and EEG components that measurably altered outcome.


  1. Top of page
  2. Abstract
  7. Acknowledgments

We retrospectively studied patients who underwent focal resections for intractable seizures at University Hospital, London, between 1989 and 1999. Those patients whose resected specimens revealed no histologic abnormality or nonspecific histologic changes constituted the patient population. Nonspecific changes included subpial or transcortical gliosis, and gliosis in the molecular layer of the hippocampal dentate region or in the amygdala without other evidence of mesial temporal sclerosis (Fig. 1).


Figure 1. Normal histology and mild diffuse astrocytosis seen best with glial fibrillary acid protein (GFAP) stain.

Download figure to PowerPoint

Exclusion criteria were macroscopic or microscopic nonvisualization of the resected mesial temporal lobe including the hippocampus, any histologic features of mesial temporal sclerosis (MTS) (20,21), and identification of a specific pathology such as neoplasm, vascular malformation, or cortical dysplasia. A specific lesion disclosed by MRI or by surgeon's inspection of the operative field excluded any patient. All patients underwent MRI scanning.

The MRI protocol varied during the period of this investigation as new techniques became available. In 1989 and 1990, axial and coronal T2 scans and coronal T1 with 5-mm slices were used. From 1991 to 1994, 3-mm slices were studied. Fluid-attenuated inversion recovery (FLAIR), high-resolution inversion recovery (STIR), and volumetric T1 with 1 or 2 mm slices were added in 1995. Small dysplasias and subtle MTS may have eluded the techniques of 1989 through 1990.

The principal epileptogenic zone was determined by clinical history, prolonged scalp interictal and ictal EEG/video monitoring, electrocorticography, and neuropsychology. Within typical seizures for each patient, earliest features of lateralizing significance (22–24) were sought through history and Epilepsy Unit documentation.

Twenty-four-hour scalp EEG monitoring used collodion-applied scalp electrodes placed according to the 10–20 system, supplemented by mandibular notch electrodes (25). Strip or grid subdural EEG clarified the epileptogenic zone in some patients. Subdural (strip or grid) EEG was performed when one or more of the following pertained: (a) EEG seizures arose from a region not implicated by ictal semeiology, (b) EEG seizure origin was not congruent with principal interictal spikes, and (c) ambiguous scalp seizure origin.

For this study, our EEG data were retrospectively obtained from our classification system (26).

Surgery was performed in these medically intractable patients when the neurology and neurosurgeon epileptologists determined that sufficient topologic congruity existed among semiologic and EEG data, the latter comprising interictal and ictal, scalp, and subdural findings. Resection topology was determined by the aforementioned data supplemented by electrocorticography. Such decisions were based on clinical judgment in each instance, not on a fixed protocol.

Patients were followed up postoperatively from 2 to 12 years (mean, 8.1 years). Seizure incidences were compared between the entire duration of follow-up and the last 12 presurgical months.


  1. Top of page
  2. Abstract
  7. Acknowledgments

Outcome after resective surgery is presented in two sections: overall and correlative. This latter contrasts the 26 seizure-free (SF) patients with the 27 patients whose disorders remained the same or worsened, similar to the analysis of Bengzon et al. (19).

Overall (70 patients)

Of the 685 patients undergoing focal resection in this interval, 70 (10%) had normal or nonspecific histology. Of these 70 patients, 19 (27%) had normal histology, and 48 (69%) had nonspecific histology (see Methods). Ten of 19 patients with normal histology had standard temporal resections, as did 31 of 48 patients with mild gliosis. Histology was unavailable in three (4%) of patients, but no lesion was seen by the surgeon. Forty-one (59%) were male patients. The ages at operation ranged from 6 to 65 years (mean, 31 years). Age at habitual seizure onset ranged from 1 to 47 years (mean, 13 years) with a duration of illness before resection ranging from 1 to 41 years (mean, 17 years).

A neurologic antecedent of questionable relevance to the seizure disorder occurred in 41 (59%) of 70 patients. Of these 41, 23 (56%) had one or more brief, nonlateralized, febrile seizures; 13 (32%) had mild closed head injuries without aspects prognostic of posttraumatic epilepsy (27). Four (10%) patients had a history of meningitis, and one had birth asphyxia without immediate sequelae.

Neuroimaging was normal in 47 (67%) of the 70 patients and showed mild, nonfocal atrophy in 23 (33%), as interpreted by our epilepsy neuroradiologist (D.H.L.).

Forty-three (61%) of the 70 patients had standard temporal lobectomy only. Other resections were carried out in the following regions: frontal, 16 (23%); temporal neocortex or standard temporal with other resections, seven (10%); occipital, six (9%); and parietal, three (4%). Some resections involved portions of more than one lobe.

A remarkable aspect was polarization of outcome: although seizures stopped in 26 (37%) of 70, of whom 10 are off medication, 27 (39%) obtained no benefit, and six (22%) have more frequent attacks (Table 2). A worthwhile result appears to have occurred in 35 (50%) patients, as seizure incidence diminished >90% in six non-SF patients, and an additional three have only nocturnal generalized attacks (outcomes I + II, Table 2). A mediocre (∼50%) improvement occurred in eight (11%).

Table 2. Outcome: standard temporal and extratemporal resections
  1. Numbers, patients; ( ), percentages calculated across; I–IV, Engel's outcome classification (30); I, II vs. III, IV, standard temporal vs. others, p = 0.0486, Fisher's exact, significant; standard temporal, maximum of 6.0–6.5 cm of anterior lateral surface for nondominant temporal lobe or 4.0–4.5 cm of the dominant temporal lobe; mesial resection included the amygdala and anterior 1.0–3.0 cm of hippocampus (33).

Neocortical and nontemporal(30)(4)(7)(59) 
Total26 (37%)9 (13%)8 (11%)27 (39%)70

Outcome was assessed for the 43 patients undergoing only a standard temporal lobectomy including its mesial structures and for all others (27 patients) including temporal neocortical resections only, combined temporal and extratemporal resections, and extratemporal resections only. Of the 43 patients undergoing standard temporal lobectomy, 26 (60%) achieved a worthwhile (I + II) outcome, more than the nine (33%) of 27 patients with temporal neocortex or extratemporal resections (p = 0.0486, significant, Fisher's exact test). Eighteen (42%) of the 43 temporal lobectomy patients became SF compared with eight (30%) of 27 with other procedures [p = 0.3244, Fisher's exact test, not significant (NS)].

Follow-up durations between SF and non-SF patients were similar. The number of antiepileptic medications (AEDs) was decreased in 26 (37%) of 70, increased in 15 (21%), and remained the same in 29 (41%).

Seventeen (24%) of 70 patients obtained some type of residual postoperative complication including a superior quadrantopia (nine patients), hemianopia (two patients), subjective decrease in memory (five patients), and mild hemiparesis (one patient). Transient abnormalities were dysphasia (11 patients) and hemiparesis (one patient). Subdural infection with meningitis occurred in one patient. Transient psychiatric disturbances appeared in five patients, principally depression.

Correlative (53 patients)


Outcome did not correlate with histology: SF-to-unhelped ratios were 9:8 for normality and 16:17 for mild gliosis. Therefore these groups are combined for subsequent analyses.


Median and mean ages at seizure onset and ages at operation did not differ significantly among outcome groups comparing SF with no change and worse. However, mean duration of epilepsy before surgery was significantly less for SF patients (12.5 years) than for those unchanged or worse (19.8 years) (p = 0.0102, unpaired t test). Presence or type of neurologic antecedent did not distinguish SF from unhelped patients.

Of 40 patients with definite aura, 22 (55%) became SF compared with four (31%) of 13 without aura (p = 0.2021, NS, Fisher's exact). Fifteen (60%) of 25 patients whose aurae clearly implicated the limbic system became SF compared with seven (47%) of 15 whose aurae did not (p = 0.5175, NS, Fisher's exact). Seizure incidence held no prognostic value: 10 (59%) of 17 with daily seizures became SF compared with 14 (42%) of 33 whose attacks occurred less often. Seizure incidence could not be reliably established in the three others. Preoperative status epilepticus, occurring in six patients, did not correlate with outcome.

Of 36 patients whose ictal semiology contained lateralizing features implicating the side of resective surgery, 19 (53%) became SF compared with seven (41%) of 17 without such features (p = 0.5587, NS). Seizures of 14 of these 17 patients contained no lateralizing components, whereas those of three contained mixed or falsely lateralizing elements. Ictal lateralizing features were motor in 23 patients, somatosensory in eight, linguistic in 14, and visual in five; 11 patients had more than one type of feature.

Outcome did not vary consistently with refinements in MRI technique (see Methods). Of the 53 patients in the SF, no-change, and worse-outcome groups, 26 underwent resection in 1989 through 1990, 12 in 1991 through 1994, and 15 from 1995 to 1999. SF proportions were 61%, 25%, and 47%, whereas no change/worse occurred in 39%, 75%, and 53% (not significant for trend for before vs. after 1990).

Scalp EEG and outcome

Some aspects of scalp EEG data distinguished SF patients from those unhelped. Scalp seizure congruency was defined as >50% of clinical attacks focally arising from a single (ultimately resected) lobe with no seizure clearly arising from another lobe. Of 25 patients in whom this occurred, 18 (72%) became SF compared with seven (28%) of the 25 others (p = 0.0042, significant, Fisher's exact; Table 3). However, this relation between seizure congruency and outcome held only for temporal lobe cases, of which 84% of congruent cases became SF versus 43% of others. Three patients had no preoperative scalp-recorded seizures.

Table 3. Scalp seizure congruencya with resection lobea and outcome
 SFNo changeWorsep Valueb
  1. SF, Seizure free; numbers, patients; percentages calculated across; NS, not significant.

  2. aCongruency: >50% of clinical seizures originating focally at lobe of later resection and no focal seizure origin from another lobe. Includes all 50 of these 53 patients with one or more preoperative recorded scalp EEG clinical seizures.

  3. bCombines no-change and worse outcomes vs. SF for Fisher's exact test.

All lobes (50 patients)
 Congruent (25)18 (72%) 610.0042, Fisher's
 Otherwise (25) 7 (28%)135 
Temporal (26 patients)
 Congruent (19)16 (84%) 210.0572, NS
 Otherwise (7) 3 (43%) 40 
Nontemporal (24 patients)
 Congruent (6) 2 (33%) 400.6181, NS
 Otherwise (18) 4 (22%) 95 

The following data derive from 51 of the 53 patients (29 temporal, 22 nontemporal) with ≥10 preoperative EEGs. Fifteen (88%) of 17 patients whose interictal scalp EEGs lacked all of the following features became SF as compared with 10 (29%) of 34 with one or more of the following: a spike focus outside the resected lobe, multiple spike foci, generalized spike–waves, and any seizure outside the resected lobe (p = 0.0001) (Table 4A). The presence of each of these EEG phenomena also was associated with a higher proportion of “no change” or “worse” outcomes than for those without each feature. However, this multiple-features relation held only for the 29 temporal lobe patients of whom about an equal number (15) had one or more unfavorable features as did not (14; Table 4B). In contrast, 19 of 22 nontemporal patients had at least one unpropitious component (Table 4C). Thirteen (93%) of 14 temporal patients without any features suggestive of epileptogenesis outside the later resected lobe became SF postoperatively compared with only five (33%) with one or more such features (p = .0017, Fisher's exact; Table 4B). Again, the presence of each of such features augured a higher proportion of unfavorable outcomes than for the remainder of the temporal group. Among the 29 temporal patients, extratemporal spikes appeared in five, only bitemporal spikes in two, and both temporal and extratemporal in four: only three (27%) of these 11 with spikes outside the resected lobe became SF compared with 15 (83%) of 18 with only resected lobe spikes (p < 0.0051).

Table 4A. Interictal and ictal scalp EEG and outcomea
 SFNo changeWorseNo change + worsep Value
  1. SF, Seizure free; MISF, multiple independent spike foci (56).

  2. For each of the above scalp EEG features, p values (Fisher's exact test) relate to SF: (no change + worse) ratios of patients with each feature to those without it. “Distant” spike or seizure focus: not from later-resected lobe. Percentages of patients in parentheses, calculated across.

  3. aFifty-one of 53 patients with ≥10 preoperative EEGs. All 29 temporal patients had ≥10 preoperative EEGs; 22 of 24 nontemporal patients had ≥10 preoperative EEGs.

Any “distant” spike focus 6 (25)16218 (75)<0.0019
MISF 4 (29) 9110 (71) 0.1164
Generalized spike–waves 7 (32)12315 (68) 0.0483
Any “distant” seizure 2 (18) 81 9 (82)<0.0385
Any of above10 (29)20424 (71) 0.0001
None of above15 (88) 02 2 (12) 
Total patients25 (49)20 (39)6 (12)26 (51) 
Table 4B. Temporal (29 patients)
 SFNo changeWorseNC + Worsep Value
Any “distant” spike focus 3 (27)718 (73)0.0051
Generalized spike–waves 2 (29)505 (71)0.0712
MISF 1 (25)303 (75)0.1389
Any “distant” seizure0 (0)11 2 (100)0.1355
Any of above 5 (33)9110 (67) 0.0017
None of above13 (93)011 (7)  
Total patients18 (62)9211 (38)  
Table 4C. Nontemporal (22 patients)
 SFNo changeWorseNC + Worsep Value
Any “distant” spike focus3 (23) 9110 (77)0.3762
Generalized spike–waves5 (33) 7310 (67)1.000 
MISF3 (30) 61 7 (70)1.000 
Any “distant” seizure2 (22) 70 7 (78)0.6478
Any of above5 (26)11314 (74)0.2273
None of above2 (67) 01 1 (33) 
Total patients7 (32)11415 (68) 
Subdural EEG and outcome

Likely reflecting the complexity or ambiguity of noninvasive clinical and EEG data, the considered need for subdural EEG to locate epileptogenesis reduced an SF outcome: from 18 (90%) of 20 without subdurals to eight (24%) of 33 with them (p < 0.0001; Table 5).

Table 5. Performance of subdural recordingsa and outcome
SubduralsSFNo changeWorsep Value
  1. SF, seizure free; numbers, patients.

  2. aIncludes strips and/or grids.

No   2018 (90%) 11<0.0001 Fisher's exact
Yes  33 8 (24%)205 test

Applying the same definition used for scalp ictal congruence to subdural EEGs, “>50% congruency,” two (14%) of 14 patients without congruence were SF compared with six (40%) of 15 with congruence (p = 0.2148, Fisher's, NS; Table 6A). Distinguishing the 13 patients whose every seizure distinctly arose from the ultimately resected lobe, “100% congruence,” from those with another ictal origin or ambiguous origin in one or more attacks (Table 6B) shows a balanced outlook for the former (46% SF) and dismal (12% SF) for the latter (p = 0.0923, Fisher's, NS).

Table 6A. Seizure congruencya with resection lobe and outcome
 SFNo changeWorseTotals
  1. Subdural recordings (29 patients), with >50% congruency. Includes only 29 patients with bilateral multilobe subdural coverage before any resective surgery. Correlations (comparing SF vs. no change + worse) not significant by Fisher's exact test.

  2. SF, seizure free; numbers, patients; percentages in parenthesis.

  3. aCongruency: >50% of clinical seizures originating focally at lobe of later resection + no focal seizure origin from another lobe.

All lobes8 (28)18329
 Congruent6 (40) 8115
 Otherwise2 (14)10214
Temporal only3 (38) 50 8
 Congruent3 (100) 00 3
 Otherwise0 (0) 50 5
Not temporal5 (24)13321
 Congruent3 (25) 8112
 Otherwise2 (22) 52 9
Table 6B. Seizure congruencya with resection lobe and outcome
 Seizure freeNot helped, worse
  1. Subdural recordings (29 patients), 100% congruency. Same patients as in Table 6A. Percentages calculated across; p = 0.0923 by Fisher's exact, NS.

  2. aAll clinical seizures focally originate from later resected lobe.

  3. bSeizure origins: variable foci, generalized, hemispheric, or ambiguous.

100% congruenta6 (46%) 7 (54%)
Othersb2 (12%)14 (88%)


  1. Top of page
  2. Abstract
  7. Acknowledgments

Nonlesional incidence in surgical series

The proportion of our patients without demonstrated specific lesions (10%) is lower than that in most epilepsy surgical series, possibly because of the strict inclusion criteria of our study and its more recent time span (3–9,11–13,15,16,28,29). Eleven of these reports specifically described pathology; of these, the proportion of all patients with normal or nonspecific pathology ranged from 6 to 58% (median, 20%; average, 25%). Series confined to the temporal lobes had a lower average percentage of normal or nonspecific pathology (16%) than did combined or extratemporal series (31%). Paradoxically the single series that had temporal and nontemporal pathologic findings separately (7,8) found a higher proportion among temporal cases. Table 7 lists eight of these series that grouped outcomes according to Engel's (1987) classification (30).

Table 7. Nonlesional surgical outcome
  1. aEngel outcome system (30).

  2. bThis study.

All lobes
 Fish et al. (1993)12 (48)13 (52)
 Jayakar (1994)15 (48)16 (52)
 Armon et al. (1996)26 (76) 8 (24)
 Spencer (1996)18 (43)24 (57)
 Zentner (1996) 4 (40) 6 (60)
 Blume et al. (2003)b35 (50)35 (50)
Temporal lobe
 Jack et al. (1994)43 (83) 9 (17)
 Berkovic et al. (1995)13 (54)11 (46)
 Blume et al. (2003)b26 (60)17 (40)

Surgical effectiveness

Surgery among our group of 70 nonlesional patients was less effective than that for other temporal and extratemporal series from our center (31–33), a conclusion reached in a majority of surgical series (see introduction).

The presence of an epileptogenic lesion indicates the general region of seizure onset. Complete lesion resection is the principal determinant of effective surgery (34), but Van Ness et al. (35) showed that epileptogenic zone resection also contributes to surgical effectiveness. In a study most relevant to ours, among 31 children with normal or nonspecific neuroimaging, extent of epileptogenic region removal correlated best with effectiveness (36). Lacking a relevant lesion removes a reliable guide to a principal epileptogenic zone, possibly contributing to the bimodal outcomes we encountered (i.e., principally either SF or unhelped; Table 2).

Clinical data

Although influencing the site chosen for surgical resection based on principles of clinical cerebral localization (22–24), the lack of correlation between clinical semiology and outcome may reflect varying local relations between such semiology and the epileptogenic zone.

Among several factors that possibly underlie the better outcomes among patients with shorter-duration epileptic disorders may simply be a delay in the surgical decision in complex cases. Our EEG data support this interpretation.

Scalp EEG

Despite a lack of mesial and inferior surface coverage, several studies have disclosed the value of scalp-recorded seizures in localizing epileptogenesis. Among studies that used M1, T1 sphenoidal, or sphenoidal electrodes supplementing the 10-20 system, the site of scalp-recorded seizures in temporal lobe epilepsy correlated with side of invasively recorded seizures or of effective lobectomy in 75–83% of cases (37–40). Among 67 nonlesional temporal patients rendered SF by surgery, Williamson et al. (41) found scalp ictal lateralizing “changes” ultimately appearing in 81% of patients; in 87% of these, the seizures occurred ipsilateral to depth EEG seizures and curative surgery. In neocortical epilepsies, 72% of patients studied by Lee et al. (42) had at least one invasive-confirmed localizing or lateralizing scalp ictal EEG. In that study, a greater proportion of occipital and temporal neocortical seizures could be localized than could frontal or parietal attacks. These data underlie our finding that surgery was more effective when a majority of scalp-recorded seizures arose from the later-resected lobe (Table 3).

In adults with temporal lobe epilepsy, the seizures of 95% of patients with predominantly unilateral interictal temporal spikes arose ipsilaterally (43). This consistent relation for temporal lobe epilepsy also was found by Gloor (44,45), Sammaritano et al. (46), and Montplaisir et al. (47). This study extends this relation of unilateral temporal spikes and effective surgery to patients without an identifiable lesion. Temporal spikes may reflect a hippocampal seizure-inhibiting process and thus paradoxically identify the epileptogenic side (48).

However, a less reliable relation between interictal spikes and epileptogenic focus in neocortical epilepsy was found in our study (Table 4) and others. Among 34 patients with lesional frontal lobe epilepsy rendered SF by focal resection, only three (9%) had focal scalp spikes in the epileptogenic area (49). Such incongruity may be found in central–parietal epilepsy (50) and in occipital seizure disorders (51). In a study of nonlesional patients, even sequential spikes constituting an ictal discharge failed to identify the ictal-onset region consistently (52). Thus congruency between spike field and region of principal epileptogenesis in some studies (32,53) may reflect the presence of a lesion as the essential linchpin for the relation.

EEG telemetry with prolonged recording also seeks the existence of factors inimical to successful surgery. As each of (a) a single interictal spike focus distant from the resected lobe, (b) multiple spike foci, (c) generalized spike–waves, and (d) any seizure distant from the ultimately resected lobe was associated postoperatively with fewer SF patients than those unchanged or worse; the markedly improved outcome when none of these features appeared is understandable (Table 4). Multifocal seizure onsets under steady-state conditions augur unfavorably for surgical effectiveness (54). However, Engel advises scrutiny of the circumstances of such seizures, possibly discounting atypical attacks. In contrast to the current study, Williamson et al. (41) found contralateral seizure onsets in 13% of nonlesional, postoperatively SF temporal lobe patients. The appearance of multiple interictal spike foci or generalized spike–waves augur an unfavorable surgical outcome likely by representing multifocal epileptogenesis (55–58).

Subdural EEG

Although determined from multiple considerations on a case-by-case basis, a decision for subdural EEG reflects either ambiguity of EEG ictal onset, incongruity of semiologic and scalp EEG data, or both. From results discussed earlier, factors underlying this decision also carry an unfavorable prognosis for surgical effectiveness, as reflected in the poorer outcomes among the 33 patients who underwent subdural recording in our comparative analysis (Table 5). Within this group, a less dismal outlook for those whose ictal origins were mostly (>50%) or always (100%) congruent with the resected lobe concurs with the finding of Siegel et al. (16) of congruency between invasively recorded ictal origin and resection site in a study of SF nonlesion patients.


  1. Top of page
  2. Abstract
  7. Acknowledgments

Do these prognostic indices guide the neurologist caring for patients with intractable, focal, nonlesional epilepsy? The poorer operative results compared with series containing lesional cases indicates scrutiny of technically advanced neuroimaging for one or more potentially epileptogenic lesions. Documentation of ictal semiology may differentiate patients with the more prognostically favorable limbic epilepsy from those without. Outpatient and several prolonged scalp EEGs would determine whether most seizures have a consistent discrete focus of origin or early involvement and whether interictal features reflecting multifocal epileptogenesis are absent. Although the threshold for invasive recordings varies among centers, practitioners should realize that ambiguous epileptogenesis prompting this decision itself augurs an unfavorable outcome. However, within this somber framework, a consistent seizure onset elevates the outlook for surgical effectiveness to equivocal.


  1. Top of page
  2. Abstract
  7. Acknowledgments

ACKNOWLEDGMENT:  Mrs. Maria Raffa carefully prepared the manuscript.


  1. Top of page
  2. Abstract
  7. Acknowledgments
  • 1
    Duncan JS. Imaging and epilepsy. Brain 1997;120: 33977.
  • 2
    Roberts RC. Adult idiopathic and cryptogenic focal epilepsies. In: OxburyJM, PolkeyCE, DuchownyM, eds. Intractable focal epilepsy. London : WB Saunders, 2000: 26976.
  • 3
    Falconer MA, Serafetinides EA, Corsellis JAN. Etiology and pathogenesis of temporal lobe epilepsy. Arch Neurol 1964;10: 23348.
  • 4
    Duncan JS, Sagar HJ. Seizure characteristics, pathology and outcome after temporal lobectomy. Neurology 1987;37: 4059.
  • 5
    Wyllie E, Lüders H, Morris HH, et al. Clinical outcome after complete or partial cortical resection for intractable epilepsy. Neurology 1987;37: 163441.
  • 6
    Fish DR, Smith SJ, Quesney LF, et al. Surgical treatment of children with medically intractable frontal or temporal lobe epilepsy: results and highlights of 40 years' experience. Epilepsia 1993;34: 2447.
  • 7
    Guldvog B, Loyning Y, Hauglie-Hanssen E, et al. Surgical treatment for partial epilepsy among Norwegian adults. Epilepsia 1994;35: 54053.
  • 8
    Guldvog B, Loyning Y, Hauglie-Hanssen E, et al. Predictive factors for success in surgical treatment for partial epilepsy: a multivariate analysis. Epilepsia 1994;35: 56678.
  • 9
    Berkovic SF, McIntosh AM, Kalnins RM, et al. Preoperative MRI predicts outcome of temporal lobectomy: an actuarial analysis. Neurology 1995;45: 135863.
  • 10
    Lorenzo NY, Parisi JE, Cascino GD, et al. Intractable frontal lobe epilepsy: pathological and MRI features. Epilepsy Res 1995;20: 1718.
  • 11
    Spencer SS. Long-term outcome after epilepsy surgery. Epilepsia 1996;37: 80713.
  • 12
    Zentner J, Hufnagel A, Ostertun B, et al. Surgical treatment of extratemporal epilepsy: clinical, radiologic, and histopathologic findings in 60 patients. Epilepsia 1996;37: 107280.
  • 13
    Bizzi JW, Bruce DA, North R, et al. Surgical treatment of focal epilepsy in children: results in 37 patients. Pediatr Neurosurg 1997;26: 8392.
  • 14
    Swartz BE, Delgado-Escueta AV, Walsh GO, et al. Surgical outcomes in pure frontal lobe epilepsy and foci that mimic them. Epilepsy Res 1998;29: 97108.
  • 15
    Ferrier CH, Engelsman J, Alarcon G, et al. Prognostic factors in presurgical assessment of frontal lobe epilepsy. J Neurol Neurosurg Psychiatry 1999;66: 3506.
  • 16
    Siegel AM, Jobst BC, Thadani VM, et al. Medically intractable, localization-related epilepsy with normal MRI: presurgical evaluation and surgical outcome in 43 patients. Epilepsia 2001;42: 8838.
  • 17
    Penfield W. Epileptogenic lesions. Acta Neurol Belg 1956;56: 7588.
  • 18
    Penfield W. Pitfalls and success in surgical treatment of focal epilepsy. Br Med J 1958;1: 66972.
  • 19
    Bengzon ARA, Rasmussen T, Gloor P, et al. Prognostic factors in surgical treatment of temporal lobe epilepsy. Neurology 1968;18: 71731.
  • 20
    Najm IM, Babb TL, Mohamed A, et al. Mesial temporal lobe sclerosis. In: LudersHO, ComairYG, eds. Epilespy surgery. 2nd ed. Philadelphia : Lippincott Williams & Wilkins, 2001: 95103.
  • 21
    Babb T. Research on the anatomy and pathology of epileptic tissue. In: LudersHO, ed. Epilepsy surgery. New York : Raven Press, 1992: 71927.
  • 22
    Penfield W, Jasper H. Epilepsy and the functional anatomy of the human brain. Boston : Little, Brown, 1954.
  • 23
    So NK. Epileptic auras. In: WyllieE, ed. The treatment of epilepsy: principles and practice. Philadelphia : Lea & Febiger, 1993: 36977.
  • 24
    Kotagal P. Psychomotor seizures: clinical and EEG findings. In: WyllieE, ed. The treatment of epilepsy: principles and practice. Philadelphia : Lea & Febiger, 1993: 37892.
  • 25
    Sadler RM, Goodwin J. Multiple electrodes for detecting spikes in partial complex seizures. Can J Neurol Sci 1989;16: 3269.
  • 26
    Lemieux JF, Vera RS, Blume WT. Database system for EEG laboratories. Electroencephalogr Clin Neurophysiol 1984;58; 50P1P.
  • 27
    Jennett WB. Epilepsy after non-missile head injuries. 2nd ed. London : William Heinemann, 1975.
  • 28
    Elwes RD, Dunn G, Binnie CD, et al. Outcome following resective surgery for temporal lobe epilepsy: a prospective follow up study of 102 consecutive cases. J Neurol Neurosurg Psychiatry 1991;54: 94952.
  • 29
    Wass CT, Rajala MM, Hughes JM, et al. Long-term follow-up of patients treated surgically for medically intractable epilepsy: results in 291 patients treated at Mayo Clinic Rochester between July 1972 and March 1985. Mayo Clin Proc 1996;71: 110513.
  • 30
    Engel J Jr. Outcome with respect to epileptic seizures. In: EngelJJr, ed. Surgical treatment of the epilepsies. 1st ed. New York : Raven Press, 1987: 55372.
  • 31
    Blume WT, Desai HB, Girvin JP, et al. Effectiveness of temporal lobectomy measured by yearly follow-up and multivariate analysis. J Epilepsy 1994;7: 20314.
  • 32
    Blume WT, Whiting SE, Girvin JP. Epilepsy surgery in the posterior cortex. Ann Neurol 1991;29: 63845.
  • 33
    Wiebe S, Blume WT, Girvin JP, et al. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med 2001;345: 3118.
  • 34
    Awad IA, Rosenfeld J, Ahl J, et al. Intractable epilepsy and structural lesions of the brain: mapping, resection strategies, and seizure outcome. Epilepsia 1991;32: 17986.
  • 35
    Van Ness PC, Awad IA, Lüders HO, et al. The relationship of epileptogenic zone resection, lesion resection and outcome in 27 cases with neocortical epilepsy. Ann Neurol 1990;28: 263.
  • 36
    Jayakar P, Duchowny M, Resnick T, et al. Epilepsy surgery in children with normal or nonspecific neuroimaging studies. Ann Neurol 1994;36: 504.
  • 37
    Engel J Jr, Rausch R, Lieb JP, et al. Correlation of criteria used for localizing epileptic foci in patients considered for surgical therapy of epilepsy. Ann Neurol 1981;9: 21524.
  • 38
    Risinger MW, Engel J Jr, Van Ness PC, et al. Ictal localization of temporal lobe seizures with scalp/sphenoidal recordings. Neurology 1989;39: 128893.
  • 39
    Walczak TS, Radtke RA, Lewis DV. Accuracy and interobserver reliability of scalp ictal EEG. Neurology 1992;42: 227985.
  • 40
    Blume WT, Holloway GM, Wiebe S. Temporal epileptogenesis: localizing value of scalp and subdural interictal and ictal EEG data. Epilepsia 2001;42: 50814.
  • 41
    Williamson PD, French JA, Thadani VM, et al. Characteristics of medial temporal lobe epilepsy, II: interictal and ictal scalp electroencephalography, neuropsychological testing, neuroimaging, surgical results, and pathology. Ann Neurol 1993;34: 7817.
  • 42
    Lee SK, Kim JY, Hong KS, et al. The clinical usefulness of ictal surface EEG in neocortical epilepsy. Epilepsia 2000;41: 14505.
  • 43
    Blume WT, Borghesi JL, Lemieux JF. Interictal indices of temporal seizure origin. Ann Neurol 1993;34: 7039.
  • 44
    Gloor P. Commentary: approaches to localization of the epileptogenic lesion. In: EngelJJr, ed. Surgical treatment of the epilepsies. New York : Raven Press, 1987: 97100.
  • 45
    Gloor P. Preoperative electroencephalographic investigation in temporal lobe epilepsy: extracranial and intracranial recording. Can J Neurol Sci 1991;18: 5548.
  • 46
    Sammaritano M, Gigli GL, Gotman J. Interictal spiking during wakefulness and sleep and the localization of foci in temporal lobe epilepsy. Neurology 1991;41: 2907.
  • 47
    Montplaisir J, Laverdiere M, Saint-Hilaire JM, et al. Sleep and focal epilepsy: a study of patients implanted with depth electrodes. In: WolfP, DamM, DreifussFE, eds. Advances in epileptology. New York : Raven Press, 1987: 7057.
  • 48
    Avoli M. Do interictal discharges promote or control seizures? Experimental evidence from an in vitro model of epileptiform discharge. Epilepsia 2001;42(suppl 3):24.
  • 49
    Quesney LF. Preoperative electroencephalographic investigation in frontal lobe epilepsy: electroencephalographic and electro-corticographic recordings. Can J Neurol Sci 1991;18: 55963.
  • 50
    Pathak P, Blume WT. Asymmetrical epileptogenicity of brain lesions. Epilepsia 1997;38(suppl 8):64.
  • 51
    Williamson PD, Thadani VM, Darcey TM, et al. Occipital lobe epilepsy: clinical characteristics, seizure spread patterns, and results of surgery. Ann Neurol 1992;31: 313.
  • 52
    Park SA, Lim SR, Kim GS, et al. Ictal electrocorticographic findings related with surgical outcomes in nonlesional neocortical epilepsy. Epilepsy Res 2002;48: 199206.
  • 53
    Salanova V, Andermann F, Olivier A, et al. Occipital lobe epilepsy: electroclinical manifestations, electrocorticography, cortical stimulation and outcome in 42 patients treated between 1930 and 1991: surgery of occipital lobe epilepsy. Brain 1992;115: 165580.
  • 54
    Engel J. Bilateral temporal lobe epilepsy. In: WolfP, ed. Epileptic seizures and syndromes. London : John Libbey, 1994: 35968.
  • 55
    Noriega-Sanchez A, Markand ON. Clinical and electroencephalographic correlation of independent multifocal spike discharges. Neurology 1976;26: 66772.
  • 56
    Blume WT. Clinical and electroencephalographic correlates of the multiple independent spike foci pattern in children. Ann Neurol 1978;4: 5417.
  • 57
    Gabor AJ, Ajmone Marsan C. Co-existence of focal and bilateral diffuse paroxysmal discharges in epileptics: clinical-electrographic study. Epilepsia 1969;10: 45372.
  • 58
    Blume WT, Pillay N. Electrographic and clinical correlates of secondary bilateral synchrony. Epilepsia 1985;26: 63641.