Brain Advance Access originally published online on November 1, 2006
Brain 2006 129(12):3307-3314; doi:10.1093/brain/awl305
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Epilepsy surgery involving the sensory-motor cortex
1 Department of Clinical Neurological Sciences, London Health Sciences Centre London, Ontario 2 Department of Clinical Neurosciences, University of Calgary Calgary, Alberta, Canada 3 Department of Neurology, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico City, Mexico
Correspondence to: Dr Samuel Wiebe, Division of Neurology, Foothills Medical Centre, 1403-29 Street N.W., Calgary, Alberta, Canada T2N 2T9 E-mail: swiebe{at}ucalgary.ca
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Summary |
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Our aim was to assess the outcome with regard to seizures and neurological function in unselected patients undergoing resective surgery involving the perirolandic area, with or without multiple subpial transections (MSTs). All patients who underwent perirolandic cortical resection or MSTs from 1979 to 2003 at the London Health Sciences Centre were identified. Patients were included if they had seizures originating in the perirolandic area, recorded with subdural electrodes, or if they had scalp recorded seizures and a congruent discrete epileptogenic lesion on MRI in the perirolandic area. Most patients had electrocorticography (ECoG) at the time of surgery. Data collected include pre-operative and post-operative neurological deficits, MRI findings, interictal and ictal scalp EEG, interictal and ictal subdural data, ECoG findings, type and extent of surgery, neuropathologic diagnoses, and seizure outcomes. We studied 52 patients (22 females). The average age at the time of surgery was 33 years, and the average post-operative follow-up was 4.2 years. The most frequent aetiologies were neoplastic in 26 patients (50%), vascular in eight (15%), malformations of cortical development in six (12%), Rasmussen's encephalitis in three (6%) and other aetiologies in nine (17%). Surgery involved the pre-central gyrus in 17 patients, pre- and post-central gyrus in 13, the inferior central region in 11, the post-central gyrus in 7, and the pre-central gyrus and mesial frontal area in 2. At last follow-up 16 patients were in Engel class I (31%), 8 (15%) in class II, 14 (27%) in class III and 14 (27%) in class IV. Residual neurological deficits were present in 26 patients (50%), occurred more frequently in patients
25 years old (P < 0.05) and were mild in 14 (54%) patients. In univariate analyses, better seizure outcomes (P < 0.05) occurred in patients whose ECoG showed infrequent post-resectional spikes and no spikes distant to the resection margin, and in resections involving the pre-central and inferior rolandic cortex. In unselected patients with intractable perirolandic epilepsy, many of whom have large, complex epileptogenic lesions, various levels of seizure improvement can be achieved in almost 75% through well-planned surgical resections. New, severe post-operative neurological deficits can occur in 23% of these patients and appear to be more frequent in older patients. Whereas scalp EEG provided limited information to guide surgery, findings on interictal ECoG predicted seizure outcome.
Key Words: extratemporal epilepsy; epilepsy surgery; perirolandic epilepsy; sensorimotor epilepsy
Abbreviations: ECoG, electrocorticography; MSTs, multiple supbial transections
Received May 24, 2006. Revised September 13, 2006. Accepted September 18, 2006.
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Introduction |
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In 1886, Victor Horsley (1886)
resected an area of post-central gliotic cortex in a 22-year-old man using electrical stimulation to map cortical function. Subsequently, Horsley (1890), Keen (1888), Nancrede (1888), Lloyd and Deaver (1888), Sachs (1935) and Putnam (1940) reported favourable results of resections of the sensorimotor cortex in patients with various types of involuntary movements, whose neurological function was preserved to variable degrees. In 1947, Pilcher et al. (1947) performed large corticectomies involving the sensorimotor cortex using cortical stimulation mapping in 41 patients with non-lesional and lesional epilepsy. Fifteen patients experienced no neurological deficit, 17 had mild weakness, and functional recovery followed more limited resections. After 6 years of follow-up, 19.5% of patients were seizure free.
In epilepsy surgery centres, 
20% of patients with partial epilepsy have extratemporal epilepsy, mostly of frontal lobe or central (perirolandic) origin (Spencer and Spencer, 1985; Kutsy, 1999; Spencer et al., 2003; Cascino, 2004). In hospital-based studies of unselected patients with epilepsy the corresponding proportion is 33% (Semah et al., 1998). In comparison, in population-based studies, the prevalence of extratemporal epilepsy is as high as 55% (Manford et al., 1992).
Surgical treatment for partial epilepsy of extratemporal origin is particularly challenging because of difficulty in localizing the epileptogenic zone, rapidity and extent of ictal spread, and the risk of neurological deficits related to excision of functional cortex. Compared with temporal lobe epilepsy, which merely requires localization to perform a standardized resection, extemporal epilepsy requires an accurate estimation of the extent of the epileptic region to know how much cortex should be resected (Kutsy, 1999; Cascino, 2004). Advances in neuroimaging have facilitated the identification of epileptogenic lesions in patients with neocortical epilepsy, allowing for more precise and safer resections. Still, perirolandic cortical excisions may be associated with substantial post-operative sensory motor deficits (Cascino, 2004). Moreover, many patients with extratemporal lobe epilepsy have normal structural neuroimaging, and elusive seizure origins (McKhann et al., 2002).
Here we describe the neurological and seizure outcomes of 52 patients who had surgery involving the perirolandic cortex for intractable epilepsy. We focus on seizure and functional outcomes as they relate to MRI findings, interictal and ictal scalp and intracranial EEG (IEEG), electrocorticography (ECoG), type and extent of surgery, and aetiology.
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Material and methods |
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Patients and methods
We identified all patients with epilepsy who were treated with surgical resection with or without multiple subpial transections (MSTs) involving the perirolandic cortex from 1979 to 2003 at the London Health Sciences Centre, Ontario, Canada. Perirolandic surgery was defined as that involving the pre-central and/or post-central gyrus, with or without adjacent cortex. Because specific surgical location determines neurological outcomes we also classified surgical resections as involving the upper, middle or inferior portions of the perirolandic cortex. Patients were included if IEEG demonstrated seizure origin in the perirolandic region, or if scalp EEG demonstrated a regional perirolandic seizure origin and MRI showed a congruent, discrete epileptogenic lesion. Standard pre-surgical evaluation included history and neurological examination, continuous scalp EEG monitoring using the 10–20 system with additional mandibular notch electrodes (Sadler and Goodwin, 1989
), MRI imaging, detailed neuropsychological testing (Jones-Gotman et al., 2000) and the sodium amobarbital (Wada) test to evaluate speech and memory in selected patients (Blume, 1986).
When necessary, IEEG monitoring was done by implanting electrode lines and strips with post-implantation imaging to confirm placement (Dubeau and McLachlan, 2000; Blume, 1986). Electrode grids were used when adjacent areas of cortical convexity needed coverage, allowing for more detailed topographical analysis. Some patients received dexamethasone (10 mg) just prior to surgery and then for 3 days on a tapering schedule to reduce post-operative discomfort (Sahjpaul et al., 2003). Lines consisted of cylindrical stainless steel contacts measuring 4 mm in length by 2 mm diameter at 10 mm intervals (McLachlan and Luba, 2002). Strips consisted of single-sided or double-sided rows of stainless steel disks with 7 mm2 of exposed surface embedded in Silastin at 10 mm intervals. Typical grids consisted of similar disks arranged in 6 x 7–8 x 7 arrays. When indicated for somatosensory, motor, visual or language mapping, cortical stimulation studies were performed as described by Blume et al. (2004). All patients had ECoG at the time of surgery. Antiepileptic drugs (AEDs) were continued unchanged after surgery for at least 6 months. Slow tapering was attempted thereafter only if patients were completely seizure free.
Outcome measures and data collection
The principal outcomes were seizures and neurological function obtained from patients' charts and prospectively using a telephone-administered standardized questionnaire. We categorized seizure outcomes using Engel's four-category classification consisting of Class I: free of disabling seizures; Class II: rare disabling seizures; Class III: worthwhile improvement; Class IV: no worthwhile improvement (Engel et al., 1993). For some analyses, we considered Engel class I, II or III, i.e. any improvement, as a favourable outcome. This was judged appropriate because seizure freedom is difficult to achieve in many patients with perirolandic epilepsy surgery (Cascino, 2004). We also collected information on the following predictor variables. (i) Type and severity of pre-operative and post-operative neurological deficits, determined at last follow-up by the treating neurologists. (ii) Aetiology, as defined by structural MRI and histopathology. (iii) Interictal and ictal scalp EEG and IEEG findings, specifically, the presence and location of epileptiform activity. (iv) Location and amount of spikes on ECoG, i.e. located only in the post-resection margin or distant to it; and amount of post-resection spikes, assessed by the electroencephalographer as frequent or none/infrequent. (v) Type and extent of surgery, i.e. complete lesionectomy and/or corticectomy versus other.
Principles of surgical management
The objective of resective surgery was the removal of a lesion when present, and any associated cortex harbouring epileptogenic activity.
Tailoring of the surgical resection was strongly influenced by the clinical semiology in addition to ECoG epileptogenic activity. This is particularly important because well-localized sensorimotor epileptogenic activity is often poorly defined in the perirolandic area, and defining a true ‘focus’ is often problematic. The hierarchy of surgical priorities was perirolandic cortical resection, resection of inferior perirolandic cortex and MSTs. Surgery was performed under local anaesthesia. Resection was carried out by typical careful subpial resective technique, with continual monitoring of the neurological function at risk. MSTs were done if, following the most extensive resection, epileptogenic activity remained in unresectable areas due to risk to neurological function. MSTs were carried out transverse to the gyral surface, over 5–10 mm spacing. Because of the known difficulty in controlling perirolandic seizures, our thrust was to perform more rather than less surgical resection or MSTs, especially in the cases with very severe intractability. In these cases there was acceptance of the potential deficits, if they were considered to justify a more satisfactory outcome of seizure control. Resection of the inferior perirolandic neocortex, i.e. head and neck representation inferior to the thumb area, most often does not result in long-lasting post-operative deficits. Intraoperative ECoG was done when pre-operative subdural ECoG was insufficient or not done. Functional cortical localization was done using 50 Hz biphasic monopolar stimuli with 0.3 ms pulse durations and 1.5–18 mA strengths were employed. At each electrode, stimulation was commenced at 1.5 mA with 1 mA increments for each subsequent stimulation until a functional alteration, an afterdischarge or 18 mA was obtained or attained (Blume et al., 2004).
Definition of deficits
We categorized deficits according to resection of the superior, middle and inferior perirolandic regions. Broadly, superior resections involved the foot and the leg area, middle resections included the arm and hand area, and inferior resections involved the face area and resections around Broca's area.
Analysis
We used continuity corrected 
2 or Fisher exact analyses to compare outcomes in such categorical variables as type of surgery, localization of the epileptic foci, aetiology and complications. Independent t-tests were used to compare continuous variables. We performed two multivariate logistic regression analyses. In the first model the dependent variable was seizure outcome (favourable outcome = Engel I, II and III), as predicted by aetiology (tumour versus other), type of resection (lesionectomy and complete resection versus other), neurological deficit (present or absent), resection site (superior, middle, inferior) and age. In the second model the dependent variable was the presence or absence of new neurological deficits, as predicted by aetiology (tumour versus other), type of resection (lesionectomy and complete resection versus other), age (25 years), resection site (superior, middle and inferior) and seizure outcome (as defined above).
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Results |
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Fifty-two patients (22 females) fulfilled eligibility criteria. At the time of surgery, the mean age (± SD) was 33 ± 14 years, and the mean number of AEDs was 1.8 (range 0–4). Sixty percent of patients were operated after 1990. The median post-surgical follow-up was 3 years (range 1–18 years) and the average was 4.2 years (SD 3.6) (Table 1).
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Type of seizures
Forty seven (90%) patients had simple partial seizures, 16 (31%) also had complex partial seizures, 17 (34%) had generalized tonic–clonic seizures and 4 (8%) had epilepsia partialis continua (Table 1).
Aetiology
The most frequent aetiologies were neoplastic [26 patients (50%)], vascular malformations [8 (15%)], neuronal migration disorders [6 (12%)] and Rasmussen's encephalitis [3 (6%)] (Table 2). Cases classified as ‘other’ included mesenchymal meningeal sarcoma (1), porencephalic cyst (1), gliosis (5), meningioangiomatosis (1) and mitochondrial encephalopathy (1). The patient with mitochondrial encephalopathy had severely disabling epilepsia partialis continua which mandated heroic surgical therapy involving extensive MSTs.
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Scalp EEG
Central spikes occurred in 32% of patients; spikes were multifocal and generalized in 24%, temporal in 10%, parietal in 6%, central-sagittal in 6% and frontal in 4%. Nine patients (18%) did not have interictal spikes. Seizure origins involved the central region exclusively in only 26% of patients. A focus could not be identified in 36% of patients. Other broad areas of seizure origin included the frontal (8%), parietal (6%) or temporal (2%) regions. Multifocal onsets occurred in 8% and generalized onset in 6%. Ambiguous or non-regional seizure origins occurred in 8%.
Type of surgery
ECoG-guided awake surgical resections were performed in all patients. Eight patients (15%) underwent resection plus MST, 11 (21%) had corticectomies, 11 (21%) had lesionectomies plus corticectomies, 11 (21%) had lesionectomies alone, 8 (15%) had a partial lesionectomy, 1 patient had only MST (3%) and 2 (4%) had partial lesionectomy and corticectomy (Table 3).
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Topography of resections
In all but one patient surgery involved a lesion identified on CT/MRI and it was congruent with the identified epileptogenic area. In one patient, the ECoG and clinical semiology guided surgery. The resection involved the pre-central gyrus in 17 patients (33%), the post-central gyrus in 7 (33%), the pre- and post-central gyri in 13 (25%), the inferior central region in 13 (25%), and the pre-central and mesial frontal region in 2 (4%) (Table 3).
Seizure outcome
At last follow-up 38 patients (73%) were improved (Engel Class I–III). Sixteen (31%) were in Engel class I (13 in IA and 3 in 1B). Eight (15%) were in class II (1 in IIA and 7 in IIB). Fourteen (27%) were in class III (10 in IIIA and 4 in IIIB), and 14 (27%) were in class IV (four in IVA, 7 in IVB and 5 in IVC) (Fig. 1). Seizure outcome was similar in patients operated on before 1980 and those operated after 1990 (good outcome in 71 and 73%, respectively).
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Type of surgery and seizure outcome
The best seizure outcome was seen in patients with lesionectomy and corticectomy, and in those with complete lesionectomy. The worst outcomes involved patients undergoing MSTs. Outcome differences between patients who had MST versus other groups (lesionectomy and corticectomy) were statistically significant (P < 0.05) (Table 3).
Topography of resection and seizure outcome
Seizure outcomes were significantly different among various surgical locations within the perirolandic cortex. Eighty-three per cent of patients with resections involving the pre-central gyrus and inferior central region had a good seizure outcome, as compared with 59% of those whose surgery involved other areas (P < 0.05). Good outcomes were similar with surgery in the right (40%) and the left hemisphere (41%) (Tables 3 and 4).
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Seizure outcomes appeared better with pre-central than post-central resections (not significant) (Table 3). However, no significant differences emerged between these groups in analyses of age, pathology, completeness of resection and presence of deficits.
Ten patients had resections around Broca's area. Nine (90%) had left hemisphere and one (10%) right hemisphere resections. Four (40%) had a complete lesionectomy, three (30%) had a partial lesionectomy, two (20%) had a partial lesionectomy plus corticectomy and one (10%) had a corticectomy. Speech deficits occurred in five patients (55%) with left sided resections and in the one patient with a right-sided resection, who had atypical language representation. Seizure outcome in these patients was Engel IA in two (20%), IIB in one (10%), IIIA in five (50%), IIIB in one (10%) and IVC in one (10%).
Neurological deficits
Twenty six patients (50%) had a new or more severe post-operative neurological deficit at last follow-up, but 10 of these (38%) had pre-existing deficits. New deficits were mild in 14 (54%) patients. As expected, most deficits involved motor function and speech (Table 5). The majority of patients (4 of 6) with speech impairment had only a mild deficit. Deficits involved motor function in all but 3 patients, and they were mild in 11 (48%). Only one patient had exclusively sensory abnormalities (mild). There was no correlation between severity of neurological deficits and the side of the surgery (Table 2). However, larger and superior-middle resections were more often associated with deficits (Table 4). There was no association between neurological deficit and seizure outcome (Table 2), i.e. better seizure outcomes were not obtained at the expense of larger deficits. The frequency of neurological deficits overall was similar in both hemispheres.
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Aetiology and seizure outcome
The best seizure outcomes were achieved in patients with DNET, oligodendrioglioma and cortical dysplasia. Worst outcomes occurred in patients with Rasmussen's encephalitis. However, the differences were not significant (Table 2).
ECoG and seizure outcome
ECoG data were available in 29 patients. The location and number of post-resection spikes were related to seizure outcome. In univariate analyses, patients who had spikes distant to the resection margin, and those with frequent post-resectional spikes had worse outcomes (P < 0.05) (Fig. 2).
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Multivariate analyses
The logistic regression analysis did not find any independent predictors of seizure outcome. Although lack of power is a plausible explanation, it is clear that the predictors explored are substantially intercorrelated. The model exploring predictors of neurological deficits showed that patients
25 years old had an almost 4-fold risk of deficits (OR 3.9, P = 0.048). Also, patients <25 years old had fewer complete or partial lesionectomies (38 versus 68%), and significantly fewer had tumours (33 versus 59%, P < 0.05). |
Discussion |
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As compared to other studies of resective perirolandic epilepsy surgery, fewer of our patients had Engel I outcomes (31%), although 73% had some improvement. This difference could be explained by the complexity of our patients' epileptogenic zones and structural abnormalities, which demanded a broad range of surgical procedures. In many of the studies of perirolandic epilepsy, most surgical procedures consisted of selected resections and lesionectomies not requiring palliative procedures such as MSTs or partial resections, and not involving patients with multifocal epilepsy. Conceivably, the epileptogenic areas in our unselected cases involved more eloquent cortex, increasing the risk of deficits and precluding the possibility of complete, curative resections. It is also conceivable that larger surgical resections in our patients, in keeping with our surgical philosophy, gave rise to a higher incidence of neurological deficits.
In analyses of Engel I and II outcomes, which are commonly reported in these studies, our results (46%) are comparable to those of Devinsky et al. (54%), Otsubo et al. (43%) and Pilcher et al. (48.7%) (Table 6), (Devinsky et al., 2003) (Pilcher et al., 1947; Otsubo et al., 2001). Two of these studies (Pilcher et al., 1947; Devinsky et al., 2003) have a larger sample size, similar to ours. Outcomes in these studies contrast with those of small studies (n < 5), such as Cukiert et al.'s (75%) and Cohen-Gadol et al.'s (80%) (Cukiert et al., 2001; Cohen-Gadol et al., 2003).
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The relation between type of resection and surgical outcome is germane. Pilcher et al.'s (1947)
and our study included many superior resections involving the leg and arm/hand area. Resections are typically more limited in these areas to avoid deficits, and could explain worse seizure outcomes. This notion is supported by the superior seizure outcomes reported by Lehman et al. (60%) (Lehman et al., 1994) and Cukiert et al. (75%) (Cukiert et al., 2001) whose patients had surgery mostly involving the face area, where resections can be more extensive.
Specific surgical procedures probably relate to seizure outcomes. Studies focusing on corticectomies and lesionectomies in selected cases such as those of Cukiert et al. and Cohen-Gadol et al. (Cukiert et al., 2001; Cohen-Gadol et al., 2003) report better outcomes (75–80% Engel I and II), than studies including patients with complex epileptogenic zones and structural abnormalities, which require a broad range of surgical procedures, e.g. ours (46%) and Pilcher et al.'s (48.7%) (Pilcher et al., 1947).
Our univariate analyses suggest that patients with complete lesionectomies, those with resections of pre-central and inferior rolandic cortex, neoplastic aetiology, and those with no or only resection-margin spikes on ECoG may have better surgical outcomes. However, multivariate logistic regression analysis failed to identify any independent predictors of seizure outcome. Possible explanations for this lack of association include a small sample size and a high level of intercorrelation of predictor variables.
Patients undergoing MSTs had poorer outcomes than in other reports (Table 3). Seven of these nine patients had >1 epileptogenic focus (range 1–5), and most were superior and mid perirolandic. Their histopathology revealed cortical dysplasia (4), Rasmussen's encephalitis (3), mitochondrial encephalopathy (1) and plasmocytoma (1). We believe that the aetiology, multifocality and location within the perirolandic cortex contributed to a poorer outcome in these patients. A meta-analysis of 211 patients undergoing MST at six centres found that 62–71% of patients had >95% seizure reduction with only MST, and 68–87% of patients with MST plus cortical resections had >95% seizure reduction (Spencer et al., 2002). Our results are substantially poorer (seizure freedom ranged from 0 to 38%) (Table 3), but they resemble Schramm et al.'s (2002), in which only 15% of patients undergoing MSTs were seizure free in long-term follow-up.
In 1947, Penfield and Rasmussen reported that large resections in the pre-central gyrus produced a complete, immediate paralysis followed by spasticity. However, significant improvement in proximal limb function with minor return of distal (finger/toe) movements occurred after 1 year. Our patients had a higher rate of post-surgical permanent deficits (50%) than that reported in several studies. In Lehman et al.'s study (1994) 40% had transient deficits and 30% had permanent deficits. One (7%) of 14 patients reported by Sandok and Cascino et al. (1998) had monoparesis after surgery. In Cukiert et al.'s series (Cukiert et al., 2001) all patients had transient but not permanent deficits. Devinsky and Cohen (Cohen-Gadol et al., 2003; Devinsky et al., 2003) reported permanent deficits in 8 and 20%, respectively. Finally, none of seven patients in a paediatric study had deficits after surgery (Otsubo et al., 2001). Although these discrepancies defy simple explanations, we postulate that many reports of perirolandic epilepsy surgery describe selected cases with lower surgical risk.
Pilcher et al. report rates of post-operative deficits similar to ours (41%) (Pilcher et al., 1947). The patient population is also similar in both studies. These were unselected cases with complex pathology, extensive epileptogenic areas involving superior, medial and inferior areas of the homunculus, pre-existing neurological deficits, and severely disabling seizures. These lesions demanded larger resections involving eloquent cortex and substantial risk to function. In addition, both studies included a large number of resections involving the superior and middle areas of the perirolandic cortex, which entail higher risks of deficits (Table 6). It is of note that new or worse deficits occurred frequently in Pilcher et al.'s (1947) and in our patients despite using cortical function mapping to guide surgical resections. In our study this is explained by our surgical philosophy of performing more rather than less surgery, and the acceptance of potential deficits when these justified a more satisfactory outcome of seizure control in highly intractable patients.
The association between age, seizure outcome and risk of neurological deficits has been explored only rarely (McLachlan et al., 1992). Our multivariate analysis identified age (25 years) as the only independent predictor of neurological deficits. Moreover, tumours occurred significantly more frequently in patients 25 years old. It is conceivable that epileptogenic lesions in older patients develop more rapidly, giving less opportunity for reorganization of eloquent perirolandic cortex. Surgical resection of overlapping epileptogenic and eloquent cortices may thus result in a higher risk of neurological deficits in these patients.
Meticulous follow-up can show improvements in post-operative deficits over many years, which may reflect neural plasticity. Chronic processes in the sensorimotor cortex have been shown to induce plastic changes in the functional organization of eloquent cortex (Merzenich and Sameshima, 1993; Rauschecker, 1997; Danckert et al., 2004; Jaillard et al., 2005). Recent evidence has shown redundant functional cortical units in regions adjacent to the sensory motor cortex, each participating in the same finger, wrist or forearm movements (Sanes et al., 1995). Although we cannot demonstrate this process in our patients, one may invoke cortical reorganization as a contributor to functional recovery, as has been shown in patients who have suffered strokes or undergone large resections in eloquent cortices.
In our study the three most important aetiologies were neoplastic (50%), cortical dysplasia (10%) and vascular (15%) (Table 2). This is in agreement with previous studies. In Sandok's study (Sandok et al., 1998) the most frequent aetiologies were tumours in 29% of patients, arteriovenous malformations in 29% and gliosis in 21%. In Lehman's study (Lehman et al., 1994) 45% had gliosis, cortical dysplasia or microgyria. Cukiert et al. (2001) report gliosis in 75%, and cortical dysplasia in 25%. Lastly, in Otsubo et al.'s series (Otsubo et al., 2001) of five children, two had cortical dysplasia, and others had tuberous sclerosis. It is clear that advances in imaging techniques have improved our ability to identify cortical developmental anomalies (Colombo et al., 2003; Huppertz et al., 2005). For example, in the oldest study of Pilcher et al. (1947) this entity was infrequent, in contrast with more recent studies (Otsubo et al., 2001; Cohen-Gadol et al., 2003).
Some controversy exists regarding the usefulness of ECoG in the localization of foci in non lesional cases (Davies and Weeks, 1995). However, we found an association between distant post-resection spikes and poorer seizure outcome (Fig. 2). This corroborates findings from previous studies of perirolandic (Lehman et al., 1994; Devinsky et al., 2003) and extratemporal epilepsy surgery (Wennberg et al., 1998, 1999). Poorer outcomes have also been associated with the presence of any extratemporal post-resectional spikes (Ferrier et al., 2001), but the number of patients without any post-resectional spikes in our study was too small to allow meaningful comparisons.
In summary, this large surgical cohort of unselected patients suffering from severe, intractable perirolandic epilepsy presents a realistic view of the outcomes resulting from extensive surgical management. Seizure and neurological outcomes in these patients may be somewhat less optimistic than those reported in series of selected patients. Finally, our data suggest that ECoG is useful in epilepsy surgery involving the sensorimotor cortex, and that increasing age may carry a higher risk of neurological deficits.
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References |
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|
TopSummaryIntroductionMaterial and methodsResultsDiscussionReferences |
|---|
Blanchette N and Smith ML. (2002) Language after temporal or frontal lobe surgery in children with epilepsy. Brain Cogn 48:280–4.[ISI][Medline]
Blume WT. (1986) Principles of clinical investigation of surgical patients. Int Anesthesiol Clin 24:47–73.[ISI][Medline]
Blume WT, Jones DC, Pathak P. (2004) Properties of after-discharges from cortical electrical stimulation in focal epilepsies. Clin Neurophysiol 115:982–9.[CrossRef][ISI][Medline]
Cascino GD. (2004) Surgical treatment for extratemporal epilepsy. Curr Treat Options Neurol 6:257–62.[Medline]
Cohen-Gadol AA, Britton JW, Collignon FP, Bates LM, Cascino GD, Meyer FB. (2003) Nonlesional central lobule seizures: use of awake cortical mapping and subdural grid monitoring for resection of seizure focus. J Neurosurg 98:1255–62.[ISI][Medline]
Colombo N, Citterio A, Galli C, Tassi L, Lo Russo G, Scialfa G, et al. (2003) Neuroimaging of focal cortical dysplasia: neuropathological correlations. Epileptic Disord 5:Suppl. 2, S67–72.
Cukiert A, Buratini JA, Machado E, Sousa A, Vieira J, Forster C, et al. (2001) Seizure's outcome after cortical resections including the face and tongue rolandic areas in patients with refractory epilepsy and normal MRI submitted to subdural grids' implantation. Arq Neuropsiquiatr 59:717–21.[Medline]
Danckert J, Mirsattari SM, Danckert S, Wiebe S, Blume WT, Carey D, et al. (2004) Spared somatomotor and cognitive functions in a patient with a large porencephalic cyst revealed by fMRI. Neuropsychologia 42:405–18.[CrossRef][ISI][Medline]
Davies KG and Weeks RD. (1995) Results of cortical resection for intractable epilepsy using intra-operative corticography without chronic intracranial recording. Br J Neurosurg 9:7–12.[CrossRef][ISI][Medline]
Devinsky O, Romanelli P, Orbach D, Pacia S, Doyle W. (2003) Surgical treatment of multifocal epilepsy involving eloquent cortex. Epilepsia 44:718–23.[CrossRef][ISI][Medline]
Dubeau F and McLachlan RS. (2000) Invasive electrographic recording techniques in temporal lobe epilepsy. Can J Neurol Sci 27:Suppl 1, S29–34.
Engel J, Van Ness PC, Rasmussen TB. (1993) Outcome with respect to epileptic seizures. Surgical treatment of the epilepsies(Raven Press, New York) pp. 609–21.
Ferrier CH, Alarcon G, Engelsman J, Binnie CD, Koutroumanidis M, Polkey CE, et al. (2001) Relevance of residual histologic and electrocorticographic abnormalities for surgical outcome in frontal lobe epilepsy. Epilepsia 42:363–71.[CrossRef][ISI][Medline]
Horsley VA. (1886) Brain surgery. Br Med J 2:670–5.
Horsley VA. (1890) Remarks on the surgery of the central nervous system. Br Med J 2:1286–92.
Huppertz HJ, Grimm C, Fauser S, Kassubek J, Mader I, Hochmuth A, et al. (2005) Enhanced visualization of blurred gray-white matter junctions in focal cortical dysplasia by voxel-based 3D MRI analysis. Epilepsy Res 67:35–50.[CrossRef][ISI][Medline]
Jaillard A, Martin CD, Garambois K, Lebas JF, Hommel M. (2005) Vicarious function within the human primary motor cortex? A longitudinal fMRI stroke study. Brain 128:1122–38.
Jones-Gotman M, Harnadek MC, Kubu CS. (2000) Neuropsychological assessment for temporal lobe epilepsy surgery. Can J Neurol Sci 27:Suppl 1, S39–43.
Keen WW. (1888) The successful cases of cerebral surgery. Am J Med Sci 96:452–65.
Kutsy RL. (1999) Focal extratemporal epilepsy: clinical features, EEG patterns, and surgical approach. J Neurol Sci 166:1–15.[CrossRef][ISI][Medline]
Lehman R, Andermann F, Olivier A, Tandon PN, Quesney LF, Rasmussen TB. (1994) Seizures with onset in the sensorimotor face area: clinical patterns and results of surgical treatment in 20 patients. Epilepsia 35:1117–24.[CrossRef][ISI][Medline]
Lloyd JH and Deaver JB. (1888) A case of focal epilepsy successfully treated by trephining and excision of the motor centres. Am J Med Sci 96:477–87.
Manford M, Hart YM, Sander JW, Shorvon SD. (1992) National General Practice Study of Epilepsy (NGPSE): partial seizure patterns in a general population. Neurology 42:1911–7.
McKhann GM, Bourgeois BF, Goodman RR. (2002) Epilepsy surgery: indications, approaches, and results. Semin Neurol 22:269–78.[CrossRef][ISI][Medline]
McLachlan RS, Chovaz CJ, Blume WT, Girving JP. (1992) Temporal lobectomy for intractable epilepsy in patients over age 45 years. Neurology 42:662–5.
McLachlan RS and Luba N. (2002) Cortical location of benign paroxysmal rhythms in the electrocorticogram. Can J Neurol Sci 29:154–8.[ISI][Medline]
Merzenich MM and Sameshima K. (1993) Cortical plasticity and memory. Curr Opin Neurobiol 3:187–96.[CrossRef][Medline]
Nancrede CB. (1888) Two successful cases of brain surgery. Med News 53:584–8.
Otsubo H, Chitoku S, Ochi A, Jay V, Rutka JT, Smith ML, et al. (2001) Malignant rolandic-sylvian epilepsy in children: diagnosis, treatment, and outcomes. Neurology 57:590–6.
Penfield W and Rasmussen T. (1947) The cerebral cortex of man; a clinical study of localization of function(McMillan, New York).
Pilcher C, Meacham WR, Holbrook TJ. (1947) Partial excision of the motor cortex in treatment of Jacksonian convulsions. Results of forty cases. Arch Surg 54:633–43.
Putnam TJ. (1940) Treatment of unilateral paralysis agitans by section of the lateral pyramidal tract. Arch Neurol Psychiatr 44:950–76.
Rauschecker JP. (1997) Mechanisms of compensatory plasticity in the cerebral cortex. Adv Neurol 73:137–46.[ISI][Medline]
Sachs E. (1935) The subpial resection of the cortex in the treatment of Jacksonian epilepsy (Horsley operation) with observations in areas 4 and 6. Brain 58:492–503.
Sadler RM and Goodwin J. (1989) Multiple electrodes for detecting spikes in partial complex seizures. Can J Neurol Sci 16:326–9.[ISI][Medline]
Sahjpaul RL, Mahon J, Wiebe S. (2003) Dexamethasone for morbidity after subdural electrode insertion—a randomized controlled trial. Can J Neurol Sci 30:340–8.[ISI][Medline]
Sandok EK and Cascino GD. (1998) Surgical treatment for perirolandic lesional epilepsy. Epilepsia 39:Suppl 4, S42–8.
Sanes JN, Donoghue JP, Thangaraj V, Edelman RR, Warach S. (1995) Shared neural substrates controlling hand movements in human motor cortex. Science 268:1775–7.
Schramm J, Aliashkevich AF, Grunwald T. (2002) Multiple subpial transections: outcome and complications in 20 patients who did not undergo resection. J Neurosurg 97:39–47.[ISI][Medline]
Semah F, Picot MC, Adam C, Broglin D, Arzimanoglou A, Bazin B, et al. (1998) Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology 51:1256–62.
Spencer DD and Spencer SS. (1985) Surgery for epilepsy. Neurol Clin 3:313–30.[ISI][Medline]
Spencer SS, Berg AT, Vickrey BG, Sperling MR, Bazil CW, Shinnar S, et al. (2003) Initial outcomes in the multicenter study of epilepsy surgery. Neurology 61:1680–5.
Spencer SS, Schramm J, Wyler A, O'Connor M, Orbach D, Krauss G, et al. (2002) Multiple subpial transection for intractable partial epilepsy: an international meta-analysis. Epilepsia 43:141–5.[CrossRef][ISI][Medline]
Wennberg R, Quesney F, Olivier A, Rasmussen T. (1998) Electrocorticography and outcome in frontal lobe epilepsy. Electroencephalogr Clin Neurophysiol 106:357–68.[CrossRef][ISI][Medline]
Wennberg R, Quesney LF, Lozano A, Olivier A, Rasmussen T. (1999) Role of electrocorticography at surgery for lesion-related frontal lobe epilepsy. Can J Neurol Sci 26:33–9.[ISI][Medline]
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