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Surgical treatment of epilepsy in adults

Surgical treatment of epilepsy in adults
Author:
Gregory D Cascino, MD
Section Editor:
Paul Garcia, MD
Deputy Editor:
John F Dashe, MD, PhD
Literature review current through: Nov 2022. | This topic last updated: Nov 11, 2022.

INTRODUCTION — Epilepsy is one of the most common chronic neurologic disorders, and approximately 20 to 30 percent of patients with epilepsy will have medically and socially disabling seizure disorders. Such patients are at increased risk for serious morbidity and mortality, including cognitive disorders, depression, physical trauma, and sudden death in epilepsy. The goals of treatment for individuals with drug-resistant epilepsy are to render the patient seizure free, avoid treatment-related adverse effects, and allow the individual to become a participating and productive member of society.

Most individuals who will respond favorably to antiseizure medications are successfully managed within the first two years of treatment. Patients who do not respond favorably to two antiseizure medications used appropriately are likely to have drug-resistant epilepsy and should be investigated for surgery and other alternative forms of treatment.

Surgical therapy is an important and underutilized treatment in patients with drug-resistant focal epilepsy. Surgical procedures for epilepsy range from focal resection of the epileptogenic cortex (antero-mesial temporal lobe and other focal cortical resections) to interventions that remove or isolate the cortex of a grossly diseased hemisphere (functional hemispherectomy, anterior corpus callosotomy, multiple subpial transections). The latter procedures are most often performed in children and are not discussed further here. In general, only complete resection of the epileptogenic brain region offers the chance of long-term seizure freedom.

This topic will discuss the surgical treatment of drug-resistant focal epilepsy in adults utilizing focal cortical resection. Epilepsy surgery in children and other aspects of epilepsy management and treatment in adults are discussed separately. (See "Overview of the management of epilepsy in adults" and "Evaluation and management of drug-resistant epilepsy" and "Seizures and epilepsy in children: Refractory seizures", section on 'Epilepsy surgery'.)

SURGICAL CANDIDATES — Focal cortical resection is a consideration in patients with drug-resistant focal epilepsy if the seizures emanate from a region that can be removed with minimal risk of disabling neurologic or cognitive dysfunction. Early referral for epilepsy surgery – as soon as drug resistance is ascertained – is supported by 2022 expert consensus recommendations from the ILAE [1].

The localization of seizure onset, underlying surgical pathology, and seizure type(s) are important determinants of surgical candidacy and outcomes. The most favorable candidates are those with magnetic resonance imaging (MRI)-identified lesions that represent both the pathologic process underlying the epileptogenic brain tissue and the location of seizure onset. Such MRI findings, together with concordant electroencephalography (EEG) data, are pivotal in selecting operative candidates and determining the strategy for the surgical procedure. (See 'Surgical evaluation' below.)

In adults, there are three major types of seizure disorders that may be remedied with focal cortical resective surgery:

Patients with mesial temporal lobe epilepsy with localization of the epileptogenic zone in the amygdala and hippocampus are the most common candidates for effective surgical therapy. As discussed below, substantial observational data and a single completed randomized trial support the superiority of surgical therapy compared with continued antiseizure medication for patients with drug-resistant temporal lobe epilepsy. (See 'Mesial temporal lobe epilepsy' below.)

Patients with lesional epilepsy due to focal structural pathology, such as a low-grade glial tumor, cavernous malformation, or malformation of cortical development (MCD) with medically refractory seizures, may also be good surgical candidates. There are important differences in the likelihood of surgical success depending on the specific pathologic finding, however. For example, operative outcomes are distinctly less favorable in individuals with focal cortical dysplasia and other MCDs. (See 'Lesional epilepsy' below.)

Patients with drug-resistant focal epilepsy and a normal brain MRI are more challenging, but some of these patients are nonetheless good surgical candidates. Localization of the epileptic brain tissue in these patients often requires long-term intracranial EEG monitoring in addition to functional and metabolic brain imaging. (See 'Neocortical epilepsy with normal brain MRI' below.)

Patients who are usually not surgical candidates for focal cortical resection include individuals with bilateral or multifocal seizure onset, those with significant medical comorbidities that preclude the surgery, and patients with generalized-onset epilepsy [2,3]. Patients in whom the site of seizure onset and initial seizure propagation is intimately associated with functional cortex may also not be appropriate candidates for resective surgery.

SURGICAL EVALUATION — The goals of the surgical evaluation are to identify the epileptogenic zone, determine the extent to which it can be resected, and avoid operative morbidity, especially injury to eloquent cortex. Standard components of the surgical evaluation are discussed below.

In general, decisions about the potential effectiveness of focal cortical resection rely most heavily on the concordance of clinical seizure semiology, ictal and interictal scalp electroencephalography (EEG) findings, and structural magnetic resonance imaging (MRI). Positron emission tomography (PET), single-photon emission computed tomography (SPECT), and magnetoencephalography (MEG) typically play a confirmative role in cases of questionable structural lesions or in patients with multiple lesions or a normal MRI. Neuropsychologic testing and functional localization techniques are used to help localize the epileptogenic zone and determine the safety of the proposed procedure, for example by estimating cognitive reserve in the contralateral hemisphere.

Clinical evaluation — A comprehensive evaluation is essential in patients with drug-resistant epilepsy. Patients should be referred to neurologists who have subspecialty expertise in epilepsy and are based at a comprehensive epilepsy center that has the necessary multidisciplinary resources and personnel. (See "Evaluation and management of drug-resistant epilepsy".)

The history and neurologic examination are critical to confirm the diagnosis and characterize seizure semiology and clinical localization. Emphasis should be placed on the presence of multiple or differing seizure semiologies, which may raise concern for multiple epileptogenic zones.

Comorbid psychiatric disease (eg, anxiety or depression) is common in patients with drug-resistant epilepsy and has been associated with worse postsurgical seizure outcomes. While the presence of a psychiatric disorder does not preclude surgery, presurgical psychiatric evaluation and psychosocial assessment are advised in order to mitigate potential complications postoperatively [4]. (See 'Psychologic sequelae' below.)

At most epilepsy centers, each patient's diagnostic evaluation is reviewed at a surgical epilepsy consensus conference before epilepsy surgery to discuss the surgical treatment plan, and to consider potential alternative treatment options.

Neuropsychologic testing — Neuropsychologic studies are performed to evaluate the presence of verbal or nonverbal learning and memory deficits. The rationale for these studies as part of a presurgical epilepsy evaluation is fourfold [5]:

To determine preoperative cognitive performance as a baseline that can be compared with a postoperative examination

To identify and quantify ictal and postictal deficits as an aid to seizure characterization, lateralization, and localization

To provide evidence-based predictions of cognitive risk associated with the proposed surgery

To provide comprehensive preoperative counseling, including neuropsychologic education of the patient and family

Neuropsychologic studies may be of highest diagnostic yield in individuals with temporal lobe epilepsy.

Intellectual disability has traditionally been a relative contraindication to temporal lobectomy because it implies bilateral and potentially diffuse rather than focal brain pathology. In some studies, low intelligence quotient (IQ) has been associated with lower postoperative seizure remission rates and increased risk of postoperative cognitive sequelae. However, intellectual disability may not be an independent predictor of surgical outcome, and some patients may still benefit from epilepsy surgery.

Routine and video-EEG — Routine EEG recording with standard activating procedure and long-term scalp-recorded video-EEG monitoring are essential to confirm and localize the site of seizure onset in individuals with focal epilepsy. Additional scalp-recorded EEG electrodes, including anterior or inferior temporal electrodes, are often placed to increase the diagnostic yield of the neurophysiologic studies. (See "Electroencephalography (EEG) in the diagnosis of seizures and epilepsy", section on 'Special electrode placement'.)

Interictal and ictal EEG patterns are utilized for surgical localization. Using computer-assisted video-EEG in an inpatient epilepsy monitoring unit, habitual seizures are recorded to determine the correlation between ictal semiology and EEG findings. The peri-ictal neurologic examination provides an additional functional assessment that can assist in lateralizing and localizing the epileptogenic zone.

High-resolution brain MRI — All patients undergoing surgical evaluation should have a high-resolution brain MRI with sequences optimized for visualization of the hippocampus and gray-white matter junction. The MRI should include coronal or oblique-coronal T1- and T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences. Postcontrast T1-weighted images are not useful in patients with mesial temporal sclerosis but should be included in the evaluation of suspected tumors or vascular anomalies. High field strength (3-Tesla) MRI is preferred for maximal sensitivity. (See "Neuroimaging in the evaluation of seizures and epilepsy", section on 'Epilepsy protocol for MRI'.)

In patients with temporal lobe epilepsy associated with hippocampal sclerosis (also called mesial temporal sclerosis), the most common imaging alteration is hippocampal atrophy with a signal intensity change that reflects gliosis (image 1 and image 2) [6]. FLAIR sequences increase the sensitivity of MRI to indicate a signal change [7]. Loss of internal structure of the hippocampus may also be seen. An MRI finding of mesial temporal lobe sclerosis is predictive of better seizure and neurocognitive outcomes following surgery [8,9].

High-resolution structural MRI also has a high diagnostic yield in patients with tumors or vascular malformations. The latter are often best visualized on gradient-echo sequences, which are sensitive for blood products. Typical imaging features of tumors and vascular malformations are discussed elsewhere. (See "Overview of the clinical features and diagnosis of brain tumors in adults", section on 'Neuroimaging features' and "Brain arteriovenous malformations", section on 'Diagnosis' and "Vascular malformations of the central nervous system", section on 'Neuroimaging'.)

In patients with focal cortical dysplasia, MRI findings may be subtle and include mild cortical thickening, a prominent deep sulcus, a cortical signal intensity change, blurring of the gray-white junction, or aberrant cortical architecture (image 3). Thin-section 3D volumetric MRI and reformatted 1.5 mm 3D spoiled gradient echo (SPGR) sequences are particularly useful, since it is difficult to resolve volume-averaged normal cortical infolding from true abnormalities if the spatial resolution of the images is coarser than 1.5 mm. Higher field strength (eg, 3-Tesla) also aids in detecting cortical dysplasia.

Advanced MRI techniques — Quantitative MRI techniques have limited diagnostic value over and above visual inspection but may provide useful prognostic information. MRI-based volumetric studies of the hippocampal formation can objectively determine the degree of hippocampal volume loss in patients with mesial temporal sclerosis using a standardized protocol; results are compared with age-matched normal controls to assign abnormal values. A unilateral reduction in hippocampal volume is a reliable indicator of the epileptogenic temporal lobe in patients with medically refractory focal epilepsy [10]. Patients with bilateral hippocampal atrophy or hippocampal atrophy contralateral to the site of seizure onset are more likely to experience adverse cognitive outcomes following temporal lobe surgery [8].

FDG-PET — Measurement of interictal cerebral glucose metabolism using [18F]-2-deoxyglucose PET (FDG-PET) is a sensitive functional neuroimaging technique in patients with temporal lobe epilepsy. Unilateral temporal lobe hypometabolism on FDG-PET (image 4) correlates strongly with the temporal lobe of seizure origin and is predictive of seizure freedom following epilepsy surgery, independent of structural MRI findings [9,11]. FDG-PET can also be clinically useful in patients with extratemporal regions of seizure onset. This includes individuals with focal cortical dysplasia who may have an unremarkable MRI study. (See "Neuroimaging in the evaluation of seizures and epilepsy", section on 'PET'.)

FDG-PET and MRI coregistration increases the diagnostic yield of preoperative imaging and may improve surgical outcome in patients with negative MRI studies and focal cortical dysplasia. In such patients, FDG-PET/MRI demonstrates a hypometabolic zone indicative of the site of focal cortical dysplasia and the region of seizure onset. This modality is highly sensitive in detecting focal cortical dysplasia type II (Taylor-type) in patients with a normal brain MRI, and it may improve outcomes. (See 'Efficacy' below.)

Ictal SPECT — Ictal SPECT studies are used to map increased cerebral blood flow during seizures to assist in localizing the epileptogenic zone (image 5). While not technically feasible at all institutions due to logistic constraints of ictal tracer injection, SPECT is particularly useful in patients with a conflicting noninvasive epilepsy evaluation with regard to localization of the epileptic brain tissue. SPECT findings can also influence the diagnostic strategy for placement of intracranial EEG electrodes. (See 'Seizure localization' below.)

SPECT studies involve cerebral blood flow imaging using radiopharmaceuticals, most often either technetium-99m-hexamethylpropylene amine oxime (99mTc-HMPAO) or 99mTc-bicisate, that have a rapid first-pass brain extraction with maximum uptake being achieved within 30 to 60 seconds of an intravenous injection. (See "Neuroimaging in the evaluation of seizures and epilepsy", section on 'SPECT'.)

Subtraction ictal SPECT coregistered to MRI (SISCOM) is a modification of the ictal SPECT technique that superimposes ictal and interictal SPECT images and brain MRI (image 5). SISCOM has been used in patients with normal MRI studies, those with multifocal EEG or MRI abnormalities, and individuals with intractable epilepsy who are being considered for reoperation. In a series of 51 patients undergoing surgical evaluation, SISCOM had a significantly higher rate of localization (88 versus 39 percent), better interobserver agreement, and better predictive value for surgical outcome compared with visual inspection of interictal and ictal images [12].

Some of the limitations of visual inspection may be overcome by statistic parametric mapping methods, which permit better localization of the focal hyperperfusion abnormality concordant with the epileptogenic zone in patients with both temporal lobe and extratemporal epilepsy [13].

Speech and language localization — In selected patients, eloquent cortex involved with speech and language function must be well defined before temporal lobe and frontal lobe resections to minimize operative morbidity. The standard method for determining critical areas of functional cortex is intraoperative electrical cortical stimulation. If necessary, this can be carried out intraoperatively in awake patients, or extra-operatively using implanted subdural electrodes for long-term intracranial EEG monitoring.

Preoperatively, functional MRI and the intracarotid amobarbital procedure (also called the Wada test) are two methods used to assess language localization and predict postoperative language and memory outcomes. Functional MRI is generally preferred over intracarotid amobarbital given its superior safety profile [14].

Functional MRI is a noninvasive neuroimaging technique that is capable of language localization as well as lateralization of language processes. In many epilepsy centers, this has largely replaced intracarotid amobarbital procedures. Functional MRI can also be used to assess sensory and motor eloquent cortices and as an alternative or adjunct to the Wada test in predicting neurocognitive sequelae after surgery [15-23]. (See "Neuroimaging in the evaluation of seizures and epilepsy", section on 'Functional MRI'.)

Numerous studies have estimated the validity of functional MRI as an alternative to the Wada test and have found an overall discordance rate of approximately 15 percent [14,24,25]. Discordance rates may be slightly higher in patients with extratemporal foci and larger lesions. In one study that measured language outcomes after anterior temporal lobectomy in patients with discordant functional MRI and Wada testing preoperatively, functional MRI provided a more accurate prediction of language outcome in 7 of 10 cases [26].

However, some patients cannot complete functional MRI, or have inconclusive results, and still require preoperative Wada testing [23]. Most centers use Wada tests only for patients with temporal lobe epilepsy at significant risk for cognitive decline (eg, left temporal lobe epilepsy with normal MRI, bilateral hippocampal atrophy, or bitemporal seizures).

Intracarotid amobarbital administration is an invasive procedure that has been used for many years in surgical candidates to determine the language-dominant hemisphere as well as assess the risk of postoperative memory decline after temporal lobectomy [27-29]. Amobarbital or another anesthetic is injected into the internal carotid artery, temporarily suppressing function on that side while language and memory tests are performed. Neuropsychologic testing after intracarotid injection of amobarbital allows for assessment of language and memory function in each hemisphere independently. While complications are reported in up to 11 percent of patients, serious adverse events (stroke, carotid dissection, localized bleeding, and infection) occur in less than 1 percent [30,31].

Other anesthetic agents such as pentobarbital, etomidate, methohexital, and propofol have been investigated as alternatives to amobarbital, which has not been consistently available. In general, these agents appear to be well tolerated and produce results similar to amobarbital for presurgical testing [32-35]. Etomidate has been associated with adrenal insufficiency when used in critically ill patients [36]. In one study, propofol was associated with a higher risk of significant side effects, especially in older patients [37].

Lack of test standardization and selection bias limit our understanding of the reliability of the Wada test as a predictive tool.

Invasive EEG monitoring — In selected cases, invasive intracranial EEG monitoring is required for localization of the epileptogenic zone before a resection can be performed. Invasive monitoring is primarily used when noninvasive techniques fail to localize the area of seizure onset or if other tests have discordant results. Although use of intracranial electrodes in mesial temporal lobe epilepsy has diminished over time, invasive monitoring continues to be used commonly in patients with neocortical focal epilepsy, particularly those with a normal MRI or bilateral seizure foci. (See 'Seizure localization' below.)

SURGICALLY REMEDIABLE EPILEPTIC SYNDROMES

Mesial temporal lobe epilepsy — Mesial temporal lobe epilepsy is the most frequently encountered surgically remediable epileptic syndrome in adults. Patients typically experience focal dyscognitive seizures, also known as complex partial seizures, with or without aura or tonic-clonic seizures. The most common pathologic substrate associated with temporal lobe epilepsy is hippocampal sclerosis (mesial temporal sclerosis), which is characterized by selected focal neuronal loss and gliosis in the hippocampus, predominantly affecting CA1, CA3, and the dentate granule cell layer. Hippocampal sclerosis is the most commonly encountered histopathologic diagnosis at the time of epilepsy surgery in adults and accounts for approximately 45 percent of all resections [38]. (See "Focal epilepsy: Causes and clinical features", section on 'Seizure semiology'.)

Patients with mesial temporal lobe epilepsy due to tumors or other structural lesions in the temporal lobe are discussed below in the context of lesional epilepsy surgery (see 'Lesional epilepsy' below), and those with extrahippocampal temporal lobe epilepsy and a normal brain magnetic resonance imaging (MRI) are discussed in the context of neocortical epilepsy with normal brain MRI. (See 'Neocortical epilepsy with normal brain MRI' below.)

Surgical techniques — The most common surgical procedure for mesial temporal epilepsy is resection of the anterior temporal pole, hippocampus, and part of the amygdala. The posterior extent of the anterior temporal resection is measured to minimize risk to the visual radiations and language cortex (4.0 to 4.5 cm back from the temporal pole on the dominant side, and 5.0 to 5.5 cm on the nondominant side). Cortical resection may also be tailored based on language mapping and intraoperative electrocorticography, as language areas in the temporal cortex are variable.

Selective amygdalohippocampectomy has been explored as an alternative to anterior temporal lobectomy that spares the temporal lobe neocortex. Seizure control rates might be similar with a selective approach, but potential differences in neurocognitive outcomes have not been well studied [39]. There are conflicting results regarding the effectiveness of the specific operative strategies to achieve seizure freedom in individuals with mesial temporal lobe epilepsy. A 2018 meta-analysis noted that the only direct evidence comparing surgical efficacy of selective amygdalohippocampectomy with anterior temporal lobectomy comes from observational studies and is therefore is of low quality [39]. Importantly, most individuals experience a significant reduction in seizure frequency with either operative approach.

Other minimally invasive techniques are being increasingly utilized in the management of drug-resistant focal epilepsy [40-44]. In a systematic review of radiosurgery for drug-resistant focal epilepsy, which included 16 studies and 170 patients, the proportion who were seizure-free or experienced rare seizures after treatment (ie, Engel Class I to II) was 58 percent [40]. However, subsequent surgery related to complications or recurrent seizures was required in 20 percent. The efficacy and safety of mesial temporal lobe epilepsy have been investigated. A systematic review and meta-analysis of surgical strategies for drug-resistant mesial temporal lobe epilepsy found that selective amygdalohippocampectomy and anterior temporal lobectomy were associated with better seizure outcomes compared with radiofrequency ablation (RFA) or laser interstitial thermal therapy (LITT) [44]. The proportion of patients who were seizure-free or near seizure-free (ie, Engel Class I) was 66 percent with selective amygdalohippocampectomy and 69 percent with anterior temporal lobectomy, compared with 57 percent with LITT and 44 percent with RFA. However, individuals undergoing the minimally invasive techniques may have fewer major complications, especially with naming or verbal memory deficits [44].

Efficacy — Patients with temporal lobe epilepsy and localization of the epileptogenic zone to the amygdala and hippocampus are extremely good candidates for resective surgery, which is associated with superior outcomes compared with continued medical management.

This was demonstrated by a randomized, controlled trial involving 80 patients with temporal lobe epilepsy whose seizures were poorly controlled with medical therapy [45]. Approximately three-quarters of the patients had magnetic resonance imaging (MRI) findings consistent with hippocampal sclerosis, 10 to 15 percent had structural lesions such as tumors or vascular malformations, and approximately 15 percent had normal MRI scans. Patients were randomly assigned to surgery or continued antiseizure medication treatment. At one year, the cumulative proportion of patients who were free of seizures that impaired awareness was significantly greater in the surgery group than the medical group (58 versus 8 percent). Quality-of-life ratings were also higher in the postsurgical group.

A second randomized, controlled study was initiated to evaluate the efficacy of early surgery versus continued medical management in patients who had failed two antiseizure medication trials, but the trial was stopped early because of slow enrollment [46,47]. After two years of follow-up, seizure remission occurred in 11 of 15 patients assigned to surgical treatment and none of 23 patients assigned to medical management. Quality-of-life measures were not different between the assigned treatment groups. However, an on-treatment analysis that included seven patients in the medical group who underwent surgery during follow-up found a significant benefit for surgery on quality of life.

Based on these and other observational studies, the most important preoperative predictors of seizure freedom after anterior temporal lobe resection for mesial temporal lobe epilepsy include [9,48-56]:

Presence of a focal brain lesion on MRI

Presence of unilateral mesial temporal sclerosis in the temporal lobe of seizure origin

Presence of a localized temporal lobe positron emission tomography (PET) abnormality, even if brain MRI is normal

Electroencephalography (EEG) data showing concordant location of ictal onset and interictal epileptiform discharges

Shorter preoperative seizure duration

Postoperatively, the strongest predictor of long-term seizure control is freedom from seizures in the first year after surgery, particularly generalized seizures or focal seizures with altered or impaired awareness [48,49,57-60]. The presence of interictal epileptiform discharges on an EEG performed within the first few years after surgery has been associated with an approximately threefold higher risk of recurrent seizures [61,62].

Taken together, patients with MRI scans showing hippocampal sclerosis who undergo anterior temporal lobectomy for intractable epilepsy have the most favorable seizure outcomes, with approximately 65 to 75 percent of patients remaining continuously seizure free or having only auras up to 10 years after surgery [63-65]. An additional 10 to 15 percent of patients will have seizures postoperatively but eventually achieve terminal remission. In highly selected series limited to patients most likely to do well with surgery (ie, positive MRI findings, pathologically proven hippocampal sclerosis, concordant EEG findings, no dual pathology or discordant preoperative data), long-term rates of seizure freedom as high as 90 percent have been reported [66].

The surgical outcome of patients with a localized temporal lobe PET abnormality and a normal MRI may be equivalent to individuals with MRI-identified unilateral hippocampal sclerosis. Seventy-six percent of patients in one series with temporal lobe PET hypometabolism and a normal MRI were seizure free following surgery [11].

For patients with mesial temporal lobe epilepsy and a normal brain MRI, rates of seizure freedom after anterior temporal lobectomy range from 50 to 60 percent. Most (70 to 87 percent) achieve at least a 75 percent reduction in seizure frequency [67-72]. In a series of 87 patients with a normal MRI undergoing anterior temporal lobectomy, 55 percent had an excellent operative outcome, defined as seizure free or auras only [73].

Neocortical epilepsy with normal brain MRI — The surgical management of focal seizures of neocortical origin (ie, extrahippocampal) can be challenging because of difficulty defining the boundaries of the epileptogenic zone that must be resected for seizure freedom. There are also increased concerns regarding clinically functional cortex.

The clinical manifestations of neocortical epilepsy depend on the area of cortex involved. Seizures arising from functional cortex can be localized based on neurologic symptoms that occur at seizure onset or during the postictal state. Compared with mesial temporal lobe seizures, lateral temporal neocortical seizures are more likely to manifest as experiential auras and less likely to manifest as epigastric auras and contralateral dystonia. Frontal lobe seizures tend to be shorter and more frequent than temporal lobe seizures, with manifestations varying from motionless staring to violent automatisms. Frontal lobe seizures are often confined to sleep. Parietal and occipital seizures typically have complex sensory symptoms such as visual hallucinations of objects or scenes. (See "Focal epilepsy: Causes and clinical features", section on 'Neocortical epilepsy'.)

Despite these general principles, extrahippocampal focal seizures often have varied clinical semiology and can be difficult to localize with scalp-recorded ictal EEG studies. In addition, ictal behaviors may relate to seizure propagation and provide few clues regarding the site of actual seizure onset. Another challenge to clinical localization in neocortical epilepsy is that seizures may be tonic-clonic without a clinically recognized focal seizure, or the focal seizure may be very brief or subtle, such as a brief stare with arrest of activity or hypermotor activity.

Seizure localization — In order to adequately localize seizures and tailor resections to spare eloquent cortex, the surgical evaluation in patients with neocortical epilepsy often includes functional or metabolic imaging and long-term intracranial EEG monitoring.

Before invasive EEG recordings, patients usually undergo functional neuroimaging to include PET and/or ictal single-photon emission computed tomography (SPECT) in an attempt to better localize the epileptogenic zone and direct intracranial electrode placement. The diagnostic yield of PET and SPECT in patients with neocortical epilepsy depends on multiple factors, including the underlying pathology, localization of the epileptogenic zone, and the specific neuroimaging technique. PET or SPECT studies may permit an anterior temporal lobe resection in patients with unilateral temporal lobe scalp-recorded seizures and negative brain MRI scans. Individuals with extratemporal seizures and normal brain MRIs almost invariably require intracranial EEG recordings or functional mapping for surgical localization, or both.

The strategy for intracranial EEG recordings often includes a combination of subdural strips or grids of electrodes and depth electrodes. Depth electrodes are implanted stereotactically by a neurosurgical team using brain imaging for localization. In two retrospective series of more than 400 patients, the major complication rate of invasive monitoring was 7 to 9 percent; the majority of these complications were either intracranial hemorrhage or infection [74,75]. Use of subdural electrodes may pose higher risk than use of depth electrodes [75-78].

Stereoelectroencephalography (SEEG) is another invasive technique that is being increasingly used to evaluate patients with nonlesional drug-resistant focal epilepsy being considered for surgical treatment [79-84]. SEEG may be preferred in individuals with epileptogenic zones that are difficult to evaluate with subdural grid recordings, such as the insula, the depth of sulci, and mesial regions of cerebral cortex. In selected patients being considered for focal cortical resection, the effectiveness and safety of SEEG compares favorably with other methodologies for intracranial EEG recording [78-80,85], with a pooled complication rate of 1.3 percent across multiple studies [86].

In some cases, patients who undergo a full surgical evaluation for nonlesional epilepsy, including intracranial EEG monitoring, are deemed poor candidates for surgery [87]. Common reasons include difficulty localizing seizure onset, multifocal seizures, overlap with functional cerebral cortex, or morbidity associated with chronic intracranial EEG recordings.

Efficacy — Even with an appropriate comprehensive presurgical evaluation, seizure outcomes tend to be less favorable in patients with neocortical epilepsy and normal MRI scans compared with those with mesial temporal lobe epilepsy due to hippocampal sclerosis or a structural lesion. Patients with extratemporal seizures do even less well.

Surgical procedures used for patients with neocortical nonlesional epilepsy include topectomy (ie, removal of cortex while sparing underlying white matter) and lobar and multilobar cortical resections. Rates of seizure freedom after such procedures range from 30 to 55 percent based on small, mostly single-center observational studies [87-91]. Predictors of better outcome include the presence of a localizing PET or SPECT study, high concordance of the noninvasive presurgical evaluation, the presence of an aura, and complete resection of areas of ictal onset [91].

Lesional epilepsy — Patients with intractable focal epilepsy due to focal brain lesions require a comprehensive epilepsy evaluation to establish the relationship between the pathologic findings and the epileptogenic zone. Common pathologic entities responsible for medically refractory lesional epilepsy include low-grade tumors, cavernous hemangiomas, and focal cortical dysplasia.

Primary brain tumors — The incidence of seizures among patients with primary brain tumors is related to tumor type and grade and cortical localization. Low-grade, slowly growing tumors are most commonly associated with a chronic seizure disorder. Gangliogliomas and dysembryoplastic neuroepithelial tumors (DNET) together account for approximately three-quarters of all tumors found in adults undergoing epilepsy surgery [38]. Other examples include pilocytic astrocytoma, gangliocytoma, pleomorphic xanthoastrocytoma, and oligodendroglioma.

Imaging features common to all these tumors include typically small size, location at or near a cortical surface, sharply defined borders, little or no surrounding edema, and, except for pilocytic astrocytoma, little or no contrast enhancement. In a series of 133 patients from one institution who underwent operations for extratemporal epilepsy, tumors were identified in 28 percent of cases. These included, in order of decreasing frequency, astrocytoma, ganglioglioma, DNET, glioneuronal hamartoma, oligodendroglioma, and oligoastrocytoma [92]. Roughly the same proportion of patients have tumors in series of patients undergoing surgery for temporal lobe epilepsy [45,93,94].

Seizure outcome in patients undergoing surgical treatment for intractable focal epilepsy due to a primary brain neoplasm is typically very good. Most individuals become seizure free or nearly seizure free [95,96]. Although complete tumor resection is the goal, tumors associated with functional cortex (eg, perirolandic lesions) may require a subtotal excision to avoid a postoperative neurologic deficit.

Some studies have suggested that DNETs are associated with higher seizure relapse rates compared with other epileptogenic tumors [63,97]. A review of 29 relevant studies found seizure-freedom rates ranging from 58 to 100 percent (median 86 percent) with a median follow-up of four years [98]. The median age at the time of surgery was 18 years. Among 12 studies that reported rates of antiseizure medication discontinuation, approximately half of seizure-free patients were off all antiseizure medications. The most commonly identified predictors of seizure freedom were younger age at the time of surgery, shorter duration of epilepsy, and complete resection. In a separate study that included 79 patients with DNET with long-term follow-up, the rate of long-term seizure freedom was 42 percent at 10 years after surgery [63].

Vascular malformations — Cavernous malformations and arteriovenous malformations are the most common vascular lesions found in patients with focal epilepsy. Venous angiomas and telangiectasias are often incidental findings in patients with seizure disorders and are not typically causative lesions. Seizures are a common presenting feature of cavernous malformation.

Resection typically leads to complete seizure control or significant improvement. In a case series of 168 patients with symptomatic epilepsy attributed to cavernous malformations, more than two-thirds of patients were seizure free at three years after surgery [99]. Predictors for good outcome included mesiotemporal location, size <1.5 cm, and the absence of secondarily generalized seizures. In another study, 87 percent of 56 patients undergoing resection of a supratentorial cavernous malformation were seizure free following surgical treatment [100].

Malformations of cortical development — Malformations of cortical development (MCDs) are an important etiology for drug-resistant focal epilepsy. Among various diffuse and focal MCDs, focal cortical dysplasia (FCD) is the most common surgically remediable lesions in adults. Before widespread availability of MRI, many culprit lesions were only diagnosed at the time of postmortem examination. Even with high-resolution structural MRI, some patients with so-called MRI-negative focal epilepsy have evidence of FCD at the time of surgery.

Not uncommonly, FCD occurs in extratemporal locations and is associated with focal seizures that are difficult to localize with scalp-recorded EEG. [18F]-2-deoxyglucose PET (FDG-PET)/MRI may be very useful in the surgical evaluation of such patients. (See 'FDG-PET' above.)

The International League Against Epilepsy has developed a multi-tier histologic classification of FCD [101,102].

FCD type I – This category is defined by architectural disorganization of the neocortex. Subtypes are characterized by abundant neuronal microcolumns (FCDIa), abnormal layering (FCDIb), and vertical and horizontal abnormalities (FCDIc). MRI studies in these patients may be normal or show very subtle blurring of the grey-white matter junction or thinning of the cerebral cortex.

FCD type II – This category delineates dysmorphic neurons (FCDIIa) and dysmorphic neurons with balloon cells (FCDIIb). MRI studies may be normal or show blurring of the grey-white matter junction, a fluid-attenuated inversion recovery (FLAIR) signal intensity alteration, a transmantle sign, or increased cortical thickness. Abnormal cortical gyration or sulcation pattern may also be evident.

FCD type III – This category distinguishes FCD characterized by cortical dyslamination associated with hippocampal sclerosis (FCDIIIa), tumor (FCDIIIb), vascular malformation (FCDIIIc), or a lesion acquired during early life, such as a stroke (FCDIIId).

White matter lesions – This category delineates mild malformations of cortical development (mMCD) that are not associated with any other lesion, such as hippocampal sclerosis, brain tumor, or vascular malformation, and primarily involve the white matter:

mMCD with excessive heterotopic neurons

mMCD with oligodendroglial hyperplasia in epilepsy (MOGHE)

No definite FCD on histopathology – This category encompasses lesions with ambiguous abnormalities of cortical organization and histopathologic findings not compatible with FCD types I, II, or III.

Importantly, the diagnostic yield of MRI is dependent on the specific pathologic alterations [101]. A normal MRI study in a patient with a drug-resistant focal epilepsy does not exclude the diagnosis of focal cortical dysplasia. Not uncommonly, MCDs associated with intractable epilepsy are extratemporal and multilobar lesions.

Efficacy — Studies based on postsurgical histopathologic diagnosis of focal cortical dysplasia (which included MRI-positive and MRI-negative lesions) suggested that epilepsy surgery was less effective for patients with focal cortical dysplasia compared with surgery for patients with other lesional pathology (eg, tumors or cavernous malformations) [103]. Challenging issues in these patients include the difficulty identifying areas of focal cortical dysplasia using MRI, the presence of extratemporal neocortical lesions, and multilobar pathology. However, patients are generally selected for epilepsy surgery based upon presurgical evaluation that includes MRI. A systematic review and meta-analysis of patients who had epilepsy surgery for MRI-diagnosed focal cortical dysplasia, which included 35 observational studies and 1353 patients, found that the overall rate of a favorable outcome (ie, seizure free, or seizure free with only auras) at ≥12 months after surgery was 70 percent (95% CI 64-75 percent) [104]. A favorable outcome was associated with complete lesion resection and location in the temporal lobe but was not associated with lesion extent or histologic subtype.

One center reported that 57 percent of 166 patients with focal cortical dysplasia followed for two years or longer after surgery were seizure free [105]. Success rates may be higher in patients with a specific form of focal cortical dysplasia type II in which dysplastic features are maximal at the bottom of the sulcus (referred to as a transmantle sign on MRI) [106-108].

FDG-PET/MRI may improve the surgical outcome in patients with focal cortical dysplasia type II associated with balloon cells (Taylor-type focal cortical dysplasia) [109]. In a study that included 23 patients who underwent SEEG and epilepsy surgery, and who had pathologically verified focal cortical dysplasia type II, MRI was negative in 13 patients and showed subtle alterations in 10 patients. FDG-PET/MRI revealed a hypometabolic zone in 22 of 23 patients. Twenty of the 23 patients (87 percent) became seizure free following surgery.

Temporal encephaloceles — Temporal encephaloceles are a relatively rare cause of drug-resistant focal epilepsy but are increasingly reported in surgical series of temporal lobe epilepsy, which likely represents increased awareness and advances in neuroimaging rather than a true increase in incidence. Detection of encephaloceles is facilitated by thin-slice 3D MRI sequences and skull base computed tomography (CT) (image 6). Their presence may be related to current or prior raised intracranial pressure, based on associated imaging findings and higher prevalence in obese patients [110,111].

Anteroinferior/basal temporal encephaloceles, rather than posterior and lateral defects, are most commonly implicated in temporal lobe epilepsy. It remains unclear whether temporal encephaloceles represent a singular epileptogenic focus that can be removed via a lesionectomy sparing the medial structures or are a part of an extensive epileptogenic network requiring treatment with anterior temporal lobectomy and amygdalohippocampectomy.

The surgical approach to encephaloceles can vary. Extratemporal cases usually undergo lesionectomy exclusively, whereas two-thirds of temporal encephalocele cases undergo anterior temporal lobectomy and amygdalohippocampectomy [112].

SURGICAL COMPLICATIONS — The morbidity and mortality associated with temporal lobe resection for epilepsy treatment are low. In the Nationwide Inpatient Sample hospital discharge database, anterior temporal lobe resections for epilepsy performed between 1988 and 2003 were associated with a 10.8 percent overall morbidity and no mortality [113].

Cognitive sequelae — Epilepsy surgery poses some risk to cognitive function. Approximately one-fourth to one-third of patients develop some degree of memory loss [114,115]. Left temporal lobe resections can result in decrements in verbal memory [114,116-119], while spatial memory and learning may be affected by right-sided surgery [120].

In a six-year follow-up study of 85 patients who had serial examinations over six years, cognition continued to decline for two years following left temporal lobe resection, but it then stabilized over the next four years [121,122]. After right temporal lobe resections, cognitive scores initially improved but returned to preoperative baseline two years after surgery. Another cohort study of patients who had temporal lobe resections reported stable cognitive function for 2 to 10 years after temporal lobe resection [123]. Patients with higher presurgical abilities are at greater risk for memory decline following temporal lobectomy compared with those with lower presurgical scores [114,124-126].

In at least one comparative study, children appeared to recover lost cognitive function more quickly and more completely than adults, presumably reflecting greater neuronal plasticity [122,127]. Older age and lower baseline verbal intelligence quotient (IQ) have also been identified as risk factors in some groups [115].

The possibility of cognitive impairment after surgery needs to be balanced against the potential for control of seizures, as this may be more important for functional outcomes. In one study of 138 patients undergoing epilepsy surgery, health-related quality of life (HRQOL) improved in all patients with seizure remission, regardless of neurocognitive sequelae [128]. However, in individuals without seizure remission, memory decline after surgery was associated with reduced HRQOL, which remained stable in the absence of this complication.

A preliminary, nonrandomized study in 112 patients after temporal lobectomy suggests that postoperative cognitive rehabilitation may be helpful in ameliorating some of these deficits, particularly a decline in verbal memory [129].

Visual field defects — Additional neurologic sequelae of temporal lobe surgery include visual field defects (VFDs), which are usually limited to a superior quadrant and may be detectable only by formal testing. VFDs are mainly due to injury to the inferior optic radiations (Meyer loop), which course anteriorly in the temporal lobe. In a systematic review of 76 studies that included data on over 1000 patients who underwent temporal lobe epilepsy surgery, the incidence of superior quadrantanopsia was 18 percent and the incidence of major field defects (homonymous hemianopsia) was 2 percent [130].

Risk may be higher for left-sided resections. In a prospective case series of 105 patients undergoing anterior temporal lobectomy, 16 had a new postoperative VFD; 12 of these occurred following a left-sided resection [131]. Risk may also vary according to the type of resection that is performed. In one retrospective study of 276 patients who underwent mesial temporal lobe epilepsy surgery, rates of homonymous scotoma within the central 20 degrees ranged from 56 percent after anterior temporal lobectomy to 21 percent after selective subtemporal amygdalohippocampectomy [132].

Some of the variability in rates of VFD may be related to significant interindividual variation in the anterior extent of Meyer loop, which is incompletely predicted preoperatively by current neuroimaging techniques [133-137]. Limited data suggest that use of intraoperative magnetic resonance imaging (MRI) with display of optic radiation tractography during surgery, where available, may help to minimize risk [138].

VFDs can improve somewhat from the initial postoperative defect, and driving restrictions based upon this deficit should be reevaluated up to one to two years later [139]. (See "Homonymous hemianopia".)

Psychologic sequelae — Psychiatric problems, including depression and psychosocial adjustment difficulties, are not uncommon after epilepsy surgery. Risk factors include a personal or family history of psychiatric disease, poor family and psychosocial support, and certain personality traits [4,140,141]. Presurgical psychiatric evaluation and psychosocial assessment and comprehensive, long-term postsurgical neuropsychologic follow-up are advised in order to mitigate these complications [4,5].

Others — Other neurologic deficits (aphasia, cranial nerve palsy, hemiparesis) occur in 6 percent and are permanent in only half of these cases [142,143]. Death associated with epilepsy surgery is extremely rare (1 in 700) [143].

ANTISEIZURE MEDICATION MANAGEMENT AFTER SURGERY — As discussed above, seizure control within the first year after surgery also predicts more favorable longer-term seizure outcomes [48,57-60]. Long remissions can occur after a relapse; however, these remissions are associated with a poorer outcome than an equivalent period of complete seizure remission immediately following surgery. Similarly, some patients will relapse after an extended period of remission, but these patients usually do not become medically intractable. Patients who develop recurrent intractability are usually identifiable within several months after surgery.

Patients and families understandably hope that antiseizure medications can be tapered and withdrawn after surgery. The rationale for reducing antiseizure medications includes avoidance of drug interactions and dose-related adverse effects, as well as concerns regarding teratogenesis. Patients often believe that medication is unnecessary if they have had "successful" surgery, and thus perceive continued use of antiseizure medications as an unwanted reminder of a disease process that is no longer an active issue for them.

There are no prospective, randomized data evaluating discontinuation of antiseizure medications following epilepsy surgery. A review of six retrospective studies including 611 children and adults followed for one to six years postoperatively noted the following [144]:

The mean seizure recurrence rate was 34 percent after planned discontinuation of antiseizure medications in patients who were seizure free after epilepsy surgery (most often temporal lobe surgery).

The seizure recurrence rate increased during years one to three of follow-up.

More than 90 percent of adults who had recurrent seizures regained control with reinstitution of previous antiseizure medication therapy.

The incidence of recurrent seizures was not affected by the duration of postoperative antiseizure medication treatment, suggesting that there is no value to treating for a specified period of time before attempting to stop therapy.

No factors were identified that predicted the risk of relapse after tapering antiseizure medications, despite looking at factors such as duration of epilepsy, age at onset of epilepsy, and preoperative magnetic resonance imaging (MRI). However, it is not clear whether any of these factors would be predictive of relapse in a prospective, randomized study.

There are compelling reasons for patients to be considered for antiseizure medication taper and withdrawal following epilepsy surgery. These include antiseizure medication adverse effects, potential drug interactions, cost of therapy, and pregnancy-related considerations. Such factors are weighed against the risk of recurrent seizures, which may affect legal driving status. In practice, most individuals are not considered for antiseizure medication withdrawal unless they are seizure free for at least one year following surgery. Those with auras or seizure activity following surgery should probably remain on antiseizure medication therapy unless they are seizure free for two to five years.

There is controversy regarding the utility of electroencephalography (EEG) postoperatively to predict the likelihood of seizure recurrence with drug discontinuation. The emergence of epileptiform activity during the drug taper may be associated with an increased risk of seizure activity. We typically determine an antiseizure medication level and perform an EEG prior to antiseizure medication taper and withdrawal. When the decision is made to taper, an antiseizure medication is usually withdrawn over several weeks. Long tapering schedules (eg, a year or longer) have not been shown to be beneficial.

Most, but not all, individuals who have seizure activity associated with antiseizure medication termination will become seizure free again with reinstitution of medical treatment. Even if all antiseizure medications cannot be tapered, many patients are successfully tapered to antiseizure medication monotherapy, which may minimize adverse effects, cost of therapy, and potential drug interactions. The goal of surgery remains to render the patient seizure free, with or without continued antiseizure medication treatment [145].

TRENDS IN EPILEPSY SURGERY — Despite a large and growing body of evidence supporting the benefit of epilepsy surgery in carefully selected patients with drug refractory epilepsy, surgery remains underutilized [146-151]. A population-based study utilizing the United States Nationwide Inpatient Sample found that there were 6653 resective surgeries from 1990 to 2008, and there was no growth trend over this time period [146]. By contrast, a similar study examining pediatric epilepsy surgery trends in the United States found that rates of epilepsy surgery incrementally rose from 1997 to 2009 [152].

At the same time, there is evidence that the patient population undergoing surgical treatment at large epilepsy centers has changed. In several studies, the absolute number of anterior temporal lobe resections, as well as the percentage of epilepsy surgeries comprising anterior temporal resections, has decreased over time [153-155]. The reasons for decreased utilization of the most common operative procedure for epilepsy are not clear. At many epilepsy centers, an increasing number of patients referred for consideration of surgery have negative magnetic resonance imaging (MRI) studies, multifocal seizures, or indeterminate outpatient diagnostic evaluations [156].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Seizures and epilepsy in adults".)

SUMMARY AND RECOMMENDATIONS

Patients with drug-resistant focal epilepsy should be referred to a comprehensive epilepsy center to confirm the diagnosis, categorize the epilepsy syndrome, and evaluate all possible treatment options, including surgery. (See "Evaluation and management of drug-resistant epilepsy".)

Surgical evaluation is recommended for patients with refractory focal seizures (Grade 1A). The most favorable candidates are those with magnetic resonance imaging (MRI)-identified lesions that correlate with the electrophysiologic localization of seizure onset. (See 'Surgical candidates' above.)

The goals of the surgical evaluation are to identify the epileptogenic zone fully and avoid operative morbidity associated with a focal cortical resection. Standard components of the surgical evaluation include detailed neurologic history and examination, neuropsychologic testing, routine electroencephalography (EEG) recordings with standard activating procedures, inpatient long-term video-EEG monitoring in an epilepsy monitoring unit, high-resolution brain MRI, and functional and metabolic imaging using positron emission tomography (PET) and/or single-photon emission computed tomography (SPECT). Preoperative formal speech and language testing and visual field examinations are also performed in selected patients. (See 'Surgical evaluation' above.)

In adult patients, mesial temporal lobe epilepsy secondary to mesial temporal sclerosis is the most frequently encountered surgically remediable epileptic syndrome. The most common surgical procedure is an anterior temporal resection in which the temporal pole is removed along with the hippocampus and part of the amygdala. The best surgical candidates are those patients with focal, unilateral brain lesions (eg, mesial temporal sclerosis, tumor, or vascular malformation) that correlate with focal-onset seizures localizing to the ipsilateral temporal lobe. (See 'Mesial temporal lobe epilepsy' above.)

Patients with focal seizures of neocortical origin and normal brain MRI scans may also be candidates for epilepsy surgery, but management is often more challenging because of difficulty lateralizing and localizing the epileptogenic zone, difficulty defining the extent of brain tissue that must be resected for seizure freedom, and concerns regarding functional cortex. (See 'Neocortical epilepsy with normal brain MRI' above.)

Low-grade primary brain tumors, vascular malformations, and malformations of cortical development (MCDs) are other causes of refractory focal epilepsy. Resection of the epileptogenic brain region often results in improved seizure control. Outcomes are typically better for patients with tumors and vascular malformations than for patients with focal cortical dysplasia. (See 'Lesional epilepsy' above.)

Epilepsy surgery is associated with low rates of morbidity and mortality when performed at specialized centers. The most common adverse effects related to epilepsy surgery are cognitive impairment and visual field defects (VFDs). (See 'Surgical complications' above.)

  1. Jehi L, Jette N, Kwon CS, et al. Timing of referral to evaluate for epilepsy surgery: Expert Consensus Recommendations from the Surgical Therapies Commission of the International League Against Epilepsy. Epilepsia 2022; 63:2491.
  2. Khoo A, de Tisi J, Mannan S, et al. Reasons for not having epilepsy surgery. Epilepsia 2021; 62:2909.
  3. Weber J, Gustafsson C, Malmgren K, et al. Evaluation for epilepsy surgery - Why do patients not proceed to operation? Seizure 2019; 69:241.
  4. Kerr MP, Mensah S, Besag F, et al. International consensus clinical practice statements for the treatment of neuropsychiatric conditions associated with epilepsy. Epilepsia 2011; 52:2133.
  5. Baxendale S, Wilson SJ, Baker GA, et al. Indications and expectations for neuropsychological assessment in epilepsy surgery in children and adults. Epileptic Disord 2019; 21:221.
  6. Kuzniecky RI, Bilir E, Gilliam F, et al. Multimodality MRI in mesial temporal sclerosis: relative sensitivity and specificity. Neurology 1997; 49:774.
  7. Jack CR Jr, Rydberg CH, Krecke KN, et al. Mesial temporal sclerosis: diagnosis with fluid-attenuated inversion-recovery versus spin-echo MR imaging. Radiology 1996; 199:367.
  8. Trenerry MR, Jack CR Jr, Ivnik RJ, et al. MRI hippocampal volumes and memory function before and after temporal lobectomy. Neurology 1993; 43:1800.
  9. Jones AL, Cascino GD. Evidence on Use of Neuroimaging for Surgical Treatment of Temporal Lobe Epilepsy: A Systematic Review. JAMA Neurol 2016; 73:464.
  10. Cascino GD, Jack CR Jr, Parisi JE, et al. Magnetic resonance imaging-based volume studies in temporal lobe epilepsy: pathological correlations. Ann Neurol 1991; 30:31.
  11. LoPinto-Khoury C, Sperling MR, Skidmore C, et al. Surgical outcome in PET-positive, MRI-negative patients with temporal lobe epilepsy. Epilepsia 2012; 53:342.
  12. O'Brien TJ, So EL, Mullan BP, et al. Subtraction ictal SPECT co-registered to MRI improves clinical usefulness of SPECT in localizing the surgical seizure focus. Neurology 1998; 50:445.
  13. Sulc V, Stykel S, Hanson DP, et al. Statistical SPECT processing in MRI-negative epilepsy surgery. Neurology 2014; 82:932.
  14. Szaflarski JP, Gloss D, Binder JR, et al. Practice guideline summary: Use of fMRI in the presurgical evaluation of patients with epilepsy: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology 2017; 88:395.
  15. Rabin ML, Narayan VM, Kimberg DY, et al. Functional MRI predicts post-surgical memory following temporal lobectomy. Brain 2004; 127:2286.
  16. Richardson MP, Strange BA, Thompson PJ, et al. Pre-operative verbal memory fMRI predicts post-operative memory decline after left temporal lobe resection. Brain 2004; 127:2419.
  17. Bartha L, Mariën P, Brenneis C, et al. Hippocampal formation involvement in a language-activation task in patients with mesial temporal lobe epilepsy. Epilepsia 2005; 46:1754.
  18. Schacher M, Haemmerle B, Woermann FG, et al. Amygdala fMRI lateralizes temporal lobe epilepsy. Neurology 2006; 66:81.
  19. Richardson MP, Strange BA, Duncan JS, Dolan RJ. Memory fMRI in left hippocampal sclerosis: optimizing the approach to predicting postsurgical memory. Neurology 2006; 66:699.
  20. Benke T, Köylü B, Visani P, et al. Language lateralization in temporal lobe epilepsy: a comparison between fMRI and the Wada Test. Epilepsia 2006; 47:1308.
  21. Lineweaver TT, Morris HH, Naugle RI, et al. Evaluating the contributions of state-of-the-art assessment techniques to predicting memory outcome after unilateral anterior temporal lobectomy. Epilepsia 2006; 47:1895.
  22. Mechanic-Hamilton D, Korczykowski M, Yushkevich PA, et al. Hippocampal volumetry and functional MRI of memory in temporal lobe epilepsy. Epilepsy Behav 2009; 16:128.
  23. Wagner K, Hader C, Metternich B, et al. Who needs a Wada test? Present clinical indications for amobarbital procedures. J Neurol Neurosurg Psychiatry 2012; 83:503.
  24. Dym RJ, Burns J, Freeman K, Lipton ML. Is functional MR imaging assessment of hemispheric language dominance as good as the Wada test?: a meta-analysis. Radiology 2011; 261:446.
  25. Janecek JK, Swanson SJ, Sabsevitz DS, et al. Language lateralization by fMRI and Wada testing in 229 patients with epilepsy: rates and predictors of discordance. Epilepsia 2013; 54:314.
  26. Janecek JK, Swanson SJ, Sabsevitz DS, et al. Naming outcome prediction in patients with discordant Wada and fMRI language lateralization. Epilepsy Behav 2013; 27:399.
  27. Kirsch HE, Walker JA, Winstanley FS, et al. Limitations of Wada memory asymmetry as a predictor of outcomes after temporal lobectomy. Neurology 2005; 65:676.
  28. Stroup E, Langfitt J, Berg M, et al. Predicting verbal memory decline following anterior temporal lobectomy (ATL). Neurology 2003; 60:1266.
  29. Simkins-Bullock J. Beyond speech lateralization: a review of the variability, reliability, and validity of the intracarotid amobarbital procedure and its nonlanguage uses in epilepsy surgery candidates. Neuropsychol Rev 2000; 10:41.
  30. Loddenkemper T, Morris HH, Möddel G. Complications during the Wada test. Epilepsy Behav 2008; 13:551.
  31. English J, Davis B. Case report: Death associated with stroke following intracarotid amobarbital testing. Epilepsy Behav 2010; 17:283.
  32. Jones-Gotman M, Sziklas V, Djordjevic J, et al. Etomidate speech and memory test (eSAM): a new drug and improved intracarotid procedure. Neurology 2005; 65:1723.
  33. Buchtel HA, Passaro EA, Selwa LM, et al. Sodium methohexital (brevital) as an anesthetic in the Wada test. Epilepsia 2002; 43:1056.
  34. Kim JH, Joo EY, Han SJ, et al. Can pentobarbital replace amobarbital in the Wada test? Epilepsy Behav 2007; 11:378.
  35. Mikati MA, Naasan G, Tarabay H, et al. Intracarotid propofol testing: a comparative study with amobarbital. Epilepsy Behav 2009; 14:503.
  36. Malerba G, Romano-Girard F, Cravoisy A, et al. Risk factors of relative adrenocortical deficiency in intensive care patients needing mechanical ventilation. Intensive Care Med 2005; 31:388.
  37. Mikuni N, Takayama M, Satow T, et al. Evaluation of adverse effects in intracarotid propofol injection for Wada test. Neurology 2005; 65:1813.
  38. Blumcke I, Spreafico R, Haaker G, et al. Histopathological Findings in Brain Tissue Obtained during Epilepsy Surgery. N Engl J Med 2017; 377:1648.
  39. Jain P, Tomlinson G, Snead C, et al. Systematic review and network meta-analysis of resective surgery for mesial temporal lobe epilepsy. J Neurol Neurosurg Psychiatry 2018; 89:1138.
  40. Eekers DBP, Pijnappel EN, Schijns OEMG, et al. Evidence on the efficacy of primary radiosurgery or stereotactic radiotherapy for drug-resistant non-neoplastic focal epilepsy in adults: A systematic review. Seizure 2018; 55:83.
  41. Englot DJ, Birk H, Chang EF. Seizure outcomes in nonresective epilepsy surgery: an update. Neurosurg Rev 2017; 40:181.
  42. Chang EF, Englot DJ, Vadera S. Minimally invasive surgical approaches for temporal lobe epilepsy. Epilepsy Behav 2015; 47:24.
  43. Brown MG, Drees C, Nagae LM, et al. Curative and palliative MRI-guided laser ablation for drug-resistant epilepsy. J Neurol Neurosurg Psychiatry 2018; 89:425.
  44. Kohlhase K, Zöllner JP, Tandon N, et al. Comparison of minimally invasive and traditional surgical approaches for refractory mesial temporal lobe epilepsy: A systematic review and meta-analysis of outcomes. Epilepsia 2021; 62:831.
  45. Wiebe S, Blume WT, Girvin JP, et al. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med 2001; 345:311.
  46. Engel J Jr, McDermott MP, Wiebe S, et al. Early surgical therapy for drug-resistant temporal lobe epilepsy: a randomized trial. JAMA 2012; 307:922.
  47. Schomer DL, Lewis RJ. Stopping seizures early and the surgical epilepsy trial that stopped even earlier. JAMA 2012; 307:966.
  48. Radhakrishnan K, So EL, Silbert PL, et al. Predictors of outcome of anterior temporal lobectomy for intractable epilepsy: a multivariate study. Neurology 1998; 51:465.
  49. McIntosh AM, Kalnins RM, Mitchell LA, et al. Temporal lobectomy: long-term seizure outcome, late recurrence and risks for seizure recurrence. Brain 2004; 127:2018.
  50. Spencer SS, Berg AT, Vickrey BG, et al. Predicting long-term seizure outcome after resective epilepsy surgery: the multicenter study. Neurology 2005; 65:912.
  51. Berkovic SF, McIntosh AM, Kalnins RM, et al. Preoperative MRI predicts outcome of temporal lobectomy: an actuarial analysis. Neurology 1995; 45:1358.
  52. McIntosh AM, Wilson SJ, Berkovic SF. Seizure outcome after temporal lobectomy: current research practice and findings. Epilepsia 2001; 42:1288.
  53. Janszky J, Janszky I, Schulz R, et al. Temporal lobe epilepsy with hippocampal sclerosis: predictors for long-term surgical outcome. Brain 2005; 128:395.
  54. Jeha LE, Najm IM, Bingaman WE, et al. Predictors of outcome after temporal lobectomy for the treatment of intractable epilepsy. Neurology 2006; 66:1938.
  55. Jeong SW, Lee SK, Hong KS, et al. Prognostic factors for the surgery for mesial temporal lobe epilepsy: longitudinal analysis. Epilepsia 2005; 46:1273.
  56. West S, Nolan SJ, Cotton J, et al. Surgery for epilepsy. Cochrane Database Syst Rev 2015; :CD010541.
  57. McIntosh AM, Kalnins RM, Mitchell LA, Berkovic SF. Early seizures after temporal lobectomy predict subsequent seizure recurrence. Ann Neurol 2005; 57:283.
  58. Radhakrishnan K, So EL, Silbert PL, et al. Prognostic implications of seizure recurrence in the first year after anterior temporal lobectomy. Epilepsia 2003; 44:77.
  59. Cohen-Gadol AA, Wilhelmi BG, Collignon F, et al. Long-term outcome of epilepsy surgery among 399 patients with nonlesional seizure foci including mesial temporal lobe sclerosis. J Neurosurg 2006; 104:513.
  60. Yoon HH, Kwon HL, Mattson RH, et al. Long-term seizure outcome in patients initially seizure-free after resective epilepsy surgery. Neurology 2003; 61:445.
  61. Jehi L, Sarkis R, Bingaman W, et al. When is a postoperative seizure equivalent to "epilepsy recurrence" after epilepsy surgery? Epilepsia 2010; 51:994.
  62. Rathore C, Radhakrishnan K. Prognostic significance of interictal epileptiform discharges after epilepsy surgery. J Clin Neurophysiol 2010; 27:255.
  63. de Tisi J, Bell GS, Peacock JL, et al. The long-term outcome of adult epilepsy surgery, patterns of seizure remission, and relapse: a cohort study. Lancet 2011; 378:1388.
  64. Edelvik A, Rydenhag B, Olsson I, et al. Long-term outcomes of epilepsy surgery in Sweden: a national prospective and longitudinal study. Neurology 2013; 81:1244.
  65. Hemb M, Palmini A, Paglioli E, et al. An 18-year follow-up of seizure outcome after surgery for temporal lobe epilepsy and hippocampal sclerosis. J Neurol Neurosurg Psychiatry 2013; 84:800.
  66. Elliott RE, Bollo RJ, Berliner JL, et al. Anterior temporal lobectomy with amygdalohippocampectomy for mesial temporal sclerosis: predictors of long-term seizure control. J Neurosurg 2013; 119:261.
  67. Uijl SG, Leijten FS, Arends JB, et al. The added value of [18F]-fluoro-D-deoxyglucose positron emission tomography in screening for temporal lobe epilepsy surgery. Epilepsia 2007; 48:2121.
  68. Holmes MD, Born DE, Kutsy RL, et al. Outcome after surgery in patients with refractory temporal lobe epilepsy and normal MRI. Seizure 2000; 9:407.
  69. Sylaja PN, Radhakrishnan K, Kesavadas C, Sarma PS. Seizure outcome after anterior temporal lobectomy and its predictors in patients with apparent temporal lobe epilepsy and normal MRI. Epilepsia 2004; 45:803.
  70. Alarcón G, Valentín A, Watt C, et al. Is it worth pursuing surgery for epilepsy in patients with normal neuroimaging? J Neurol Neurosurg Psychiatry 2006; 77:474.
  71. Bell ML, Rao S, So EL, et al. Epilepsy surgery outcomes in temporal lobe epilepsy with a normal MRI. Epilepsia 2009; 50:2053.
  72. Fong JS, Jehi L, Najm I, et al. Seizure outcome and its predictors after temporal lobe epilepsy surgery in patients with normal MRI. Epilepsia 2011; 52:1393.
  73. Burkholder D, Vlastimil S, Hoffman E, et al. Scalp electroencephalography and intraoperative electrocorticography and temporal lobe epilepsy surgical outcomes in patients with normal MRI. Neurology 2013; 80:Abstact PD4.006.
  74. Van Gompel JJ, Worrell GA, Bell ML, et al. Intracranial electroencephalography with subdural grid electrodes: techniques, complications, and outcomes. Neurosurgery 2008; 63:498.
  75. Wellmer J, von der Groeben F, Klarmann U, et al. Risks and benefits of invasive epilepsy surgery workup with implanted subdural and depth electrodes. Epilepsia 2012; 53:1322.
  76. Hedegärd E, Bjellvi J, Edelvik A, et al. Complications to invasive epilepsy surgery workup with subdural and depth electrodes: a prospective population-based observational study. J Neurol Neurosurg Psychiatry 2014; 85:716.
  77. Schmidt RF, Wu C, Lang MJ, et al. Complications of subdural and depth electrodes in 269 patients undergoing 317 procedures for invasive monitoring in epilepsy. Epilepsia 2016; 57:1697.
  78. Jehi L, Morita-Sherman M, Love TE, et al. Comparative Effectiveness of Stereotactic Electroencephalography Versus Subdural Grids in Epilepsy Surgery. Ann Neurol 2021; 90:927.
  79. Gonzalez-Martinez J, Mullin J, Bulacio J, et al. Stereoelectroencephalography in children and adolescents with difficult-to-localize refractory focal epilepsy. Neurosurgery 2014; 75:258.
  80. Serletis D, Bulacio J, Bingaman W, et al. The stereotactic approach for mapping epileptic networks: a prospective study of 200 patients. J Neurosurg 2014; 121:1239.
  81. Tandon N, Tong BA, Friedman ER, et al. Analysis of Morbidity and Outcomes Associated With Use of Subdural Grids vs Stereoelectroencephalography in Patients With Intractable Epilepsy. JAMA Neurol 2019; 76:672.
  82. Cardinale F, Rizzi M, Vignati E, et al. Stereoelectroencephalography: retrospective analysis of 742 procedures in a single centre. Brain 2019; 142:2688.
  83. Samanta D. Recent developments in stereo electroencephalography monitoring for epilepsy surgery. Epilepsy Behav 2022; 135:108914.
  84. Oluigbo CO, Gaillard WD, Koubeissi MZ. The End Justifies the Means-A Call for Nuance in the Increasing Nationwide Adoption of Stereoelectroencephalography Over Subdural Electrode Monitoring in the Surgical Evaluation of Intractable Epilepsy. JAMA Neurol 2022; 79:221.
  85. Yan H, Katz JS, Anderson M, et al. Method of invasive monitoring in epilepsy surgery and seizure freedom and morbidity: A systematic review. Epilepsia 2019; 60:1960.
  86. Mullin JP, Shriver M, Alomar S, et al. Is SEEG safe? A systematic review and meta-analysis of stereo-electroencephalography-related complications. Epilepsia 2016; 57:386.
  87. Noe K, Sulc V, Wong-Kisiel L, et al. Long-term outcomes after nonlesional extratemporal lobe epilepsy surgery. JAMA Neurol 2013; 70:1003.
  88. See SJ, Jehi LE, Vadera S, et al. Surgical outcomes in patients with extratemporal epilepsy and subtle or normal magnetic resonance imaging findings. Neurosurgery 2013; 73:68.
  89. Wetjen NM, Marsh WR, Meyer FB, et al. Intracranial electroencephalography seizure onset patterns and surgical outcomes in nonlesional extratemporal epilepsy. J Neurosurg 2009; 110:1147.
  90. Schwartz TH, Jeha L, Tanner A, et al. Late seizures in patients initially seizure free after epilepsy surgery. Epilepsia 2006; 47:567.
  91. Kim DW, Lee SK, Moon HJ, et al. Surgical Treatment of Nonlesional Neocortical Epilepsy: Long-term Longitudinal Study. JAMA Neurol 2017; 74:324.
  92. Frater JL, Prayson RA, Morris III HH, Bingaman WE. Surgical pathologic findings of extratemporal-based intractable epilepsy: a study of 133 consecutive resections. Arch Pathol Lab Med 2000; 124:545.
  93. Wolf HK, Campos MG, Zentner J, et al. Surgical pathology of temporal lobe epilepsy. Experience with 216 cases. J Neuropathol Exp Neurol 1993; 52:499.
  94. Tassi L, Meroni A, Deleo F, et al. Temporal lobe epilepsy: neuropathological and clinical correlations in 243 surgically treated patients. Epileptic Disord 2009; 11:281.
  95. Vannemreddy PS, Kanner AM, Smith MC, et al. Chronic epilepsy due to low grade temporal lobe tumors and due to hippocampal sclerosis: do they differ in post-surgical outcome? J Neurooncol 2013; 115:225.
  96. Giulioni M, Marucci G, Pelliccia V, et al. Epilepsy surgery of "low grade epilepsy associated neuroepithelial tumors": A retrospective nationwide Italian study. Epilepsia 2017; 58:1832.
  97. Nolan MA, Sakuta R, Chuang N, et al. Dysembryoplastic neuroepithelial tumors in childhood: long-term outcome and prognostic features. Neurology 2004; 62:2270.
  98. Bonney PA, Boettcher LB, Conner AK, et al. Review of seizure outcomes after surgical resection of dysembryoplastic neuroepithelial tumors. J Neurooncol 2016; 126:1.
  99. Baumann CR, Acciarri N, Bertalanffy H, et al. Seizure outcome after resection of supratentorial cavernous malformations: a study of 168 patients. Epilepsia 2007; 48:559.
  100. Kwon CS, Sheth SA, Walcott BP, et al. Long-term seizure outcomes following resection of supratentorial cavernous malformations. Clin Neurol Neurosurg 2013; 115:2377.
  101. Blümcke I, Thom M, Aronica E, et al. The clinicopathologic spectrum of focal cortical dysplasias: a consensus classification proposed by an ad hoc Task Force of the ILAE Diagnostic Methods Commission. Epilepsia 2011; 52:158.
  102. Najm I, Lal D, Alonso Vanegas M, et al. The ILAE consensus classification of focal cortical dysplasia: An update proposed by an ad hoc task force of the ILAE diagnostic methods commission. Epilepsia 2022; 63:1899.
  103. Lamberink HJ, Otte WM, Blümcke I, et al. Seizure outcome and use of antiepileptic drugs after epilepsy surgery according to histopathological diagnosis: a retrospective multicentre cohort study. Lancet Neurol 2020; 19:748.
  104. Willard A, Antonic-Baker A, Chen Z, et al. Seizure Outcome After Surgery for MRI-Diagnosed Focal Cortical Dysplasia: A Systematic Review and Meta-analysis. Neurology 2022; 98:e236.
  105. Kim DW, Lee SK, Chu K, et al. Predictors of surgical outcome and pathologic considerations in focal cortical dysplasia. Neurology 2009; 72:211.
  106. Wang DD, Deans AE, Barkovich AJ, et al. Transmantle sign in focal cortical dysplasia: a unique radiological entity with excellent prognosis for seizure control. J Neurosurg 2013; 118:337.
  107. Harvey AS, Mandelstam SA, Maixner WJ, et al. The surgically remediable syndrome of epilepsy associated with bottom-of-sulcus dysplasia. Neurology 2015; 84:2021.
  108. Macdonald-Laurs E, Maixner WJ, Bailey CA, et al. One-Stage, Limited-Resection Epilepsy Surgery for Bottom-of-Sulcus Dysplasia. Neurology 2021; 97:e178.
  109. Chassoux F, Rodrigo S, Semah F, et al. FDG-PET improves surgical outcome in negative MRI Taylor-type focal cortical dysplasias. Neurology 2010; 75:2168.
  110. Urbach H, Jamneala G, Mader I, et al. Temporal lobe epilepsy due to meningoencephaloceles into the greater sphenoid wing: a consequence of idiopathic intracranial hypertension? Neuroradiology 2018; 60:51.
  111. Tse GT, Frydman AS, O'Shea MF, et al. Anterior temporal encephaloceles: Elusive, important, and rewarding to treat. Epilepsia 2020; 61:2675.
  112. Giulioni M, Licchetta L, Bisulli F, et al. Tailored surgery for drug-resistant epilepsy due to temporal pole encephalocele and microdysgenesis. Seizure 2014; 23:164.
  113. McClelland S 3rd, Guo H, Okuyemi KS. Population-based analysis of morbidity and mortality following surgery for intractable temporal lobe epilepsy in the United States. Arch Neurol 2011; 68:725.
  114. Baxendale S, Thompson PJ, Duncan JS. Improvements in memory function following anterior temporal lobe resection for epilepsy. Neurology 2008; 71:1319.
  115. Baxendale S, Thompson P, Harkness W, Duncan J. Predicting memory decline following epilepsy surgery: a multivariate approach. Epilepsia 2006; 47:1887.
  116. Chelune GJ, Naugle RI, Luders H, et al. Individual change after epilepsy surgery: practice effects and base-rate information. Neuropsychology 1993; 7:41.
  117. Davies KG, Maxwell RE, Beniak TE, et al. Language function after temporal lobectomy without stimulation mapping of cortical function. Epilepsia 1995; 36:130.
  118. Ivnik RJ, Sharbrough FW, Laws ER Jr. Effects of anterior temporal lobectomy on cognitive function. J Clin Psychol 1987; 43:128.
  119. Selwa LM, Berent S, Giordani B, et al. Serial cognitive testing in temporal lobe epilepsy: longitudinal changes with medical and surgical therapies. Epilepsia 1994; 35:743.
  120. Dulay MF, Levin HS, York MK, et al. Changes in individual and group spatial and verbal learning characteristics after anterior temporal lobectomy. Epilepsia 2009; 50:1385.
  121. Alpherts WC, Vermeulen J, Hendriks MP, et al. Long-term effects of temporal lobectomy on intelligence. Neurology 2004; 62:607.
  122. Alpherts WC, Vermeulen J, van Rijen PC, et al. Verbal memory decline after temporal epilepsy surgery?: A 6-year multiple assessments follow-up study. Neurology 2006; 67:626.
  123. Andersson-Roswall L, Engman E, Samuelsson H, Malmgren K. Cognitive outcome 10 years after temporal lobe epilepsy surgery: a prospective controlled study. Neurology 2010; 74:1977.
  124. Harvey DJ, Naugle RI, Magleby J, et al. Relationship between presurgical memory performance on the Wechsler Memory Scale-III and memory change following temporal resection for treatment of intractable epilepsy. Epilepsy Behav 2008; 13:372.
  125. Chelune GJ, Naugle RI, Lüders H, Awad IA. Prediction of cognitive change as a function of preoperative ability status among temporal lobectomy patients seen at 6-month follow-up. Neurology 1991; 41:399.
  126. Dulay MF, Levin HS, York MK, et al. Predictors of individual visual memory decline after unilateral anterior temporal lobe resection. Neurology 2009; 72:1837.
  127. Gleissner U, Sassen R, Schramm J, et al. Greater functional recovery after temporal lobe epilepsy surgery in children. Brain 2005; 128:2822.
  128. Langfitt JT, Westerveld M, Hamberger MJ, et al. Worsening of quality of life after epilepsy surgery: effect of seizures and memory decline. Neurology 2007; 68:1988.
  129. Helmstaedter C, Loer B, Wohlfahrt R, et al. The effects of cognitive rehabilitation on memory outcome after temporal lobe epilepsy surgery. Epilepsy Behav 2008; 12:402.
  130. Hader WJ, Tellez-Zenteno J, Metcalfe A, et al. Complications of epilepsy surgery: a systematic review of focal surgical resections and invasive EEG monitoring. Epilepsia 2013; 54:840.
  131. Jeelani NU, Jindahra P, Tamber MS, et al. 'Hemispherical asymmetry in the Meyer's Loop': a prospective study of visual-field deficits in 105 cases undergoing anterior temporal lobe resection for epilepsy. J Neurol Neurosurg Psychiatry 2010; 81:985.
  132. Schmeiser B, Daniel M, Kogias E, et al. Visual field defects following different resective procedures for mesiotemporal lobe epilepsy. Epilepsy Behav 2017; 76:39.
  133. Barton JJ, Hefter R, Chang B, et al. The field defects of anterior temporal lobectomy: a quantitative reassessment of Meyer's loop. Brain 2005; 128:2123.
  134. Powell HW, Parker GJ, Alexander DC, et al. MR tractography predicts visual field defects following temporal lobe resection. Neurology 2005; 65:596.
  135. Pathak-Ray V, Ray A, Walters R, Hatfield R. Detection of visual field defects in patients after anterior temporal lobectomy for mesial temporal sclerosis-establishing eligibility to drive. Eye (Lond) 2002; 16:744.
  136. Yogarajah M, Focke NK, Bonelli S, et al. Defining Meyer's loop-temporal lobe resections, visual field deficits and diffusion tensor tractography. Brain 2009; 132:1656.
  137. Winston GP, Daga P, Stretton J, et al. Optic radiation tractography and vision in anterior temporal lobe resection. Ann Neurol 2012; 71:334.
  138. Winston GP, Daga P, White MJ, et al. Preventing visual field deficits from neurosurgery. Neurology 2014; 83:604.
  139. Yam D, Nicolle D, Steven DA, et al. Visual field deficits following anterior temporal lobectomy: long-term follow-up and prognostic implications. Epilepsia 2010; 51:1018.
  140. Wrench JM, Rayner G, Wilson SJ. Profiling the evolution of depression after epilepsy surgery. Epilepsia 2011; 52:900.
  141. Wilson SJ, Wrench JM, McIntosh AM, et al. Profiles of psychosocial outcome after epilepsy surgery: the role of personality. Epilepsia 2010; 51:1133.
  142. Engel J Jr, Wiebe S, French J, et al. Practice parameter: temporal lobe and localized neocortical resections for epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology, in association with the American Epilepsy Society and the American Association of Neurological Surgeons. Neurology 2003; 60:538.
  143. Nadkarni S, LaJoie J, Devinsky O. Current treatments of epilepsy. Neurology 2005; 64:S2.
  144. Schmidt D, Baumgartner C, Löscher W. Seizure recurrence after planned discontinuation of antiepileptic drugs in seizure-free patients after epilepsy surgery: a review of current clinical experience. Epilepsia 2004; 45:179.
  145. Schiller Y, Cascino GD, So EL, Marsh WR. Discontinuation of antiepileptic drugs after successful epilepsy surgery. Neurology 2000; 54:346.
  146. Englot DJ, Ouyang D, Garcia PA, et al. Epilepsy surgery trends in the United States, 1990-2008. Neurology 2012; 78:1200.
  147. Jette N, Quan H, Tellez-Zenteno JF, et al. Development of an online tool to determine appropriateness for an epilepsy surgery evaluation. Neurology 2012; 79:1084.
  148. de Flon P, Kumlien E, Reuterwall C, Mattsson P. Empirical evidence of underutilization of referrals for epilepsy surgery evaluation. Eur J Neurol 2010; 17:619.
  149. Haneef Z, Stern J, Dewar S, Engel J Jr. Referral pattern for epilepsy surgery after evidence-based recommendations: a retrospective study. Neurology 2010; 75:699.
  150. Cukiert A, Cukiert CM, Argentoni M, et al. Outcome after corticoamygdalohippocampectomy in patients with refractory temporal lobe epilepsy and mesial temporal sclerosis without preoperative ictal recording. Epilepsia 2009; 50:1371.
  151. Burneo JG, Shariff SZ, Liu K, et al. Disparities in surgery among patients with intractable epilepsy in a universal health system. Neurology 2016; 86:72.
  152. Pestana Knight EM, Schiltz NK, Bakaki PM, et al. Increasing utilization of pediatric epilepsy surgery in the United States between 1997 and 2009. Epilepsia 2015; 56:375.
  153. Van Gompel JJ, Ottman R, Worrell GA, et al. Use of anterior temporal lobectomy for epilepsy in a community-based population. Arch Neurol 2012; 69:1476.
  154. Jehi L, Friedman D, Carlson C, et al. The evolution of epilepsy surgery between 1991 and 2011 in nine major epilepsy centers across the United States, Germany, and Australia. Epilepsia 2015; 56:1526.
  155. Helmstaedter C, May TW, von Lehe M, et al. Temporal lobe surgery in Germany from 1988 to 2008: diverse trends in etiological subgroups. Eur J Neurol 2014; 21:827.
  156. Bien CG, Raabe AL, Schramm J, et al. Trends in presurgical evaluation and surgical treatment of epilepsy at one centre from 1988-2009. J Neurol Neurosurg Psychiatry 2013; 84:54.
Topic 91820 Version 42.0

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