statement of epilepsy surgery editorial purpose purpose the epilepsy board review manual is a study...

Hospital physician Board Review Manual www.turner-white.com

EpilEpsy Board rEviEw Manual

Statement of editorial PurPoSe

The Epilepsy Board Review Manual is a study guide for trainees and practicing physicians preparing for board examinations in epilepsy. Each manual reviews a topic essential to the current management of patients with epilepsy.

PuBliSHinG Staff

PRESIDENT, GRouP PuBLISHERBruce M. White

SENIoR EDIToRRobert Litchkofski

ExEcuTIvE vIcE PRESIDENTBarbara T. White

ExEcuTIvE DIREcToR of oPERaTIoNS

Jean M. Gaul

NoTE fRoM THE PuBLISHER:This publication has been developed without involvement of or review by the American Board of Psychiatry and Neurology.

Epilepsy surgeryContributor and Editor:Thomas R. Henry, MD Professor of Neurology, Director, Comprehensive Epilepsy Center, University of Minnesota Medical School, Minneapolis, MN

Contributors:paramita Das, MDResident Physician of Neurosurgery, Department of Neurosurgery, University of Minnesota Medical School, Minneapolis, MN

Aviva Abosch, MD, phD Associate Professor of Neurosurgery, Department of Neurosurgery and the Comprehensive Epilepsy Center, University of Minnesota Medical School, Minneapolis, MN

introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1

Refractory Epilepsy: Definition, Epidemiology, and Consequences . . . . . . . . . . . . . . . . . . . . . . . .1

principles of selection for Epilepsy surgery . . . .2

surgical procedures and Outcomes . . . . . . . . . . .2

Board Review Questions . . . . . . . . . . . . . . . . . . .12

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12

Table of Contents

E p i l e p s y S u r g e r y

www.turner-white.com Epilepsy Volume 2, Part 1 1

EpilEpsy BOARD REviEw MAnuAl

Epilepsy surgeryParamita Das, MD, Thomas R. Henry, MD, and Aviva Abosch, MD, PhD

introduction

Clinicians who are managing patients with drug-resistant epilepsy must consider wheth-er epilepsy surgery is a reasonable alterna-tive for these individuals. Practitioners therefore should understand the indications, risks, and benefits of surgery, as well as the durability of the surgical outcomes. In this article, we re-view the most common and efficacious surgi-cal interventions for epilepsy, including tem-poral lobectomy, amygdalohippocampectomy, cerebral lesionectomy with or without addition-al cortical resection, nonlesional corticectomy, corpus callosotomy, and multiple subpial transections.

refractory ePilePSy: definition, ePidemioloGy, and conSequenceS

Epilepsy affects nearly 1% of the U.S. population. Treatment with an antiepileptic medication re-sults in seizure remission in only 60% to 70% of patients.1 Seizure control is crucial for clinical as well as psychosocial reasons. Patients with

epilepsy are at greater risk of death than are age-matched controls without epilepsy.2 This in-creased risk is mostly seen in young people with treatment-refractory epilepsy. Trauma, suicide, pneumonia, and status epilepticus have all been identified as causes of death in people with epi-lepsy, and are seen more frequently in these in-dividuals than in the general population.3,4 Sud-den unexpected death in epilepsy (SUDEP) is also increasingly recognized as a cause of death in this patient population, especially in those who experience more than 3 generalized tonic-clonic seizures per month.5 The fear of personal injury or injury to others results in restrictive lifestyle changes, such as limitations on driving.6 There is also a societal stigma associated with epilepsy, and patients may at times feel as if they are a burden to others.7 Women trying to conceive have to be concerned with the teratogenic nature of all antiepileptic medications. Epilepsy, even when well controlled, is not a benign condition and has clinical and psychosocial consequenc-es. For all of these reasons, surgical approaches should be considered for patients with medically refractory epilepsy.

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2 Hospital physician Board Review Manual www.turner-white.com

PrinciPleS of Selection for ePilePSy SurGery

Although antiepileptic drugs (AEDs) should be considered the first line of therapy for the treatment of epilepsy, there are specific epileptic syndromes that respond poorly to medications and yet are associated with excellent outcomes in response to surgery. Early intervention in these patients provides the best opportunity for seizure freedom and complete psychosocial rehabilitation. It is esti-mated that only 1500 of the nearly 100,000 eligible patients in the United States undergo such surgical procedures annually.8 There are many potential ex-planations for the small number of epilepsy surger-ies, including patient concerns about complications as well as misconceptions about epilepsy surgery candidacy among referring physicians,9 but the root cause(s) remains an area of active inquiry.

Ideally, the goals of resective surgery for the treatment of epilepsy are freedom from seizures, elimination of the need for anticonvulsant medica-tions, and absence of injury to eloquent cortex (with potentially permanent new deficits in motor, senso-ry, or language functions) and other complications of the surgery. With improvements in preoperative evaluations and surgical technique, children under the age of 3 years, as well as patients older than 50, are now considered for epilepsy surgery.10,11 The American Academy of Neurology (AAN) has published clinical practice guidelines recommend-ing that patients with disabling complex partial seizures who have failed first-line AEDs should be considered for epilepsy surgery.8 The definition of “failure of first-line AEDs” is not delineated in this recommendation, and no definitive guidelines are provided about when to refer children for surgical evaluation. In practice, however, clinicians often wait longer because there can be regression of

seizures in children with epilepsy. The International League Against Epilepsy (ILAE) recommends consideration of surgery for children with uncon-trolled seizures—defined as failure of 2 or more appropriate drugs—or disabling seizures, or with disabling side effects from AEDs. The ILAE also recommends surgical referral for children without an electroclinical syndrome when there is a le-sion amenable to removal, and for any infant or toddler with seizures. Patients with drug-resistant epilepsy should be reconsidered for epilepsy sur-gery at least every 3 years, as new technologies are developed on a regular basis. Finally, although not addressed in either the AAN or ILAE guide-lines, women interested in becoming pregnant should be considered for epilepsy surgery be-cause of the teratogenic nature of many antiseizure medications.12

SurGical ProcedureS and outcomeS

The following sections describe the most com-mon epilepsy conditions for which surgery might be appropriate, as well as the preoperative evaluation, surgical indications, risks, and potential benefits for each; a brief description of the surgical procedures is also provided. Outcomes of surgery are most commonly classified using Engel’s system (Table).

TEMporal loBEcToMy and aMygdalohippocaMpEcToMy for TEMporal loBE EpilEpsy

Evaluation Patients with unilateral mesial temporal lobe

epilepsy (MTLE) are in general among the most favorable of candidates for epilepsy surgery, al-though patients with the less common syndromes of neocortical temporal lobe epilepsy (TLE) also can benefit considerably from resective therapy.



Patients with MTLE typically display a characteris-tic symptom complex (see Epilepsy Board Review Manual [EBRM], Volume 1, Part 113). MTLE often begins in the latter part of the first decade of life and initially responds to medication, but disabling complex partial seizures return in adolescence and become refractory to antiepileptic medication. A rather different natural history of seizure progres-sion attends severe limbic system insults of early or later adulthood, such as herpes encephalitis, in which some patients move rapidly from acute seizures during the acute injury through an abbre-viated latent phase into highly refractory complex partial seizures of MTLE. Various other temporal patterns of seizure progression and refractoriness

are common. The auras may be viscerosensory or experiential in nature, with a rising epigastric sensation typical of the former and a déjà-vu sen-sation typical of the latter. Interestingly, febrile sei-zures are observed in 3% of all children, but 40% of all patients with MTLE have a history of febrile seizures in childhood. A history of febrile seizures has also been shown to be a strong predictor of a good surgical outcome.14

Mesial temporal sclerosis represents a specific pattern of pyramidal cell loss and gliosis, with sec-tor CA1 of Lorente de Nó most severely affected, followed by the hilus of the dentate gyrus and adja-cent sector CA3. Relative preservation of neurons in CA2 and subiculum of the granule cell layer

Table. Engel’s Classification of Postoperative Outcome

class i: free of disabling seizures*A: Completely seizure free since surgery

B. Nondisabling simple partial seizures only since surgery

C. Some disabling seizures after surgery, but free of disabling seizures for at least 2 years

D. Generalized convulsions with antiepileptic drug discontinuation only

class ii: rare disabling seizures (“almost seizure free”)A. Initially free of disabling seizures but has rare seizures now

B. Rare disabling seizures since surgery

C. More than rare disabling seizures since surgery, but rare seizures for the last 2 years

D. Nocturnal seizures only

class iii: worthwhile improvement†

A. Worthwhile seizure reduction

B. Prolonged seizure-free intervals amounting to greater than half the followed-up period, but not less than 2 years

class iv: no worthwhile improvementA. Significant seizure reduction

B. No appreciable change

C. Seizures worse

*Excludes early postoperative seizures (first few weeks).

†Determination of “worthwhile improvement” will require quantitative analysis of additional data such as percentage of seizure reduction, cognitive function, and quality of life.

Adapted with permission from Engel J Jr, Van Ness PC, Rasmussen TB. Outcome with respect to epileptic seizures. In: Engel J Jr, ed. Surgical treatment of the epilepsies. 2nd ed. New York: Lippincott-Raven; 1993:609–21.



of the dentate gyrus is usually seen (see EBRM, Volume 1, Part 315).16 There are varying degrees of involvement of the hippocampus. In more severe hippocampal sclerosis, mossy fiber sprouting can be identified in the dentate gyrus, in addition to granule cell dispersion and depletion in the dentate gyrus. Sclerosis is often found in the amygdala and in the parahippocampal gyrus as well.

The standard presurgical evaluation for patients with MTLE includes a careful history and physical examination. Ictal and interictal electroencepha-lography (EEG) and video-EEG with extracranial electrodes, magnetic resonance imaging (MRI) with specific sequences, and neuropsychological and neuropsychiatric assessment are also usu-ally performed (see EBRM, Volume 1, Parts 2 and 315,17). Functional imaging with positron emis-sion tomography (PET) or single-photon emission computed tomography (SPECT) is often utilized (see EBRM, Volume 1, Part 418). More invasive testing is considered, if needed. Historical details should include the age of seizure onset, presence of febrile seizures in early childhood, and any family history of epilepsy or unexplained deaths. Familial MTLE exists but is thought to be clini-cally and histopathologically indistinguishable from sporadic MTLE.19,20 There is currently no genetic determinant for predicting outcome after epilepsy surgery.21 An accurate description of semiology, meaning the phenotype of the seizures, must be obtained, as the auras, automatisms, and postictal findings can help support the diagnosis of MTLE. For instance, 40% to 80% of patients with MTLE manifest aural or manual automatisms, include lip-smacking, chewing, and picking.22

Ictal EEG recording is a major component of the preoperative evaluation for surgical consider-ation. Various ictal rhythms have been described, including background attenuation, start-stop-start

phenomenon, irregular 2- to 5-Hz lateralized ac-tivity, and 5- to 10-Hz sinusoidal waves or repeti-tive epileptiform discharges.23 Postictal delta can be lateralized in 60% of patients with TLE and is concordant with the side of seizure onset in most patients. The standard scalp EEG electrode can detect up to 58% of all spikes.24 More invasive electrodes have been used to further evaluate sei-zure foci, and include sphenoidal, nasopharyngeal, anterior temporal, and surface electrodes overlying the mandibular notch or zygoma.25,26 If surface EEG yields inconclusive results, intracranial elec-trodes using subdural or intracerebral depth elec-trodes can be used to improve diagnostic accuracy (see EBRM, Volume 1, Part 217). No prospective studies have yet established the minimum number of ictal recordings necessary to prove lateraliza-tion and localization of seizure-onset zone. How-ever, Sirven and colleagues reported that among a group of patients with bilateral seizure foci, all patients demonstrated contralateral seizure onset by the fourth recorded seizure.27 Blum used a statistical model to demonstrate that 5 recorded seizures were required to yield a 95% chance of avoiding a conflicting seizure, and only 4 seizures were required if all interictal spikes were noted to be unilateral.28

In patients with medically refractory TLE, visual-ization of a lesion or evidence of mesial temporal sclerosis on MRI has been shown to be a prognos-tic indicator of good surgical outcome.29–34 MRI can suggest both the likely side of seizure onset as well as the probable surgical pathology, and therefore plays a critical role in the preoperative evaluation of patients. The widely accepted features of mesial temporal sclerosis on MRI include increased hip-pocampal signal intensity, reduced hippocampal volume, atrophy of hippocampal collateral white matter, enlarged temporal horn, reduced gray-



white matter demarcation in the temporal lobe, and decreased temporal lobe volume.35 Preop-erative MRI evaluation should therefore include a T1-weighted volumetric acquisition allowing quan-titative assessment of the hippocampal volume, T2-weighted coronal sequences, fluid-attenuated inversion recovery (FLAIR) images to detect in-creased signal in the hippocampus, and inversion recovery images to detect the loss of internal struc-ture of the hippocampus (see EBRM, Volume 1, Part 315).

In addition to MRI, electroclinical correlation is recommended to confirm the epileptogenicity of the structural abnormality. There are 2 main types of surgically remediable TLE: MTLE and lateral or neocortical TLE. The latter may be unac-companied by MRI findings but still benefit from surgical intervention.35 Immonen and colleagues found that 40% of 38 patients with MRI-negative TLE who underwent surgery achieved an Engel I seizure outcome (free of disabling seizures).36 Bell and colleagues reported that 60% of TLE patients with normal MRI achieved an Engel I surgical outcome.37 Therefore, patients with suspected “non-lesional” epilepsy based on MRI should not be denied access to a preoperative surgical evaluation.

In patients with normal MRI, greater emphasis is placed on ictal recordings and functional imaging, including PET and SPECT.38 Although the underly-ing pathophysiology has not been completely elu-cidated, a subset of these patients demonstrate lat-eralized temporal lobe seizures on ictal EEG, often with significant focal temporal hypometabolism on PET and yet normal MRI.39 In patients with hip-pocampal atrophy on MRI, PET typically reveals hypometabolism in the ipsilateral temporal lobe (see EBRM, Volume 1, Part 418). The presence of contralateral or bilateral temporal hypometabolism

may suggest bilateral temporal lobe pathology with seizures arising independently from both hip-pocampi. Ictal SPECT is a useful adjunctive study in patients with negative MRIs and inconclusive EEGs. Studies have shown that if the radio-labeled tracer injection is given within 30 seconds of seizure onset, hyperperfusion can be identified at the site of the seizure focus in more than 90% of patients (see EBRM Volume 1, Part 418). The sensitivity of interictal SPECT drops to nearly 50%, and there-fore this study is not very useful in localizing seizure focus.40

surgical procedure For many years, standard anterior temporal lobe

resection was the most frequently used proce-dure for TLE. Several variants of this procedure have evolved, including a transcortical amygda-lohippocampectomy41 as well as a trans-Sylvian amygdalohippocampectomy.42 The rationale for these variants includes relative sparing of temporal neocortex, with the potential benefit to postopera-tive language and cognitive function that this rela-tive tissue sparing might provide.43,44 Once surgical intervention is selected, the surgical procedure generally involves the use of intraoperative image guidance, which helps in the planning of position-ing and the surgical approach. The surgery itself can be performed using general endotracheal anesthesia or awake if there is concern about language function. It is worth emphasizing that language representation in the dominant hemi-sphere can vary substantially in patients who have had epilepsy from an early age.45 With an awake, cooperative patient, cortical mapping using electrical stimulation can be performed intraop-eratively to confirm the location of language areas, using complex protocols to assure patient electri-cal safety and adequacy of functional mapping



(see EBRM, Volume 1, Part 217). Resection of the temporal lobe typically extends approximately 6 to 6.5 cm posterior to the temporal pole on the nondominant side and 4.5 cm in the dominant temporal lobe (figure 1). Hippocampal resection generally terminates posteriorly at the level of the tectal plate.46 Extent of resection should be con-firmed on postoperative MRI. Amygdalohippo-campectomy can avoid resection of temporal lobe neocortex, or amygdalohippocampectomy may be combined with resection of neocortex of the anterior temporal pole, leaving large lateral and inferior portions of temporal neocortex intact (figure 2). Some groups tailor their hippocampal resection based on intraoperative electrocorti-cography of this structure.47 Presumably, amyg-dalohippocampectomy will reduce the likelihood

of iatrogenic language and other deficits due to neocortical injury,48 although this expectation has not been confirmed by a randomized prospective trial of amygdalohippocampectomy versus “full” temporal lobectomy with margins tailored to ex-clude eloquent cortex that has been mapped with direct cortical electrical stimulation at the time of surgery.

Although anterior temporal lobectomy is con-sidered the intervention of choice for intractable MTLE, radiosurgery targeting the mesial struc-tures is an attractive option given its noninvasive nature, and has been the focus of much recent work. A drawback of radiosurgery is the lack of immediate seizure control—an average of 10 to 12 months is required until maximum seizure freedom is achieved.49–51 Post-procedural cerebral edema

figure 1. Anterior temporal lobectomy. The right lateral and inferior cerebral views show typical resection margins, which differ for language dominant versus nondominant lateral resection, as shown. (Adapted with permission from Wiebe S, Blume WT, Girvin JP, Eliasziw M; Effectiveness and Efficiency of Surgery for Temporal Lobe Epilepsy Study Group. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med 2001;345:313.)

Maximal lateral resection

Minimal mesial resection

Amygdala

Hippocampus

6.0–6.5 cm Nondominant4.0–4.5 cm Dominant

1.0–3.0 cm



has been documented, and this can require an ex-tended duration of steroid therapy. The multicenter National Institutes of Health–funded Radiosurgery or Open Surgery for Epilepsy (ROSE) trial was recently closed due to lack of enrollment, but on-going analysis of the accumulated results of this study might further elucidate the efficacy of radio-surgery in this patient population.

risks of surgeryIn addition to the standard risks of a craniotomy,

postoperative amnesia is a specific risk of tem-poral lobe surgery. Formal neuropsychological testing is used to provide a baseline assessment of cognitive functioning across all domains, to as-sess the risk of postoperative memory loss, and to help with localizing seizure focus by identifying the laterality of specific deficits in memory or other cognitive function. In patients with both verbal and nonverbal deficits, or with deficits ascribed to the side contralateral to the proposed side of surgery,

an intracarotid amobarbital procedure (or “Wada test”) is used to establish language lateralization and whether the contralateral temporal lobe will be capable of sustaining memory function postop-eratively. Studies examining the use of the Wada test for presurgical evaluation show wide varia-tions in the use of the test,52–54 with 25% to 35% of all surgical patients undergoing Wada testing. The lack of more widespread use of preoperative Wada testing is in part due to its requirement for invasive cerebral angiography, which carries a risk of stroke (up to 10% in some centers) and other complications.55 For this reason, much interest has centered on the use of noninvasive techniques such as language-activation functional MRI, but to date no noninvasive technique for language later-alization has supplanted Wada testing in terms of accuracy.56

From an anatomical standpoint, visual pathway fibers are located in the roof of the temporal horn as they extend forward from the lateral geniculate

figure 2. Amygdalohippocampectomy and temporal neocortical resections. These T1-weighted, single-axial images show typical anatomical results of (a) focal amygdalohippocampectomy, (B) amygdalohippocampectomy with anterior temporal pole resection, and (c) full anterior temporal lobectomy. (Adapted with permission from Helmstaedter C, Richter S, Röske S, et al. Differential ef-fects of temporal pole resection with amygdalohippocampectomy versus selective amygdalohippocampectomy on material-specific memory in patients with mesial temporal lobe epilepsy. Epilepsia 2008;49:90.)

a B c



body before turning posterior to reach the calca-rine cortex. Since the location of these fibers is not always predictable, standard anterior temporal resections can result in a “pie in the sky” superior quadrantanopsia in the contralateral visual field. This postoperative deficit has been documented in 35% to 50% of patients undergoing surgery for MTLE.57 Worsened or new postoperative memory problems are expected in 1% to 4% of patients.58–60 Preoperative risk factors for decreased memory function following surgery include dominant TLE, lack of hippocampal sclerosis on MRI or histo-pathology, normal baseline neuropsychological functioning, and later age of seizure onset. Post-operative hemiparesis occurred in 2% to 5% of patients,59 and is a consequence of anterior cho-roidal artery injury or direct injury to the cerebral peduncle, which lies medial to the hippocampus. Other series report much lower rates of hemipa-resis,61,62 and emphasize marked improvement in acute postoperative motor deficits during chronic recovery.

seizure outcome and overall outcome Despite the risks of surgery, surgical therapy for

mesial temporal sclerosis has been demonstrated to be superior to optimal medical therapy. Evalu-ation of outcome is based on seizure frequency, cognitive outcome, and quality-of-life measures. Wiebe and colleagues in 2001 reported the results of their prospective trial of 80 patients randomly as-signed to receive either temporal lobectomy or op-timal medical therapy.61 The proportion of patients who were free of seizures impairing awareness at 1 year was 58% in the surgical group and only 8% in the best-medical-therapy group (P < 0.001). The proportion of patients who were free of all seizures, including aura, was 38% in the surgical group and 3% in the medical group (P < 0.001).61

Quality of life was also shown to be better in the surgical group at both 6 months and 1 year follow-ing surgery. There was no difference in psychiatric comorbidities between the 2 groups. Psychopa-thology and depression were assessed using the General Health Questionnaire and the depression scale of the Center for Epidemiological Studies, respectively. All of these instruments have demon-strated reliability and validity in assessing patients with epilepsy and were self-administered at base-line and at 3, 6, 9, and 12 months. Four patients had adverse effects from surgery. A small thalamic infarct developed in 1 patient, causing sensory ab-normalities in the left thigh; in 2 patients, there was a decline in verbal memory that interfered with the patients’ occupations at 1 year. Asymptomatic, su-perior subquadrantic visual-field defects occurred in 22 patients in the surgical group (55%), as ex-pected. No neurologic abnormalities occurred in the patients in the medical group. Depression oc-curred in 7 patients in the surgical group (18%) and 8 patients in the medical group (20%). Transient psychosis developed in 1 patient in each group. These findings strongly support the use of ante-rior temporal lobectomy over best medical therapy alone for the treatment of MTLE.

The Early Randomized Surgical Epilepsy Trial (ERSET) was a randomized, controlled clinical trial performed at 16 U.S. epilepsy surgery centers.62 The 38 MTLE patients had disabling seizures for less than 2 years, with adequate trials of 2 antisei-zure medications. Participants were randomly as-signed to ongoing trials of antiseizure drugs (medi-cal group) or to temporal resection (surgical group), and seizures were followed for 2 years. None of 23 patients in the medical group became seizure-free after 2 years of further medication trials, but 11 of 15 in the surgical group were seizure-free during year 2 of follow-up (P < 0.001). The sample was



too small to permit definitive conclusions about treatment group differences in cognitive outcomes. Adverse events in the medical group included 3 cases of status epilepticus, and in the surgical group included a postoperative stroke with only transient neurologic deficit.

Systematic reviews of the current literature dem-onstrate that even after 5 years, the proportion of seizure-free patients is preserved.63,64 Recently, attention has been paid to the seizure outcome in patients who do not become entirely seizure-free after surgery. Most such patients experience major overall seizure reduction, although in some instances the reduction in complex partial seizures is greater than the relative reduction in grand mal seizures.65,66 A more common outcome pattern is to become free of seizures that cause impaired awareness but to continue to experience isolated auras, often with aura symptoms that are similar in preoperative and postoperative periods.67 The overall effects of amygalohippocampectomy with regard to seizure freedom and semiological al-terations during seizures that recur after surgery appear rather similar to those of anterior temporal lobectomy.68

corTicEcToMy and cErEBral lEsionEcToMy

EvaluationIn approaching refractory epilepsies with features

of neocortical (non-limbic system) seizures, local-ization of the cortex with earliest ictal discharges may in some cases be sufficient to direct surgery in the absence of a cerebral lesion. In general, the localization process is more likely to be successful and the outcome of resection to be efficacious in controlling seizures when a causative lesion is im-aged with MRI.69–71 It is often quite difficult to local-ize ictal onset zones in frontal lobe limbic structures such as the insula and orbitofrontal and cingulate cortices in the absence of a lesion imaged on MRI, but subdural and intracerebral (depth) electrodes can be used to do so.72,73 Neocortical ictal onset zones on the dorsolateral surfaces of the cerebral hemispheres are readily studied with subdural grid arrays, which also support functional mapping by direct cortical electrical stimulation (as reviewed in EBRM, Volume 1 Part 217). The anatomical out-come of corticectomy is readily evaluated with MRI (figure 3).

Certain types of intracranial lesions are more likely to be epileptogenic, particularly those involv-

figure 3. Corticectomy. These T1-weighted coronal and parasagittal images show anatomical results of a resection of a frontal opercular ictal onset zone. (Adapted with permission from Proserpio P, Cossu M, Francione S, et al. Insular-opercular seizures manifesting with sleep-related paroxysmal motor behaviors: a stereo-EEG study. Epilepsia 2011;52:1787.)



ing exposure of cortex to hemosiderin or calcium (see EBRM, Volume 1, Part 315). Such lesions in-clude neoplasms (eg, astrocytoma, ganglioglioma, pleomorphic xanthoastrocytoma, and dysembryo-plastic neuroepithelial tumor), vascular lesions (eg, cavernous hemangioma and arteriovenous malformation), and dysgenetic lesions (eg, micro-dysgenesis, focal or diffuse dysplasia, Sturge-Weber syndrome, and tuberous sclerosis), or may be traumatic/ischemic in nature. Why lesions cause seizures is unknown, but seizures might occur as a consequence of synaptic reorganization or changes in extracellular ion concentration, inhibitory inter-neurons, intrinsic neuronal channels, or expression of gap junctions; or they may occur due to vascular changes or hemosiderin deposition, or in GABA or NMDA channels.

Although advances in structural and functional MRI have allowed for identification of more subtle lesions, 20% to 30% of patients with temporal epi-lepsy and 20% to 40% of those with extratemporal epilepsy have no clear lesion on currently available clinical MRI.74–76 Nonlesional, refractory partial epi-lepsies appear to be more common among frontal lobe epilepsies than in TLE.

seizure outcomeThe highest rate of seizure reduction has been

reported when there is congruence between the location of the lesion on MRI and the location of the seizure focus on EEG. Overall, electrophysi-ologically guided corticectomy in the absence of an associated MRI-defined lesion results in full seizure control in 20% to 50% of cases, while elec-trophysiologically guided corticectomy coupled with resection of an associated lesion offers full seizure control in 50% to 80% of cases, in review of multiple series.69–71 The surgical approach in such patients is then one of removing the le-

sion if one is present, and also the electrophysi-ologically defined seizure-onset zone. A recent meta-analysis by Tellez-Zenteno and colleagues77 demonstrated that the odds of being seizure-free 1 year or later after epilepsy surgery were 2.5 to 2.8 times higher in patients with a lesion identi-fied by MRI or histopathology. Certain lesions, including cavernous malformations and small focal dysplasias, appear to offer higher rates of full sei-zure control with corticectomy-lesionectomy, while large and incompletely resected malformations of cortical development and glial neoplasia are as-sociated with lower rates of postresective seizure control.78–82

corpus callosoToMy for EpilEpTic drop aTTacks in syMpToMaTic gEnEralizEd EpilEpsiEs

Seizure generalization requires bilateral syn-chrony and spread through subcortical structures, including the corpus callosum. Subtotal or staged total corpus callosotomy is used as a palliative treatment in patients with generalized tonic-clonic seizures and unresectable seizure foci and drop attacks. Drop attacks are caused by tonic or atonic seizures and can result in significant injury due to falls.

seizure outcomes and risks of surgeryCallosotomy is considered palliative, as result-

ing rates of complete seizure freedom are low. The main goals of callosotomy are to alleviate seizure severity and to eliminate drop attacks. Various studies support the finding that callosotomy results are best in patients with generalized tonic-clonic seizures and drop attacks.83–90 The relapse rate for drop attacks is low, especially following complete corpus callosotomy, with one study documenting a 13% relapse rate at 6 years after surgery.91 When



partial callosotomy was employed, 91% of patients were seizure-free at 1 year, but this dropped to 58% at 6 years. This decreased long-term efficacy of partial callosotomy has been illustrated several times.88,92,93

Complete initial corpus callosotomy engenders a higher risk of postoperative disconnection syn-drome. Symptoms of disconnection syndrome include left tactile anomia, left-sided dysprax-ia, pseudo-hemianopsia, right-sided anomia for smells, difficulty with right-hand spatial synthesis, decreased spontaneity of speech, and inconti-nence. For this reason, if a complete callosotomy is required for symptom control, it is generally staged by sectioning the anterior two-thirds first and later doing the posterior third. If patients develop dis-connection syndrome after partial callosotomy, it can resolve in a few days, but sometimes requires up to 2 to 3 months for resolution.94 Although the actual incidence is unknown, disconnection syn-drome can be permanent in those who undergo total callosotomy. This outcome is less likely with a staged procedure, however.95

Lennox-Gastaut syndrome is one form of epi-lepsy that responds favorably to corpus calloso-tomy. This syndrome usually begins between the ages of 1 and 8 years, and persists into adult-hood. It is refractory to antiepileptic medications and results in cognitive decline and behavioral problems in affected individuals. The most com-mon seizure pattern in these patients is noctur-nal tonic seizures, but others include axial tonic, atonic, atypical absence, and myoclonic seizures. The syndrome is known to result from intrauter-ine infections and vascular injury to the brain, but can also be cryptogenic in origin. The pathologi-cal basis seems to include neuronal migrational abnormalities and late effects of central nervous system infection. EEG usually demonstrates high-

voltage, bifrontal 1.5- to 2.5-Hz spike-and-wave complexes interictally and attenuation with parox-ysmal fast activity from 10 to 13 Hz during the ictal phase.96

surgical procedureModern corpus callosotomy is done with the aid

of a neuronavigational guidance system. The ap-proach is generally from the nondominant side for language, with care taken to preserve the superior sagittal sinus and large draining veins during dural incision and cerebral retraction in order to avoid significant venous infarct. Callosal sectioning is usually carried out from the posterior margin of the callosotomy to the anterior margin. The posterior border of resection typically lies within 5 cm of the callosal genu. In complete callosotomy, visualiza-tion of arachnoid covering the vein of Galen and internal cerebral veins establishes the posterior edge of resection.97

MulTiplE suBpial TransEcTion for nEocorTical EpilEpsiEs

When the seizure-onset zone is situated partly or wholly in eloquent cortex, total lesionectomy is not possible given the likelihood of postoperative neurological deficits. The technique of multiple subpial transections (MSTs) was therefore devel-oped as an option for epileptogenic lesions that are situated in eloquent cortex. Neuroanatomical studies have shown that the basic functional corti-cal unit is arranged vertically, whereas epileptic ac-tivity spreads horizontally through the cortex. From a theoretical basis, therefore, vertical incisions in the cortex can be expected to interrupt transverse synaptic connections, preventing seizures from propagating while preserving the vertical column that is critical to neuronal function. Because a minimal contiguous cortical surface area is neces-



sary for the maintenance of cortical activity, the subpial transections are separated by 5 mm, as this distance leads to spike foci becoming inde-pendent. The efficacy of MSTs as the sole surgical treatment is low, and when used today, it is gen-erally in conjunction with lesionectomy or cortical resection. However, this technique is particularly well-suited for those with Landau-Kleffner syn-drome, characterized by abrupt or subacute pre-sentation with mutism, apparent deafness, behav-ioral abnormalities, an epileptiform EEG pattern, and seizures in approximately 70% of patients.98

Multiple subpial transections seem to be effective in language recovery for these patients. There is an observed long-term recurrence rate of nearly 20% in patients who initially have a postoperative improvement.99 For this reason, MSTs are gener-ally reserved for patients in whom seizures are re-fractory and primary lesionectomy cannot be per-formed because the lesion is situated in eloquent cortex.

surgical procedureThe initial procedure was described by Morrell in

1989,100 and although there have been some small variations in the technique, the concept remains the same as when initially described (figure 4). The location of the area of interest is identified by cortical stimulation and electrocorticography prior to the start of the procedure. A fine wire with a 4- to 5-mm up-angled tip is used to puncture the cortex. Transections are placed 5 mm from each other and electrocorticography is performed intraoperatively to check for residual significant spiking, in which case further transections are carried out.101

referenceS

1. Sander JW. The epidemiology of epilepsy revisited. Curr Opin Neurol 2003;16:165–70.

2. Bell GS, Sander JW. The epidemiology of epilepsy: the size of the problem. Seizure 2001;10:306–14.

3. Nilsson L, Ahlbom A, Farahmand BY, et al. Risk factors for suicide in epilepsy: a case control study. Epilepsia 2002;43:644–51.

4. Wu YW, Shek DW, Garcia PA, et al. Incidence and mortal-ity of generalized convulsive status epilepticus in Califor-nia. Neurology 2002;58:1070–6.

5. Walczak TS, Leppik IE, D'Amelio M, et al. Incidence and

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Go to www.turner-white.com and select Epilepsy from the drop-down menu of specialties.

figure 4. Multiple subpial transection. This schematic coro-nal view shows insertion of the sectioning device in a sulcus with the arrow indicating the direction of the insertion; the in-set shows the path of withdrawal intended to slice subcortical fibers without damaging the gyral crest. (Adapted with permis-sion from Morrell F, Whisler WW, Bleck TP. Multiple subpial transection: a new approach to the surgical treatment of focal epilepsy. J Neurosurg 1989;70:231–9.)



risk factors in sudden unexpected death in epilepsy: a pro-spective cohort study. Neurology 2001;56:519–25.

6. Ficker D. Sudden unexplained death and injury in epilepsy. Epilepsia 2000;Suppl;2:S7–S12.

7. Odell C WJ, Cloyd J. The Personal and Financial Impact of repetitive or prolonged Seizures on the Patient and Family. J Child Neurol 2007;22:61S–70S.

8. Engel J Jr, Wiebe S, French J, et al. Practice parameter: temporal lobe and localized neocortical resections for epi-lepsy: 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;60:538–47.

9. Wiebe S, Jette N. Epilepsy surgery utilization: who, when, where and why? Curr Opin Neurol 2012;25:187–93.

10. Dunkley C, Kung J, Scott RC, et al. Epilepsy surgery in children under 3 years. Epilepsy Res 2011;93:96–106.

11. Murphy M, Smith PD, Wood M, et al. Surgery for temporal lobe epilepsy associated with mesial temporal sclero-sis in the older patient: a long-term follow-up. Epilepsia 2010;51:1024–9.

12. Harden CL, Meador KJ, Pennell PB, et al. Practice pa-rameter update: management issues for women with epilepsy--focus on pregnancy (an evidence-based re-view): teratogenesis and perinatal outcomes: report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and American Epilepsy Society. Neurology 2009;73:133–41.

13. Henry TR. Seizures and epilepsy: pathophysiology and principles of diagnosis. Hospital Physician Epilepsy Board Review Manual. Vol. 1, Part 1. October 8, 2012. www.epilepsy-digital.com/epilepsy/2012vol1pt1#pg1.

14. Lindsay J, Ounsted C, Richards P. Long Term outcome in children with temporal lobe seizures: IV: Genetic factors, febrile convulsions and the remission of seizures. Dev Med Child Neurol 1980;22:429–39.

15. McKinney AM IV, Henry TR. Seizures and epilepsy: structural brain imaging in chronic epilepsies. Hospital Physician Epilepsy Board Review Manual. Vol. 1, Part 3. November 5, 2012. www.epilepsy-digital.com/epilepsy/ 2012vol1pt3#pg1.

16. Blumcke I, Coras R, Miyata H, Ozkara C. Defining clinico-neuropathological subtypes of mesial temporal lobe epilepsy with hippocampal sclerosis. Brain Pathol 2012;22:402–11.

17. Sha ZY, Henry TR. Seizures and epilepsy: electrophysi-ological diagnosis. Hospital Physician Epilepsy Board Review Manual. Vol. 1, Part 2. October 22, 2012. www.epilepsy-digital.com/epilepsy/ 2012vol1pt2#pg1.

18. McKinney AM IV, Henry TR. Seizures and epilepsy: struc-

tural brain imaging in acute seizures and functional neu-roimaging in the epilepsies. Hospital Physician Epilepsy Board Review Manual. Vol. 1, Part 4. November 19, 2012. www.epilepsy-digital.com/epilepsy/ 2012vol1pt3#pg4.

19. Cendes F, Lopes-Cendes I, Andermann E, Andermann F. Familial temporal lobe epilepsy: a clinically heterogeneous syndrome. Neurology 1998;50:554–57.

20. Morita ME, Yasuda CL, Betting LE, et al. MRI and EEG as long-term seizure outcome predictors in familial mesial temporal lobe epilepsy. Neurology 2012;79:2349–54.

21. Kasperaviciute D, Catarino CB, Heinzen EL, et al. Common genetic variation and susceptibility to partial epilepsies: a genome-wide association study. Brain 2010;133:2136–47.

22. Fogarasi A TI, Jansky J, Janszky I, et al. Age-dependent seizure semiology in temporal lobe epilepsy. Epilepsia 2007;48:1697–1702.

23. Risinger MW, Engel J Jr, Van Ness PC, et al. Ictal localiza-tion of temporal seizures with scalp-sphenoidal recordings. Neurology 1989;39:1288–93.

24. Sadler RM, Goodwin J. Multiple electrodes for detect-ing spikes in partial complex seizures. Can J Neurol Sci 1989;16:326–9.

25. Nuwer MR. Recording electrode site nomenclature. J Clin Neurophysiol 1987;4:121–33.

26. Silverman D. The anterior temporal electrode and the ten-twenty system. Electroencephalogr Clin Neurophysiol 1960;12:735–7.

27. Sirven JI, Liporace JD, French JA, et al. Seizures in tem-poral lobe epilepsy: I. Reliability of scalp/sphenoidal ictal recording. Neurology 1997;48:1041–6.

28. Blum D. Prevalence of bilateral partial seizure foci and implications for electroencephalographic telemetry moni-toring and epilepsy surgery. Electroencephalogr Clin Neu-rophysiol 1994;91:329–36.

29. Berkovic SF, McIntosh AM, Kalnins RM, et al. Preoperative MRI predicts outcome of temporal lobectomy: an actuarial analysis. Neurology 1995;45:1358–63.

30. Burgerman RS, Sperling MR, French JA, et al. Com-parison of mesial versus neocortical onset temporal lobe seizures: neurodiagnostic findings and surgical outcome. Epilepsia 1995;36:662–70.

31. Garcia PA, Laxer KD, Barbaro NM, Dillon WP. Prognostic value of qualitative magnetic resonance imaging hip-pocampal abnormalities in patients undergoing temporal lobectomy for medically refractory seizures. Epilepsia 1994;35:520–4.

32. Jack CR Jr, Sharbrough FW, Cascino GD, et al. Magnetic resonance image-based hippocampal volumetry: correla-tion with outcome after temporal lobectomy. Ann Neurol 1992;31:138–46.

33. Janszky J, Janszky I, Schulz R, et al. Temporal lobe epi-



lepsy with hippocampal sclerosis: predictors for long-term surgical outcome. Brain 2005;128:395–404.

34. Jeong SW, Lee SK, Hong KS, et al. Prognostic factors for the surgery for mesial temporal lobe epilepsy: longitudinal analysis. Epilepsia 2005;46:1273–9.

35. Kilpatrick C, O'Brien T, Matkovic Z, et al. Preoperative evaluation for temporal lobe surgery. J Clin Neurosci 2003;10:535–9.

36. Immonen A, Jutila L, Muraja-Murro A, et al. Long-term epilepsy surgery outcomes in patients with MRI-negative temporal lobe epilepsy. Epilepsia 2010;51:2260–9.

37. Bell ML, Rao S, So EL, et al. Epilepsy surgery outcomes in temporal lobe epilepsy with a normal MRI. Epilepsia 2009;50:2053–60.

38. Engel J Jr, Henry TR, Risinger MW, et al. Presurgical evaluation for partial epilepsy: Relative contributions of chronic depth electrode recordings versus FDG-PET and scalp-sphenoidal ictal EEG. Neurology 1990;40: 1670–7.

39. Dupont S, Semah F, Clemenceau S, et al. Accurate pre-diction of postoperative outcome in mesial temporal lobe epilepsy: a study using positron emission tomography with 18fluorodeoxyglucose. Arch Neurol 2000;57:1331–6.

40. Newton MR, Berkovic SF, Austin MC, et al. Dystonia, clinical lateralization, and regional blood flow changes in temporal lobe seizures. Neurology 1992;42:371–7.

41. Olivier A. Transcortical selective amygdalohippocam-pectomy in temporal lobe epilepsy. Can J Neurol Sci 2000;27:S68–76.

42. Yasargil MG, Weiser HG, Valavanis A, et al. Surgery and results of selective amygdala-hippocampectomy in one hundred patients with nonlesional limbic epilepsy. Neuro-surg Clin N Am 1993;4:243–61.

43. Helmstaedter EC, Hufnagel A, Zenter J, Schramm J. Dif-ferent effects of left anterior temporal lobectomy, selective amygdalohippocampectomy, and temporal cortical lesio-nectomy on verbal learning, memory, and recognition. J Epilepsy 1996;9:39–45.

44. Helmstaedter C, Richter S, Roske S, et al. Differential ef-fects of temporal pole resection with amygdalohippocam-pectomy versus selective amygdalohippocampectomy on material-specific memory in patients with mesial temporal lobe epilepsy. Epilepsia 2008;49:88–97.

45. Haglund MM, Berger MS, Shamseldin M, et al. Cortical localization of temporal lobe language sites in patients with gliomas. Neurosurgery 1994;34:567–76.

46. Wyler AR, Hermann BP, Somes G. Extent of medial temporal resection on outcome from anterior temporal lobectomy: a randomized prospective study. Neurosurgery 1995;37:982–91.

47. McKhann GM 2nd, Schoenfeld-McNeil J, Born DE, et al.

Intraoperative hippocampal electrocorticoagraphy to pre-dict the extent of hippocampal resection in temporal lobe epilepsy surgery. J Neurosurg 2000;93:44–52.

48. Sagher O, Thawani JP, Etame AB, Gomez-Hassan DM. Seizure outcomes and mesial resection volumes following selective amygdalohippocampectomy and temporal lobec-tomy. Neurosurgical Focus 2012;32:E8.

49. Barbaro NM, Quigg M, Broshek DK, et al. A multicenter, prospective pilot study of gamma knife radiosurgery for mesial temporal lobe epilepsy: seizure response, adverse events, and verbal memory. Ann Neurol 2009;65:167–75.

50. Bartolomei F, Hayashi M, Tamura M, et al. Long-term effi-cacy of gamma knife radiosurgery in mesial temporal lobe epilepsy. Neurology 2008;70:1658–63.

51. Regis J, Bartolomei F, Rey M, et al. Gamma knife surgery for mesial temporal lobe epilepsy. Epilepsia 1999;40: 1551–6.

52. Baxendale SA, Thompson PJ, Duncan JS. Evidence-based practice: a reevaluation of the intracarotid amobar-bital procedure (Wada test). Arch Neurol 2008;65:841–5.

53. Haag A, Knake S, Hamer HM, et al. The Wada test in Austrian, Dutch, German, and Swiss epilepsy centers from 2000 to 2005: a review of 1421 procedures. Epilepsy Behav 2008;13:83–9.

54. Kemp S, Wilkinson K, Caswell H, et al. The base rate of Wada test failure. Epilepsy Behav 2008;13:630–3.

55. Loddenkemper T, Morris HH, Moddel G. Complications during the Wada test. Epilepsy Behav 2008;13:551–3.

56. Wagner HC, Hader C, Metternich B, et al. Who needs a Wada test? Present clinical indications for amobarbital pro-cedures. J Neurol Neurosurg Psychiatry 2012;83:503–9.

57. Nilsson D, Malmgren K, Rydenhag B, Frisen L. Visual field defects after temporal lobectomy-comparing meth-ods and analyzing resection size. Acta Neurol Scand 2004;110:301–7.

58. King DW, Flanigin HF, Gallagher BB, et al. Temporal lobec-tomy for partial complex seizures: evaluation, results, and 1-year follow-up. Neurology 1996;36:334–9.

59. Pilcher WH, Rusyniak WG. Complications of epilepsy sur-gery. Neurosurg Clin N Am 1993;4:311–25.

60. Walczak TS, Radtke RA, McNamara JO, et al. Anterior temporal lobectomy for complex partial seizures: evalua-tion, results, and long-term follow-up in 100 cases. Neurol-ogy 1990;40:413–8.

61. Wiebe S, Blume WT, Girvin JP, Eliasziw M. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med 2001;345:311–8.

62. Engel J Jr, McDermott MP, Wiebe S, et al. Early surgical therapy for drug-resistant temporal lobe epilepsy: a ran-domized trial. JAMA 2012;307:922–30.

63. Tellez-Zenteno JF, Dhar R, Wiebe S. Long-term seizure



outcomes following epilepsy surgery: a systematic review and meta-analysis. Brain 2005;128:1188–98.

64. Ozkara C, Uzan M, Benbir G, et al. Surgical outcome of patients with mesial temporal lobe epilepsy related to hip-pocampal sclerosis. Epilepsia 2008;49:696–9.

65. Henry TR, Drury I, Schuh LA, Ross DA. Increased second-ary generalization of partial seizures following temporal lobectomy. Neurology 2000;55: 1812–7.

66. Sarkis RA, Jehi L, Bingaman W, Najm IM. Seizure wors-ening and its predictors after epilepsy surgery. Epilepsia 2012;53:1731–8.

67. Blume WT, Girvin JP. Altered seizure patterns after tempo-ral lobectomy. Epilepsia 1997;38:1183–7.

68. Abosch A, Bernasconi N, Boling W, et al. Factors predictive of suboptimal seizure control following selective amygdalo-hippocampectomy. J Neurosurg 2002;97:1142–51.

69. Ficker DM, So EL, Mosewich RK, et al. Improvement and deterioration of seizure control during the postsurgical course of epilepsy surgery patients. Epilepsia 1999;40: 62–7.

70. Schuele SU, Luders HO. Intractable epilepsy: manage-ment and therapeutic alternatives. Lancet Neurology 2008;7:514–24.

71. Spencer S, Huh L. Outcomes of epilepsy surgery in adults and children. Lancet Neurology 2008;7:525–37.

72. Henry TR, Ross DA, Schuh LA, Drury I. Indications and outcome of ictal recording with intracerebral and subdural electrodes in refractory complex partial seizures. J Clin Neurophysiol 1999;16:426–38.

73. Proserpio P, Cossu M, Francione S, et al. Insular-oper-cular seizures manifesting with sleep-related paroxysmal motor behaviors: a stereo-EEG study. Epilepsia 2011;52: 1781–91.

74. Carne RP, O'Brien TJ, Kilpatrick CJ, et al. MRI-negative PET-positive temporal lobe epilepsy: a distinct surgically remediable syndrome. Brain 2004;127:2276–85.

75. Hong KS, Lee SK, Kim JY, et al. Pre-surgical evaluation and surgical outcome of 41 patients with non-lesional neo-cortical epilepsy. Seizure 2002;11:184–92.

76. Kutsy RL. Focal extratemporal epilepsy: clinical features, EEG patterns, and surgical approach. J Neurol Sci 1999;166:1–15.

77. Tellez-Zenteno JF, Hernandez Ronquillo L, Moien-Afshari F, Wiebe S. Surgical outcomes in lesional and non-lesional epilepsy: a systematic review and meta-analysis. Epilepsy Res 2010;89:310–8.

78. Chang EF, Wang DD, Barkovich AJ, Tihan T, et al. Predic-tors of seizure freedom after surgery for malformations of cortical development. Ann Neurol 2011;70:151–62.

79. Chung CK. Lee SK. Kim KJ. Surgical outcome of epilepsy caused by cortical dysplasia. Epilepsia 2005;46 Suppl

1:25–9.80. Sarkis RA, Jehi LE, Bingaman WE, Najm IM. Surgical

outcome following resection of rolandic focal cortical dys-plasia. Epilepsy Res 2010;90:240–7.

81. Stavrou I, Baumgartner C, Frischer JM, et al. Long-term seizure control after resection of supratentorial caverno-mas: a retrospective single-center study in 53 patients. Neurosurgery 2008;63:888–9.

82. Pondal-Sordo M, Diosy D, Tellez-Zenteno JF, et al. Epi-lepsy surgery involving the sensory-motor cortex. Brain 2006;129:3307–14.

83. Andermann F. Clinical indications for hemispherectomy and callosotomy. In: Theodore WH, ed. Surgical Treatment of Epilepsy. New York: Elsevier Science; 1992:189–99.

84. Engel J Jr, Van Ness PC, Rasmussen T. Outcome with respect to epileptic seizures. In: Engel J Jr, ed. Surgical treatment of the epilepsies. New York: Lippincott-Raven Publishers; 1993: 609–21.

85. Fuiks KS WA, Hermann BP, Somes G. Seizure outcome from anterior and complete corpus callosotomy. J Neuro-surg 1991;74:573–8.

86. Gates JR, Rosenfeld WE, Maxwell RE, Lyons RE. Re-sponse of multiple seizure types to corpus callosum sec-tion. Epilepsia 1987;28:28–34.

87. Gates JR, Wada JH, Reeves A. Reevaluation of corpus callosotomy. In: Engel J Jr, ed. Surgical treatment of the epilepsies. Philadelphia: Lippincott-Raven Publishers; 1993:637–48.

88. Maehara T, Shimizu H. Surgical outcome of corpus callos-tomy in patients with drop attacks. Epilepsia 2001;42:67–71.

89. Mamelak AN, Barbaro NM, Walker JA, Laxer KD. Corpus callosotomy: a quantitative study of the extent of resection, seizure control, and neuropsychological outcome. J Neu-rosurg 1993;79:688–95.

90. Tanriverdi T, Olivier A, Poulin N, et al. Long-term seizure outcome after corpus callosotomy: a retrospective analysis of 95 patients. J Neurosurg 2009;110:332–42.

91. Sunaga S, Shimizu H, Sugano H. Long-term follow-up of seizure outcomes after corpus callosotomy. Seizure 2009;18:124–8.

92. Pinard JM, Delalande O, Chiron C, et al. Callosotomy for epilepsy after West syndrome. Epilepsia 1999;40: 1727–34.

93. Spencer SS, Spencer DD, Williamson PD, et al. Corpus callosotomy for epilepsy. I. Seizure effects. Neurology 1988;38:19–24.

94. Fuiks KS, Wyler AR, Hermann BP, Somes G. Seizure out-come from anterior and complete corpus callosotomy. J Neurosurg 1991;74:573–8.

95. Kim DS, Yang KH, Kim TG, et al. The surgical effect of



callosotomy in the treatment of intractable seizure. Yonsei Medical J 2004;45:233-40.

96. Crumrine PK. Management of seizures in Lennox-Gastaut syndrome. Paediatr Drugs 2011;13:107–18.

97. Quinones-Hinojosa A. Schmidek and Sweets operative neurosurgical techniques. Philadelphia (PA): Elsevier Saun-ders; 2012.

98. Irwin K, Birch V, Lees J, et al. Multiple subpial transec-tion in Landau-Kleffner Syndrome. Dev Med Child Neurol

2001;43:248–52.99. Orbach D, Romanelli P, Devinsky O, Doyle W. Late seizure

recurrence after multiple subpial transections. Epilepsia 2001;42:1316–9.

100. Morrell F, Whisler WW, Bleck TP. Multiple subpial transec-tion: a new approach to the surgical treatment of focal epilepsy. J Neurosurg 1989;70:231–9.

101. Mulligan LP, Spencer DD, Spencer SS. Multiple subpial transections: the Yale experience. Epilepsia 2001;42:226–9.

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