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The Neurosurgical Treatment of Epilepsy
William O. Tatum, IV, DO;
Selim R. Benbadis, MD;
Fernando L. Vale, MD
Arch Fam Med. 2000;9:1142-1147.
ABSTRACT
Despite the new advancements in antiepileptic drug development, thousands of people with epilepsy will remain intractable to medication. For a considerable proportion of these people, epilepsy surgery is a consideration for better control of their seizures. Resective surgery is now standard practice for patients with medication-refractory epilepsy. Temporal lobectomy continues to be the most common surgery performed. Once patients fail 2 to 3 optimal trials of antiepileptic medication, further drug therapy offers a minimal number of patients freedom from seizures. In contrast, temporal lobectomy in carefully selected patients may result in seizure-free outcomes in more than 70% to 90% of patients with intractable seizures. As technology and drug availability increases in the new millennium, it is important for the primary care physician to be aware of epilepsy surgery as a means to treat patients with antiepileptic drug–refractory epilepsy.
INTRODUCTION
Of 150 000 people who develop epilepsy each year, 20% have seizures that are medically intractable.1 At a population level, epilepsy that is manifest by complex partial seizures is the most frequently occurring single seizure type and comprises up to 55% of adult seizures2 with a cumulative incidence of 3% by age 75 years.3 Temporal lobe epilepsy is common, with large surgical centers reporting 70% to 85% of complex partial seizures originating in the temporal lobes.4 Patients with temporal lobe epilepsy may be remarkably resistant to treatment with antiepileptic drugs.5 Complex partial seizures demonstrate impairment of consciousness, automatisms, and focal epileptiform discharges on electroencephalogram (EEG) recordings. Poorly controlled seizures may result in treatment with 2 or more antiepileptic drugs, clinical toxic effects, continued seizures, and subsequent deterioration of educational, psychosocial, and cognitive skills.6-7 With the frequency of temporal lobe–complex partial seizures, it is of no surprise that the temporal lobes are the most common target in epilepsy surgery.8 Surgery performed after medical intractability may limit the deterioration in quality of life.9-11
SURGICAL CANDIDACY
When medical management has failed, surgery should be considered.12-13 There are several caveats that favor surgical referral. First, the seizures are disabling and intractable to high therapeutic levels of first-line antiepileptic drugs. Second, if resective surgery is considered, a well-defined epileptogenic zone must be localized. Additionally, the epileptogenic zone must be surgically accessible and in a functionally silent cortex.
MEDICAL INTRACTABILITY
Before surgery is considered, a patient must meet the basic premise of medical intractability. Exclusion of nonepileptic seizures and patient noncompliance that may be responsible for apparent "intractability" are necessary starting points.14 Stability of the epileptogenic zone must be established. At least 2 years of a persistent and stable epilepsy pattern are generally required to ensure that several major antiepileptic drugs have been pushed to their therapeutic limits and that the likelihood of spontaneous improvement has diminished.15 A toxic dose cannot be defined as one that is beyond a certain predetermined laboratory range, but rather as one that produces evidence of clinical toxic effects. This is highly individualized. Medical intractability is not only seizure persistence to maximal tolerated antiepileptic drug doses, but includes adverse effects or idiosyncratic reactions (ie, rash) that prevent efficacious use. Aggressive monotherapy may be superior to polypharmacy in some patients.16 Improved seizure control, better tolerability, reduced drug interaction and expense, and better compliance are benefits of monotherapy.
When considering neurosurgical intervention for intractable epilepsy, it is important to understand that social disability and the effect of the patient seizure type(s) are unique to each individual. Some patients may be medically intractable but well compensated, while others, owing to physical, mental, or emotional ramifications, may derive only marginal overall benefit. Patients with refractory, disabling, complex partial seizures of a single and stereotyped behavior and a unilateral temporal epileptiform discharge noted on EEG readings are the best candidates for surgery. The patients who should be referred for epilepsy surgery early in the course of treatment are those in whom there is a lesion identified on neuroimaging studies. Psychosis or serious psychiatric problems are a relative contraindication. Likewise, patients with limited support at home, or for whom control of the seizures will make little difference are probably less appropriate candidates for surgery. Severely retarded individuals, those with only minor motor seizures or simple partial seizures, or those with difficulty cooperating throughout the presurgical process are limited candidates for resective surgery.
PRESURGICAL EVALUATION
The goal of the presurgical evaluation is to characterize the seizure type(s) and ascertain from where they originate in the brain to best determine the precise neurosurgical approach to treatment. When hemispherectomy is considered, presurgical evaluation needs to identify the hemisphere involved. If the epileptogenic zone seems to be multifocal or so diffuse, vagus nerve stimulation or section of the corpus callosum to inhibit seizures or their spread may help limit seizures and their consequences. The presurgical evaluation in these situations need only exclude focal excision as a treatment. For focal excision, lateralization and localization of the epileptogenic zone must be known. In addition, the extent and relationship of the functional cortex surrounding the region being considered for ablation must be known.
MAGNETIC RESONANCE IMAGING
Magnetic resonance imaging (MRI) of brain anatomy is the most important imaging technique used during preoperative evaluation. The principal role is to anatomically localize the epileptogenic zone. Regarding partial epilepsy, MRI is clearly superior to computed tomography scanning in the detection of structural lesions.17-18 High-resolution techniques and specialized sequences augment routine imaging with MRI. Using thin-section coronal images and special sequences that include fluid-attenuated inversion recovery sequences, mesial temporal focal pathological features are more distinct.19 Gadolinium–diethylenetriamine pentaacetic acid does not enhance detection of small lesions in patients with epilepsy and should be used only when a mass lesion or breakdown of the blood-brain barrier is present.20 Magnetic resonance imaging has an overall sensitivity of 86% compared with the simple use of surgical pathologic findings.21
Magnetic resonance spectroscopy is a neuroimaging technique that uses the same instruments as MRI but incorporates specially designed software to noninvasively measure the chemical components of the tissue that has been imaged. Its role is to develop a chemical spectra that is displayed on film media to measure in vivo cellular metabolism. Magnetic resonance spectroscopy can reliably lateralize and detect neuronal loss and glial proliferation in intractable temporal lobe epilepsy.22 Proton magnetic resonance spectroscopy measures N-acetylaspartate, which reflects neuronal activity and lateralizes subtle neurochemical abnormalities not noted with standard quantitative MRI.23
Functional MRI (fMRI) also uses the same instrument as MRI but measures rapid variations in cerebral blood flow using blood oxygenation level–dependent contrast to visualize task-specific changes in regional cerebral blood flow and metabolic function. Functional MRI has been shown to remain in agreement with the Wada test in correctly lateralizing language function.24 Detecting asymmetries in memory activation can also be shown using fMRI.25 Together, the successful lateralization of language and memory promises fMRI to become a noninvasive alternative to the Wada test.
FUNCTIONAL NEUROIMAGING
While various functional imaging modalities have been used in the study of partial epilepsy, positron emission tomography (PET) using fluorodeoxyglucose has assumed the bulk of use. With PET scanning, unilateral hypometabolism, usually in the temporal lobe, is found in 70% to 80% of patients with complex partial seizures.25 Scans using PET during the seizures (ictal) have not been as accurate owing to the imaging of regions of seizure propagation, as well as the altered peri-ictal metabolic patterns imaged. Single-photon emission computed tomography (SPECT) to measure regional cerebral blood flow or receptor binding is more readily available and features a reproducible and reliable localizing capability. While focal interictal hypoperfusion is unreliable, ictal SPECT correlates very well with seizure onset, making this technique a more practical approach than PET.26-27
VIDEO EEG MONITORING
Seizure Behavior
Closed-circuit television with videotaping and simultaneous EEG record allows the documentation, storage, and review of the seizures. Recording 3 or more seizures is the standard practice in some centers during presurgical evaluation. Video EEG monitoring for 3 to 7 days may be necessary. The characteristics of the aura and seizure behavior (semiology) of partial seizures help to localize brain regions of seizure origin. The hemispheric lateralization or lobar localization value of auras, motor patterns, or automatisms suggest the site of the seizure's origin or later propagation.28 Useful lateralizing features include unilateral clonic activity, dystonic posturing, or tonic posturing, and these findings denote a contralateral seizure origin in most patients. Speech during a seizure suggests a focus contralateral to the language-dominant hemisphere. Unilateral automatisms suggest ipsilateral seizure onset. Sustained forced head rotation for longer than 10 seconds prior to secondarily generalized tonicoclonic seizures is a highly reliable sign for seizure onset contralateral to the seizure focus.
Scalp EEG Recording
Electroencephalogram monitoring with recording electrodes attached to the scalp is performed initially to obtain interictal (between seizures) and ictal (during seizures) information regarding seizure onset. Scalp-based monitoring using extracranial electrodes is essential to verify that the seizures are indeed epileptic and to help localize the zone of seizure onset. Because many epileptic foci lie in the medial temporal, basal temporal, or basal frontal areas distant from the scalp, special electrodes may provide additional useful data. Sphenoidal electrodes are commonly used given their inferior frontotemporal position subserved, suitability for long-term EEG monitoring, and less tendency for artifact (as compared with nasopharyngeal electrodes). Electroencephalogram morphological activity during seizures is variable, can begin after clinical onset, and may be obscured by artifact. Most patients with temporal lobe seizures have anterior temporal interictal spikes.29 While the reliability of using scalp EEG monitoring for ictal localization has been questioned, one study30 comparing scalp EEG monitoring and depth electrodes on intracranial recording found that unilateral temporal and sphenoidal ictal patterns strictly defined and correctly predicted findings from the depth recordings in 82% to 94% of cases. Scalp and sphenoidal recordings are subject to error and false lateralization on occasion and should never be used in isolation for presurgical localization. When a gross structural lesion is known to exist, it should be suspected to be the cause until proven otherwise, even when extracranial EEG evidence points to the contrary.31 Most patients with unilateral temporal lobe epilepsy have bitemporal epileptiform discharges on EEG and need not be eliminated from the surgical selection process.32 Surgery for epilepsy can be performed without implanted or intracranial electrodes if scalp EEG localization is appropriate for the video-observed clinical seizures in association with supporting evidence from neuroimaging, neuropsychological testing, and Wada testing.
Intracranial EEG Recording
When localization from scalp EEG is not obtained, invasive recordings may be required for definitive localization.33 Surgically implanted indwelling intracranial electrodes record EEG readings to identify the seizure focus so that resective surgery can be performed. Intracranial electrodes are commonly depth probes implanted directly into the brain parenchyma or subdural space. Grid or strip electrodes enmeshed in plastic record from the brain surface. Other arrays of electrodes include pegs, strips, and grids. Spikes are frequent and are usually multifocal in the intracranial EEG reading.34 When an intracranial EEG recording is used, analysis of the seizure recordings supplies the critical pieces of information. All types of intracranial electrodes lie closer to the anticipated generator and are implanted in an arrangement based on the noninvasive clinical workup. It is difficult to compare one electrode type with another because of the heterogeneity of individual patients. Depth and subdural strip electrodes are often used and have been used together. Comparison of bilateral depth recordings and simultaneous subdural temporal strip recordings showed that subdural strips alone may fail to localize seizure onset in some patients with seizures localized by depth EEG.35-36 Additionally, electrical brain stimulation may be performed using subdural strips or grids to help localize functional cortical regions and devise a preoperative functional brain map.
NEUROPSYCHOLOGICAL EVALUATION AND THE INTRACAROTID AMOBARBITAL PROCEDURE (WADA TEST)
Neuropsychological evaluation is routinely performed as part of the presurgical evaluation to aid in the preoperative localization of cerebral dysfunction. A variety of selected cognitive, language, and memory tests are performed such that the results of all tests combined form a pattern that may point to the dysfunctional cortical region(s). Initial memory and language evaluations are subsequently evaluated with the Wada (intracarotid sodium amobarbital) test. This procedure involves the temporary chemical inactivation of each hemisphere by injection of amobarbital into the carotid artery, with testing of memory and language function in the "awake" hemisphere. While initially used to predict the site of language function, prediction of postoperative memory function and seizure outcome is a principal role.37
SURGERY
The largest group of surgical candidates comprises patients with complex partial seizures of temporal lobe origin.1 The term temporal lobectomy describes various surgical procedures directed at the temporal lobe. An en bloc anterior temporal lobectomy is a standardized operative technique at which excision of the anterior medial temporal lobe in a single block of tissue occurs. It begins with suction aspiration through the temporal horn exposing the amygdala and the anterior aspect of parahippocampal gyrus and hippocampus, which is then removed.38 Variations include resection based on intraoperative EEG, anteromedial temporal lobectomy with limited lateral resection, and more restricted removal of the amygdala and hippocampus only (amygdalohippocampectomy). Intraoperative electrocorticography records EEG readings obtained from the cortex and may define a zone of frequent interictal spiking. However, "chasing spikes" has not been convincingly shown to improve outcomes of resective epilepsy surgical procedures. Identification of the primary motor cortex using cortical stimulation or evoked potentials is preferable if localization of rolandic motor areas is needed. The most common cause of failure of temporal lobectomy is inadequate medial temporal lobe excision.39 Extratemporal epilepsies typically require more invasive recordings for definitive localization and are based on clinical and ancillary data (eg, interictal EEG abnormalities, MRI, PET).
HEMISPHERECTOMY
In children with congenital or postencephalitic hemiplegia, hemispherectomy usually dramatically arrests focal motor and generalized convulsive seizures. Total anatomic hemispherectomy has given rise to functional hemispherectomy, which is anatomically incomplete but physiologically complete with the removal of the central and temporal portion of the hemisphere and severing of all commissural projections connecting the hemisphere.40
CORPUS CALLOSAL SECTION
Corpus callosotomy (of a partial or complete section of the corpus callosum) is often a palliative form of epilepsy surgery. Recurrent seizure-related injury and morbidity related to generalized tonic or atonic seizures (drop attacks) respond best.41 Corpus callosal section to limit seizure injury may be helpful in patients for whom resective surgery is inappropriate (multifocal or widespread epileptogenicity) or impractical owing to severe mental dysfunction.
VAGUS NERVE STIMULATION
Vagus nerve stimulation is an alternative to brain surgery. It uses a nonpharmacologic, surgically implanted device for patients with drug-resistant seizures via intermittent electrical stimulation of the left vagus nerve. Vagus nerve stimulation involves the surgical placement of a generator (similar to a cardiac pacemaker) in the chest with electrodes connected subcutaneously to the vagus nerve in the neck. Intermittent electrical stimulation occurs at preprogrammed cycle rates. Settings involving current, frequency, and duration of stimulation are regulated by a computer. Standard stimulus settings for an electrical current that is delivered for 30 seconds every 5 minutes may be adjusted. Approximately 30% to 40% of patients experienced a 50% seizure reduction.42-43 As with corpus callosotomy, a relatively limited number of patients are rendered seizure free. Though approved for use in patients older than 12 years, efficacy in children and patients with symptomatic generalized epilepsy seems particularly promising. Hoarseness, throat pain, coughing, and tingling at the electrode site are potential adverse effects experienced during the time of stimulation. No cardiac or pulmonary residual effects have been noted.42, 44 Unlike antiepileptic drugs, systemic and idiosyncratic adverse effects have not been noted. A favorable attribute is 100% compliance and the potential for concomitant drug reduction.45
OUTCOME
Patients with temporal lobectomy, extratemporal resection, hemispherectomy, corpus callosotomy, or vagus nerve stimulation have different pathologic mechanisms, surgical approaches, complications, and outcomes. A 4-level outcome classification for resective surgery has been proposed by Engel46: class 1, seizure-free with or without auras; class 2, rare seizures ("almost seizure free"); class 3, worthwhile postoperative improvement (>90% reduction from preoperative frequency); and class 4, no worthwhile improvement.4, 46 Several large published series have documented seizure outcomes with 70% to 90% seizure-free rates, with prolonged efficacy seen at 5-years' follow-up.47-48 Patients with temporal lobe epilepsy as well as certain subgroups such as those with structural lesions typically have higher seizure-free rates. Limiting the deleterious effects of seizures on educational, social, behavioral, and cognitive functioning early on in the course of refractory epilepsy, may result in marked gains in pediatric epilepsy surgery.49
COMPLICATIONS
The mortality rate following temporal lobe resection is less than 1%.50 Visual field defects are not uncommon following temporal lobectomy; however, patients rarely notice visual dysfunction. Up to 30% may experience mild naming and verbal problems as a result of surgery in the language-dominant hemisphere, with fewer than 2% of patients encountering permanent or denser speech difficulties.50 Hemiparesis seen in 5% of older series has been reported in fewer patients recently.50 Patients with good postoperative seizure control have had improvement in full-scale IQ tests regardless of the side of the brain on which surgery is performed, whereas those with poorly controlled seizures incurred little change or mild losses.51 Several variables modulate the frequency and severity of memory deficits. Favorable seizure control, nature and extent of resection, dominance, and baseline function or dysfunction all affect individual outcome.
Hemispherectomy previously performed with complete anatomic hemispheric evacuation yielded major morbidity and mortality in patients and has been significantly reduced using a "functional" approach to incompletely remove an entire hemispere.40 While complications of infection, hemorrhage, and hydrocephalus can occur, these potential complications are affected based on the volume involved in resection. Complications of corpus callosal section have included transient left-sided neglect, apraxia, mutism or stuttering, cerebral infarction, hemorrhage, or infrequently, death.
In conclusion, epilepsy surgery should be considered for certain patients with complex partial seizures that are poorly controlled by antiepileptic drugs. While the development of new antiepileptic drugs to appear in the new millennium brings the hope of new and improved efficacy and tolerability, the number of patients with intractable seizures will remain high. For certain patients, resective surgical procedures for temporal lobe epilepsy, epilepsy with a lesion on neuroimaging studies, and hemispherectomy are subpopulations of patients for whom surgery is an early consideration. A team approach to the neurosurgical treatment of epilepsy is essential. An understanding of the surgical evaluation and a close working relationship with the primary care physician as part of the epilepsy surgery team is crucial for cohesive and successful management of epilepsy.
AUTHOR INFORMATION
Accepted for publication September 11, 2000.
Corresponding authors and reprints: William O. Tatum IV, DO, 13801 Bruce B. Downs Blvd, Suite 401, Tampa, FL 33613 (e-mail: WOTIV{at}aol.com).
From the Departments of Neurology (Drs Tatum and Benbadis) and Neurosurgery (Drs Benbadis and Vale), Tampa General Hospital Epilepsy Center, University of South Florida, Tampa.
REFERENCES
| |
1. National Institutes of Health Consensus Development Conference Statement: Surgery for Epilepsy, March 19-21, 1990. Epilepsia. 1990;31:806-812.
ISI
| PUBMED
2. Lechtenberg R. Types of seizures and classes of epilepsy. In: Seizure Recognition and Treatment. New York, NY: Churchill-Livingstone; 1990:36-41.
3. Hauser WA, Hesdorffer DC. Epilepsy: Frequency, Causes, and Consequences. New York, NY: Demos Medical Publishing; 1990.
4. Cahan LD, Sutherling W, McCullough MA, Rausch R, Engel J Jr, Crandall PH. Review of the 20-year UCLA experience with surgery for epilepsy. Cleve Clin Q. 1984;51:313-318.
ISI
| PUBMED
5. Mattson RH, Cramer JA, Collins JF, et al. Comparison of carbamazepine, phenobarbital, phenytoin, and primidone in partial and secondarily generalized tonic-clonic seizures. N Engl J Med. 1985;313:145-151.
ABSTRACT
6. Aldenkamp AP, Alpherts WC, Sandstedt P, et al. Antiepileptic drug-related cognitive complaints in seizure-free children with epilepsy before and after drug discontinuation. Epilepsia. 1998;39:1070-1074.
FULL TEXT
|
ISI
| PUBMED
7. Nichols ME, Meador KJ, Loring DW. Neuropsychological effects of antiepileptic drugs: a current perspective. Clin Neuropharmacol. 1993;16:471-484.
ISI
| PUBMED
8. Penfield W, Flanigin H. Surgical therapy of temporal lobe seizures. Arch Neurol Psychiatry. 1950;64:491-500.
FREE FULL TEXT
9. Vickrey BG, Hays RD, Engel J Jr, et al. Outcome assessment for epilepsy surgery: the impact of measuring health-related quality of life. Ann Neurol. 1995;37:158-177.
FULL TEXT
|
ISI
| PUBMED
10. Devinsky O, Cramer JA. Quality of life in epilepsy. Epilepsia. 1993;34(suppl 4):S4-S70.
11. Engel J Jr. Outcome with respect to epileptic seizures. In: Engel J Jr, ed. Surgical Treatment of the Epilepsies. New York, NY: Raven Press; 1987:553-572.
12. Ward AA Jr. Perspectives for surgical therapy of epilepsy. In: Ward AA Jr, Penry JK, Purpura D, eds. Epilepsy. New York, NY: Raven Press; 1983:371-390.
13. Wyllie E. Focal cortical resections: general principles. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. Philadelphia, Pa: Lea & Febiger; 1993:999-1008.
14. Lindsay J, Ounsted C, Richards P. Long-term outcome in children with temporal lobe seizures, IV: genetic factors, febrile convulsions and remission of seizures. Dev Med Child Neurol. 1980;22:429-440.
ISI
| PUBMED
15. Kutt H. Relation of plasma concentration to seizure control. In: Woodbury DM, Penry JK, Pippenger CE, eds. Antiepileptic Drugs. New York, NY: Raven Press; 1982:241-246.
16. Lesser RP, Pipenger CE, Luders H, Dinner DS. High dose monotherapy in treatment of intractable seizures. Neurology. 1984;34:707-711.
FREE FULL TEXT
17. Boon P, Williamson P. Presurgical evaluation of patients with partial epilepsy: indications and evaluation techniques for resective surgery. Clin Neurol Neurosurg. 1989;91:3-11.
FULL TEXT
|
ISI
| PUBMED
18. Sperling MR, Wilson G, Engel J Jr, Babb TW, Phelps M, Bradley W. Magnetic resonsance imaging in intractable partial epilepsy: correlative studies. Ann Neurol. 1986;20:57-62.
FULL TEXT
|
ISI
| PUBMED
19. Jack CR, Rydberg CH, Krecke KN, et al. Mesial temporal sclerosis: diagnosis with fluid-attenuated inversion-recovery versus spin-echo MR imaging. Radiology. 1996;199:367-373.
FREE FULL TEXT
20. Cascino GD, Hirschorn KA, Jack CR, Sharbrough FW. Gadolinium-DTPA-enhanced magnetic resonance imaging in intractable partial epilepsy. Neurology. 1989;39:1115-1118.
FREE FULL TEXT
21. Bronen RA, Fulbright RK, Spencer DD, et al. Refractory epilepsy: comparison of MR imaging, CT, and histopathologic findings in 117 patients. Radiology. 1996;201:97-105.
FREE FULL TEXT
22. Cendes F, Andermann F, Preul PC, Arnold DL. Lateralization of temporal lobe epilepsy based on regional metabolic abnormalies in proton MRS. Ann Neurol. 1994;35:211-216.
FULL TEXT
|
ISI
| PUBMED
23. Kuzniecky R, Hugg J, Hetherington H, et al. Relative utility of 1H spectroscopic imaging and hippocampal volumetry in lateralization of mesial temporal lobe epilepsy. Neurology. 1998;51:66-71.
FREE FULL TEXT
24. Binder JR, Swanson SJ, Hammeke TA, et al. Determination of language dominance using functional MRI: a comparison with the Wada test. Neurology. 1996;46:978-984.
FREE FULL TEXT
25. Detre JA, Maccotta L, King D, et al. Functional MRI lateralization of memory in temporal lobe epilepsy. Neurology. 1998;50:926-932.
FREE FULL TEXT
26. Newton MR, Berkovic SF, Austin MC, Rowe CC, McKay WJ, Bladin PF. SPECT in the localization of extratemporal and temporal seizure foci. J Neurol Neurosurg Psychiatry. 1995;59:26-30.
FREE FULL TEXT
27. Tatum WO, Sperling M, O'Connor M. Interictal SPECT in the presurgical evaluation of intractable partial epilepsy. Epilepsia. 1990;31:670-671.
28. Marks WJ Jr, Laxer KD. Semiology of temporal lobe seizures: value in lateralizing the seizure focus. Epilepsia. 1998;39:721-726.
FULL TEXT
|
ISI
| PUBMED
29. Goodin DS, Aminoff MJ, Laxer KD. Detectin of epileptiform activity by different noninvasive EEG methods in complex partial epilepsy. Ann Neurol. 1990;27:330-334.
FULL TEXT
|
ISI
| PUBMED
30. Risinger MW, Engel J Jr, Van Ness PC, Henry TR, Crandall PH. Ictal localization of temporal lobe seizures with scalp/sphenoidal recordings. Neurology. 1989;39:1288-1293.
FREE FULL TEXT
31. Sammaritano M, deLotbiniere A, Andermann F, et al. False lateralization by surface EEG of seizure onset in patients with temporal lobe epilepsy and gross focal cerebral lesions. Ann Neurol. 1987;21:361-369.
FULL TEXT
|
ISI
| PUBMED
32. So N, Olivier A, Andermann F, Gloor P, Quesney LF. Results of surgical treatment in patients with bitemporal epileptiform abnormalities. Ann Neurol. 1989;25:432-439.
FULL TEXT
|
ISI
| PUBMED
33. Spencer SS. Selection of candidates for invasive monitoring. In: Cascino GD, Jack CR, eds. Neuroimaging in Epilepsy: Principles & Practice. Newton, Mass: Butterworth-Heinemann; 1996:216-234.
34. 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;40:1670-1677.
FREE FULL TEXT
35. Spencer SS, Spencer DD, Williamson PD, Mattson R. Combined depth and subdural electrode investigation in uncontrolled epilepsy. Neurology. 1990;40:74-79.
FREE FULL TEXT
36. Sperling MR, O'Connor MJ. Comparison of depth and subdural electrodes in recording temporal lobe seizures. Neurology. 1989;39:1497-1504.
FREE FULL TEXT
37. Sperling MR, Saykin AJ, Glosser G, et al. Predictors of outcome after anterior temporal lobectomy: the internal carotid amobarbital test. Neurology. 1994;44:2325-2330.
FREE FULL TEXT
38. Crandall PH. Standard en bloc anterior temporal lobectomy. In: Spencer SS, Spencer DD, eds. Surgery for Epilepsy. Boston, Mass: Blackwell Scientific Publications; 1991:118-129.
39. Wyler AR, Herman BP, Richey ET. Results of reoperation for failed epilepsy surgery. J Neurosurg. 1989;71:815-819.
ISI
| PUBMED
40. Villemure JG. Anatomical to functional hemispherectomy from Krynauw to Rasmussen. Epilepsy Res Suppl. 1992;5:209-215.
PUBMED
41. Nordgren RE, Reeves AG, Viguera AC, Roberts DW. Corpus callosotomy for intractable seizures in the pediatric age group. Arch Neurol. 1991;48:364-372.
FREE FULL TEXT
42. Handforth A, DeGiorgio CM, Schacter SC, et al. Vagus nerve stimulation therapy for partial-onset seizures: a randomized active-control trial. Neurology. 1998;51:48-55.
FREE FULL TEXT
43. Handforth A, DeGiorgio CM, Schachter SC, et al. Vagus nerve stimulation therapy for partial-onset seizures: a randomized active-control trial. Neurology. 1998;51:48-55.
44. Tatum WO, Moore DB, Stecker MM, et al. Ventricular asystole during vagus nerve stimulation for epilepsy in humans. Neurology. 1999;52:1267-1269.
FREE FULL TEXT
45. Tatum WO, Ferreira JA, Benbadis SR, Vale FL. Vagus nerve stimulation and antiepileptic drug reduction [abstract]. Epilepsia. 1999;40:223.
46. Engel J Jr. Outcome with respect to epileptic seizures. In: Engel J Jr, ed. Surgical Treatment of the Epilepsies. New York, NY: Raven Press; 1987:553-571.
47. Sperling MR, O'Connor MJ, Saykin AJ, Plummer C. Temporal lobectomy for refractory epilepsy. JAMA. 1996;276:470-475.
FREE FULL TEXT
48. Engel J Jr. The timing of surgical intervention for mesial temporal lobe epilepsy. Arch Neurol. 1999;56:1338-1341.
FREE FULL TEXT
49. Benbadis SR, Chelune GL, Stanford LD, Comair YG. Outcome and complications of epilepsy surgery. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. 2nd ed. Baltimore, Md: Williams & Wilkins; 1996:1103-1118.
50. Jensen I. Temporal lobe surgery around the world: results, complications and mortality. Acta Neurol Scand. 1975;52:354-373.
FULL TEXT
|
ISI
51. Katz A, Awad I, Kong A, Chelune G. Extent of resection in temporal lobectomy for epilepsy, II: memory changes and neurologic complications. Epilepsia. 1989;30:763-771.
ISI
| PUBMED
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