home : about us : ahead of print : current issue : archives search instructions : subscriptionLogin 
Users online: 158      Small font sizeDefault font sizeIncrease font size Print this page Email this page


 
INVITED REVIEW
Year : 2008  |  Volume : 3  |  Issue : 1  |  Page : 74-81
 

Presurgical evaluation of epilepsy


1 Department of Neurosurgery, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, India
2 Department of Neurology, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad, India

Correspondence Address:
Manas Panigrahi
Dept. of Neurosurgery, Nizam's Institute of Medical Sciences, Punjagutta, Hyderabad
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1817-1745.40593

Rights and Permissions

 

   Abstract 

The objective of the multimodality presurgical evaluation in patients with refractory epilepsy is to establish sufficient concordance among the various investigations. There should be maximum overlap in the epileptogenic zone, the irritative zone, the ictal onset zone, the functional deficit zone and the symptomatogenic zone. The ictal and interictal electroencephalogram measures the localization of epileptiform discharges, which should be concordant with structural abnormalities noted on MRI brain and functional abnormalities in the form of a zone of hypometabolism on fluorodeoxyglucose positron emission tomography, interictal single photon emission computerized tomography (SPECT) or hyperperfusion of the epileptogenic zone on ictal SPECT for a good surgical outcome. There should be no conflicting data from any of these studies, neuropsychological evaluation or seizure semiology.


Keywords: Epilepsy surgery, epileptogenic zone, electroencephalography, imaging


How to cite this article:
Panigrahi M, Jayalakshmi SS. Presurgical evaluation of epilepsy. J Pediatr Neurosci 2008;3:74-81

How to cite this URL:
Panigrahi M, Jayalakshmi SS. Presurgical evaluation of epilepsy. J Pediatr Neurosci [serial online] 2008 [cited 2017 Apr 30];3:74-81. Available from: http://www.pediatricneurosciences.com/text.asp?2008/3/1/74/40593



   Introduction Top


Approximately 60% of all patients with epilepsy suffer from focal epilepsy syndromes. In about 15% of these patients, the seizures are not adequately controlled with anticonvulsive drugs and such patients are potential candidates for surgical treatment. [1] The average seizure-free rate after epilepsy surgery is ~60% in large epilepsy centers. The goals of presurgical evaluation are [2] 1. to establish the diagnosis of epileptic seizures, 2. define the electro-clinical syndrome, 3. delineate the lesion(s) responsible for the seizures, 4. evaluate the past antiepileptic drug (AED) treatments and make sure that an adequate medical treatment had been provided, 5. select ideal surgical candidates with optimal electro-clinico-radiologic correlation, 6. ensure that the surgery will not result in disabling neuropsychological deficits.


   Aim and Concept of Surgery for Epilepsy Top


The main aim of presurgical evaluation in patients with intractable epilepsy is the identification of the cortical area capable of generating seizures and whose removal or disconnection will result in seizure freedom. This area is called the epileptogenic zone. [3] Different diagnostic tools are being used by epileptologists to identify different cortical zones - symptomatogenic zone, irritative and ictal onset zones, epileptogenic lesion and functional deficit zone, each one of which is more or less a precise index of the epileptogenic zone [4] [Table - 1]. In the ideal surgical candidate, all five zones will show a high degree of overlap, and the resection can be performed with high likelihood of seizure freedom; but in most patients, the different cortical zones are somewhat discordant in location or extent and the final decision about surgery should be taken after careful weighing of the significance of each one of these areas, based on the information provided in various investigations.

The current diagnostic techniques used in the definition of these cortical zones are video electroencephalography (EEG) monitoring, magnetic resonance imaging (MRI), ictal single photon emission computerized tomography (SPECT) and positron emission tomography (PET). A detailed neuropsychological evaluation is an indispensable tool for prognosis of neuropsychological deficits after surgery and may significantly influence the final decision about surgery. [5] The intracarotid amobarbital procedure (Wada test) provides additional information about lateralized deficits and may help to localize the epileptogenic zone. [6],[7] Interictal SPECT is less reliable than interictal PET for identifying dysfunctional cortex with hypometabolism. 1 H magnetic resonance spectroscopy ( 1 H MRS) provides information about metabolic derangement and may be used as an adjunctive to the other data. Magnetoencephalography (MEG) can complement the scalp EEG data in defining the extent and location of the epileptogenic zone. [8]


   Role of Imaging in the Presurgical Evaluation of Epilepsy Top


The goals of neuroimaging in patients with medically refractory epilepsy are 1. delineation of structural and functional abnormalities in the suspected epileptogenic region, 2. prediction of nature of structural pathology, 3. detection of abnormalities distant from the epileptogenic region (dual pathology) and 4. identification of eloquent brain regions such as language, memory and sensorimotor areas and the relation of these regions to the epileptogenic region. [9],[10] The images should be reviewed by radiologists specially interested and experienced in the evaluation of patients with epilepsy.


   Structural Imaging Top


Magnetic resonance imaging

The common abnormalities identified by MRI in patients with refractory epilepsy are mesial temporal atrophy and sclerosis (MTS), malformations of cortical development, primary brain tumors, vascular malformations and focal atrophic lesions. The structural MRI protocol for patients with chronic epilepsy is summarized in [Table - 2]. [11]

In mesial temporal sclerosis and atrophy, the hippocampus is best visualized by acquiring thin slices (1-3 mm) orthogonal to its long axis. The important MRI features of MTS are:

  1. Abnormal increased signal of hippocampus and amygdala relative to other gray matter on T2 W images
  2. Atrophic changes in hippocampus/amygdala or temporal lobe in T1 W images
  3. Abnormal increased signal in gray/white matter of the temporal lobe relative to the gray matter elsewhere
  4. Atrophy of ipsilateral fornix
  5. Dilatation of the temporal horn
  6. Blurring of gray and white matter margin in the temporal neocortex


In addition, there may be lesions associated with ipsilateral MTS, such as migrational disorders, porencephalic cysts and neoplasms (dual pathology). [10]

MTS has been classified into four groups as follows. [12] Group 1 - high T2 W signal and atrophy of hippocampus/amygdala with atrophy of temporal lobe [Figure - 1]; Group 2 - high T2 W signal and atrophy of hippocampus/amygdala only; Group 3 - high signal in hippocampus/amygdala without atrophy; and Group 4 - hippocampal/amygdalar atrophy only without T2 W signal changes. Visual assessment may reliably detect hippocampal volume asymmetry of more than 20%; however, lesser degrees of asymmetry require quantitative volumetric analysis. [13] Quantification of T2 relaxation time is an objective way to assess hippocampal damage. An increased hippocampal T2 time reflects underlying gliosis and neuronal loss. Volumetric studies of entorhinal cortex may identify occult damage ipsilateral to the seizure focus that is not evident on visual inspection. In patients with bilateral MTS, volumetry helps to identify the side maximally affected. [14] MRI has about 90% sensitivity and specificity in detecting MTS and other abnormalities in the rest of the temporal lobe. [15] Malformations of cortical development are being increasingly recognized in patients with refractory epilepsy. They may be focal cortical dysplasia (FCD), lissencephalies, heterotopia, polymicrogyria, schizencephaly. [13] Patients with low-grade primary brain tumors frequently present with seizures. The underlying histopathologies include dysembryoplastic neuroepithelial tumors, ganglio-glioma, gangliocytoma and pilocytic and fibrillary astrocytoma. These lesions have low signal on T1 and high signal on T2 W images. Cyst formation and enhancement with gadolinium may occur. Calcification is present in some cases. Cavernous angiomas are circumscribed and have the characteristic appearance of a range of blood products on MRI. Newly developed MRI techniques, diffusion-weighted imaging (DWI), diffusion tensor imaging (DTI), tractography improve the sensitivity of MRI. [13],[16]


   Functional Imaging Top


Role of SPECT and PET in the presurgical evaluation of epilepsy

Ictal SPECT and interictal PET remain important imaging tools in the presurgical evaluation of patients with refractory partial epilepsy. The two commonly used tracers for SPECT are 99m Tc - Hexamethylene propylene amine ( 99m Tc HMPAO) and 99m Tc-ethyl cysteinate dimer ( 99m Tc - ECD). SPECT measures blood flow; and comparing interictal and ictal SPECT studies, the increase in blood flow of certain brain regions during the ictal phase with respect to the interictal period can be evaluated. During ictal SPECT, due to epileptic activation, the neurons located in these areas are hyperactive and there is an increase in blood flow as an autoregulatory response. Thus ictal SPECT can evaluate all brain areas with similar accuracy, including deep regions of gray matter that are difficult to monitor with scalp and even with invasive EEG. [17],[18] The limitations of ictal SPECT are - 1. the dye reaches the brain at least one minute after the seizure onset, a time at which significant seizure spread has already occurred; 2. the spatial resolution of the images is low. An ictal SPECT displays both the ictal onset zone and seizure propagation pathways. In common practice, the region with largest and most intense hyperperfusion is considered as the ictal onset zone [Figure - 2]. However, these regions may also represent ictal propagation. [19] An ictal injection delay of less than 20 seconds after seizure onset significantly correlates with correct localization [20] . The sensitivity of ictal SPECT is 89-95% in temporal lobe epilepsy. [21],[22],[23] Subtraction ictal SPECT co-registered with MRI (SISCOM) improves the localization of the area of hyperperfusion. Extratemporal seizures are brief, and it is difficult to obtain an ictal SPECT. Post-ictal injections are easier to perform than ictal injections and have a sensitivity of 70% in temporal lobe seizures and 46% in extratemporal lobe epilepsy. [13] In conclusion ictal SPECT, as ictal EEG, can only define approximately the location and extent of the ictal onset zone and provides complementary information to the EEG data with respect to the ictal onset zone.

Interictal SPECT provides information about dysfunctional cortex with decreased blood perfusion. It is used as a baseline exam for comparison with scans obtained during the ictal phase as this method is moderately sensitive (40-50% correct localization), has high false-positive rate. [13]

18 F-deoxyglucose (FDG) PET measures changes in cerebral glucose metabolism and has higher spatial resolution and more reliable quantitation than SPECT, but the temporal resolution of PET with 18 FDG is unfavorable for ictal studies. [24] PET maps cerebral glucose metabolism using FDG PET and cerebral blood flow using 15 O-labelled water. Regional hypometabolism is best analyzed with co-registration of PET scans to MR images. The sensitivity of FDG PET is 60-90% for the detection of interictal temporal lobe hypometabolism. [21],[25],[26],[27]

18 FDG PET detects interictal glucose hypometabolism ipsilateral to the seizure focus in 60-90% of temporal lobe epilepsy (TLE) patients. Unilateral or asymmetric bilateral diffuse regional hypometabolism usually extends mesiolaterally in the temporal lobe. Some patients also have changes in extratemporal cortical areas or in the basal ganglia or thalamus. 15 OH 2 O studies generally show hypoperfusion in the same areas as glucose hypometabolism but are less sensitive and associated with more frequent false lateralization. [13]

18 FDG PET is more useful for lateralizing than localizing the epileptic focus. Patients with MTS have low glucose metabolism in the whole temporal lobe [Figure - 3], while patients with mesiobasal temporal tumors show only a slight decrease in metabolism. There is no correlation found between the degree of hypometabolism and the location of epileptic focus. Unilateral focal temporal hypometabolism in 18 FDG PET predicts good outcome of surgery for TLE. [13] However, absence of unilateral hypometabolism does not preclude a favorable outcome. Symmetric bilateral temporal hypometabolism, severe extratemporal cortical or thalamic hypometabolism is associated with higher incidence of postoperative seizures. The diagnostic sensitivity of FDG PET as analyzed by statistical parametric mapping (SPM) was 44% in patients with refractory partial epilepsy and normal MRI. [28] 18 FDG PET has lower sensitivity for lateralization of epileptic foci in extratemporal epilepsies than in TLE, and SPM improves diagnostic yield of 18 FDG PET and assists the planning of implantation of intracranial electrodes in patients with refractory partial epilepsy with nonlocalizing MRI or scalp EEG.

Magnetic resonance spectroscopy (MRS)

1 H MRS provides measurement of metabolites like N-acetylaspartate (NAA), choline, creatinine, lactate γ-aminobutyric acid (GABA) and glutamate; 31 P MRS measures phosphorus-containing compounds. 1 H MRS lateralizes seizure focus in up to 80-90% of the patients with TLE. [13],[29] Patients with MTS show decrease in NAA and increase in choline, creatinine and myo-inositol signals ipsilaterally; 20-50% of patients with unilateral TLE have bilateral temporal abnormalities in 1 H MRS. The role of 1 H MRS in predicting outcome of temporal lobe epilepsy surgery is not clear, and its role in extratemporal lobe epilepsy is uncertain.

Functional magnetic resonance imaging

Functional MRI (fMRI) helps to visualize regional brain activity. It provides a reliable way to lateralize language dominance and eliminates the need for invasive intracarotid amobarbital test (IAT) in 80% or more patients. [13] A series of related tests, such as verbal fluency and language comprehension, should be performed for functional language mapping. Language fMRI has limited correlation with the IAT, especially in patients with left TLE and with mixed speech dominance. [30] Functional MRI with memory paradigms may be incorporated into the presurgical assessment of TLE to minimize the adverse cognitive sequelae of anterior temporal lobe resection, and this will result in less use of IAT. fMRI of memory-induced mesial temporal lobe activation lateralizes the side of seizure onset in patients with refractory symptomatic TLE and may provide complementary information for presurgical evaluation. [31] fMRI may be used to identify sensorimotor cortex when planning neocortical resections.


   Role of EEG in Presurgical Evaluation Top


Non invasive EEG monitoring

Long-term noninvasive video EEG monitoring in presurgical evaluation is performed to differentiate seizure versus nonseizure events, classification of seizure types and localization of seizure onset. It is expensive and labor intensive. At least two to five habitual seizures should be recorded after gradual AED withdrawal.

Analysis of events - Ictal semiology : The clinical features distinguishing between temporal and extratemporal complex partial seizures are given in [Table - 3]. [2],[32] Ictal semiology that helps to lateralize complex partial seizures (CPS) of temporal lobe origin is contralateral dystonic posturing of upper limb; ipsilateral limb automatism, associated with behavioral arrest, is seen in most cases [Table - 4]. [33],[34]

Interictal EEG : Interictal epileptiform discharges (EDs) are good indices of the epileptogenic temporal lobe. [35],[36] Bilateral independent EDs are seen in 15-30% of patients with intractable TLE. Excellent surgical results are obtained in patients with unilateral preponderance of EDs of 3:1, along with ipsilateral ictal onset on ictal EEG. [37],[38],[39],[40] The other interictal EEG abnormalities seen in TLE are temporal intermittent rhythmic delta activity (TIRDA) and focal delta activity and generalized EDs.

Ictal EEG : The most reliable ictal EEG pattern in TLE is a rhythmic buildup of 5-7 Hz theta activity over one temporal region preceding the clinical event [41] [Figure - 4]. The initial pattern of ictal discharge on scalp EEG can assist in distinguishing seizures of temporal neocortical onset from those of hippocampal onset, and this information can be used to identify patients for invasive monitoring [42] [Table - 5]; the ictal discharges in extratemporal epilepsy present as low-voltage fast activity, an incrementing or a recruiting rhythm, repetitive spikes or spikes and slow waves, rhythmic slow waves, high-voltage sharp waves or focal or widespread attenuation or a flattening of the background. [43] Spike and wave, paroxysmal fast and beta frequency discharges with rapid spread are more likely to be seen with extratemporal and particularly, frontal seizures. Sphenoidal electrodes have an advantage over laterally placed scalp electrodes in detecting inferiorly directed mesial temporal discharges. [44] They sometimes detect interictal spikes and seizures not seen with scalp electrodes. Anterior temporal electrodes detect interictal and ictal epileptiform phenomena and may replace sphenoidal electrodes as they do not require expertise for their placement and create no discomfort. [45]

Role of invasive EEG in presurgical evaluation : Intracranial EEG recording with seizure monitoring is indicated when exact localization of the epileptogenic zone is required to plan a precise surgical resection for treatment of medically refractory seizures or when exact localization of functional cortex is required to plan a safe resection. Stereotactically inserted depth electrodes are indicated when EEG recording is needed from buried gray matter that is not accessible with other electrodes. [46] Bilateral depth electrodes are indicated when the surface EEG is suggestive of bilateral independent ictal pattern and when the ictal pattern is first seen in the contralateral temporal lobe on surface EEG in a case of unilateral mesial temporal lobe epilepsy. [47],[48],[49] According to Mayo Clinic experience, invasive recordings in TLE were deemed necessary due to (a) inability to accurately localize the site of seizure onset by surface EEG, (b) suspected multifocal onset and (c) discrepancies between MRI findings and video EEG monitoring. [50] Stereotactic depth recordings, when combined with scalp EEG recording, the so-called stereo EEG (SEEG), help in well delineation of the epileptogenic zone in complex cases. The complications of depth electrodes are intracerebral hemorrhage, in 1-4% cases with rare fatalities and infection. [51] Subdural strip and grid electrodes, inserted through burr holes or craniotomy, are indicated when neocortical seizure onset is suspected. Foramen ovale electrode recordings from the mesial aspect of the temporal lobe are indicated in patients with temporal lobe epilepsy. [46] Epidural peg electrodes are now used as sentinel electrodes, often in combination with other invasive techniques, for obtaining epidural ictal recordings.

Magnetoencephalography (MEG) in presurgical evaluation : Whole-head MEG facilitates simultaneous recording from the entire brain surface. Localizations of interictal spike zone with MEG showed excellent agreement with invasive EEG recordings. MEG is useful for the study of patients with nonlesional neocortical epilepsy and in patients with large lesions; it provides unique information on the epileptogenic zone. MEG can be used to map the sensorimotor cortex and language cortex. Both EEG and MEG yield complementary and confirmatory information. [52]

Neuropsychology and psychiatry workup in presurgical evaluation : The primary goal for neuropsychological evaluation is to characterize the patient's intellectual level, intelligence quotient (IQ) with the Wechsler Adult Intelligence Scale (WAIS) or a revision of it (WAIS-R), the Minnesota Multiphasic Personality Inventory (MMPI) and the Washington Psychosocial Seizure Inventory (WPSI). [53] An epileptic dysfunction in a silent cortical area will have less influence on IQ area. Discriminative neuropsychology has several tests in store, as reviewed by Jones Gotman et al. [54] Neuropsychology provides information about size, location and degree of epileptic dysfunction. Preoperative evaluation assists in predicting epilepsy surgery outcome and thus helps in selecting ideal candidates for surgery. [55] Epilepsy surgery can be performed without any neuropsychology at all, but it helps in the preoperative counseling of the patients and their caregivers. It provides baseline values against which the postoperative values can be compared.

Epilepsy, especially TLE, is often associated with psychiatric disorders such as behavioral changes, major mood disorders or psychosis. Presurgical psychiatric workup is a must for documentation of psychiatric disorders. This should be followed by postsurgical psychiatric documentation. [56] It is important to determine whether the association is casual and when postoperatively new psychiatric disorders occur, what the casual mechanism is. [57]

The role of Wada's test in the presurgical evaluation: The intracarotid amobarbital test (IAT) (or Wada's test) is commonly used to assess the hemispheric functions in patients being evaluated for epilepsy surgery. It helps in lateralization of language and to identify temporal lobe surgical candidates at risk for global amnesia and lateralization of the epileptic zone. [58],[59] Memory assessment during Wada's test produces a state of temporary, reversible dysfunction ipsilateral to the side of surgery; it thus helps to know the effect of temporal lobectomy on memory before surgical resection. However, a relative failure of a side in Wada's memory test does not reliably predict postoperative amnesia. Wada's test involves selective internal carotid artery catheterization through transfemoral route. Selective posterior cerebral artery amobarbital test can reliably predict postoperative memory function in patients with TLE. [60],[61] A practice test is performed prior to actual Wada's test one day before. A transfemoral intercarotid angiogram is performed and sodium amobarbital 125 mg is injected. The patient will develop hemiplegia on the contralateral side and global aphasia if speech-dominant hemisphere is injected. Memory for the items presented during the period of hemiparesis is tested approximately ten minutes after the time of injection, when the strength and language functions have returned to normal. The Wada's test is most commonly performed in patients who are candidates for temporal lobectomy, for the evaluation of language and memory and for language lateralization in patients with extratemporal lobe epilepsy. The Wada's test is used mostly in left-handed patients or in those who demonstrate bilateral or contralateral hemisphere damage or with confusing findings on neuropsychological testing. fMRI is a promising noninvasive technique to replace IAT for language lateralization as several studies which compared language lateralization by fMRI and IAT have shown a strong correlation between Wada testing and fMRI. [62],[63],[64]

Successful epilepsy surgery requires a multidisciplinary team approach with discussion of individual patient presurgical evaluation data in detail in a patient management conference. It will improve patient care and communication among members of the team.

In conclusion, none of the currently available preoperative workups can exactly delineate the epileptogenic zone. However, with the multimodality presurgical evaluation approach, sufficient concordance should be established among various independent investigations, thus identifying location and extent of the epileptogenic zone with a high degree of confidence. This will result in a good surgical outcome.

Words/Group of words/Corrections that need to be checked/verified have been highlighted or commented upon. Those abbreviations used for the first time in the article but not spelt out are highlighted; along with the abbreviations, their expanded forms need to be given at the place where the abbreviations are first used.

 
   References Top

1.Engel J Jr. Update on surgical treatment of the epilepsies: Summary of the Second International Palm Desert Conference on the Surgical Treatment of the Epilepsies (1992). Neurology 1993;43:1612-7.  Back to cited text no. 1  [PUBMED]  
2.Kurupath R. Medically refractory epilepsy. In : Kurupath R, editor. Medically refractory epilepsy - SCTIMS and Technology: 1999. p. 1-39.  Back to cited text no. 2    
3.Carreno M, Luders HO. General principles of presurgical evaluation. In : Luders HO, Comair YG, editor. Epilepsy surgery, 2 nd ed. Lippincott Williams and Williams: 2001. p. 185-200.  Back to cited text no. 3    
4.Luders HO, Engel J Jr, Munari C. General principles. In : Engel J Jr, editor. Surgical treatment of the epilepsies, 2 nd ed. Raven Press: New York; 1993. p. 137-53.  Back to cited text no. 4    
5.Chelune GJ, Naugle RI, Lüders H, Awad IA. Prediction of cognitive change as a function of preoperative abiity status among temporal lobectomy patients seen at 6-month follow-up. Neurology 1991;41:399-404.  Back to cited text no. 5    
6.Kanemoto K, Kawasaki J, Takenouchi K, Hayashi K, Kubo H, Morimura T, et al . Lateralized memory deficits on the Wada test correlate with the side of lobectomy only for patients with unilateral medial temporal lobe epilepsy. Seizure 1999;8:471-5.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Acharya JN, Dinner DS. Use of the intracarotid amobarbital procedure in the evaluation of memory. J Clin Neurophysiol 1997; 14:311-25.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Cohen D, Cuffin BN, Yunokuchi K, Maniewski R, Purcell C, Cosgrove GR, et al . MEG versus EEG localization test using implanted sources in the human brain. Ann Neurol 1990;28:811-7.  Back to cited text no. 8  [PUBMED]  
9.Commission on Neuroimaging of the International League Against Epilepsy. Guidelines for neuroimaging evaluation of patients with uncontrolled epilepsy considered for surgery. Epilepsia 1998;39:1375-6.  Back to cited text no. 9  [PUBMED]  
10.Cendes F, Cook MJ, Watson C, Andermann F, Fish DR, Shorvon SD, et al . Frequency and characteristics of dual pathology in patients with lesional epilepsy. Neurology 1995;45:2058-64.  Back to cited text no. 10  [PUBMED]  
11.Gupta AK. The role of imaging in presurgical evaluation of epilepsy. In : Kurupath R, editor. Medically refractory epilepsy - SCTIMS and Technology: 1999. p. 1-39.  Back to cited text no. 11    
12.Lee DH, Gao F, Rogers JM, Gulka I, Mackenzie IR, Parrent AG, et al . MR in temporal lobe epilepsy: Analysis with pathologic confirmation. AJNR Am J Neuroradiol 1998;19:19-27.  Back to cited text no. 12    
13.Salmenpera TM, Duncan JS. Imaging in epilepsy. J Neurol Neurosurg Psychiatry 2005;76:2-10.  Back to cited text no. 13    
14.King D, Spencer SS, McCarthy G, Luby M. Spencer DD. Bilateral hippocampal atrophy in medial temporal lobe epilepsy. Epilepsia 1995;36:905-10.  Back to cited text no. 14    
15.Jackson GD. Visual analysis in mesial temporal sclerosis. In : Cascino GD, Jack CR Jr, editors. Neuroimagaing in epilepsy. Butterworth-Heinemann: Boston; 1996. p. 73-110.  Back to cited text no. 15    
16.Assaf BA, Mohamed FB, Abou-Khaled KJ, Williams JM, Yazeji MS, Haselgrove J, et al . Diffusion tensor imaging of the hippocampal formation in temporal lobe epilepsy. AJNR Am J Neuroradiol 2003;24:1857-62.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Spanaki MV, Spencer SS, Corsi M, MacMullan J, Seibyl J, Zubal IG. Sensitivity and specificity of quantitative difference SPECT analysis in seizure localization. J Nucl Med 1999;40:730-6.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]
18.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.  Back to cited text no. 18  [PUBMED]  [FULLTEXT]
19.Dupont P, Van Paesschen W, Palmini A, Ambayi R, Van Loon J, Goffin J, et al . Ictal perfusion patterns associated with single MRI-visible focal dysplastic lesions: Implications for the noninvasive delineation of the epileptogenic zone. Epilepsia 2006;47:1550-7.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Lee SK, Lee SY, Yun CH, Lee HY, Lee JS, Lee DS. Icgal SPECT in neocortical epilepsies: Clinical usefulness and factors affecting the pattern of hyperperfusion. Neuroradiology 2006;48:678-84.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]
21.Ho SS, Berkovic SF, Berlangieri SU, Newton MR, Egan GF, Tochon-Danguy HJ, et al . Comparison of ictal SPECT and interictal PET in the presurgical evaluation of temporal lobe epilepsy. Ann Neurol 1995;37:738-45.  Back to cited text no. 21  [PUBMED]  
22.Lee SK, Lee SH, Kim SK, Lee DS, Kim H. The clinical usefulness of ictal SPECT in temporal lobe epilepsy: The lateralization of seizure focus and correlation with EEG. Epilepsia 2000;41:955-62.  Back to cited text no. 22  [PUBMED]  
23.Newton MR, Berkovic SF, Austin MC, Rowe CC, McKay WJ, Bladin PF. Ictal postictal and interictal single-photon emission tomography in the lateralization of temporal lobe epilepsy. Eur J Nucl Med 1994;21:1067-71.  Back to cited text no. 23  [PUBMED]  
24.Mazziotta JC, Engel J Jr. The use and impact of positron computed scanning in epilepsy. Epilepsia 1984;25:S86-104.  Back to cited text no. 24    
25.Engel J Jr, Henry TR, Risinger MW, Mazziotta JC, Sutherling WW, Levesque MF, 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.  Back to cited text no. 25  [PUBMED]  
26.Theodore WH, Newmark ME, Sato S, Brooks R, Patronas N, De La Paz R, et al . Fluorodeoxyglucose positron emission tomography in refractory complex partial seizures. Ann Neurol 1983;14:429-37.  Back to cited text no. 26  [PUBMED]  
27.Ryvlin P, Philippon B, Cinotti I, Froment JC, Le Bars D, Mauguiθre F. Functional neuroimaging strategy in temporal lobe epilepsy: A comparative study of FDG-PET and Tc-HMPAO-SPECT. Ann Neurol 1992;31:650-6.  Back to cited text no. 27    
28.Lee SK, Lee SY, Kim KK, Hong KS, Lee DS, Chung CK. Surgical outcome and prognostic factors of cryptogenic neocortical epilepsy. Ann Neurol 2005;58:525-32.  Back to cited text no. 28  [PUBMED]  [FULLTEXT]
29.Cendes F, Caramanos Z, Andermann F, Dubeau F, Arnold DL. Proton magnetic resonance spectroscopic imaging and magnetic resonance imaging volumetry in the lateralization of temporal lobe epilepsy: A series of 100 patients. Ann Neurol 1997;42:737-46.  Back to cited text no. 29  [PUBMED]  
30.Benke T, Koylu B, Visani P, Karner E, Brenneis C, Bartha L, et al . Language lateralization in temporal lobe epilepsy: A comparison between fMRI and the Wada Test. Epilepsia 2006;47:1308-19.  Back to cited text no. 30    
31.Jokeit H, Okujava M, Woermann FG. Memory fMRI lateralizes temporal lobe epilepsy. Neurology 2001;57:1786-93.  Back to cited text no. 31  [PUBMED]  [FULLTEXT]
32.Gil-Nagel A, Risinger MW. Ictal semiology in hippocampal versus extrahippocampal temporal lobe epilepsy. Brain 1997;120:183-92.  Back to cited text no. 32  [PUBMED]  [FULLTEXT]
33.Marks WJ Jr, Laxer KD. Semiology of temporal lobe seizures: Value in lateralizing the seizure focus. Epilepsia 1998;39:721-6.  Back to cited text no. 33  [PUBMED]  
34.Fakhoury T, Abou-Khalil B, Peguero E. Differentiating clinical features of right and left temporal lobe seizures. Epilepsia 1994;35:1038-44.  Back to cited text no. 34  [PUBMED]  
35.Quesney LF, Abou-Khalil B, Cole A, Olivier A. Preoperative extracranial and intracranial EEG investigation in patients with temporal lobe epilepsy: Trends, results and review of pathophysiologic mechanisms. Acta Neurol Scand 1988;78:52-60.  Back to cited text no. 35    
36.Quesney LF. Clinical and EEG features of complex partial seizures of temporal lobe origin. Epilepsia 1986;26:S27-46.  Back to cited text no. 36    
37.Chung M, Walezak T, Lewis D, Dawson B, Radtke R. Temporal lobectomy and independent bitemporal interictal activity: What degree of lateralization is sufficient? Epilepsia 1991;32:195-201.  Back to cited text no. 37    
38.Blum D. Prevalence of bilateral partial seizure foci and implications for electroencephalographic telemetry monitoring and epilepsy surgery. Electroencephalogr Clin Neurophysiol 1994;91:329-36.  Back to cited text no. 38  [PUBMED]  
39.Holmes MD, Dodrill CB, Wilensky AJ, Ojemann LM, Ojemann GA. Unilateral focal preponderance of interictal epileptiform discharges as predictor of seizure origin. Arch Neurol 1996;53:228-32.  Back to cited text no. 39  [PUBMED]  
40.Holmes MD, Dodrill CB, Ojemann GA, Wilensky AJ, Ojemann LM. Outcome following surgery in patients with bitemporal interictal epileptiform patterns. Neurology 1997;48:1037-40.  Back to cited text no. 40  [PUBMED]  
41.Sharbrough FW. Scalp-recorded ictal patterns in focal epilepsy. J Cin Neurophysiol 1993;10:262-7.  Back to cited text no. 41    
42.Ebersole JS, Pacia SV. Localization of temporal lobe foci by ictal EEG patterns. Epilepsia 1996;37:386-99.  Back to cited text no. 42  [PUBMED]  
43.Barbara F, Westmoreland. The EEG findings in extratemporal seizures. Epilepsia 1998;39:S1.  Back to cited text no. 43    
44.Sperling MR, Guina L. The necessity for sphenoidal electrodes in the presurgical evaluation of temporal lobe epilepsy: Pro position. J Clin Neurophysiol 2003;20:299-304.  Back to cited text no. 44  [PUBMED]  [FULLTEXT]
45.Blume WT. The necessity for sphenoidal electrodes in the presurgical evaluation of temporal lobe epilepsy: Con position. J Clin Neurophysiol 2003;20:305-10.  Back to cited text no. 45  [PUBMED]  [FULLTEXT]
46.Zumsteg D, Wieser HG. Presurgical evaluation: Current role of invasive EEG. Epilepsia 2000;41:S55-60.  Back to cited text no. 46  [PUBMED]  
47.Sammaritano M deLotbiniere A anderman F, Olivier A, Gloor P, Quesnay LF. False lateralization by surface EEG of seizure onset in patients with temporal lobe epilepsy and gross focal cerebral lesions. Ann Neurol 1987;21:361-9.  Back to cited text no. 47    
48.Williamsen PD, French JA, Thadani VM, Kim JH, Novelly RA, Spencer SS, et al . Characteristics of medial temporal lobe epilepsy: II, Interictal and ictal scalp electroencephalography, neuropsychological testing, neuroimaging, surgical results and pathology. Ann Neurol 1993;34:781-7.  Back to cited text no. 48    
49.Diehl B, Luders HO. Temporal lobe epilepsy: When are invasive recordings needed? Epilepsia 2000;41:S61-74.  Back to cited text no. 49    
50.Schiller Y, Cascino GD, Sharbrough FW. Chronic intracranial EEG monitoring for localization of the epileptogenic zone: An electroclinical correlation. Epilepsia 1998;39:1302-8.  Back to cited text no. 50  [PUBMED]  
51.Van Buren JM. Complications of surgical procedures in the diagnosis and treatment of epilepsy. In : Engel J, editor. Surgical treatment of the epilepsies. Raven Press: New York; 1987. p. 465-75.  Back to cited text no. 51    
52.Pataraia E, Baumgartner C, Lindinger G, Deeke L. Magnetoencephalography in presurgical epilepsy evaluation. Neurosurg Rev 2002;25:141-59.  Back to cited text no. 52    
53.Jones-Gotman M. Presurgical neuropsychological evaluation for localization and lateralization of seizure focus. In : Luders HO, editor. Epilepsy surgery. Raven Press: New York; 1991. p. 469-75.  Back to cited text no. 53    
54.Jones-Gotman M, Smith ML. Zatorre RJ. Neuropsycholgoical testing for localizing and lateralizing the epileptogenic region. In : Engel J Jr, editor. Surgical treatment of the epilepsies. 2 nd ed. Raven Press: New York; 1993. p. 245-62.  Back to cited text no. 54    
55.Silfvenius H. The role of neuropsychological evaluation in epilepsy surgery. In : Kurupath R, editor. Medically refractory epilepsy - SCTIMS and Technology: 1999. p. 145-57.  Back to cited text no. 55    
56.Elger G, Elger CE. Presurgical psychiatric workup. In : Luders HO, Comair YG, editor. Epilepsy surgery, 2 nd ed. Lippincott Williams and Williams: 2001. p. 469-74.  Back to cited text no. 56    
57.Taylor DC. Overview: Psychiatric issues. In : Engel J Jr, Pedley TA, editors. Epilepsy: A comprehensive textbook. Lippincott Raven Publishers: Philadelphia; 1997. p. 2039-43.  Back to cited text no. 57    
58.Wada J, Rasmussen T. Intracarotid injection of sodium amytal for the lateralization of cerebral speech dominance: Experimental and clinical observations. J Neurosurg 1960;27:266-82.  Back to cited text no. 58    
59.Rausch R, Babb TL, Engel J Jr, Crandalll PH. Memory following intracarotid amobarbital injection contralateral to hippocampal damage. Arch Neurol 1989;46:783-8.  Back to cited text no. 59    
60.Yen DJ, Lirng JF, Shih YH, Shan IK, Su TP, Chen C, et al . Selective posterior cerebral artery amobarbital test in patients with temporal lobe epilepsy for surgical treatment. Seizure 2006;15:117-24.  Back to cited text no. 60  [PUBMED]  [FULLTEXT]
61.Stabell KE, Bakke SJ, Andressen S, Bjornaes H, Borchgrevink HM, Due-Tonnessen P, et al . Selective posterior cerebral artery amobarbital test: Its role in presurgical memory assessment in temporal lobe epilepsy. Epilepsia 2004;45:817-25.  Back to cited text no. 61    
62.Binder JR, Swanson SJ, Hammeke TA, Morris GL, Mueller WM, Fischer M, et al . Determination of language dominance using functional MRI: A comparison with the Wada test. Neurology 1996;46:978-84.  Back to cited text no. 62  [PUBMED]  
63.Desmond JE, Sum JM, Wagner AD, Demb JB, Shear PK, Glover GH, et al . Functional MRI measurement of language lateralization in Wada-tested patients. Brain 1995;118:1411-9.  Back to cited text no. 63  [PUBMED]  [FULLTEXT]
64.Bahn MM, Lin W, Silbergeld DL, Miller JW, Kuppusamy K, Cook RJ, et al . Localization of language cortices by functional MR imaging compared with intracarotid amobarbital hemispheric sedation. AJR Am J Roentgenol 1997;169:575-9.  Back to cited text no. 64  [PUBMED]  [FULLTEXT]


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]
 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5]


This article has been cited by
1 Relation between electroencephalogram and neuroimaging present in children with epilepsy of difficult control | [Relación entre electroencefalograma y neuroimagen en niños con epilepsia focal de difícil control]
Valdivia Álvarez, I., Aguilar Fabré, L., Francisco Pérez, A.
Revista Cubana de Pediatria. 2009; 81(3): 2
[Pubmed]



 

Top
Print this article  Email this article
Previous article Next article

    

 
  Search
 
   Next article
   Previous article 
   Table of Contents
  
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (90 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
    Introduction
    Aim and Concept ...
    Role of Imaging ...
    Structural Imaging
    Functional Imaging
    Role of EEG in P...
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed8849    
    Printed197    
    Emailed0    
    PDF Downloaded440    
    Comments [Add]    
    Cited by others 1    

Recommend this journal