Predictive value of magnetic resonance imaging in temporal lobe epilepsy surgery . Arch Neu rol 1993 ; 50 ( 1 ): 65 \200\223 9 . 53. Pataraia E , Simos PG , Castillo EM , Billingsley RL , Sarkari S , Wheless JW , et al . Does magnetoencephalography add to scalp video-EEG as a diagnostic tool in epilepsy surger y? Neurology 2004 : 62 ( 6 ): 943 \200\223 8 . 34. Carne RP , O \200\231Brien TJ , Kilpatrick CJ , MacGregor LR , Hicks RJ , Murphy MA , e t al . MRI-negative PET-positive temporal lobe epilepsy: a distinct surgically remediable syndrome . Brain 2004 ; 127 (Pt 10 ): 2276 \200\223 85 . 54. Wheless JW , Willmore LJ , Breier JI , Kataki M , Smith JR , King DW , et al . A comparison of magnetoencephalography, MRI, and V-EEG in patients evaluated for ep ilepsy surgery . Epilepsia 1999 : 40 ( 7 ): 931 \200\223 41 . 55. Kral T , Clusmann H , Bl mcke I , Fimmers R , Ostertun B , Kurthen M , et al . Outcome of epilepsy surgery in foca l cortical dysplasia . J Neurol Neurosurg Psychiatry 2003 : 74 : 183 \200\223 8 . 35. Murphy MA , O \200\231Brien TJ , Morris K , Cook MJ . Multimodality image-guided surgery for the treatment of medically refractory epilepsy . J Neurosurg 2004 ; 100 : 452 \200\223 62 . 36. Knowlton RC . The role of FDG-PET, ictal SPECT, and MEG in the epilepsy surgery evaluat ion . Epilepsy Behav 2006 ; 8 ( 1 ): 91 \200\223 101 . 37. Ryvlin P , Bouvard S , Le Bars D , De Lam rie G , Gr goire MC , Kahane 56. Fabinyi G . Operative diagnostic methods in the treatment of epilepsy . In: Kaye AH , B lack PM (eds) Operative Neurosurgery , pp. 1251 \200\2238. London : Churchill Livingstone , 2000 . P , et al . Clinical utility of \202 umazenil-PET versus 18F \202 uorodeoxyglucose-PET and MRI in refractory partial epilepsy . A prospective study in 100 patients. Brain 1998 ; 121 (Pt 11 ): 2067 \200\223 81 . 57. Jayakar P . Invasive EEG monitoring in children: When, where and what? J Clin Neurophysiol 1999 ; 16 : 408 \200\223 18 . 38. Gaillard WD , Bhatia S , Bookheimer SY , Fazilat S , Sato S , Theodore WH . FDG-PET and volumetric MRI in the evaluation of patients with partial epilepsy . Neuro logy 1995 ; 45 ( 1 ): 123 \200\223 6 . 58. Bruce DA , Bizzi JWJ . Surgical technique for the insertion of grids and strips for invasive monitoring in children with intractable epilepsy . Child \200\231s Nerv Syst 2000 ; 16 : 724 \200\223 30 . 39. Locharernkul C , Tepmongkol S , Limotai C , Loplumlert J . Positron emission tomography (PET) scan in epilepsy . Asian Biomed 2008 ; 2 ( 1 ): 3 \200\223 17 . 59. Risinger MW . Electroencephalographic strategies for determining the epileptogenic zone . In: L ders H (ed) Epilepsy Surgery , pp. 337 \200\22347. New York: Ra ven Press , 1992 . 40. la Foug re C , Rominger A , F rster S , Geisler J , Bartenstein P . PET and SPECT in epilepsy: A critical review . Epilepsy Behav 2009 ; 15 ( 1 ): 50 \200\223 5 . 60. Roper SN . Implantation of grid and strip electrodes . Tech Neurosurg 1995 ; 1 : 5 \200\223 10 . 61. Jennum P , Dhuna A , Davies K , Fiol M , Maxwell R . Outcome of 41. O \200\231Brien TJ , Hicks RJ , Ware R , Binns DS , Murphy M , Cook MJ. resective surgery for intractable partial epilepsy guided by subdural electrode arrays . Ac ta Neurol Scand 1993 ; 87 : 434 \200\223 7 . T he utility of a 3-dimensional, large- \201 eld-of-view, sodium iodide crystal-based PET scanner in the presurgical evaluation of partial epilepsy . J Nucl Med 2001 ; 42 : 1158 \200\223 65 . 62. Wyler AR , Ojemann GA , Lettich E , Ward AA Jr . Subdural strip electrodes for localizi ng epileptogenic foci . J Neurosurg 1984 ; 60 : 1195 \200\223 200 . 42. Vinton AB , Carne R , Hicks RJ , Desmond PM , Kilpatrick C , Kaye AH , et al . The exte nt of resection of FDG-PET hypometabolism relates to outcome of temporal lobectomy . Brain 2007 ; 130 (Pt 2 ) :548 \200\223 60 . 43. Willmann O , Wennberg R , May T , Woermann FG , Pohlmann-Eden 63. Hong SC , Kang KS , Seo DW , Hong SB , Lee M , Nam DH , et al . Surgical treatment of intractable epilepsy accompanying cortical dysplasia . J Neurosurg 20 00 ; 93 : 766 \200\223 73 . B . The contribution of 18F-FDG PET in preoperative epilepsy surgery evaluation for patient s with temporal lobe epilepsy A meta-analysis . Seizure 2007 : 16 ( 6 ): 509 \200\223 20 . 64. Spencer SS , Spencer DD , Williamson PD , Mattson R . Combined depth and subdural electrode investigation in uncontrolled epilepsy . Neurology 1990 ; 40 : 74 \200\223 9 . 44. Rathore C , Kesavadas C , Ajith J , Sasikala A , Sarma SP , Radhakrishnan K . Cost-effe ctive utilization of single photon emission computed tomography (SPECT) in decision making for epilepsy surgery . Seizure 2011 : 20 ( 2 ): 107 \200\223 14 . 65. Brekelmans GJ , van Emde Boas W , Velis DN , Lopes da Silva FH , van Rijen PC , van Vee len CW . Comparison of combined versus subdural or intracerebral electrodes alone in presur gical focus localization . Epilepsia 1998 ; 39 ( 12 ): 1290 \200\223 301 . 45. Zubal IG , Spencer SS , Imam K , Seibyl J , Smith EO , Wisniewski G , Hoffer PB . Difference images calculated from ictal and interictal technetium-99m-HMPAO SPE CT scans of epilepsy . J Nucl Med 1995 : 36 ( 4 ): 684 \200\223 9 . 66. Engel J . Approaches to localization of the epileptogenic lesion . In: Engel J (ed) Surgical Treatment of the Epilepsies , pp.75 \200\22396. New York : Raven Pres s , 1987 . oxford textbook of epilepsy and epileptic seizures 306 epileptogenic process and surgical approach . Acta Neurochir (Wien) 1994 ; 130 ( 101 \200 \223110 ): 101 . 67. Fountas KN , Smith JR . Subdural electrode-associated complications: a 20-year experien ce . Stereotact Funct Neurosurg , 2007 ; 85 : 264 \200\223 72 . 89. Lowe AJ , David E , Kilpatrick CJ , Matkovic Z , Cook MJ , Kaye A , et al . Epilepsy su rgery for pathologically proven hippocampal sclerosis provides long term seizure control an d improved quality of life . Epilepsia 2004 ; 45 : 237 \200\223 42 . 68. Ruggieri PM , Najm I , Bronen R , Campos M , Cendes F , Duncan JS , et al . Neuroimagin g of the cortical dysplasias . Neurology 2004 ; 62 (Suppl 3 ): S27 \200\223 9 . 69. Widdess-Walsh P , Diehl B , Najm I . Neuroimaging of focal cortical 90. Schiller Y , Cascino GD , Sharbrough FW . Chronic Intracranial EEG dysplasia . J Neuroimaging 2006 ; 16 : 185 \200\223 96 . Monitoring for Localizing the Epileptogenic Zone: An Electroclinical Correlation . Epilepsi a 1998 ; 39 ( 12 ): 1302 \200\223 8 . 70. Widdess-Walsh P , Jeha L , Nair D , Kotagal P , Bingaman W , Najm I . Subdural electrode analysis in focal cortical dysplasia . Neurology 2007 ; 69 : 660 \200 \223 7 . 91. Schulz R , L ders HO , Tuxhorn I , Ebner A , Holthausen H , Hoppe M , et al . Localiza tion of epileptic auras induced on stimulation by subdural electrodes . Epilepsia 1997 . 38 ( 12 ): 1321 \200\223 9 . 71. Drake J , Hoffman HJ , Kobayashi J , Hwang P , Becker LE . Surgical management of children with temporal lobe epilepsy and mass lesions . Neurosurgery 1987 ; 2 1 : 792 \200\223 7 . 92. Cohen-Gadol AA , Bradley CC , Williamson A , Kim JH , Westerveld M , Duckrow RB , et al . Normal magnetic resonance imaging and medial temporal lobe epilepsy: t he clinical syndrome of paradoxical temporal lobe epilepsy . J Neurosurg 2005 ; 102 : 902 \200\223 9 . 72. Berger MS , Kincaid J , Ojemann GA . Brain mapping techniques to maximize resection, safety, and seizure control in children with brain tumors . Neurosurger y 1989 ; 25 : 786 \200\223 92 . 93. Cunha I , Oliveira J . Quality of life after surgery for temporal lobe epilepsy: a 5-ye ar follow-up . Epilepsy Behav 2010 ; 17 ( 4 ): 506 \200\223 10 . 73. Yeh HS , Kashiwagi S , Tew JM Jr , Berger TS . Surgical management of epilepsy associat ed with cerebral arteriovenous malformations . J Neurosurg 1990 ; 72 : 216 \200\223 23 . 94. Mihara T , Inoue Y , Matsuda K , Tottori T , Otsubo T , Watanabe Y , et al . Recommenda tion of early surgery from the viewpoint of daily quality of life . Epilepsia 1996 ; 37(Sup pl 3) : 33 \200\223 6 . 74. Weber JP , Silbergeld DL , Winn HR . Surgical resection of epileptogenic cortex associa ted with structural lesions . Neurosurg Clin North Am 1993 ; 4 : 327 \200\223 36 . 95. Kellett MW , Smith DF , Baker GA , Chadwick DW . Quality of life after epilepsy surgery . J Neurol Neurosurg Psychiatry 1997 ; 63 ( 1 ): 52 \200\223 8 . 96. McLachlan RS , Rose KJ , Derry PA , Bonnar C , Blume WT , Girvin JP . Health-related quality of life and seizur e control in temporal lobe epilepsy . Ann Neurol 1997 ; 41 ( 4 ): 482 \200\223 9 . 75. Morris K , O \200\231Brien TJ , Cook MJ , Murphy M , Bowden SC . A Computer generated s tereotactic \200\230virtual subdural grid \200\231 to guide resective epilepsy surgery . A m J Neuroradiol 2004 ; 25 : 77 \200\223 83 . 76. Cukiert A , Buratini JA , Machado E , Sousa A , Vieira JO , Argentoni M , et al . Resul ts of surgery in patients with refractory extratemporal epilepsy with normal or nonlocalizi ng magnetic resonance \201 ndings investigated with subdural grids . Epilepsia 2001 ; 42 ( 7 ): 889 \200\223 94 . 77. Wieser HG , Yas argil MG . Selective amygdalohippocampectom y as a 97. Spencer SS , Berg AT , Vickrey BG , Sperling MR , Bazil CW , Haut S , et al . Health-re lated quality of life over time since resective epilepsy surgery . Ann Neurol 2007 ; 62 ( 4 ): 327 \200\223 34 . 98. Jehi LE , Silveira DC , Bingaman W , Najm I . Temporal lobe epilepsy surgical treatment of mesiobasal limbic epilepsy . Surg Neurol 1982 ; 17 ( 6 ): 445 \200 \223 57 . surgery failures: predictors of seizure recurrence, yield of reevaluation, and outcome foll owing reoperation . J Neurosurg 2010 ; 113 ( 6 ): 1186 \200\223 94 . 78. Popovic EA , Fabinyi GC , Brazenor GA , Berkovic SF , Bladin PF . Temporal lobectomy for epilepsy \200\224 complications in 200 patients . J Clin Neurosci 1 995 ; 2 : 238 \200\223 44 . 99. Ramos E , Benbadis S , Vale FL . Failure of temporal lobe resection for epilepsy in pat ients with mesial temporal sclerosis: results and treatment options . J Neurosurg 2009 ; 11 0 ( 6 ): 1127 \200\223 34 . 79. Walczak TS , Radtke RA , McNamara JO , Lewis DV , Luther JS , Thompson E , et al . Anterior temporal lobectomy for complex partial seizures: evaluation, results, and long-term follow-up in 100 cases . Neurology 1990 ; 40 ( 3 Pt 1 ): 413 \200 \2231 8 . 100. Lowe NM , Eldridge P , Varma T , Wieshmann UC . The duration of temporal lobe epilepsy and seizure outcome after epilepsy surgery . Seizure 2010 ; 19 ( 5 ): 261 \200\223 3 . 80. McIntosh AM , Kalnins RM , Mitchell LA , Berkovic SF . Early seizures after temporal lo bectomy predict subsequent seizure recurrence . Ann Neurol 2005 ; 57 ( 2 ): 283 \200\223 8 . 101. Abosch A , Bernasconi N , Boling W , Jones-Gotman M , Poulin N , Dubeau F , et al . Fa ctors predictive of suboptimal seizure control following selective amygdalohippocampectomy . J Neurosurg 2002 ; 97 ( 5 ): 1142 \200\223 51 . 81. Malla BR , O \200\231Brien TJ , Cascino GD , So EL , Radhakrishnan K , Silbert P , 102. Awad IA , Nayel MH , L ders H . Second operation after the failure of previous resect ion for epilepsy . Neurosurgery 1991 ; 28 ( 4 ): 510 \200\2231 8 . 103. Germano IM , Pouli n N , Olivier A . Reoperation for recurrent temporal et al . Acute postoperative seizures following anterior temporal lobectomy for intractable partial epilepsy . J Neurosurg 1998 ; 89 : 177 \200\223 82 . 82. T llez-Zenteno JF , Dhar R , Hernandez-Ronquillo L , Wiebe S . Long- lobe epilepsy . J Neurosurg 1994 ; 81 ( 1 ): 31 \200\223 6 . term outcomes in epilepsy surgery: antiepileptic drugs, mortality, cognitive and psychosoci al aspects . Brain 2007 ; 130 (Pt 2 ): 334 \200\223 45 . 83. Tellez-Zenteno JF , Dhar R , Wiebe S . Long-term seizure outcomes following epilepsy surgery: a systematic review and me ta-analysis . Brain 2005 ; 128 (Pt 5 ): 1188 \200\223 98 . 104. Gonz lez-Mart nez JA , Srikijvilaikul T , Nair D , Bingaman WE . Long-term seizure outcome in reoperation after failure of epilepsy surgery . Neurosurgery 2 007 ; 60 ( 5 ): 873 \200\223 80 ; discussion 873 \200\22380 . 105. Salanova V , Markand O , Worth R . Temporal lobe epilepsy: analysis of failures and the role of reoperation . Acta Neurol Scand 2005 ; 111 ( 2 ): 126 \200\223 33 . 84. Schramm J , Kral T , Grunwald T , Bl mcke I . Surgical treatment for neocortical tempo ral lobe epilepsy: clinical and surgical aspects and seizure outcome . J Neurosurg 2001 ; 9 4 ( 1 ): 33 \200\223 42 . 106. Wyler AR , Hermann BP , Richey ET . Results of reoperation for failed epilepsy surgery . J Neurosurg 1989 ; 71 ( 6 ): 815 \200\2231 9 . 85. Tonini C , Beghi E , Berg AT , Bogliun G , Giordano L , Newton RW , et al . Predictors of epilepsy surgery outcome: a meta-analysis . Epilepsy Res 2004 ; 62 ( 1 ): 75 \200\223 87 . 107. Wetjen NM , Cascino GD , Fessler AJ , So EL , Buchhalter JR , Mullan BP , et al . Subt raction ictal single-photon emission computed tomography coregistered to magnetic resonance imaging in evaluating the need for repeated epilepsy surgery . J Neurosurg 2006 ; 105 : 71 \200\223 6 . 86. McIntosh AM , Kalnins RM , Mitchell LA , Fabinyi GC , Briellmann RS , Berkovic SF . Temporal lobectomy: long-term seizure outcome, late recurrence and risks for seizure recurrence . Brain 2004 ; 127 (Pt 9 ): 2018 \200\223 30 . 108. Margerison JH , Corsellis JA . Epilepsy and the temporal lobes . A clinical, electroencephalographic and neuropathological study of the brain in epilepsy, wit h particular reference to the temporal lobes . Brain 1966 ; 89 ( 3 ): 499 \200\223 530 . 87. Paolicchi JM , Jayakar P , Dean P , Yaylali I , Morrison G , Prats A , et al . Predicto rs of outcome in pediatric epilepsy surgery . Neurology 2000 ; 54 : 642 \200\223 7 . 109. Schiller Y , Cascino GD , So EL , Marsh WR . Discontinuation of 88. Rossi GF , Colicchio G , Scerrati M . Resection surgery for partial epilepsy: relation of surgical outcome with some aspects of the antiepileptic drugs after successful epilepsy surgery . Neurology 2000 ; 54 ( 2 ): 346 \200\223 9 . CHAPTER 29 Resective Surgery of Extratemporal Epilepsy Shahram Amina and Hans O. L ders Introduction Up to a third of patients have epilepsy that is intractable to medical treatme nt. Despite the availability of many new antiepileptic medi- cations in recent decades, the percentage of medically intractable cases remains relatively unchanged (1). As discussed i n Chapter 27, surgical treatment is an alternative option for drug-resistant focal epilepsi es and in appropriately selected cases, resective surgery can result in either complete sei zure freedom or signi \201 cant seizure reduction. The availability of modern neuroimaging techniques, digital electroencephalogram (EEG), and advanced neurosurgical equipment in ma ny epilepsy centers has now made surgical options available for a far greater number of pat ients than was previously feasible. modern era are of extratemporal epilepsies (3). These surgeries range from lesionectomies t o large multilobar resections and hemispherectomies. In this chapter we only discuss region al resec- tions. Hemispherectomies and disconnection procedures are discussed in Chapter 31 . The most common extratemporal surger- ies are frontal resections followed by parietal and occipital resec- tions. Most of these surgeries are carried out in \200\230lesional \200 \231 cases with identi \201 able brain abnormalities on neuroimaging studies (2). Classi \201 cation of extratemporal epilepsies We routinely use a classi \201 cation syst em (the Cleveland classi \201 ca- tion) which has been in use for more than two decades in our insti- tution and several other major epilepsy centers around the world. This system c lassi \201 es epilepsy for each patient in four dimensions: (1) location of the epileptoge nic zone, (2) etiology of epileptic seizures, (3) seizure symptomatology , and (4) other re lated medical conditions . Based on the complexity of each case, different investi- gations may be needed to de \201 ne these four dimensions of epilepsy with greater precision. For example, in pharmacoresponsive cases of epilepsy, a detailed history and physical exam, ba sic neuroimag- ing, and a routine EEG may usually suf \201 ce. However, in a complex case of drug-resistant epilepsy an extensive work-up (discussed in Chapter 27) may be needed to determine surgical candidacy based on these four dimensions. A full discussion of this clas si \201 cation system can be found elsewhere (4 \200\2236). From a surgical perspective, epilepsies can be classi \201 ed into two major categories, n amely epilepsies arising from the temporal lobe (mainly anterior mesiotemporal region) and epilepsies of extratem- poral origin. The main reasons for this classi \201 cation are the high epileptogenicity of the mesiotemporal structures (hippocampus, amygdala, and parahipp ocampal gyri), the high frequency of mesial temporal sclerosis in the refractory population , and the relatively high representation of temporal lobe epilepsy in the surgically remedi able epilepsies. In contrast, extratemporal lobe epilepsies consist of heterogeneous neuroa natomical regions with often ill-de \201 ned borders and more heterogeneous aetiologies wh ich in general make identi \201 cation of the epileptogenic zone more dif \201 - cult (2) . In particular with cases which are magnetic resonance imaging (MRI)-negative or \200\230 non-lesional \200\231, localizing the epilep- togenic zone can be quite challenging. Surgic ally, the structures that are usually resected in mesiotemporal epilepsies are \200\230sta ndard- ized \200\231 (i.e. amygdala, hippocampus, parahippocampal gyri) whilst in extratemp oral epilepsies, the epileptogenic structures vary for each case. Another challenge with su rgical resections in extratem- poral epilepsies is the possibility of the overlapping of th e epilep- togenic zone and eloquent cortices. In such cases, careful mapping of eloquent co rtex is essential for the avoidance of signi \201 cant and permanent neurological de \201 cits. These factors are some of the main reasons why favorable outcomes are more common in the resective surgery of mesiotemporal epilepsies. Extratemporal epilepsies are commonly classi \201 ed according to the presumed anatomical localization of the epileptogenic zone. Such a classi \201 cation can be based on lobar re gions, i.e. into frontal, parietal, occipital, or insular. The anatomical localization can also be speci \201 ed with more precision. For example, frontal lobe epilepsies can be sub divided into lateral frontal, mesial frontal, prefrontal, basal frontal, and orbitofrontal. One should also note that multiple lobar or sublobar territorial overlap may occur (Fig. 2 9.1 ). Epileptogenic and symptomatogenic zones In any discussion of surgical therapy in epilepsy, the important concepts of the epileptogenic zone, seizure onset zone, irritative zone, symp tomatogenic zone, functional de \201 cit zone, epileptogenic lesion zone, and their mutual spatial relationships need to be fully Although historically the \201 rst epilepsy surgeries were carried out in extratemporal c ases, large published series from different epi- lepsy centers suggest that only 30 \200 \22340 % of surgical resections in the oxford textbook of epilepsy and epileptic seizures 308 Operctilum parietale Sulcus praecentralis sup. Gyrus praecentralis Sulcus centralis Pars operoularis gyri frontalis inferioris Gyrus postcentralis Sulcus postcentralis Gyrus frontalis superior Gyrus circumflexus Sulcus interparietalis Gyrue frontalie medius Gyrus angularis Labulus parie- talis superior Lobulus parie- talis inferior Sulcus parieto- accipitalis (Polus frontalis) Pars triangularis gyrifront. zinferioris fissurae cercbri lateralis ramus frontalis ramus parietalis Gyri occipi- talss laterales fisscva cerebri lateralis (Polus temporalis) Gyrus temporalis superior Sulcus temporalis superior (Polus occipitalis) Sulcus occipitalis transversus Sulcus temperalis superior Gyrus temporalis medius Sulcus temporalis medius Fissura cerebri lateralis, ramus occipitalis Gyrus temporalis inferior Truncus corporis callosi Sulcus cinguli 37 Columna fornicis Crus fornicis Commissura rostralis (ant.) Sulcus sub- parietalis Sulcus parieto- occipitalis Septum pellucidum Fissura calcarina Gyrus occipito temp. medialis Splenium cor- poris callosi Isthamus gyri cing. Genu cor- poris callosi Bulbus olfactorius Gyrus occipito temp. lateralis Rostram corporis callosi Gyrus paraterminolis Gyrus fasciolaris Gyrus dentatus Area subcallosa Fimbria hippocampi Lamina terminalis Sulcus collateralis Chiasma fasciculorum optic. Fig. 29.1 Anatomical classi \201 cation of the human brain. appreciated (Chapter 27). By de \201 nition, the epileptogenic zone is the area of cortex that is indispensable for the generation of epilep- tic seizures and its total removal resu lts in seizure freedom. In other words, if surgical resection renders complete seizure free dom, a conclusion can be made that the epileptogenic zone was included in the resected cort ex (7). However, there is no direct method to measure the epileptogenic zone. Detailed surg ical work-up allows more or less precise measurement of the other \201 ve zones mentioned (seizure onset zone, irritative zone, symptomatogenic zone, epilep- togenic lesion, functi onal de \201 cit zone), all of which have a close spatial relationship with the epileptoge nic zone. Their analysis allows the epileptologist to establish a more or less reliable hyp oth- esis regarding the location and extent of the epileptogenic zone. The symptomatogenic zone is de \201 ned as an area of cortex whose ictal activation produc es the initial ictal symptoms. Careful analy- sis of seizure semiology helps to identify th is zone. Not uncom- monly, seizures arise from a relatively silent region in the brain and do not become symptomatic until they propagate to eloquent cortex. In other words, seizure semiology points to the symptoma- togenic zone which frequently does not overlap with the e pilep- togenic zone. Figs. 29.2 \200\22329.4 illustrate the symptomatogenic zones and seizu re types (8). Some of these seizure semiologies are repro- ducible through direct cortical stimulation of the symptomatogenic cortex in patients with subdural and depth electrodes. T he exact symptomatogenic regions of some seizure semiologies are less understood and remain controversial, perhaps due to involvement CHAPTER 29 resective surgery of extratemporal epilepsy 309 of more complex neural networks. In our institution we use a semiological classi \201 cati on of epileptic seizures to describe each seizure type and its topography. Often clinical s eizures consist of more than one seizure type component and in this classi \201 cation, ev olution and propagation of seizures can be described by linking seizure components. Here we only discuss the seizure semiologies of particular interest in extratemporal epilepsies an d a full discus- sion of epileptic seizures and semiological classi \201 cation can be fou nd in published references (4, 8). Primary motor (4, 6) Somatosensory (1, 2, 3) Auditory aura (14) Negative motor (24) Speech (22, 39) Visual aura (17, 18) Common seizure semiologies which can be seen in frontal lobe epilepsies include simple moto r, hypermotor, complex motor, and dialeptic seizures. Because of the connectivity of the la teral orbitof- rontal lobe to the anterior temporal lobe, epilepsies of these regions can m imic temporal lobe epilepsy. Seizures with brief duration, nocturnal predominance, minimal postictal confusion, and rapid generalization are more characteristic of frontal lobe epile psies. While hypermotor and complex motor seizures are often indica- tive of frontal lobe i nvolvement, the exact symptomatogenic zones of these seizures are not well known. Ictal act ivation of primary motor cortex often produces contralateral clonic activity in a topograph ical manner and marching of the clonic activity is indicative of seizure spread over the mo tor strip (Jacksonian march). Ictal activation of supplementary motor cortex (SMA) typicall y produces bilateral asymmetric tonic posturing with preserved consciousness. Often, a fenc ing posture, vocalization or speech arrest is seen in these seizures. Activation of the fro ntal eye \201 eld usually leads to contralateral versive movement of the eyes and head (v ersive seizure). Olfactory auras can occur when the orbitofrontal region and rectus gyrus a re activated. Auditory auras occur with activation of Heschl \200\231s gyrus. Ictal activat ion of the oper- culum and insula are thought to produce salivation, mastication and swallo wing movements, laryngeal constriction, unpleasant sensations in the pharyngolaryngeal regi on, and a feeling of stran- gulation. Because of the strong connectivity of the anterior in sula and mesiotemporal structures, insular epilepsies can also mimic temporal lobe epilepsy . It has been proposed that ictal involvement of cingulate gyrus is responsible for automat isms (automotor sei- zures) but this has not been reproduced by conventional cortical stimu lation methods and remains controversial. Seizures originat- ing from the parietal lobe can be divided into those of post-central gyral origin and posterior parietal gyral origin. Po st-central gyrus ictal activation often produces contralateral positive somatosen- sory sym ptoms such as tingling sensation. Less commonly these seizures are associated with numbness or pain. Posterior parietal activation can produce somatic or visual illusions. Seizures o f the occipital lobe often result in primary visual phenomena of \202 ashing or \202 ic kering white and colored lights if the primary visual cortex is activated. Complex visual h allucinations can occur with activa- tion of association visual cortex. One should keep in mind that epi- lepsies of a certain lobe can also spread to other lobes to produce symptoms and secondary generalized tonic \200\223clonic seizures can occur in any focal epilepsy (4 , 8, 9). Speech (44) Fig. 29.2 Symptomatogenic zones in convexity regions identi \201 ed by electrical stimulat ion. Reproduced from Hans O. L ders, Soheyl Noachtar. Atlas of Epileptic Seizures and Synd romes . W.B. Saunders Company, 2001. Primary motor (4) Focal tonic (6) Somatosensory (1, 2, 3) Negative motor (8) Automatisms (24) (Controversial) Visual aura (17, 18) Olfactory aura (11) Psychic aura (27, 28, 34) Speech (35, 36) Fig. 29.3 Symptomatogenic zones in mesial cortices identi \201 ed by electrical stimulatio n. Reproduced from Hans O. L ders, Soheyl Noachtar. Atlas of Epileptic Seizures and Syndro mes . W.B. Saunders Company, 2001. Taste Swallowing Hearing Digestive tract Etiology Whilst the etiology of most epilepsies is likely to be multifactorial (i.e. suscep tibility genes plus exogenous factors plus one or more neuropathological lesions), here we refer to etiology mainly as an identi \201 able neuropathology. From an aetiological stand point, focal Fig. 29.4 Symptomatogenic zones in the insula and operculum identi \201 ed by electrical s timulation. Reproduced from Hans O. L ders, Soheyl Noachtar. Atlas of Epileptic Seizures a nd Syndromes . W.B. Saunders Company, 2001. oxford textbook of epilepsy and epileptic seizures 310 can be helpful in the non-invasive mapping of eloquent cortex. While fMRI usually reliably localizes the primary motor cortex, its reliability in lateralization and localization of l anguage areas depend on the subject \200\231s cooperation and the experience of the centers utilizing this investigation (10, 11). epilepsies can be classi \201 ed into two major groups, namely MRI negative or \200\230no n-lesional \200\231 and MRI positive or \200\230lesional \200\231 epilepsies (10, 11). Thi s distinction is particularly signi \201 cant because most surgical series have shown that the presence of an identi \201 able pathology on MRI is associated with a more favorable surgical outcome (12 \200\22314). We prefer the term \200\230MRI negative \200\231 over th e expression \200\230non-lesional \200\231 which can give the wrong impression of a comple te absence of an identi \201 able pathology. Interictal positron emission tomography (PET) scanning often plays an important role in non -lesional temporal lobe epilep- sies but its role in extratemporal epilepsies is less clear ly de \201 ned. More recently, it has been reported that the overlaying of MRI and PET ima ges can be a powerful tool in the identification of abnormalities that are not visually det ectable by either method used separately (30). MRI positive aetiologies include neoplasms, vascular malforma- tions (arteriovenous malform ation (AVM), cavernous angioma), malformations of cortical development (MCDs), tuberous scl ero- sis, non-speci \201 c encephalomacias, and gliosis (from remote strokes, traumatic br ain injuries, encephalitis, and anoxic brain injuries). Neoplasms and MCDs are the two majo r groups representing 30 \200\22370 % of the aetiologies in reported surgical series. Neopl asms that are seen in patients with chronic epilepsy include low-grade astrocytic tumors, o ligodendrogliomas, gangliogliomas, dysem- bryoplastic neuroepithelial tumors, and pleomorph ic xanthoastrocytomas (14 \200\22317). Ictal SPECT (single-positron emission computed tomography) with technetium 99-m has been fo und very useful in identifying seizure onset area in some centers (21, 22). SISCOM, is a st atistical method expressing in z-values the difference of ictal from interictal SPECT and s uperimposing the z-values on an MRI. SISCOM is often used to identify areas of hypermetabol ism during ictal activation of the cortex. One should be aware of technical and interpretat ional limitations of this method which may lead to false localization of the epileptogenic zone elucidating areas of seizure propagation instead of the seizure onset zone. Focal cortical dysplasia without balloon cells is the etiology in most cases with negative MRIs. Identi \201 cation of the epileptogenic zone in these cases is challenging but surgi cal outcome can be excellent if neurophysiology and other presurgical techniques de \201 n e a limited focus with clear borders located at a safe distance from eloquent cortex. Taylo r type cortical dysplasia (with balloon cells) can usually be seen in high-resolution MRI a nd is classi \201 ed under lesional epilepsies (18). All surgical patients should also have a neuropsychological evaluation to determine their n eurocognitive baseline and to identify possible preoperative de \201 cits. Neuropsychologi cal data can be helpful in predicting postoperative neurocognitive outcome. The Wada test i s still the gold standard study in lateral- izing the dominant hemisphere for language and may need to be done in extratemporal cases when there is concern for developing language de \201 cits from resective surgery. Presurgical work-up The presurgical work-up of extratemporal epilepsies follows the same ap proach and rationale as temporal lobe epilepsies. Non- lesional cases and patients in whom the epileptogenic zone is in close proximity, or even overlaps with eloquent cortex, almost invariably require chronic invasive EEG recordings and detailed brain mapping by direct el ectrical stimulation. In general EEG plays a critical role in localizing the seizure onset and irritative zones. However, in extratemporal epilepsies, scalp EEG may not show any inte rictal abnormality. Besides, early ictal changes may not be detectable until seizure activi ty has spread to the brain con- vexity (19, 20). This is due to limitations of scalp EEG in detecting epileptiform activity from deeper brain regions which include a large portion of extratemporal cortex. The common problem areas for scalp EEG in detecting interictal and i ctal discharges include mesial frontal cortex (i.e. the SMA), the orbitofrontal cortex (whi ch can be semiologically indistinguishable from temporal lobe seizures), and also small foc i in the primary motor or sensory cortex which can produce clinical seizures but remain und etected by scalp EEG because of the relatively restricted area of cortex involved. Ictal EE G changes may also be obscured by muscle arte- fact that, not infrequently, occurs simultan eously with EEG seizure onset in extratemporal lobe epilepsies. Invasive (intracranial) EEG is the gold standard for the precise identi \201 cation of the ictal onset and irritative zones. Essentially, almost all cases with negative MRI and thos e cases in which the epileptogenic lesion is close to eloquent cortex will need invasive EE G (23 \200\22325). Careful planning of subdural or depth electrodes placement is essential, based on analysis of the information gath- ered from all non-invasive studies. A clear hyp othesis with regard to the localization of the epileptogenic zone should be formulated and appropriate invasive studies capable of con \201 rming the hypoth- esis as well as de \201 ning with precision the location and extent of the epileptogenic zone, should be plann ed. Invasive EEG studies should be carried out in experienced centers that bene \201 t fro m modern neurophysiological and neurosurgical technologies with highly skilled epileptologi sts and neurosurgeons. In more challenging cases, invasive EEG studies may need to be stage d into more than one implantation operation. During the second stage, more elec- trodes may need to be inserted for accurate localization of the epi- leptogenic zone based on informa tion derived from the \201 rst stage. Direct electrical stimulation of the cortex remains the gold stand- ard for brain mapping. Detailed and careful mapping of eloquent cortex can be done extraoperatively in the epilepsy monitoring unit while patients are fully awake an d cooperative. Cortical mapping needs to be performed by a trained and experienced neurophy si- ologist. Intraoperative mapping is more limited because of time constraints in the oper ative room and technical dif \201 culties in per- forming craniotomies under awake conditi ons. However, mapping in the operative room can be done for patients who do not undergo chr onic invasive EEG recordings or in order to con \201 rm the results of extraoperative mapp ing. MRI is the cornerstone of any search for structural neuropathol- ogies and obtaining a high -resolution epilepsy protocol MRI is crucial in all surgical candidates. Focal cortical dys plasia can be very dif \201 cult to detect on routine MRI. High-resolution, 3 Tesla MRIs r ead by experienced neuroradiologists may not reveal a sub- sequently pathologically con \201 rmed abnormality. Functional MRI (fMRI) is becoming more available in major epilepsy c enters and CHAPTER 29 resective surgery of extratemporal epilepsy 311 dysplasia and generalized ictal EEG patterns have been reported to be other predictors of p oorer surgical outcomes in frontal epilepsy resections. Surgical methods and outcomes Lesionectomy is the most common type of surgical resection in extratemporal epilepsy. In most cases, complete resection of the visible MRI lesion is nec essary to achieve seizure freedom. However, in the majority of the patients, additional res ection of the area surrounding the lesion is also necessary for a successful outcome. The e xtent of perilesional resection is determined by the pathology of the lesion and also the r esults of invasive ictal and interictal EEG recordings. Besides, mapping of possible adjace nt eloquent cortex will also in \202 uence the extent of the cortical resection. In cases with no identi \201 able lesion on MRI the extent of the topectomy is de \201 ned primari ly by functional data (ictal and interic- tal EEG,). Modern neurosurgical operating rooms b ene \201 t from neuronavigation and stereotactic systems that can aid surgery with more pr ecise resection. In large retrospective series, the occurrence of complications have been reported as 0.4 % for perisurgical death, 5 % for infec- tion, 6 % for neurological de \201 cits (3 % were t ransient), and 6 % for behavioral and cognitive complications (26, 29). Case studies Case A A 59-year-old woman with a history of epilepsy since age 25. Her seizur es consisted of stereotyped hypermotor movements of the right upper extremity with no alter ation of awareness, occa- sionally followed by secondary generalized tonic \200\223clonic s eizures. Seizures occurred up to 20 times per day mostly during sleep. Her epilepsy remaine d intractable despite treatment with different antiepileptic medications. She had a surgica l evaluation with inva- sive EEG recording more than 30 years ago, prior to availability of MRI as an investigational tool. At that time she underwent bifron- tal depth electrode pla cement through burr holes. This evaluation failed to lateralize the origin of her seizures and no surgical resec- tion was performed. She underwent another surgical evaluation more r ecently. A presurgical MRI showed bifrontal encephaloma- lacia and gliosis under the previo us surgical burr holes. Due to lack of prior MRI for comparison, a differentiation between the possi- bilities of primary lesions versus postsurgical changes from prior depth electro des placements could not be made. Scalp EEG was negative interictally and showed no changes during her habitual seizures. She underwent stereotactic placement of multiple depth elect rodes in both frontal lobes in two stages. Perilesional, anterior cingulate, orbitofrontal, frontal pole, and lateral frontal areas were sampled bilaterally. After recording numerous seizures it was con- cluded that the seizures originated primarily in the right perile- si onal area and rapidly propagated to the contralateral frontal lobe. She underwent a partial right frontal lobectomy which included There has not been a prospective controlled study in extratem- poral resective surgery and outcomes from published retrospective surgical series vary widely. This outcome variability is likely related to the heterogeneity of these cases, selection biases, different inves- tigational approaches, and the variability of surgical methods amongst different epilepsy c enters. Nevertheless, it is clear that in comparison to temporal lobectomies, seizure-free outcomes are lower in extratemporal resections (2). In a systemic review of out- come data in 298 neocortical resections from 24 published studies with more than 1-year follow-up, a seizure-free rate of 50 % and an improvement rate of 79 % were found (26). Another meta-ana lysis of surgical outcomes found long-term (more than 5 years follow- up) seizure-free rate s of 34 % for extratemporal resections (27). Results from a major epilepsy center showed th at the seizure-free rate for frontal lobe resections drops from 56 % at 1-year follow-up to 30 % at 5 years (28). So far, the existence of an identi \201 able struc- tural lesion is the single most important factor for the prediction of a favorable surgical outcome in ext ratemporal resections. Cortical Fig. 29.5 Bifrontal lesions. Note the burr hole defects in the skull from previous surgery overlying the lesions. oxford textbook of epilepsy and epileptic seizures 312 Fig. 29.6 (See also Color plate 18.) Location of depth electrodes can be determined by the fusion of high-resolution computed tomography images (taken after placing the electrodes) w ith preoperative MRI. The red circle shows the area of seizure onset around the right mesio frontal lesion.