medication-resistant generalized epilepsy . Neurology 1999 ; 52 : 1510 \200\223 12 . 72. Arthur TM , Saneto RP , Sotero de Menezes M , Devinsky O , LaJoie J , 51. Quintana C , Tecoma ES , Iragui VJ . Evidence that refractory partial onset and general ized epilepsy syndromes respond comparably to adjunctive vagus nerve stimulation therapy . Epilepsia 2002 ; 43 (S 7 ): 344 \200\223 5 . et al . Vagus nerve stimulation in children with mitochondrial electron transportation chai n de \201 ciencies . Mitochondrion 2007 ; 7 : 279 \200\223 83 . 73. Koutroumanidis M , Binnie CD , Henessy MJ , Alarcon G , Elwes RDC , Toone BK , et al . VNS in patients with previous unsuccessful resective epilepsy surgery: antiepileptic and ps ychotropic effects . Acta Neurol Scand 2003 ; 107 : 117 \200\223 21 . 52. Michael NG and Devinsky O . Vagus nerve stimulation for refractory idiopathic generalized epilepsy . Seizure 2004 ; 13 : 176 \200\223 8 . 53. Kostov H , Lars son PG, Roste GK . 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Cardiorespiratory variables and sensation during stimulation of the left vagus in patients with epilepsy . Epilepsy Res 1999 ; 35 : 1 \200\223 11 . 77. Charous SJ , Kempster G , Man ders E , Ristanovic R . The effect of vagal 56. Hosain S , Nikalov B , Harden C , Li M , Fraser R , Labar D . Vagus nerve stimulation t reatment for Lennox-Gastaut syndrome . J Child Neurol 2000 ; 15 : 509 \200\223 12 . nerve stimulation on voice . Laryngoscope 2001 ; 111 : 2028 \200\223 31 . 78. Ben Menachem E . Vagus nerve stimulation, side effects and long-term safety . J Clin Neurophysiol 2001 ; 18 : 415 \200\223 18 . 57. Helmers S , Al-Jayyousi M , Madsen J . Adjunctive treatment in 79. Clarke BM , Upton ARM , Grif \201 n HM . Cognitive motor function after electrical sti mulation of the vagus nerve . Pacing Clin Electrophysiol 1992 ; 15 : 1603 \200\223 7 . Lennox-Gastaut syndrome using vagal nerve stimulation . Epilepsia 1998 ; 39 (S 6 ): 169 . 58. Murphy J , Hornig G . Chronic intermittent stimulation of the left vagal nerve in nine children with Lennox-Gastaut syndrome . Epilepsia 1998 ; 39 (S 6 ): 169 . 80. Clarke BM , Upton ARM , Kamath M , Grif \201 n HM . Electrostimulation effects of the vagus nerve on balance in epilepsy . Pacing Clin Electrophysiol 1992 ; 15 : 1614 \200\223 30 . CHAPTER 30 vagal nerve stimulation and deep brain stimulation in epilepsy 325 101. Davis R . Cerebellar stimulation for cerebral palsy spasticity, function 81. Clarke BM , Upton ARM , Kamath M , Grif \201 n HM . Acute effects of high frequency va gal nerve stimulation on balance and cognitive motor performance in epilepsy: three case st udy reports . Pacing Clin Electrophyisol 1992 ; 15 : 1608 \200\223 13 . and seizures . Arch Med Res 2000 ; 31 : 290 \200\223 9 . 102. Wright GD , McLellan DL , Brice JC . A double-blind trial of chronic cerebellar stimulation in twelve patients with severe epilepsy . J Neurol Neurosurg Psychia try 1984 ; 47 : 769 \200\223 74 . 82. 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No evidence for cognitive side eff ects afer 6 months of vagus nerve stimulation in epilepsy patients . Epilepsy Behav 2001 ; 2 : 351 \200\223 6 . 85. Espinosa J , Aiello MT , Naritoku DK . Revision and removal of 105. Benabid A , Minotti L , Koudsie A , de Saint Martin A , Hirsch E . stimulating electrodes following long-term therapy with the vagus nerve stimulator . Surg N eurol 1999 ; 51 : 659 \200\223 64 . Antiepileptic effects of high-frequency stimulation of the subthalamic nucleus (corpus Luys i) in a case of medically intractable epilepsy caused by focal dysplasia: a 30-month follow -up: technical case report . Neurosurgery 2002 ; 50 : 1385 . 86. Tatum WO , Moore DB , Stecker MM . Ventricular asystole during vagus nerve stimulation for epilepsy in humans . Neurology 2000 ; 52 : 1267 \200\223 9 . 106. Alaraj A , Commair Y , Mikati M , Wakim J , Louak E , Atweh S . Subthalamic nucleus deep brain stimulation: a novel method for the treatment of non-focal i ntractable epilepsy . Neuromodulation: de \201 ning the future, poster presentation Clevel and Ohio 2001 . 107. Loddenkemper T , Pan A , Neme S , Baker KB , Rezai AR , Dinner DS , et al . Deep brain stimulation in epilepsy . J Clin Neurophysiol 2001 ; 18 : 514 \200\223 32 . 87. Asconape JJ , Moore DD , Zipes DP , Hartman LM , Duffell WH . Bradycardia and asystole with the use of vagus nerve stimulation for the treatment of epile psy: a rare complication of intraoperative device testing . Epilepsia 1998 ; 39 : 998 \200 \223 1000 . 88. Ali I , Pirzada N , Kanjwal Y . Complete heart block with ventricular asystole during left vagus nerve stimulation for epilepsy . Epilepsy Behav 2004 ; 5 : 768 \200\223 71 . 108. Handforth A , DeSalles A , Krahl SE . Deep brain stimulation of the subthalamic nucleu s as adjunct treatment for refractory epilepsy . Epilepsia 2006 ; 47 ( 7 ): 1239 \200\223 41 . 89. Andriola MR , Rosenweig T , Vlay S , Brook S . Vagus nerve stimulator (VNS): induction of asystole during implantations with subsequent succesfull stimulation . Epilepsia 2000 ; 41 (s 7 ): 223 . 109. Vesper J , Steinhoff B , Rona S , Wille C , Bilic S , Nikkhah G , et al . Chronic high-frequency deep brain stimulation of the STN/SNr for progressive myoclonic epil epsy . Epilepsia 2007 ; 48 ( 10 ): 1984 \200\223 9 . 110. Velasco M , Velasco F , Velasco AL . Centromedian-thalamic and hippocampal electrical stimulation for the control of intrac table epileptic seizures . J Clin Neurophysiol 2001 ; 18 : 495 \200\223 513 . 90. Ardesch JJ , Buschman HP , van der Burgh PH , Wagener-Schimmel LJ , van der Aa HA, Hage man G . Cardiac responses of vagus nerve stimulation: intraoperative bradycardia and subseq uent chronic stimulation . Clin Neurol Neurophysiol 2007 ; 109 : 849 \200\223 52 . 91. Amark P. Stodberg T , Wallstedt L . Late onset bradyarrhythmia during vagus nerve stimulation . Epilepsia 2007 ; 48 ( 5 ): 1023 \200\223 5 . 111. Velasco F , Velasco M , Jimenez F , Velasco AL , Rojas B , Perez ML . Centromedian nucleus stimulation for epilepsy. Clinical, electroencephalographic and behavi oral observations . Thal Syst 2002 ; 1 : 387 \200\223 98 . 92. Nyenhuis JA , Bourland JD , Foster KS , Graber GP , Terry RS , Adkins RA . Testing of M RI compatibility of the cyberonics model 100 NCP and model 300 series lead . Epilepsia 1997 ; 38 (S 8 ): 140 . 112. Velasco A , Velasco F , Jimenez F , Velasco M , Castro G , Carrillo-Ruiz 93. Benbadis SR , Nyhenhuis J , Tatum WO , Murtagh FR , Gieron M , Vale JD , et al . Neuromodulation of the centromedian thalamic nuclei in the treatment of genera lized seizures and the improvement of the quality of life in patients with Lennox-Gastaut s yndrome . Epilepsia 2006 ; 47 ( 7 ): 1203 \200\223 12 . FL . MRI of the brain is safe in patients implanted with the vagus nerve stimulator . Seizu re 2001 ; 10 : 512 \200\223 15 . 94. Duncan J . The current status of neuroimaging for epilepsy . Curr Opin Neurol 2003 ; 16 : 163 \200\223 4 . 113. Fisher RS , Uematsu S , Krauss GL , Cysyk BJ , McPherson R , Lesser RP , et al . Place bo-controlled pilot study of centromedian thalamic stimulation in treatment of intractable seizures . Epilepsia 1992 ; 33 : 841 \200\223 51 . 95. Achten E , Jackson GD , Cameron JA , Abbott DF , Stella DL , Fabinyi GCA . Presurgical evaluation of the motor hand area with functional MR imaging in patients with tumors and dysplastic lesions . Radiology 1999 ; 210 : 529 \200\223 38 . 114. Parain D , Blondeau C , Peudenier S , Delangre T . Vagus nerve stimulation in refracto ry childhood absence epilepsy . Epilepsia AES abstract , 2003 . 96. Sucholeiki R , Alsaadi TM , Morris GL , III , Ulmer JL , Biswal B , Mueller WM . fMRI i n patients implanted with a vagal nerve stimulator . Seizure 2002 ; 11 : 157 \200\223 62 . 115. Hodaie M , Wennberg R , 102. Wright GD , McLellan DL , Brice JG . A double-blind trial of chronic cerebellar stimulation in twelve patients with severe epile psy . J Neurol Neurosurg Psychiatry 1984 ; 47 : 769 \200\223 74 . 116. Andrade DM , Zumste g D , Hamani C . Long-term follow-up (up to 97. Bohning DE , Lomarev MP , Denslow S , Nahas Z , Shastri A , George MS . Feasibility of vagus nerve stimulation-synchronized blood oxygenation level-dependent functional MRI . Inv est Radiol 2001 ; 36 : 470 \200\223 9 . 7 years) of patients with thalamic deep brain stimulation for epilepsy . Neurology 2006 ; 6 6 : 1571 \200\223 3 . 98. Narayanan JT , Watts R , Haddad N , Labar DR , Li PM , Filippi CG . 117. Kerrigan JF , Litt B , Fisher RS , Cranstoun S , French JA , Blum DE , et al . Cerebral activation during vagus nerve stimulation: a functional MR study . Epilepsia 2002 ; 43 : 1509 \200\223 14 . Electrical stimulation of the anterior nucleus of the thalamus for the treatment of intract able seizures . Epilepsia 2004 ; 45 : 346 \200\223 54 . 99. Lomarev M , Denslow S , Nahas Z , Chae JH , George MS , Bohning DE . 118. Wiebe S , Blume WT , Girvin JP , Eliasziw M . A randomized, controlled Vagus nerve stimulation (VNS) synchronized BOLD fMRI suggests that VNS in depressed adults has frequency/dose dependent effects . J Psychiatr Res 2002 ; 36 : 219 \200\223 27 . trial of surgery for temporal lobe epilepsy . N Engl J Med 2001 ; 345 : 311 \200\223 18 . 119. Bragin A , Wilson CL , Engel J . Chronic epileptogenesis requires 100. Proctor M , Gale K . Basal ganglia and brain stem anatomy and development of a network of pathologcially interconnected neuron clusters: a hypothesis . E pilepsia 2000 ; 41 : S144 \200\223 52 . physiology . In: Engel J , Pedley TA (eds) Epilepsy: The Comprehensive CD Rom . Philadelphi a, PA: Lippincot Williams and Wilkins , 1999 . oxford textbook of epilepsy and epileptic seizures 326 (5 Hz) frequency on afterdischarges in kindled rats . Epilepsy Res 2010 ; 88( 2 \200\2233 ) : 239 \200\223 46 . 120. Kemppainen S , Jolkkonen E , Pitkanen A . Projections from the posterior cortical nucl eus of the amygdala to the hippocampal formation and parahippocampal region in rat . Hippoc ampus 2002 ; 12 ( 6 ): 735 \200\223 55 . 126. Wyckhuys T , Boon P , Raedt R , Van Nieuwenhuyse B , Vonck K , Wadman W . Suppression of hippocampal epileptic seizures in the kainate rat by Poisson dist ributed stimulation . Epilepsia 2010 ; 51 ( 11 ): 2297 \200\223 304 . 121. Wilson CL , Engel J : Electrical stimulation of the human epileptic limbic cortex . In: Devinsky O , Beric A , Dogali M (eds) Electric and magnetic stimulation of the brain and spinal cord , pp. 103 \200\223 13 . New York : Raven Press , 1993 . 127. Bragin A , Wilson CL , Engel J . Increased afterdischarge treshold during kindling in epileptic rats . Exp Brain Res 2002 ; 144 : 30 \200\223 7 . 122. Lian J , Bikson M , Sciortino C , Stacey WC , Durand DM . Local 128. Velasco M , Velasco F , Velasco AL , Boleaga B , Jimenez F , Brito F , et al . Subacut e electrical stimulation of the hippocampus blocks intractable temporal lobe seizures and p aroxysmal EEG activities . Epilepsia 2000 ; 41 : 158 \200\223 69 . suppression of epileptiform activity by electrical stimulation in rat hippocampus in vitro . J Physiol 2003 ; 547 : 427 \200\223 34 . 123. Su Y , Radman T , Vaynshteyn J , Parra LC , Bikson M . Effects of high-frequency stimulation on epileptiform activity in vitro: on/off control paradigm . Epi lepsia 2008 ; 49 ( 9 ): 1586 \200\223 93 . 129. Tellez-Zenteno JF , McLachlan RS , Parrent A , Kubu CS , Wiebe S . Hippocampal electrical stimulation in mesial temporal lobe epilepsy . Neurol 2006 ; 66 : 14 90 \200\223 4 . 124. Wyckhuys T , De Smedt T , Claeys P , Raedt R , Waterschoot L , Vonck K , et al . High frequency deep brain stimulation in the hippocampus modi \201 es seizure characteristics i n kindled rats . Epilepsia 2007 ; 48 : 1543 \200\223 50 . 130. Velasco A , Velasco F , Velasco M , Trejo D , Castro G , Carrillo-Ruiz JD . Electrical stimulation of the hippocampal epileptic foci for seizure control: a double-blind, long-te rm follow-up study . Epilepsia 2007 ; 48 ( 10 ): 1895 \200\223 903 . 125. Wyckhuys T , Raedt R , Vonck K , Wadman W , Boon P . Comparison of hippocampal deep br ain stimulation with high (130 Hz) and low CHAPTER 31 Other Surgeries for Epilepsy and New Approaches Kitti Kaiboriboon and Samden D. Lhatoo Introduction In this chapter, we describe epilepsy surgeries at two ends of the spectrum in terms of the volume of brain tissue subjected to sur- gery. Hemispherectomies, at the one end, represent extensive, complex, unilateral resections and removal of close to entire hem i- spheres of epileptogenic brain whilst multiple hippocampal transections (a new surgical technique) at the other end, constitute discrete, limited transections of just one hippocam pus. Although resection of the epileptogenic zone offers the most effective method of obtai ning seizure freedom as detailed in previous chapters, this is not always possible. Unaccep table proximity of the epileptogenic zone to eloquent cortex can contraindicate wide resect ion as can multifocal epilepsy where multiple resections are impractical or dangerous. In t he generalized epilepsy syndromes, resection is clearly not possible. In many of these situ ations, an attempt at sei- zure freedom or a substantial reduction in seizure burden can st ill be made through additional surgical techniques that do not involve removal of the epile ptogenic zone or stimulator implantation. track (2). This process is continued over the selected area until the abnormal discharges o n simultanous electrocorticography is minimized or abolished (Fig. 31.2). The utility of MST in epilepsy can be measured by assessing postoperative functional de \201 cits (if any) and seizure control. In general, it is accepted that MST leads to minima l long-term functional de \201 cits. However, initial neurological de \201 cits can be qu ite common (3 \200\2238). Recent functional magnetic resonance imag- ing (MRI) (9), positro n emission tomography (PET) (10), and transcranial magnetic stimulation studies (11) con \201 rm that MST does not interfere with the functioning of transected cortical regions. On the other hand, the ef \201 cacy of MST in controlling seizures has been debated. Seizu re freedom outcomes vary from study to study depending primarily on the indications for sur gery and whether cortical resection is performed to supplement MST. In general, a combinati on of MST and resection has a higher rate of seizure freedom than pure MST (1, 5, 7, 8, 12 \200\22315). A meta-analysis evaluating 211 patients, most of whom underwent MST combined w ith cortical resection, demonstrated that MST with and without accompanying resection had a more than 95 % reduction in seizure frequency (16). Interestingly, approximately 15 \200 \22320 % of patients had increased frequency of simple partial seizures after MST, pre- sum ably due to disconnection of inhibitory inputs from neigh- bouring cortex (16). Late seizur e recurrence can occur in some patients who initially experience good seizure control and c on- versely, late improvement in patients with initial, relatively poor outcome has been ob served (7, 17). The mechanisms of late seizure recurrence or late improvement of seizure co ntrol are unknown. Multiple subpial transection The principle behind multiple subpial transection (MST) epito- mizes the classical situation where resection of a brain region iden- ti \201 ed as the l ikely epileptogenic zone would probably result in signi \201 cant and unacceptable neurolo gical de \201 cits and where resec- tive surgery would therefore be impractical (Box 31.1 ). Morrell et al. (1) initially described MST for this particular scenario. The technique i s based on the columnar organization of normal human cortex, the hypothesis that synchroniz ation and propagation of epileptic spikes and/or seizures often occurs horizontally and tha t a critical mass of cortex is required to generate seizures. MST cuts horizontally oriente d cortical \201 bres while preserving vertically ori- ented \201 bres as well as blood vessels (Fig. 31.1), thereby blocking the synchronization of epileptogenic neurons without causing functional de \201 cit. The plan for MST (e.g. de \201 ning the cortical area tha t will be transected) is critical and the distance between cuts should be approximately 5 m m. Transections are made by passing a modified right-angled hook transector deep into the g yrus (Fig. 31.1) which is then swept forward perpendicular to the corti- cal surface toward s the opposite sulci. The tip of the transector is raised and pulled backwards underneath t he pia, creating a small Box 31.1 Candidates for multiple subpial transection \227\206 Intractable focal or multifocal epilepsy involving eloquent cortex \227\206 Epilepsia partialis continua or refractory focal status epilepticus \227\206 Landau \200\223Kleffner syndrome \227\206 Rasmussen \200\231s encephalitis with functional use of hand and/or language. oxford textbook of epilepsy and epileptic seizures 328 A B Fig. 31.1 Artist \200\231s drawings to illustrate the technique of insertion and movement o f the subpial transector (A) and the anatomical principles involved in multiple subpial tra nsection (B) where horizontally oriented nerve \201 bres are transected whilst vertically oriented \201 bres are spared. Reproduced permission of Journal of Neurosurgery , Americ an Assn. of Neurosurgeons (1). atypical LKS or autistic epileptiform regression, only a temporary response to MST has been demonstrated (31, 32). The application of MST in patients with multifocal epilepsy who are not candidates for conv entional surgery has shown promising results. A study of 13 patients with independent multi focal epilep- togenic foci demonstrated that cortical resection combined with MST in eloque nt cortex improved seizure outcome in 77 % (15). The best results were observed in patients with discrete epilep- togenic foci limited to two lobes. Another study of 61 patients with multifocal epilepsy who underwent MST with and without cortical resection found no signi \201 cant differences in seizure outcomes between the two groups (18). Approximately half o f their patients were seizure free. Several MST series have contained patients with Rasmussen \200\231s encephalitis (3, 5, 6, 13, 33). Since Rasmussen \200\231s encephalitis is a progressive disease, most patients wit h this condition either did not have good outcome or achieved only temporary relief. In the se patients, therefore, MST should be considered as a mainly pallia- tive intervention to d elay hemispherectomy in patients who have functional use of hand and/or language (13). An improvement in seizure control after MST has been reported in a few patients with infant ile spasms (18, 34). In a report of two patients with infantile spasms (34), one patient de veloped infantile spasms after meningoencephalitis with a resulting diffuse struc- tural ab normality on MRI and focal metabolic abnormality on PET. The other patient had cortical dys plasia with focal metabolic abnormality on PET. Both patients had reduction of seizures fre - quency. In another report (18), two patients with infantile spasms underwent MST in both hemispheres. One patient became seizure free whereas the other patient did not show any imp rovement. In the same series (18), three patients with Lennox \200\223Gastaut syndrome also improved after MST. MST combined with cortical resection has also been used suc- cessfully in stopping seizures in patients with refractory focal status epilepticus or epilepsia partialis continua (19 \200\22324). In this situation, pure MST has been used in cortical dysplasia of the left mo tor cortex (25) and of the angular gyrus, superior temporal gyrus, and suprasylvian frontal lobe in another case (26). MST has also been used in a variety of epilepsy syndromes including Landau \200\223Kleffner syndrome (LKS), Rasmussen \200\231s encephalitis, Lennox \200\223Gastaut syndrome, and inf antile spasms (Box 31.1 ). However, no clear recommendations can be made for MST in these s yndromes based on the very small number of patients reported. A few surgical series of pati ents with LKS have demonstrated signi \201 cant improvement in language function after MST (27, 28) but this, however, has not been reproduced by others (8, 29, 30). Patient selecti on and resolution of the severe epilepti- form abnormality are important factors in predict ing good out- come (13). Incorrect diagnoses may contaminate some of the poorer reported re sults. In general, continued recovery of language function can be seen at least 6 months af ter surgery and adjunctive, intensive speech therapy is usually necessary. For patients wit h Multiple hippocampal transection Approximately 30 \200\22360 % of patients who undergo lang uage domi- nant anterior temporal lobectomy experience a signi \201 cant decline in verbal memory and visual naming postoperatively (35 \200\22338). Several studies suggest that pat ients with mild or moderate hippocampal neuronal loss have the greatest risk of postoperati ve memory decline (36, 39, 40). The severity of postoperative memory deterioration depends on the extent of removal of non-lesional hippocampus (41). CHAPTER 31 other surgeries for epilepsy and new approaches 329 A B Fig. 31.2 A) Electrocorticographic recordings obtained following removal of a cystic mening ocerebral scar from the right parietal cortex. Electrodes were placed as indicated on the s uperimposed diagram. Epileptiform potentials can be readily identi \201 ed in the channels labeled with electrodes numbered 12, 13, 15, 16. Overt symptoms were reported by the patie nt during the time intervals marked by upturned arrows. The electrographic accompaniments o f these symptoms may be discerned in derivations from electrodes 15 and 16. EKG = electroca rdiographic tracing. Reproduced permission of Journal of Neurosurgery , American Assn. of N eurosurgeons (1). B) Electrocorticographic recordings obtained following multiple subpial t ransection (MST) of the precentral gyrus and a small portion of the postcentral gyrus super ior to the ablation in the same patient. The ablated region is stippled; the zone subjected to MST is shown by diagonal lines. Electrode positions are shown on the superimposed diagr am. The electrical records from derivations overlying the transected zone (channels 9 to 16 ) reveal no trace of the epileptiform abnormality so prominently shown in (A). Reproduced p ermission of Journal of Neurosurgery , American Assn. of Neurosurgeons (1). oxford textbook of epilepsy and epileptic seizures 330 In order to minimize the impact of adverse neuropsychological outcomes, more limited resect ions of the mesial temporal struc- tures such as selective amygdalohippocampectomy or more restricted variants of anterior temporal lobectomy have been used. A recent review of diffe rent surgical approaches in mesial temporal lobe epilepsy demonstrated that more restricted or selective approaches provide good seizure outcome similar to standard or more extensive approaches (42). However, selective approaches yield better postoperative cognitive and me mory outcomes (42 \200\22345). Nonetheless, left-sided hippocampectomy can still result in signi \201 - cant memory decline (41, 46). av CA2 CA3 iv f dg CA1 CA4 ce sbc Recently, the principle of MST has been applied to the hippoc- ampus in patients with domin ant mesial temporal lobe epilepsy in order to preserve verbal memory (47, 48). The techniqu e of multi- ple hippocampal transection (MHT) (Fig. 31.3) was developed based on the hypoth esis that disruption of horizontal connections in the pyramidal layer of the hippocampus ca n interrupt synchro- nization and spread of epileptic activity without interfering with mem ory function (48). To avoid the disruption of direct hippoc- ampal pathways, the hippocampu s is accessed via a small corticot- omy on the anterior superior temporal gyrus along the s ylvian veins (47). Intraoperative electrocorticography in the amygdala and hippocampus is n ecessary to determine the extent of transec- tion. When the amygdala produces epileptic dis charges, it is also resected. After the extent of MHT is determined, the pyramidal cell lay er and the dentate gyrus are transected sequentially from ante- rior to posterior using sma ll ring transectors (Fig. 31.3). The epi- leptic discharges in the hippocampus can complete ly disappear after transection is completed (Fig. 31.4). In some cases, resection of the an terior basal temporal and MST in the posterior basal temporal lobe may be required. A Shimizu et al. (47, 48) \201 rst reported MHT as an effective surgical approach with exce llent seizure and memory outcomes for patients with unilateral mesial temporal lobe epileps y. Between 2001 and 2006, 35 cases of intractable unilateral mesial temporal lobe epi- leps y with normal MRI underwent this procedure at their center. Twenty-two patients underwent l eft MHT and 23 patients had right MHT. Of the 23 patients who had more than 1 year follow-u p postoperatively, 78 % were seizure free and 17 % had rare seizures. Verbal memory was eva luated in 13 patients who underwent left MHT. Twelve of these patients did not show verbal memory decline at 6 months after surgery. Besides unilateral temporal lobe epi- lepsy, bila teral MHT was performed in 10 patients with bilateral temporal lobe epilepsy. However, 60 % of the patients had poor outcomes and one patient had severe memory de \201 cits (48) sug - gesting that the procedure is best restricted to unilateral mesial temporal lobe epilepsy . B Fig. 31.3 A) A schematic drawing of hippocampal transection. After the alveus is incised with micro-scissors, the pyramidal cell layer and dentate gyrus are transected using ring t ransectors with 2 mm and 4 mm diameters. ce, collateral eminence; iv, inferior ventricle; a v, alveus; f, \201 mbria; sbc, subiculum; dg, dentate gyrus. B) Intraoperative view of hi ppocampal transection is shown. Schematic drawing on the right illustrates transection line s (gray solid lines) being placed along the digitations marks at the hippocampal head and s mall surface vessels in the remaining area (47). Reproduced with permission from Journal of Clinical Neuroscience , Science Direct. carried out either as the sole procedure or with removal of the amygdala and temporal pole. In a more recent report of 10 patients with unilateral mesial tem- poral lobe epilepsy (49) , all patients had MHT with MST in the neocortex and some had resections of the temporal ti p. The median follow-up was 21 months (range 10 \200\22334 months). Nine patients had excel lent seizure outcomes, seven of whom were seizure free. Among patients who had pre- and pos toperative memory testing, 62 % had improvement of verbal memory, 37 % had improvement of v isual memory, and 37 % had a slight decline in visual memory. At our center, MHT is offered to patients with unilateral domi- nant, non-lesional mesial temporal lobe epilepsy and nor mal or excellent verbal memory indices. All such patients undergo intrac- ranial monitoring to con \201 rm mesial temporal epilepsy and MHT is MHT appears a logical approach for patients with unilateral, non-lesional mesial temporal l obe epilepsy, particularly where chances of signi \201 cant postoperative memory declines are otherwise high, and has a sound biological basis. The results from different groups so far are encouraging but short follow-up periods empha- size the requirement for larger seri es with long-term outcomes. Corpus callosotomy The rationale of surgical division of corpus callosum is to limit the pr opagation of epileptic activity to one hemisphere. This procedure CHAPTER 31 other surgeries for epilepsy and new approaches 331 A B Fig. 31.4 Electrocorticography over the hippocampus is recorded to determine the extent of the epileptic areas (A). The upper four leads are recorded from the hippocampal head and th e lower four from the hippocampal body and tail. After completion of hippocampal transectio n, active epileptic discharges over the hippocampus are abolished (B) (47) Reproduced with permission from Journal of Clinical Neuroscience , Science Direct. report that anterior section is as effective as complete section (58, 59). Currently, many centers prefer sectioning of the anterior two- thirds or three-quarters initially and reser ve the complete resection only for patients who do not have suf \201 cient improvement fol low- ing the initial procedure (53, 55, 60). Nevertheless, an upfront one-stage complete ca llosal section might be an optimal choice for patients with non-functional, severe global d evelopmental delay (54, 57, 61). was \201 rst performed in patients with epilepsy based on the observa- tions that the cor pus callosum was the major route of seizure prop- agation and that seizures usually improve d after occurrence of stroke or tumor involving the corpus callosum (50). Corpus cal- losot omy is considered palliative surgery for patients with severe medically intractable epileps y with major motor manifestations such as tonic, atonic, myoclonic, or generalized tonic \200\223clonic sei- zures. Among these, drop attacks elicited by tonic or atonic sei- zures are most likely to improve (51). Patients with diffuse or multifocal pathologies who are n ot eligible for resective surgery such as infantile hemiplegia, Rasmussen \200\231s encepha litis, Lennox \200\223 Gastaux syndrome, Sturge \200\223Weber syndrome, and tuberous sclero sis might receive some bene \201 t. In general, patients with any debilitating non-resecta ble epilepsy should be considered for corpus callosot- omy regardless of age or type of epi lepsy (Box 31.2 ). Seizure improvement and reduction of bisynchronous discharges after corpus callosotomy has been well documented. Between 50 \200\22380 % of the patients who underwent callosotomy hav e at least 50 % seizure reduction (51, 55, 61 \200\22364). Atonic seizures usually respond best to callosotomy compared to other types of seizures (53) while focal motor seizures rec eive the least bene \201 t. Partial seizures can be worsened and sometimes new types of se izures can emerge after callosotomy, especially in patients with independent bifrontal epil eptogenic foci (60, 65, 66). A variety of techniques of corpus callosotomy have been described over the years. The moder n techniques are mainly restricted to division of the corpus callosum and the hippocampal c ommissure (52). However, how much of the structure is divided remains unclear. Some studies showed that the extent of callosal sections correlated with seizure outcome and, therefore , more extensive sections yielded better results (53 \200\22357). Other studies Several studies have investigated prognostic factors for callosot- omy outcomes. The result s from these studies, however, are con- \202 icting. For example, a few studies did not \201 nd age at seizure onset or at the time of surgery to have prognostic signi \201 canc e (58, 59, 62) whereas other studies suggest that younger age at the time of sur- gery or e arlier seizure onset have better outcomes including improvement in quality of life, family satisfaction, and fewer com- plications (67, 68). The presence of signi \201 cant cognitiv e impair- ment and/or mixed cerebral dominance are associated with poor outcome in a few st udies (58, 60, 67, 69). However, these \201 ndings have not been con \201 rmed by others (59, 70, 71). Moreover, recent series of callosotomy in children with severe mental retard ation demonstrate favorable results (61, 72). Ictal and interictal EEG have been found to b e prognostically useful in some studies (59, 67, 70, 71, 73). Ictal patterns of generalized slow spike wave dis- charges, electrodecrement, and non-evolving low amplitude fast activi ty have been associated with excellent outcomes (71). A few studies have shown that bilater al independent spikes are indicative of poor outcomes after callosotomy (67, 73). Disruptio n of syn- chrony as well as reduction of generalized bilateral synchronous spikes in the in traoperative or postoperative electroencephalogram (EEG) recordings are good indicators for favorable outcomes (59, 70). Some studies, however, have not found clear relationships bet ween EEG \201 ndings and outcomes after callosotomy (74, 75). Box 31.2 Candidates for corpus callosotomy Intractable generalized seizures with: \227\206 Drop attacks \227\206 Generalized tonic \200\223clonic seizures \227\206 Myoclonic seizures \227\206 Other major motor manifestations. Patients with diffuse or multifocal pathologies, e.g.: \227\206 Rasmussen \200\231s encephalitis \227\206 Lennox \200\223Gastaux syndrome \227\206 Sturge \200\223Weber syndrome \227\206 Tuberous sclerosis. oxford textbook of epilepsy and epileptic seizures 332 Corpus callosotomies can result in acute as well as chronic dis- connection syndromes. In t he acute setting, an apathetic mutism lasting days to weeks can occur, usually related to t he extent of cal- losal section. Other de \201 cits including hemiparesis and a variety of apraxias can also occur. In the chronic setting, de \201 cits can be more subtle. Poor na ming of objects in the dominant hemi \201 eld or of those held in the dominant hand can be observed. This is most likely due to a disruption of the pathways from the non-dominant he misphere where sensation or vision is perceived, to the domi- nant hemisphere where languag e is necessary to express receipt of these inputs. Several other, more subtle de \201 cits of motor, language and other functions may also exist. Box 31.3 Candidates for hemispherectomy a \227\206 Infantile spasms due to focal lesions (localization related) \227\206 Rasmussen \200\231s encephalitis \227\206 Sturge \200\223Weber syndrome \227\206 Hemispheric malformations of cortical development such as hemimegalencephaly, sch izencephaly, and cortical dysplasia involving signi \201 cant region of a hemisphere. \227\206 Porencephaly syndrome \227\206 Hemiplegia hemiconvulsion epilepsy syndrome (HHE). a There may be overlap between these categories. Hemispherectomy When seizures arise from multiple regions in one hemisphere, removal of the abnormal hemisphere seems a logical approach to getting rid of seizures. Drastic as this m ight seem, applied to the correct clinical situations and with the right expertise, it is a dra- matically effective intervention in many, both in the short and long term. Seizure fr eedom and cognitive outcomes can be impressive with postoperative de \201 cits that are ac ceptable enough to allow functionality. ipsilateral temporal lobe. The extent of the resection can vary to include the superolatera l frontal and parietal lobes but the poste- rior quadrant and anterior frontal lobes are us ually left intact. The blood supply to these structures is left undisturbed. The entire cor pus callosum is disconnected as are the white matter connec- tions of the remaining frontal lobe and the parietal and occipital lobes. The ipsilateral cingulate gyrus is also disconn ected. Complete disconnection can be technically dif \201 cult to achieve and up to a \201 fth of patients are subsequently found to have incomplete discon- nections, many of wh om continue to have seizures (84). Anatomical hemispherectomy, where the entire hemisphere is removed, was successfully perfor med with encouraging results in the late 1960s (76). However, severe late complications inc luding hydrocephalus and super \201 cial haemosiderosis occurred in up to one-third of the patients (77, 78). In order to reduce the risk of postoperative complications, several tec hnical modi \201 cations of hemispherectomy have been introduced, variously referred to as functional hemispherectomy, hemispherotomy, hemicorticec- tomy, peri-insularhemispherotomy , and hemispheric deafferenta- tion (79). In these, the anatomical cortical resection is su btotal rather than total but coupled with a physiological hemispherec- tomy where deafferen tation or disconnection is carried out. This approach of \200\230functional \200\231 hemis pherectomy is to minimize cortical resection and functionally isolate abnormal hemisphere b y dis- rupting neuronal \201 bre connections (80). A large meta-analysis of data from 11 epilepsy centers demonstrated that the new tech- niques that focused on disconnection were as good or slightly better with a clear bene \201 t in perisurgical morbidity compared to the old techniques involving large resections (79). Although anatomical hemispherectomies a re now rare in epilepsy surgery practice, these are still used in patients who failed funct ional hemi- spherectomies where there is a strong case for epilepsy arising from remnant br ain tissue. Peri-insular hemispherotomy and hemispheric deafferentation both emphasize disconnection. T he former uses a peri-insular, suprasylvian and infrasylvian approach to a transventricular corpus callosotomy and removal of the mesial temporal structures. The latter uses a standa rd temporal lobectomy for ventricular access and subsequent callosotomy. Hemidecortication is an infrequently used technique where gray matter is removed or \200\230degloved \200 \231 from underlying white matter. The overall rates of complete or near complete seizure freedom vary between 50 \200\22394 % (85 \200\22387). Seizure outcome is in \202 uenced by