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A Practical Approach to Stereo EEG

A Practical Approach to Stereo EEG

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A Practical Approach to Stereo EEG

1,152 pages
12 heures
Dec 16, 2020


Stereo EEG has revolutionized the way invasive EEG explorations are performed, facilitating the assessment of more complex cases with increased precision, a lower surgical risk, and better patient outcomes. A Practical Approach to Stereo EEG is the first dedicated reference on stereoelectroencephalography written for trainees, physicians, and technologists involved in invasive EEG evaluation and monitoring. This go-to resource provides a practical overview of the concepts, methodology, technical requirements, and implantation strategies for common and uncommon surgical epilepsies amenable to stereo EEG. Including over three hundred detailed figures, anatomical drawings, and MRI correlations, this guidebook is an indispensable tool for anyone training, practicing, and teaching in the field.

With chapters written by leading experts from around the world, the book is divided into 10 sections covering noninvasive evaluation, technical aspects, electrode planning, practical approach for specific epilepsies, surgical placement in adults and children, interpretation, brain mapping, surgical procedures, and outcomes. Chapters integrate highlighted key concepts with illustrative case examples throughout to enhance clinical applicability. Four detailed case discussions of specific epilepsy syndromes covered in the book are also available online to demonstrate the process of patient evaluation, surgical planning, and decision-making in a multidisciplinary patient management conference.

A Practical Approach to Stereo EEG is the essential comprehensive clinical handbook for practitioners at any level of training or experience involved in invasive EEG evaluations or working at surgical epilepsy centers.

Key Features:

  • Covers all practical aspects of stereo EEG, including the methodology, technical requirements, and strategies to successfully perform and interpret invasive monitoring
  • Highly illustrated cases are interwoven within chapters to heighten clinical use
  • World-class contributors with global expertise provide hands-on experience in successful use of stereo EEG in complex situations
  • Additional online chapter-based narrated cases discuss specific epilepsy syndromes
Dec 16, 2020

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A Practical Approach to Stereo EEG - Springer Publishing Company

Section I. Introduction

The History and Principles of Stereo EEG

Patrick Chauvel


Stereoelectroencephalography (SEEG) was invented in the late 50s by Jean Talairach, a neurosurgeon, and Jean Bancaud, a neuropsychiatrist and electroencephalographer.¹ This method was based upon recording of brain electrical activity by intracerebral electrodes, stereotactically implanted in preidentified cortical and subcortical structures. When the technique was developed only electrocorticography (ECoG) was utilized. ECoG was an interictal investigation that did not provide any information on actual seizure onset. Furthermore, ECoG had to be carried out after craniotomy, so the decision of whether and how to operate had to be made at the same time in the operating room. In contrast, SEEG offered a method that allowed the investigative presurgical and therapeutic surgical stages to be separated. Using data from ictal and interictal EEG recordings, complemented with the results of local electrical stimulation applied through adjacent contacts of the implanted electrodes, surgical planning could be rationally prepared.²

The impetus for Bancaud and Talairach to start an epilepsy surgery program can be traced back to Henry Hécaen, a neuropsychologist who visited the Montreal Neurological Institute (MNI) and examined postsurgical patients with Wilder Penfield and Brenda Milner. After a year of study in 1952, Hécaen returned to Hospital Sainte-Anne, Paris, full of enthusiasm for surgical treatment of epilepsy. He convinced Gabriel Mazars, a neurosurgeon, that he should not wait to start an epilepsy surgery program based on the MNI method. At that time, Jean Talairach worked in the Department of Neurosurgery at the same hospital with his mentor Marcel David.³ Since 1946 he had been developing stereotactic approaches to functional neurosurgery for chronic pain and movement disorders.⁴ Jean Bancaud was a pupil of Henri Fischgold and had presented a doctoral thesis on the relationship between neuropsychological deficits and EEG features in patients with cerebral tumors. Then Fischgold’s group joined David’s in Sainte-Anne. Bancaud and Talairach met. They were instantly immersed in an outstanding medical and scientific environment, they were Mr. and Mrs. Dell in neurophysiology, H. Hécaen and J. de Ajurriaguera in neuropsychology.

Sainte-Anne was a psychiatric hospital founded in 1651. In the 50s, the department of psychiatry was dynamic and renowned as a pioneer group in biological psychiatry: Jean Delay, Pierre Deniker, with Henri Laborit demonstrated the neuroleptic effects of chlorpromazine in 1952. Hécaen had clearly a strong influence on Bancaud, who absorbed the lessons of Penfield on localization, and understood at a very early stage the complementary information provided by clinical signs and symptoms and the EEG, whether due to lesions or occurring during seizures. This insight led him to look for methods more accurate than ECoG for localization.


Meanwhile, Talairach was coming to a decisive turning point in his own methodological process. He had worked on the design of a surgical frame that would fit human brains of various sizes and would allow accurate repositioning. In 1947, the Talairach frame was born and improved over the years. Obsessed by increasing the accuracy of stereotaxic localization of deep structures, Talairach had also invented in 1949 the double grid system, a device made of two parallels grids attached to the stereotaxic frame, and through which locator needles or electrodes could be guided into the brain (Figure 1.1). The double grids served to minimize distortion due to X-ray diffraction in ventriculography images and thus offered the opportunity to precisely align radiological and postmortem anatomical data. Note that to further reduce distortion, Talairach later conceived a very large surgery room so that the X-ray tube was placed almost 5 m away from the grids.²

His vision was at that time very unusual. He regarded stereotactic methods as optimal for analysis of human brain anatomy in three-dimensional space, rather than as merely an instrument for reaching a target in the brain. Talairach built up a coordinate system based on the anterior commissure (AC) to posterior commissure (PC) base line and studied human neuroanatomy in reference to this line. This method also allowed the normalization of anatomical data from different brains such that data from the functional investigations of different patients could be displayed on the same summarizing chart. This enormous body of work led to the publication of two anatomical atlases. The stereotaxic frame, the double grids, and the AC–PC system were put together by Talairach to precisely map the anatomic stereotaxy of basal ganglia. In 1957 he published the first stereotaxic atlas of basal ganglia,⁵ a book that soon became a reference for neurophysiologists and neurosurgeons. It took Talairach 10 years more to extend the stereotaxic approach to the entire brain. For this, he implemented the concept of proportional scaling to account for differences in brain size in the three directions of the AC–PC system. Working with a rare tenacity, he validated the concept in tens of postmortem studies and published in 1967 a second stereotaxic atlas devoted to the telencephalon, which also became a reference and a basis for SEEG.⁶

Bancaud became more and more attracted to Talairach’s method, which promised to localize the sources of scalp EEG discharges. However, at that time, stereotaxy was oriented toward pain, dyskinesias, parkinsonian tremor, and some otherwise inoperable tumors. Working with M. B. Dell, Bancaud got progressively convinced of the clinical utility of epilepsy surgery but considered that methods of investigation current at that time were poorly adapted to epileptic phenomena.

After Talairach’s completion of the 1957 anatomical atlas, Marcel David took Talairach’s views into account and supported a project to create an operating room dedicated to stereotactic surgery. This theater needed to be large enough to satisfy the physical requirements of teleradiography and allow parallel X-ray beams in order to avoid distortions of skull, vessels, ventricles, and, crucially, the frame and double grids used for guiding the placement of intracranial electrodes. The concept of a stereotactic surgery room was born, and such a suite was opened in Sainte-Anne in 1959 in the walls of an ancient chapel. Bancaud saw the potential of a spatial conceptualization of the human brain promoted by Talairach’s method and began working with him to develop applications of stereotactic functional exploration to presurgical investigations of intractable epilepsies. In the minds of Talairach and Bancaud, Penfield’s localization approach could be thoroughly applied only through electrophysiological recording of seizures directly from the involved brain structures. This goal was achieved in 1959 using Talairach’s stereotactic method to accurately place intracerebral electrodes with respect to reliable anatomical markers and then record the electrical activity of multiple cerebral structures during the course of a seizure.

FIGURE 1.1  The Talairach stereotaxic frame with the double grids allowing orthogonal and oblique electrodes implantation (circa 1962).

Benefiting from this extraordinary technical achievement, Bancaud developed a careful analysis of anatomical–physiological–clinical correlations that could directly determine surgical strategy by utilizing electrophysiological recordings of seizures precisely localized in cerebral space. With these data, Bancaud studied the spatiotemporal dynamics of seizure discharges with respect to their clinical features. In particular, he first described the respective contributions of medial and lateral cortical areas in the organization of temporal and frontal seizures: the role of amygdala and hippocampus versus the temporal neocortex in temporal seizures (Figure 1.2),⁸,³⁴ and the role of supplementary motor area and cingulate area 24 versus the dorsolateral, ventrolateral, and ventromedial frontal cortices.⁹ These studies had immediate repercussion on the practice of epilepsy surgery.

FIGURE 1.2  Stereo EEG recording in temporal lobe epilepsy circa 1962. Seizure onset with a fast activity in left amygdala (NAG) and left hippocampus (CAG) spreading to the posterior parahippocampal gyrus (gyr pH post G). The two bottom traces are scalp EEG, that was simultaneously recorded.


Intracerebral ictal recordings provided data so complex that their interpretation needed a strategic roadmap. The designations of the cortical areas according to their hierarchical involvement in the epileptogenic process required precise definitions. The region where seizures originate was obviously in the forefront of presurgical planning. The epileptogenic zone was differentiated from the space occupied by interictal activity, or the irritative zone, and from the space occupied by any morphological alteration or lesion supposed to be related to the epilepsy, or the lesional zone. Talairach and Bancaud showed that the lesional and irritative zones had a variable topographic relationship with the epileptogenic zone.¹⁰ Talairach and Bancaud developed a new type of epilepsy surgery, based on a three-dimensional representation of the epileptogenic, irritative, and lesional zones. With this novel method, the surgical plan could be carefully prepared and adapted to the individual patient’s case by referring radiological, physiological, and clinical data by physical matching to the same patient through the stereotaxic method.

The epileptogenic and lesional zones' relationship depending on their cortical localization and on the different types of lesions underwent ongoing evaluation and validation. Today the use of neuroimaging has simplified the question of the lesional zone. At that time, only pneumoencephalography, lipiodol ventriculography, and cerebral angiography were available. Talairach looked for localizing and then operating responsible lesions with the help of localizing the epileptogenic zone. SEEG was so precise that he discovered numerous pseudotumoral, nonexpansive lesions (they would be identified later as dysembryoplastic neuroepithelial tumor and cortical malformations) that had not been previously shown by the neuroradiological techniques. He therefore encouraged Bancaud to find electrical criteria for detecting lesions. In SEEG terminology, the term lesional zone referred to the area occupied by various types of slow-wave activity (characterized by waveform, frequency, and reactivity). The correlations were clearly superior to those given by the available neuroradiological images. Talairach and Bancaud, using the SEEG method, extended its application to map better the extent and anatomical location of astrocytomas or oligodendrocytomas. They correlated SEEG findings with the results of stereotaxic biopsies.¹¹ According to histopathology, surgical resections avoiding functional deficits or targeting stereotactic interstitial radiotherapy could be preplanned. The topographic transitions between electrical silence inside glial tumors, slow waves, spiking, subclinical paroxysms, and seizure activity were analyzed. Beyond their clinical utility for tumor surgery, all this collection of anatomical-electrical data served as a model to interpret SEEG in cases of epilepsy. Definitions were less precise for the cortical areas producing interictal spikes and ictal discharges. When Bancaud began to record seizures using intracerebral electrodes, he noticed that the respective topography of the two types of discharge, interictal and ictal, were far from fully overlapping. He therefore used the terms irritative zone and epileptogenic zone to describe and differentiate the spatial extent of interictal spiking and ictal discharges respectively. The term epileptogenic zone thus referred to the anatomical structure(s) where primary organization of seizures took place.¹² The role of fast synchronizing discharges that might involve more often distinct but interconnected regions than a single region was emphasized.

Even though they could not give it a scientific content, the concept of epileptogenic zone was central to the development of SEEG. Bancaud and Talairach were immediately convinced to use it as the basis of their surgical strategy rather than the location of interictal discharges used by Penfield. Since the seizure was the symptom to be cured, it was the area of seizure organization that had to be determined. However, a strict correlation between the area(s) of seizure onset and emergence of clinical semiology was often difficult to establish in practice, because ictal signs and symptoms appeared and overlapped in time as the ictal discharge propagated to different cerebral structures. Understanding the spatiotemporal dynamics of the seizure as revealed by the sequence of signs allowed Bancaud to elaborate an extrapolation of its anatomical origin. This was a genial intuition. With this principle of extrapolation, the characterization of the initial symptom(s) or sign(s) appeared to be no more important than any later part of the seizure. Bancaud’s seizure patterns included order and sequence of semiological elements as their crucial features and were always referred to anatomy.¹³

Bancaud and Talairach definitely regarded a static view of seizure genesis represented by the gross topography of interictal and/or ictal onset abnormalities as insufficient for determining the area and volume of brain tissue to resect. They believed that a dynamic model of the discharge should be inferred from detailed consideration of all the data giving good discrimination between pacemakers versus active and passive relays of propagation. This was a prerequisite for surgical therapy in order to remove the smallest possible volume, and an intellectual discipline able to provide sound outcome information for further refinement of surgical criteria. With time the novel technique of Bancaud and Talairach evolved into a comprehensive and established method, where electrophysiological advances increased knowledge of anatomo-functional correlations giving rise to the beginnings of the functional exploration of networks.


Fixating double grids onto the stereotactic frame ensured safe implantation of intracerebral electrodes recording from lateral and medial areas of the cerebral cortex. Safety was further guaranteed by routine stereotactic angiography, allowing electrode placement that avoided vulnerable blood vessels. The practice of stereotactic angiography was associated with a very low risk. The stereotactic atlas of the telencephalon, containing frontal, axial, and sagittal brain slices referenced to the AC–PC baseline, was used as a guide to the topography of cortical areas. The Talairach grid system based on AC–PC provided a statistical representation of the spatial distribution of cortical sulci. The accuracy of this approach was satisfactory for designing electrode implantations or for comparing patients but was insufficient for detailed interpretation of an individual patient’s SEEG data. A reconstruction of the precise position of the electrode contacts after implantation relative to the individual patient’s anatomy was still necessary. Fortunately, Gabor Szikla had taken advantage of the need for stereotactic angiography and had carefully described cerebral cortical blood vessels and their close relationships to the convolutions of gyri and sulci. He showed that cortical vessels mold themselves to the form of the gyri. He was able to extract gyral form and dimensions from a meticulous analysis of vascular anatomy. This discovery led to the concept that vascular lamina could provide constant landmarks for interpretation of anatomical variability among individuals and turned out to be a very precise tool for deducing the actual location of electrode contacts before the availability of modern imaging methods.¹⁴

The anatomical method of Talairach has not only survived the development of magnetic resonance-derived stereotactic techniques but continues to be the referential basis for SEEG.¹⁵


SEEG offered high spatial and temporal resolution and a high power of localization. This was immediately evident in the early 1960s when the role of amygdala and hippocampus in temporal lobe seizures was discovered.¹⁶ During the next decade a major pitfall was to confuse stereotactic depth electrode explorations and real SEEG. This former type of implantation could be targeted for instance to preselected sites thought to be the source of paroxysmal activity on the basis of empirical arguments. This could be bilateral and symmetrical electrodes in mesial temporal structures only in cases of temporal lobe epilepsy. In contrast, SEEG is displaying the spatiotemporal dynamics of seizures in relation to the anatomy. This was contingent on using multiple multilead electrodes to give a distribution of spatial sampling sufficient to capture as much of the paroxysmal activity associated with the seizure as possible. A too compartmentalized or restricted view of ictal intracerebral activity would be insufficient to understand correlations with clinical semiology.

The essential question of reliable spatial sampling was whether recording from too restricted a brain area would prevent SEEG from providing an accurate view of the electrical organization of the entire epileptogenic zone. An ideal distribution of sites for intracerebral recordings provides the neurophysiologist with an immediate view of the dynamics of ictal and interictal events. Physiological interpolation between the recording sites would thus depend on a correct strategy of implantation, which requires that the implantation be managed within a coherent method based on the individual patient’s symptoms. In this context, a strategy of electrode implantation demands a clear hypothetical framework regarding the distribution of the epileptogenic and lesional zones derived from a detailed analysis of the electrophysiological features of the interictal state, the video-EEG electrical–clinical correlations of the ictal state, and their relation to anatomical anomalies. SEEG was conceived for its capability to validate or invalidate a principal hypothesis, and at the same time to support or eliminate an alternative hypothesis.

This anatomo-electro-clinical method produced types of data sets that may interact and validate one another. For example, the coincidence of clinical and electrical onset, or the precedence of electrical onset to clinical onset, both tend to confirm accurate positioning of a recording electrode. An indispensable tool is provided by intracerebral stimulation through stereotactically implanted electrodes, a technique proven reliable for showing the relationships between the different involved areas and the ictal semiology. Electrical stimulation can confirm topography of the ictal onset by provoking a habitual seizure and gives useful insight into the organization of the epileptogenic zone, by separating relay and subrelay areas essential for building up individual ictal symptoms and signs, as well as their modes of clustering. Such data are helpful to the surgeon in planning a strategy of removal and/or disconnection.

The ultimate objective of SEEG is to provide the surgeon with an integrated view of the epileptogenic process, based on the definition of the epileptogenic zone and its overlap with the lesional zone. Eventual matching of clinical, physiological, and anatomical data is essential, and the role of this stereotactic method in preoperative planning is exactly to achieve this objective. During surgery, anatomical and physiological data that describe the epilepsy and the function of related cortical areas are referenced to three-dimensional coordinates, which allows the surgeon to perform a comprehensively preplanned cortectomy within predetermined functional and vascular constraints.


The development of SEEG ushered in a new era that coincided with a complete structural reorganization of the Sainte-Anne Department of Neurosurgery. Alain Bonis, a neurologist and pupil of Raymond Garcin, joined the team, completed by Gabor Szikla, an emigrant from Hungary in 1956, who was to devote his career to anatomy and stereotactic surgery under Jean Talairach. In 1960, David and Fischgold moved away to La Pitié-Salpétriere, and Talairach became the head of a new Department of Functional Neurosurgery at Hospital Sainte-Anne.

This was a period of scientific productivity. The role of temporal limbic structures, the amygdala, and the hippocampus in clinical symptomatology and electroclinical organization of temporal lobe seizures was demonstrated. Clinical manifestations of absences that had been attributed to discharge of centrencephalic nuclei and as such considered as signs of generalized epilepsies by Penfield, Gastaut, and others could be elicited by stimulation of frontal anterior and intermediate areas, especially from their medial aspect.¹⁷ The anatomical-functional organization of the supplementary motor area was described as a part of the premotor systems and considered distinct from language areas.¹⁸

The first milestone in the establishment of SEEG fundamentals was the book La Stéréoelectroencéphalographie dans l’Épilepsie published in 1965.¹⁹ A modern and dynamic view of the focal epilepsies emerged from the observations, reflections, and discussions it collected. This book marked a break with the past, and, beyond the specific questions it raised in the field of epilepsy surgery, it provided an authoritative justification of the critical necessity for studying seizures when studying epilepsy.

SEEG offered the opportunity of analyzing the dynamics of epileptic phenomena in humans, but also represented a remarkable tool for the study of normal neurophysiology. Pierre Buser, a prominent neurophysiologist interested in the cerebral cortex, undertook such studies in cooperation with Bancaud after 1964. He worked on motor systems, particularly the pyramidal system and sensory polymodal afferents to the frontal cortex. One of the models he used was the startle reaction in the anesthetized cat. This led to a better understanding of startle physiology, and the startle epilepsies in hemiplegic children being investigated by Bancaud.²⁰ Buser influenced Bancaud’s work on various aspects of epilepsies with motor manifestations. Besides the startle epilepsies, they worked on the connections of the supplementary motor area,²¹ and together demonstrated the cortical origin of myoclonus and seizures in the Kojevnikov’s syndrome or epilepsia partialis continua,²² as well as the cortical origin of postanoxic action myoclonus (Lance and Adams syndrome).²³ Buser used SEEG not only for functional mapping, but also to study corticocortical connections and their facilitation inside the epileptogenic zone.²⁴ He was the first to use single pulse electrical stimulation to explore the excitability of corticocortical pathways and was in fact the pioneer of the technique named cortico-cortical evoked potentials (CCEPs) some 30 years later.²⁵ These anatomical and physiological advances eventually convinced Talairach that he should add a significant section on SEEG and neurophysiology to his stereotactic anatomical atlas of the telencephalon in 1967.⁶

The Institut National de la Santé et de la Recherche Médicale Research Unit entitled Stereotaxic Functional Exploration and Surgical Treatment of the Epilepsies headed by Talairach was created in 1970. This new facility helped Bancaud to approach some basic problems in the electrophysiological investigation of the human epilepsies and set new trends in the characterization of frontal lobe seizures.

Bancaud and Talairach paid more attention and invested much more time to write books than journal articles. They considered that the challenge posed by human intracerebral recordings, the new concepts on epilepsies they were generating, and their consequences for surgical strategy were so complex that they could not be thoroughly described and properly discussed in a limited article format. They had themselves been inspired by the detailed clinical experience handed on from their predecessors. As a matter of proof, at the end of my first interview with Bancaud in 1971, I was given the five books of Penfield to read before getting back to him.

In the same period, Bancaud returned to the questions of scalp EEG interpretation raised in his doctoral thesis and clarified many of them on the basis of data accumulated from comparisons between EEG and SEEG. The 1973 book EEG et SEEG dans les Tumeurs Cérébrales et l’Épilepsie was especially dedicated to electroencephalographers and collected unique and important data on simultaneous recordings of EEG and SEEG during numerous investigations of cerebral tumors and epilepsies in the stereotaxy chapel. Nowadays, it remains a valuable and useful guide to understanding what we record and what we miss in surface recordings of slow waves, spikes, and seizures.²⁶

Between 1970 and 1973, with the help of Stéphane Geier, the recording period of SEEG lengthened, and from acute, SEEG became chronic. Technically speaking, intracerebral electrodes were significantly reduced in size and adapted to the new mode of recording while the patient was freely moving. Telemetry was used, as well as video-recording with EEG and video signals being retrospectively matched.²⁷ These new types of recording out of the operating room allowed a much better study of gestural automatic behavior that characterize certain complex partial seizures. In particular gestural manifestations, correlated with anterior frontal lobe paroxysmal discharges, were identified.²⁸ Their phenomenology, duration, and mode of association differentiated them from gestural automatisms of temporal lobe origin.²⁹ Some observations made at this time suggested an epileptogenic zone distributed between frontal and temporal lobe areas, leading to the concept of frontotemporal epilepsy, and to a concomitant change in surgical strategy. In the search for mechanisms of automatisms, Bancaud and his coworkers reported the behavioral effects of anterior cingulate gyrus stimulation which essentially consisted of complex hand–mouth coordinated movements with mood alteration toward disinhibition.⁹,³⁰

The continuing collaborative work of Jean Talairach and Jean Bancaud culminated in a global report presented in 1974 to the Société de Neurochirurgie de Langue Française, entitled Approche Nouvelle de la Neurochirurgie de I’Epilepsie, and published as a supplement volume of the Neurochirurgie journal.³¹ This presentation specified the successive and multidisciplinary steps of the method and made clear the importance of making the surgical operation fit the seizure semiology through a meticulous and rational correlative approach.

So remarkably extensive was the range of research and curiosity of Talairach and Bancaud that it is difficult to highlight the major elements of their scientific legacy. Surely one of their most important contributions is the emphasis they have placed on the value of clinical semiology and its integration through the anatomo-electro-clinical correlations of a patient’s seizures. The body of work that has been produced from these principles has transformed what was at the beginning a technique of stereotactic functional exploration into a general method of studying a patient with epilepsy. In a sense, they have fashioned a tool that has turned out to be fundamental, as proven by the fact that it has survived the development of imaging and other noninvasive techniques.³² Indeed, not only has it survived, but it has framed a preinvasive rationale for the current imaging techniques by providing a referential system perfectly suited to the investigation of this anatomo-functional crossroad.³³


A serendipitous encounter between Jean Talairach and Jean Bancaud in the late 50s marked the origins of a new conception in presurgical exploration of epilepsy. They named it stereoelectroencephalography or SEEG, meaning that it was based on a multidimensional (supplied by stereotaxy) recording of multiple brain areas (through multilead depth electrodes) simultaneously. This novel method allowed for separating a presurgical localization from a surgical treatment phase. A closed skull setup enabled intracerebral seizure recording for the first time in a fully interacting patient. SEEG interpretation was based on ictal anatomo-electro-clinical correlations. A better comprehension of seizure build-up in the human brain led to major pathophysiological advances. SEEG-guided epilepsy surgery was performed only in Paris during the first 25 years, and then adopted in Switzerland and Canada. Ten years later, its practice developed in France (Rennes and Grenoble), and also in Italy (Milan). Its recent worldwide expansion confirms its universally recognized rationality and its perfect adjustment to brain imaging.



1. Talairach J. Souvenirs Des Etudes Stereotaxiques Du Cerveau Humain: Une Vie, Une Equipe, Une Methodologie: L’ecole de Sainte-Anne . John Libbey Eurotext; 2007.

15. Talairach J, Tournoux P. Co-Planar Stereotaxic Atlas of the Human Brain. 3-Dimensional Proportional System: An Approach to Cerebral Imaging . Georg Thieme Verlag; 1988.

19. Bancaud J, Talairach J, Bonis A, et al. La Stéréo-Electroencéphalographie dans l’épilepsie. Informations neurophysiopathologiques apportées par l’investigation fonctionnelle stéréotaxique . Masson & Co; 1965.

29. Geier S, Bancaud J, Talairach J, et al. The seizures of frontal lobe epilepsy. A study of clinical manifestations. Neurology . 1977;27(10):951–958. doi:10.1212/wnl.27.10.951

30. Talairach J, Bancaud J, Geier S, et al. The cingulate gyrus and human behaviour. Electroencephalogr Clin Neurophysiol . 1973;34(1):45–52. doi:10.1016/0013-4694(73)90149-1

31. Talairach J, Bancaud J, Szikla G, et al. [New approach to the neurosurgery of epilepsy. Stereotaxic methodology and therapeutic results. 1. Introduction and history]. Neurochirurgie . 1974;20(suppl 1):1–240.

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3. David M, Talairach J, Hecaen H. Perspectives thérapeutiques issues de la méthode de repérage et de coagulation localisée des structures cérébrales sous-corticales. Bull Mem Soc Med Hop Paris . 1949;65(11–12):459-461.

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Section II. Noninvasive Evaluation

Phase I Evaluation

Allyson A. Pickard and Christopher T. Skidmore


•The epileptogenic zone (EZ) is the region of brain that causes epilepsy and, once removed, can provide a cure.

•The EZ cannot be evaluated directly, but rather approximated through evaluation of alternate regions for which testing is available.

•These regions include the symptomatogenic zone, the irritative zone, the ictal onset zone, the functional deficit zone, the epileptogenic lesion, and the eloquent cortex.

•Sometimes the data obtained from study of these zones are discordant and a more invasive evaluation is required.


Epilepsy surgery is a powerful treatment that can offer a cure for patients suffering from seizures. The main goal of a presurgical workup is to identify who may benefit from surgery. This is done with precise seizure localization and determination of any risks or deficits from the proposed surgery.

The first step to this goal is through noninvasive testing. Several so-called zones of the brain—to distinguish the term from anatomical regions—and their relationship to one another are to be defined and used to help guide an evaluation for surgery. They include the symptomatogenic zone, the irritative zone, the ictal onset zone, the functional deficit zone, the epileptogenic lesion, and the eloquent cortex.¹ The final region, called the epileptogenic zone (EZ), is the ultimate goal and is defined as the minimal area of brain to be removed or disconnected to render the patient seizure free. The EZ cannot be directly tested and is therefore theoretical in nature, approximated by careful analysis of the other areas for which testing modalities are available.

In this chapter we illustrate how an understanding of these zones helps to approximate the EZ and describe the common methodologies utilized to assess each zone. This chapter is not meant to be an exhaustive discussion of each area and several of the techniques/technologies that will be mentioned will be discussed in more detail in the following chapters.

To help give context and understanding to these regions throughout this chapter, consider a straightforward, hypothetical patient:

A 46-year-old right-handed man presents with medically refractory epilepsy since onset at age 28. He has no risk factors for epilepsy. He continues to have seizures on high doses of zonisamide and oxcarbazepine. He has previously taken levetiracetam, valproate, and lacosamide at their maximal doses without improvement. He has focal impaired awareness seizures lasting about 1 minute once per month and has focal to bilateral tonic-clonic seizures about once per year.

His workup will highlight the important points of a noninvasive presurgical evaluation.


The symptomatogenic zone is defined as the region which generates the initial seizure semiology. Note that this is often not the same region as an ictal onset as a seizure must frequently evolve and spread after onset for a clinical change to occur. However, overlap between the two regions is possible.

This zone is best identified by obtaining a detailed description of the behavior experienced by the patient or seen by others. This can be achieved by both a careful and sequential history of the seizure as well as a video of the seizure itself, whether captured by a family witness or with dedicated video-monitoring equipment in an epilepsy monitoring unit. Attention to key components can help structure analysis. The presence of an aura, whether it be somatosensory, visual, auditory, and/or focal clonic activity at onset, is helpful as it is the first symptom of a seizure and occurs before a seizure has significantly spread.² Each of these possible symptoms implicates a very specific region of the cortex as the primary area of concern, though there are potential alternative regions as well. Somatosensory auras, for instance, would suggest a possible primary sensory cortex localization or perhaps the second sensory cortex located in the posterior regions of the superior temporal gyrus. Therefore, it may give insight into a more precise symptomatogenic zone than a seizure that occurs without an aura. There are numerous lateralizing and localizing signs that, when identified, can also help determine the region of interest or at least lateralize the location of the seizure onset. A detailed description of these signs is beyond the scope of this chapter, but a very nice summary of the most common signs can be found in a review article written by Dr. Loddenkemper and Dr. Kotagal.³ Common semiologic features associated with various cortical regions of onset have been summarized in Table 2.1 and will be discussed in what follows.⁴ Finally, the early impairment of language without alteration of awareness or consciousness helps to confirm a seizure’s initial presence in the dominant hemisphere, an important consideration when planning an invasive EEG implant and eventually determining the extent of a surgical operation.

Temporal Lobe Seizures

The temporal lobe is the most common location for seizures to begin. The mesial temporal lobe frequently has a semiology that begins with a viscerosensory or fear aura. Patients may describe a sudden sense of dread or a feeling of déjà vu. Oral and manual automatisms are common though secondary generalization is rare and often occurs late in the seizures if present. The lateral temporal lobe, by contrast, has frequent rapid secondary generalization. Additionally, an auditory aura is typically described and due to its proximity to Wernicke’s area, the patient may become aphasic, which typically becomes apparent postictally.

Frontal Lobe Seizures

Seizures arising from the frontal lobes can be varied, with several locations each resulting in a different semiology.⁵ A supplementary sensorimotor seizure for instance presents with focal asymmetric tonic posturing, head version typically contralateral to the symptomatogenic zone, speech arrest, and vocalization. An orbitofrontal seizure, by contrast, may present with complex motor automatisms and olfactory hallucinations. Occasionally, these automatisms are dramatic and atypical, leading to an erroneous diagnosis of psychogenic nonepileptic seizures. Care must be taken to appreciate that the semiology is stereotyped in these patients.


Parietal Lobe Seizures

Due to the proximity to the primary and supplementary sensory cortices, parietal lobe seizures frequently begin with a somatosensory aura such as tingling or numbness. These are typically contralateral to the symptomatogenic zone, though they may be bilateral. Very frequently, there is spread to the adjacent motor cortex resulting in motor involvement as well. It should be noted, however, that a painful somatosensory aura is more typical of an insular lobe seizure and its presence should lead to consideration of this alternate region.

Occipital Lobe Seizures

The occipital lobe controls and processes visual information and as such seizures from this lobe often have visual auras. Other symptoms could include ictal blindness, ocular movement, and blinking. There is also frequently rapid spread to other lobes, resulting in respective contributions to semiology that can cause ambiguity and misidentification for the initial seizure semiology.

Returning to the hypothetical patient, the semiological description obtained after three typical seizures were captured on video is as follows:

He sits in bed working on a computer when he suddenly stops and looks up. He presses the seizure button and states he is about to have one and states he is having a déjà vu sensation. He begins to make chewing movements and rubs the fingers of his left hand. The nurse enters the room and the patient initially is unable to speak but does follow simple motor commands. After approximately 30 seconds, he stops following all commands. He rubs his thigh. A code word is given. After approximately 1 minute, the patient again interacts with the nurse. He does not remember the code word nor the chewing or rubbing movements.

This is a typical semiology of a mesial temporal lobe seizure with an aura of déjà vu and the presence of automatisms. The early retained awareness with loss of speech is consistent with a seizure in the hemisphere dominant for language which for the right-handed patient is the left side of the brain. In summary, the patient’s symptomatogenic zone is the left mesial temporal lobe. We could summarize the semiology as: psychic (déjà vu) aura → aphasic seizure → automotor seizure, capturing the most pertinent aspects of the semiology.


The irritative zone is the cortical region that generates interictal epileptiform activity. This is the location of the spikes and sharp waves detected on an EEG or magnetoencephalography (MEG). Not every patient with epilepsy generates this abnormality and occasionally they can be quite rare, necessitating prolonged EEG monitoring for detection. Epileptiform discharges are more commonly seen during nonREM sleep than during wakefulness and REM sleep. However, epileptiform discharges from REM sleep and wakefulness may be more geographically restricted and have a potentially higher degree of correlation with the ictal onset zone.⁶ Discharges may also become more prevalent after seizures.

Precise localization of the epileptiform discharges, and therefore the irritative zone, is often limited by the technical limitations of the EEG. To detect a discharge on scalp EEG, approximately 6 cm² of cortex must be involved with discharges of a smaller area not appearing at all on scalp EEG tracings.⁷ Furthermore, each discharge must pass through the meninges and bone of the skull, which may distort the localization of the activity. A discharge may be seen more prominently in the anterior temporal region while another discharge may be maximal in the midtemporal region within the same study.⁸ Other modalities may be required to help reconcile if these two locations are in fact generated by one focus, or if two nearby foci must be considered. A somewhat more precise map may be generated with a dense array EEG which can allow for up to 256 channels modelling the suspected source on the patient’s own MRI. Electrical source imaging can then be utilized to account for the impacts the bone and soft tissues have on the electrical potential to suggest a probable cortical source.

The hypothetical patient’s interictal EEG is demonstrated in Figure 2.1. In the first image a sharp wave is seen with maximal negativity at T1. In the second image, recorded a few hours later, the maximal negativity is seen at T3. Note that in both images the field is broad, extending to the temporal-occipital region. The patient’s irritative zone is best described as being located in the left anterior to midtemporal region.

An alternative to scalp EEG in determining the irritative zone is MEG. An epileptic discharge generates an electrical dipole that is perpendicular to the cortical surface. This dipole, in turn, generates a magnetic field that can be detected and localized on a brain MRI.⁹ Unlike scalp EEG, MEG is not subject to the distortions created by passing through meninges and skull. It does, however, require somewhat frequent epileptic discharges to reliably localize the irritative zone. Unfortunately, this technology is limited by availability and decreased recording time as compared to continuous EEG recordings.

FIGURE 2.1  Interictal EEG findings of the hypothetical patient. There is variability of the maximal negativity between left anterior (T1) and mid (T3) temporal.


The same modalities used to identify the irritative zone are used to help characterize the ictal onset zone, or the area of brain where a seizure first begins electrically. The same limitations present for EEG for evaluation of the irritative zone again limit the evaluation of ictal onset. Focal aware seizures may not appear on scalp EEG due to a small area of cortical involvement. Frontal seizures may poorly lateralize or have only subtle ictal changes. Seizures with a prolonged aura may have a delayed EEG onset, reflecting a spread pattern rather than the onset zone of interest. It is important to remember that even a precise localization of ictal onset does not guarantee seizure freedom as the EZ may go beyond the recorded seizure onset. This can be a reflection of the limitations of EEG, the multifactorial nature of the EZ, or both.

Many epilepsy centers use an additional modality to help confirm the ictal onset zone using ictal single-photon emission computed tomography (SPECT).¹⁰ This technique uses a radiotracer to help measure cerebral blood flow, which is increased in an area with high metabolism, such as the cortex involved in seizure onset. Ideally, the maximum blood flow and metabolism is seen at the origin of a seizure and the areas where a seizure initially spreads. This requires injection of the isotope within seconds of seizure onset. A delay in injection or a rapid ictal spread pattern will significantly lower the accuracy of the study. Ictal SPECT does, however, offer the advantage over EEG of evaluating all areas of the brain including areas often missed by EEG such as deep cortical structures.

Due to the limited recording time inherent to MEG, it is rare to record seizures during a MEG study. However, seizures that are recorded can be localized utilizing the same principles for localizing interictal epileptiform discharges.

An ictal EEG of the hypothetical patient is shown in Figure 2.2. Note that the patient felt his first symptoms several seconds before an ictal change is seen on EEG. The final report gives the following electrographic description:

A 6–8 Hz rhythmic discharge is seen maximal at T1 for 9 seconds. This evolves to slower delta rhythms (3–4 Hz) with spread to the left posterior temporal and parietal regions. There is further evolution to 2 Hz rhythmic spiking activity before an abrupt offset is seen. The electrographic seizure lasts 52 seconds.

FIGURE 2.2  Ictal EEG findings of the hypothetical patient. The first ictal changes are seen maximally in the left anterior temporal region before evolution across the left temporal region and hemisphere occurs.


A structural abnormality that is thought to give rise to seizures is known as the epileptogenic lesion. Nearly every patient receives some form of head imaging after a first time seizure, initially using CT. This will help identify more extensive lesions, such as high-grade tumors as well as hemorrhages, that may have caused the seizure. Patients with longstanding epilepsy, however, require a more detailed image to identify more subtle lesions, such as mesial temporal sclerosis or focal cortical dysplasia. An MRI is most commonly used providing higher resolution, correlating with stronger magnetic fields, for the best quality image. As the imaging technology improves, smaller abnormalities are able to be identified including heterotopias, encephaloceles, and other abnormalities of cerebral development. PET utilizing specific ligands have also been developed to identify functional or specific structural lesions such as cortical tubers in individuals with tuberous sclerosis. This will be covered in the chapter on PET imaging.

Figure 2.3 shows the coronal MRI of the hypothetical patient. Left mesial temporal sclerosis is demonstrated by the hyperintensity and atrophy of the hippocampus.


A patient with medically refractory epilepsy may present with a chronic clinical deficit that persists in the interictal period, such as a poor category-specific memory or hemiparesis. The area responsible for this interictal finding is the functional deficit zone. This may be due to a visible structural lesion, abnormal neuronal networks, or inadequate neuronal signaling in the region. It may become larger or more significant over time as seizures continue. Neurological examination may be able to detect more severe deficits such as sensory loss or weakness. Deficits that may impact the patient’s ability to perform their job, such as moderate memory loss, may not be detected on routine examination though the patient may report declining work performance.

FIGURE 2.3  Coronal T1-weighted (A) and T2-weighted (B) fluid-attenuated inversion recovery MRI of the hypothetical patient showing severe left mesial temporal sclerosis.

A detailed neuropsychological assessment may be used to identify and describe these more nuanced deficits. A better understanding of any functional deficits can be used to both predict an area of brain that may be affected as well as any impact of surgery. General intelligence including verbal, perceptual, and general intelligence quotient modalities may be tested. Verbal and visual memory testing can be helpful to identify specific memory deficits while testing naming and verbal fluency may uncover a language abnormality. Screening for anxiety and depression are also frequently done as these may significantly impact patient quality of life during the presurgical evaluation and postsurgical recovery if unrecognized and untreated.¹¹

The detailed neuropsychological report of the hypothetical patient includes assessments of his general intelligence, visual memory, verbal memory, naming, verbal fluency as well as anxiety and depression indexes. An excerpt from the report follows.

A general ability index (GAI) is used as a substitute for a Full Scale Intelligence Quotient and is average at 102 (55th percentile). His verbal memory using a list delayed recall and a prose passage immediate recall for assessment was borderline impaired in the 7th percentile. His visual memory was average in the 56th percentile after testing immediate and delayed recall of object designs. His naming was found to be impaired at the 4th percentile when he was only able to name 48 out of 60 objects. Verbal fluency was similarly impaired with phonemic fluency at the 10th percentile and semantic fluency at the 1st percentile. Anxiety and depression were evaluated using standardized assessments and found to be minimal with the patient reporting mild symptoms.

The impairment of naming and verbal fluency suggests dysfunction in the dominant hemisphere. This is further narrowed with the observed impairment of verbal memory, suggesting dominant temporal lobe dysfunction.

Like the ictal SPECT showing hypermetabolism during a seizure, the interictal PET can show hypometabolism between seizures in the same area. Even if a structural abnormality is not seen on a MRI, a hypometabolic area on an interictal PET scan indicates an area of dysfunction. The PET scan indicating left temporal lobe hypometabolism found for the hypothetical patient is shown in Figure 2.4. Interictal SPECT may also be used; however it has lower resolution than PET leaving its utility in establishing a baseline image for an ictal SPECT study limited. Some researchers have found the fluorodeoxyglucose-PET imaging with concordant semiology, interictal and ictal EEG for mesial temporal onset epilepsy is as positive a predictor of surgical success as mesial temporal sclerosis on MRI imaging.¹²

FIGURE 2.4  PET imaging of the hypothetical patient. This coronal image shows decreased radiotracer uptake in the left temporal lobe, maximally medially, indicated by the arrows. This corresponds to hypometabolism in this region.


As important as the accurate estimation of the EZ in the presurgical evaluation is for seizure freedom, the identification of eloquent cortex is equally as important to determine the functional outcome of surgery. A patient who loses the ability to understand or speak as a result of epilepsy surgery may become seizure-free but may remain disabled and unable to return to work. As such, part of the presurgical evaluation includes identification of the eloquent cortex to help understand and define boundaries for surgery.

Functional MRI (fMRI) can be used to identify eloquent cortex through evaluation of neuronal networks and any restructuring of these networks. Similar to the SPECT and PET modalities, this study evaluates the blood flow and metabolism of the brain. With fMRI, however, these changes are measured in response to certain tasks, such as motor function, movement, or language.¹³ A patient is asked to perform a movement, or remember a set of words, and the resultant change in cerebral blood flow found on the image indicates the area of brain responsible for that task. After a series of tasks, a map of functional cortex can be generated. Any deviation from the expected norms can be used in the interpretation and evaluation of the functional deficit zone previously discussed. These images can be combined with MRI diffusion tensor imaging images, which permit the visualization of structural connectivity in the form of white matter tracks traveling between cortical regions of interest. This helps to identify white matter bundles which need to be avoided during surgery. Figure 2.5 shows a normal fMRI with intact language areas identified in the left hemisphere. For the hypothetical patient, any surgical plans will need to consider preservation of these areas.

Evoked potentials and transcranial magnetic stimulation are additional noninvasive studies that could be performed. Stimulation is applied and the resultant action or signal can be used to map eloquent cortex. The Wada test (named after Juhn Wada, also known as intracarotid ambobarbital test) is an invasive test often performed prior to the implantation of intracranial electrodes and for that reason is mentioned here. It involves the injection of an anesthetic agent such as amobarbital into the carotid artery to selectively anesthetize the cerebral hemisphere ipsilateral to the injection. This permits the neurologist or neuropsychologist to test the remaining awake hemisphere for memory, language, and motor function.

FIGURE 2.5  fMRI of the hypothetical patient. The MRI sequences have been superimposed with evidence of cerebral activation during a sentence completion task, measured as changes in blood flow. The bottom right image is a reconstruction showing all language activation.

fMRI, functional MRI; L, left; R, right.


With evaluation of the previously discussed zones, summarized in Table 2.2, the theoretical EZ can be constructed. A minimum workup for every patient to provide an adequate depiction of this zone includes a history and physical examination, video-EEG monitoring, MRI, and neuropsychological testing often referred to as a Phase 1 evaluation. Many centers find additional testing such as the PET, MEG, or fRMI to help further refine the hypothesis of the EZ.

Often the patient’s individual findings are summarized and discussed at a surgical conference with epileptologists, neurosurgeons, and neuropsychologists present. Table 2.3 shows the findings of the hypothetical patient. His findings strongly suggest an EZ in the left anterior temporal region. Some may argue that for this patient, further workup may not be needed and that he could proceed to resective surgery with an anterior temporal lobectomy.¹² The extent of his resection, however, may need to be limited by the posterior Wernicke’s area to preserve language. Additionally, due to his verbal memory impairment, he is at risk of further verbal memory decline with an anterior temporal lobectomy.¹⁴ This may lead some centers to consider laser interstitial thermal therapy (or laser ablation) to target just his mesial temporal sclerosis in an attempt to preserve memory outcome and speed patient recovery following the procedure. Alternately, some centers may wish to more precisely evaluate the EZ using intracranial EEG to help minimize the extent of resection.


DTI, diffusion tensor imaging; EZ, epileptogenic zone; fMRI, functional MRI; MEG, magnetoencephalography; SPECT, single photon emission computerized tomography.


EZ, epileptogenic zone; fMRI, functional MRI.

Note: The data obtained from the hypothetical patient’s workup is concordant and gives rise to a single leading hypothesis of the EZ.

Not every patient is as straightforward. Rarely is there complete agreement between the identified zones. Sometimes two or more hypotheses are generated from the noninvasive evaluation due to discordant data. Consider the findings of an alternate patient in Table 2.4. With this evaluation, the MRI showed a right frontal abnormality suggesting a potential epileptogenic lesion in this area. However the symptomatogenic zone determined by clinical history and video analysis supports a mesial temporal onset. There is additional supporting evidence for each of these potential locations as well as other possibilities not completely assessed with the studies performed, such as the bilateral irritative zone or the left mid to posterior temporal ictal onset zone findings. Which hypothesis is correct? To help answer this question and reconcile the findings, an invasive study using intracranial EEG is needed in the presurgical evaluation.


EZ, epileptogenic zone; fMRI, functional MRI.

Note: The data obtained from the alternate patient is discordant, leading to several differing hypotheses of the EZ.


The EZ, if correctly hypothesized, can allow surgery to provide a cure for epilepsy. Approximation of this ultimate goal is done through analysis and understanding of several alternate regions including the symptomatogenic zone, the irritative zone, the ictal onset zone, the functional deficit zone, the epileptogenic lesion, and the eloquent cortex. There are many noninvasive tools for evaluation of the alternate zones including history, video, imaging, EEG, and neuropsychological assessment. Occasionally these results, when examined, provide a clear picture of the likely EZ. However, they are often not in complete agreement and a more invasive approach is required to provide the best hypothesis.



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2. Lüders H, Fernandez-Baca Vaca G, Akamatsu N, et al. Classification of paroxysmal events and the four-dimensional epilepsy classification system. Epileptic Disord . 2019;21(1):1–29 doi:10.1684/epd.2019.1033

4. Skidmore CT. Adult focal epilepsies. Continuum (Minneap Minn) . 2016;22(1 Epilepsy):94–115. doi:10.1212/CON.0000000000000290

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1. Lüders H, Comair YG. Epilepsy Surgery . 2nd ed. Lippincott Williams & Wilkins; 2001.

2. Lüders H, Fernandez-Baca Vaca G, Akamatsu N, et al. Classification of paroxysmal events and the four-dimensional epilepsy classification system. Epileptic Disord . 2019;21(1):1–29 doi: 10.1684/epd.2019.1033

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4. Skidmore CT. Adult focal epilepsies. Continuum (Minneap Minn) . 2016;22(1 Epilepsy):94–115. doi:10.1212/CON.0000000000000290

5. Bagla R, Skidmore CT. Frontal lobe seizures. Neurologist . 2011;17(3):125–135. doi:10.1097/NRL.0b013e31821733db

6. Sammaritano M, Gigli GL, Gotman J. Interictal spiking during wakefulness and sleep and the localization of foci in temporal lobe epilepsy. Neurology . 1991;41(2(Pt 1)):290–297. doi:10.1212/wnl.41.2_part_1.290

7. Cooper R, Winter AL, Crow HJ, et al. Comparison of subcortical, cortical and scale activity using chronically interdwelling electrodes in man. Electroencephalogr Clin Neurophysiol . 1965;18:217–228. doi:10.1016/0013-4694(65)90088-x

8. Goncharova II, Spencer SS, Duckrow

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