**1. Introduction**

Stereotactic electroencephalography (SEEG) is the study of the electrical activities of the brain by means of implantation of electrodes into brain parenchyma with the aid of stereotactic navigation [1].

It was first developed by Jean Talairach and Jean Bancaud in France in the late 1950s. Talairach was a renowned stereotactic neurosurgeon who developed the frame-based coordinate system of the human brain based on the anatomical AC-PC (anterior commissure – posterior commissure) line, while Bancaud put forth the presurgical evaluation of drug-resistant epilepsy (DRE) with the use of the Talariach method. Bancaud described the organization of temporal lobe seizure with respect to the mesial temporal structures and the temporal neocortex [2]. This laid the foundation of SEEG as the presurgical workup for refractory epilepsy. It was then used in France, Italy and Canada for some time.

Only till 2010s, it was adopted in the United States and gained popularity because of its attractive safety profile and the capacity to perform spatiotemporal analysis

of the progression of the epileptiform discharge and bilateral cerebral hemisphere simultaneously, in comparison with subdural grid and depth electrodes which study cases that were already lateralized and/or partially localized [3].

Moreover, as the technology improves, SEEG could combine with lesioning technique to eradicate the epileptogenic zone, for example, radiofrequency ablation (RFA) [4]. This therapeutic use became more popular since the 2000s. Besides, as the electrodes were getting smaller and smaller, it had its potential in the application in brain-computer interface and the development of neuroprosthesis, in contrast to the traditional use of electrocorticography (ECoG).

Thus, this chapter aims to review the roles of SEEG as:


## **2. Diagnostic use**

#### **2.1 Definition and epileptogenesis**

To start with, it is important to clarify the concepts of drug-resistant epilepsy (DRE), zonification of epileptogenesis, and a proper presurgical workup.

Drug-resistant epilepsy, aka medical refractory epilepsy, is defined as the failure of adequate trials of two well-tolerated, appropriately chosen and used antiepileptic drug schedules, be it monotherapy or polytherapy, according to the International League Against Epilepsy (ILAE) consensus in 2009 [5]. Patients with DRE is eligible for presurgical evaluation.

In case of focal epilepsy, an *epileptogenic zone* (EZ) may be identified where cure of epilepsy could be achieved if it is resected. For the terminology in epileptogenesis, *epileptogenic lesion* is the anatomical abnormality which could be identified in structural imaging such as MRI [6]. *Ictal onset zone* is the origin of the seizure which could be the brain parenchyma without the lesion. Epileptogenic lesion and the ictal onset zone, together, form the EZ. However, sometimes when the epileptiform discharges propagate to the other parts of the brain causing symptoms. Those part would be named *symptomatogenic zone*. Most of the time, the symptoms could be the more obvious part of the seizure semiology which could make the localization of the EZ confusing. For example, a temporal EZ could transmit the epileptiform discharge to the frontal lobe via white matter tracts such as uncinate fasciculus and arcuate fasciculus, leading to the clinical impression of frontal epilepsy. On the other hand, *irritative zone* refers to the area which produces interictal epileptiform discharge. *Functional deficit zone* refers to the area of hypometabolism in functional imaging i.e. interictal PET scan. Irritative and functional deficit zones could overlap with the EZ but the areas represented are often exaggerated. This zonification concept forms the foundation of *localization* of the culprit of the epilepsy (**Table 1**) (**Figure 1**). On the other hand, *lateralization* of the epilepsy to either left or right side is also crucial but could be difficult at times, especially in frontal epilepsy in which synchronization of the bilateral cerebral hemisphere could be quick via commissural fibers such as corpus callosum.


#### **Table 1.**

*Zonification of epileptogenesis.*

**Figure 1.** *Zonification of epileptogenesis.*
