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Definition and localization of the epileptogenic zone
The epileptogenic zone: general principles
Hans O Lüders, Imad Najm, Dileep Nair, Peter Widdess-Walsh, William Bingman
The concept of the epileptogenic zone: a modern look at Penfield and Jasper’s views on the role of interictal spikes
Andre Palmini
epileptogenic zone was based on and has evolved from the recording of interictal spikes, both in the scalp electroencephalogram (EEG) and, particularly, in the acute electrocorticogram (ECoG). Because the role of interictal spikes is still not always clear in the decision-making process of epilepsy surgery, the relevance of these spikes in the definition of the epileptogenic zone is reviewed here, starting with the pioneering work of the Montreal school.
The Bancaud and Talairach view on the epileptogenic zone: a working hypothesis
Philippe Kahane, Elisabeth Landré, Lorella Minotti, Stafano Francione, Philippe Ryvlin
recordings. It takes into account not only the anatomical location of the “site of the beginning and of the primary organization” of the epileptic discharge, but also how this discharge gives rise to the accompanying clinical symptoms. This definition is different from the North American view since, for the french authors, the epileptogenic zone is not synonymous with what can be called the “what-to-remove area”. In fact, it is above all a conceptual definition which emphazises the importance of studying the spatio-temporal dynamics of seizure discharges, and not only their starting point.
Definition of the epileptogenic zone in a patient with non-lesional temporal lobe epilepsy arising from the dominant hemisphere
Imad M Najm, Richard Naugle, Robyn M Busch, William Bingaman, Hans Lüders
of the epileptogenic zone, and the planning of the extent of the surgical resection. We report on the case of a 42-year-old, right-handed male who presented with recurrent daily seizures that were resistant to antiepileptic drugs. Multiple, non-invasive (scalp) video-EEG evaluations revealed focal epilepsy arising from the left fronto-temporal region. Multiple high resolution MRIs that were performed at multiple Epilepsy Centers failed to show any abnormality. Fluoro-deoxyglucose PET scan showed extensive, left antero-mesial temporal hypometabolism, and ictal SPECT showed increased perfusion in the left insula in addition to the left mesial and anterior temporal pole. Neuropsychological testing and intracarotid methohexital testing revealed excellent memory to the left, dominant side. A two-stage invasive evaluation with subdural grid electrodes followed by depth electrode recordings allowed the localization of the epileptogenic region to the temporal pole. A selective resection of the left temporal pole (that spared the hippocampal formation) resulted in a seizure-free outcome (one year follow-up) with no significant consequences on memory function. We conclude that targeted, invasive recording techniques should be used for the accurate localization and delineation of the extent of the epileptogenic zone in cases of suspected, non-lesional, dominant hemisphere, temporal lobe epilepsy with preserved memory function. The use of the staged invasive approach may increase the chances for memory (function) sparing through tailored, temporal resection.
Avoid falling into the depths of the insular trap
Philippe Ryvlin
lobe epilepsy (NFLE). To illustrate some of the issues raised by these observations, we report our first two patients with suspected TLE and NFLE, respectively, in whom we originally demonstrated an insular ictal onset zone. Patient 1 suffered from daytime seizures characterised by a rising and distressing epigastric sensation rapidly followed by oro-alimentary automatisms, associated with right temporal scalp-EEG ictal discharge. Neuroimaging showed consistent right temporal abnormalities, including MRI signs of hippocampal sclerosis, anterior and mesial glucose hypometabolism, and mesial decrease of benzodiazepine receptors. Intra-cerebral EEG investigation was primarily performed because of several ictal signs and symptoms suggesting a rapid involvement of the perisylvian region, and showed that the patient suffered two types of seizure, one of which arose from the mesial temporal structures, the other was sleep-related and originated in the posterior-inferior portion of the insula. Anterior temporal lobectomy failed to control this second type of seizure. Patient 2 suffered from brief, nocturnal, hypermotor seizures characterised by an indefinable aura followed by agitation, body rolling, scream and pelvic thrust. Interictal and ictal scalp-EEG failed to detect epileptiform discharges, whereas neuroimaging showed left mesial frontal, glucose hypometabolism and decreased benzodiazepine receptors associated with a left fronto-basal arachnoidal cyst. Invasive EEG monitoring was performed with the aim of identifying an orbital or mesial frontal ictal onset, but eventually demonstrated that the seizure originated in the anterior-superior portion of the left insula. The patient did not undergo surgery and died of SUDEP two years later. We discuss the heterogeneity of insular seizure semiology according to functional anatomy, the clinical signs and symptoms that might suggest an insular ictal onset, the indications and types of invasive EEG monitoring that are needed to identify an insular epileptogenic zone definitively, as well as potential surgical treatment.
A case of auditory auras: application of general principles to define and localize the epileptogenic zone
Ajay Gupta
of various diagnostic tools is discussed in this case using the North American approach to the localization of the epileptogenic zone. Whenever possible, the differences and similarities between the North American and the French/Italian approach for the localization of the epileptogenic zone are discussed.
Towards a definition of the “practical” epileptogenic zone: a case of epilepsy with dual pathology
Serge Chassagnon, Maria Paola Valenti, Cécile Sabourdy, Philippe Esposito, Pierre Kehrli, Alexis Arzimanoglou, Philippe Ryvlin, Philippe Kahane, Edouard Hirsch
the available mehods to directly measure the actual seizure-onset zone and to define “the minimum amount of cortical tissue that must be resected to produce seizure-freedom” have significant limitations.We report on the case of a patient with dual pathology (hippocampal sclerosis and a post-traumatic scar) and discuss the contribution of the various presurgical investigations that led to surgery and seizure-freedom.
