La notion d’épilepsie insulaire est longtemps restée inconnue. En raison de sa situation, profondément enfouie sous les opercules et recouverte par le réseau artérioveineux sylvien, l’insula est longtemps restée inaccessible aux explorations intracrâniennes et son rôle dans les épilepsies partielles est demeuré peu connu jusqu’à ce jour. Les progrès des techniques réalisés dans les explorations intracrâniennes nous ont permis de réaliser l’enregistrement électroencéphalographique (EEG) et des stimulations électriques directes du cortex insulaire au moyen de 472 électrodes insulaires implantées au total chez 164 patients. La sémiologie clinique des crises insulaires était dominée par deux groupes de symptômes : des manifestations somatosensitives, volontiers étendues à de vastes champs cutanés, à tonalité hyperthermiques ou douloureuses, de topographie régulièrement bilatérale ou homolatérale au foyer épileptogène ; les manifestations viscérosensitives et viscéromotrices centrées sur la sphère digestive. Cette étude décrit le spectre clinique des crises insulaires et notamment les éléments permettant de les distinguer des crises du lobe temporal. Sa présence chez un patient atteint d’épilepsie du lobe temporal devrait inciter à réaliser une exploration EEG intracrânienne préalable à toute décision chirurgicale afin d’identifier une éventuelle extension de la zone épileptogène au cortex insulaire.

The role of the insular lobe in temporal lobe epilepsy (TLE) has often been suggested but never directly demonstrated. In this article, we review data from recent literature and from our own stereo-electroencephalographic (SEEG) recordings in patients referred for temporal lobe epilepsy surgery. Our description of the clinical features of insular lobe seizures is based on data from video and SEEG ictal recordings and direct electric cortical stimulation in a population of 50 consecutive patients whose seizures, on the basis of scalp video EEG recordings, were suspected to originate from, or to rapidly propagate to, the perisylvian cortex. One hundred and forty-four intrainsular electrodes have been implanted in this series of patients. In six patients a stereotyped sequence of ictal symptoms could be identified on the basis of electroclinical correlations. The clinical presentation of insular lobe seizures is that of simple partial seizures occurring in full consciousness, beginning with a sensation of laryngeal constriction followed by paresthesiae that were often unpleasant and affected large cutaneous territories. These initial symptoms were eventually followed by dysarthric speech and/or elementary auditory hallucinations, and seizures often ended with focal dystonic postures. The insular origin of these symptoms was supported by the data from functional cortical mapping of the insula using direct cortical stimulations from a total of 472 intrainsular electrodes in 164 consecutive patients. We were able to reproduce several of the spontaneous ictal symptoms in the six patients with insular seizures. Moreover, from the whole set of insular stimulations that we performed it could be concluded that the insular cortex is involved in somatic, vegetative and visceral functions to which spontaneous ictal insular symptoms are related. The observation of the insular symptoms sequence at the onset of seizures in patients who are candidates for TLE surgery strongly suggests that the epileptic focus is located in the insular lobe. It entails the risk of unsuccessful temporal lobectomy and should lead to reconsider the indication of temporal lobectomy and to explore directly the ictal activity of both mesiotemporal and insular cortices before making any decision regarding epilepsy surgery.