Abstracts

Rationale: Painful somatosensory seizures are some of the most rarely observed partial seizures and their physiopathogenesis remains poorly understood. We report the case of a patient presenting pure painful somatosensory seizures, in whom a SEEG exploration: 1)localized the epileptic zone (EZ) in the insular cortex; 2)showed the functional organization of the cortical systems involved in the perception of pain. Methods: A 22-year-old patient consulted for presurgical evaluation for drug-resistant epilepsy. For the preceding 2 months he had had painful, recurrent partial simple seizures several times a week. These were dysesthetic hallucinations of a burning sensation or tearing of soft tissues over a more or less extended area of the left hemibody. Extremely intense, the pain seemed to continue for the first 15 seconds and then pulsated and progressively decreased over the following 2 min. MRI of the brain detected a 2-cm claustral spherical lesion, suggesting cortical dysplasia (CD) next to the right posterior insular cortex. The clinical exam, EEG, and FdG-PET scan were not contributive. SEEG exploration was planned using ten electrodes implanted in the insular-perisylvian and parietal area of the right hemisphere. Results: The seizure began as a high-frequency, low-amplitude discharge confined to the insular lesion for approximately 15 sec. This discharge was then interrupted and, over several dozen seconds, replaced with high repetitive spikes always collected by the intralesional contacts as well as in the middle part of the cingular gyrus and the parietal operculum, i.e. the secondary somato senitive cortex(SII). The passage from the first to the second period of the seizure was marked by the transformation from continuous to pulsating pain. Throughout the discharge, the cingular and SII spikes were repeated with a perfectly stable delay lasting 30 msec compared to the insular spikes. Conclusions: In this case, the painful seizures were associated with a critical discharge beginning in the insular cortex. Secondly, the paroxystic activities propagated from the insula to the secondary somatosensory areas and to the mid-cingular gyrus, precisely the structures that have been identified in functional imaging studies investigating nociception in humans. The pain in this case was produced by the pathological activation of the physiological network involved in nociception. Invasive presurgical evaluation of partial epilepsy with painful seizures should attempt to arrange electrodes in direct contact with the insulo-operculo-cingular cortices or risk mistaking the localization of the EZ.