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Modification of brain conductivity in human focal epilepsy: A model‐based estimation from stereoelectroencephalography
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International audience. Objective: We have developed a novel method for estimating brain tissue electri-cal conductivity using low-intensity pulse stereoelectroencephalography (SEEG)stimulation coupled with biophysical modeling. We evaluated the hypothesisthat brain conductivity is correlated with the degree of epileptogenicity in pa-tients with drug-resistant focal epilepsy.Methods: We used bipolar low-intensity biphasic pulse stimulation (.2 mA) fol-lowed by a postprocessing pipeline for estimating brain conductivity. This pro-cessing is based on biophysical modeling of the electrical potential induced inbrain tissue between the stimulated contacts in response to pulse stimulation. Weestimated the degree of epileptogenicity using a semi-automatic method quan-tifying the dynamic of fast discharge at seizure onset: the epileptogenicity index(EI). We also investigated how the location of stimulation within specific ana-tomical brain regions or within lesional tissue impacts brain conductivity.Results: We performed 1034 stimulations of 511 bipolar channels in 16 patients.We found that brain conductivity was lower in the epileptogenic zone (EZ; un-paired median difference = .064, p < .001) and inversely correlated with the epi-leptogenic index value (p < .001, Spearman rho = −.32). Conductivity values werealso influenced by anatomical site, location within lesion, and delay betweenSEEG electrode implantation and stimulation, and had significant interpatientvariability. Mixed model multivariate analysis showed that conductivity is sig-nificantly associated with EI (F = 13.45, p < .001), anatomical regions (F = 5.586,p < .001), delay since implantation (F = 14.71, p = .003), and age at SEEG (F = 6.591,p = .027), but not with the type of lesion (F = .372, p = .773) or the delay since lastseizure (F = 1.592, p = .235).
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