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Objective: We aimed at providing an accurate estimation of human brain tissue electrical conductivity in clinico, using local, low-intensity pulsed stimulation. Methods: Using the quasi-static approximation of Maxwell equations, we derived an analytical model of the electric field generated by intracerebral stereotactic-EEG (SEEG) electrodes. We coupled this electric field model with a model of the electrode–electrolyte interface to provide an explicit, analytical expression of brain tissue conductivity based on the recorded brain tissue response to pulse stimulation. Results: We validated our biophysical model using saline solutions calibrated in electrical conductivity, rat brain tissue, and electrophysiological data recorded in clinico from two epileptic patients during SEEG. Conclusion: This new model-based method offers a fast and reliable estimation of brain tissue electrical conductivity by accounting for contributions from the electrode–electrolyte interface. Significance: This method outperforms standard bioimpedance measurements since it provides absolute (as opposed to relative) changes in brain tissue conductivity. Application for diagnosis is envisioned since conductivity values strongly differ when estimated in the healthy versus hyperexcitable brain tissue. [ABSTRACT FROM AUTHOR]

The pathophysiological interpretation of EEG signals recorded with depth electrodes [i.e., local field potentials (LFPs)] during interictal (between seizures) or ictal (during seizures) periods is fundamental in the presurgical evaluation of patients with drug-resistant epilepsy. Our objective was to explain specific shape features of interictal spikes in the hippocampus (observed in LFPs) in terms of cell- and network-related parameters of neuronal circuits that generate these events. We developed a neural network model based on "minimal" but biologically relevant neuron models interconnected through GABAergic and glutamatergic synapses that reproduce the main physiological features of the CA1 subfield. Simulated LFPs were obtained by solving the forward problem (dipole theory) from networks including a large number ( ∼ 3000) of cells. Insertion of appropriate parameters allowed the model to simulate events that closely resemble actual epileptic spikes. Moreover, the shape of the early fast component ("spike'') and the late slow component ("negative wave'') was linked to the relative contribution of glutamatergic and GABAergic synaptic currents in pyramidal cells. In addition, the model provides insights about the sensitivity of electrode localization with respect to recorded tissue volume and about the relationship between the LFP and the intracellular activity of principal cells and interneurons represented in the network. [ABSTRACT FROM AUTHOR]