Carrie Newbold

Cochlear implant stimulation creates a reduction in electrode impedance that returns to pre-stimulation levels following cessation of stimulation and is presumed to be associated with the fibrous tissue covering over the electrode array. This study assessed the possibility that transitory impedance reduction originates from a change in the membrane permeability of cells on the electrode (electropermeabilization). These changes can be recorded using the dye propidium iodide, which fluoresces upon entry into the leaky cell. The in vitro model used showed impedance reduction and dye uptake into adherent cells overlying planar gold electrodes stimulated with as little as 5 min of clinically relevant cochlear implant stimulation. The delayed additions of propidium iodide showed a similar dye uptake to those groups with concurrent dye addition, suggesting the electropermeabilization was not reversible. Further understanding of the mechanisms behind these impedance and cell permeability ch...

This study was undertaken to assess the contribution of protein adsorption and cell growth to increases in electrode impedance that occur immediately following implantation of cochlear implant electrodes and other neural stimulation devices. An in vitro model of the electrode-tissue interface was used. Radiolabelled albumin in phosphate buffered saline was added to planar gold electrodes and electrode impedance measured using a charge-balanced biphasic current pulse. The polarization impedance component increased with protein adsorption, while no change to access resistance was observed. The maximum level of protein adsorbed was measured at 0.5 µg cm(-2), indicating a tightly packed monolayer of albumin molecules on the gold electrode and resin substrate. Three cell types were grown over the electrodes, macrophage cell line J774, dissociated fibroblasts and epithelial cell line MDCK, all of which created a significant increase in electrode impedance. As cell cover over electrodes increased, there was a corresponding increase in the initial rise in voltage, suggesting that cell cover mainly contributes to the access resistance of the electrodes. Only a small increase in the polarization component of impedance was seen with cell cover.

The impedance of stimulating electrodes used in cochlear implants and other neural prostheses often increases post-implantation, and is thought to be due to fibrous tissue encapsulation of the electrode array. Increased impedance results in higher power requirements to stimulate target neurons at set charge densities. We developed an in vitro model to investigate the electrode-tissue interface in a highly controlled environment. This model was tested using three cell types, with and without charge-balanced biphasic electrical stimulation. Under standard tissue culture conditions, a monolayer of cells was grown over the electrode surface. Electrode impedance increased in proportion to the extent of cell coverage of the electrode. Cell type was a significant factor in the amount of impedance increase, with kidney epithelial cells (MDCK) creating the greatest impedance, followed by dissociated rat skin fibroblasts and then macrophages (J774). The application of electrical stimulation to cell-covered electrodes caused impedance fluctuations similar to that seen in vivo, with a lowering of impedance immediately following stimulation, and a recovery to pre-stimulation levels during inactive periods. Examination of these electrodes suggests that the stimulation-induced impedance changes were due to the amount of cell cover over the electrodes. This in vitro technique accurately models the changes in impedance observed with neural prostheses in vivo, and shows the close relationship between impedance and tissue coverage adjacent to the electrode surface. We believe that this in vitro approach holds great promise to further our knowledge of the mechanisms contributing to electrode impedance.