Anin vitromodel for investigating impedance changes with cell growth and electrical stimulation: implications for cochlear implants

Abstract

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.

Effects of Hearing Preservation on Psychophysical Responses to Cochlear Implant Stimulation

“…We note that average impedances for group II animals were significantly higher than those for group I. This might have been due to greater tissue growth in the neomycin-treated ears as has been suggested in previous studies (Newbold et al 2004). We did not see evidence of this in the histology of the current study, but that may have been missed due to the small number of neomycin-treated animals that underwent histological examination and possible disruption of tissue when the implant was extracted.…”

A new type of recording chamber with an easy-to-exchange microdrive array for chronic recordings in macaque monkeys

“…A challenging problem in chronic recordings is long-term stability of electrodes and recording sites, i.e., obtaining single-and multiunit activity even several months or years following implantation (Hatsopoulos and Donoghue 2009; Polikov et al 2005;Zhong and Bellamkonda 2008). Within cortical tissue, chronically implanted electrodes are likely to induce foreign body reactions like local inflammation processes (Biran et al 2005;McConnell et al 2009), encapsulation of the recording surface (Schmidt et al 1976;Szarowski et al 2003;Turner et al 1999), and formation of glial scars (Griffith and Humphrey 2006), thereby increasing electrode impedance (Grill and Mortimer 1994;Newbold et al 2004;Williams et al 2007) and the distance between electrode tips and nearby neurons (Liu et al 1999). Strategies to minimize these tissue reactions include use of biocompatible materials such as polymers (Musallam et al 2007;Rousche et al 2001;Schmidt et al 1988;Suner et al 2005) and ceramics (Moxon et al 2004;Singh et al 2003) for electrode insulation as well as coating electrodes with antiinflammatory agents (Kim and Martin 2006;Bellamkonda 2005, 2007).…”

Gellan gum doped polypyrrole neural prosthetic electrode coatings

“…4,5 Slippage and micromotion of the electrode at its implantation site is thought to cause chronic inflammation because of disparity in mechanical properties between the electrode and host neural tissue. 6 Inflammatory events initiate encapsulation of the electrode within a sheath of scar tissue, decreasing the neuronal density at the electrode 3 and increasing the distance across which stimulation and recording currents must be transduced, 7,8 both of which are detrimental to the device performance. Furthermore, inert noble metal NPEs bear little biochemical resemblance to the neural tissue and therefore are not conducive to amiable tissueelectrode interaction.…”