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Electrode impedance changes after implantation of a dexamethasone-eluting intracochlear array
Karina Needham1,2,3, Dimitra Stathopoulos1,2, Carrie Newbold1,2,3
1The HEARing CRC, Carlton, Australia.
Cochlear Implants International
|October 18, 2019
Summary
Intracochlear dexamethasone did not reduce fibrotic tissue around cochlear implants. However, it altered electrode impedance, suggesting localized changes at the tissue-electrode interface, particularly with electrical stimulation.
Area of Science:
- Biomedical Engineering
- Neuroscience
- Otolaryngology
Background:
- Postoperative inflammation and fibrotic tissue formation around intracochlear electrode arrays negatively impact cochlear implant outcomes.
- Reducing this tissue response is crucial for improving hearing restoration success.
Purpose of the Study:
- To evaluate the efficacy of intracochlear dexamethasone delivery via drug-eluting electrode arrays in minimizing fibrotic tissue formation.
- To assess the impact of dexamethasone on electrode impedance as a surrogate for tissue response.
Main Methods:
- Adult guinea pigs received bilateral cochlear implants: a dexamethasone-eluting array (left) and a standard array (right).
- Electrical stimulation was applied daily for 4 weeks post-implantation.
- Monopolar and four-point electrode impedance were measured, alongside histological assessment of fibrotic tissue, bone growth, and neuron density.
Main Results:
- Dexamethasone-eluting arrays did not significantly reduce monopolar electrode impedance or observable fibrotic tissue, bone growth, or spiral ganglion neuron density.
- Four-point electrode impedance, reflecting the neural-tissue interface, was significantly lower with dexamethasone.
- Daily electrical stimulation altered the relationship between four-point impedance and fibrotic tissue/bone growth for standard arrays.
Conclusions:
- Intracochlear dexamethasone influences four-point electrode impedance and the correlation between impedance and tissue encapsulation.
- Sustained, localized dexamethasone release appears to modify the tissue-electrode interface, particularly when combined with electrical stimulation.
