Loss of Residual Hearing Initiated by Cochlear Implantation: Role of Inflammation-Initiated Cell Death Pathways, Wound Healing and Fibrosis Pathways, and Potential Otoprotective Therapies

Abstract

Cochlear implantation with electrode array insertion, even in the best of surgical hands, can be traumatic, causing the release of pro-inflammatory and apoptotic factors that lead to loss of auditory hair cells that are critical for the retention of a cochlear implant patient’s residual hearing. The chronic inflammatory process following cochlear implantation can lead to cochlear fibrosis and increased cochlear implant (CI) impedance. This can interfere with function of the implant alone or when combined with acoustic stimulation as in electroacoustic stimulation of the auditory system. Less-traumatic surgical techniques have been developed and electrode arrays have been modified to reduce trauma associated with cochlear implantation. In addition, several drug therapies have been shown to reduce postoperative inflammation and conserve residual hearing in animal models of electrode insertion trauma-induced hearing loss. These drug therapies show promise for future use in CI patients, where conservation of residual hearing is a goal and these promising therapies need to be tested in clinical trials. Preserving residual low-frequency hearing in CI patients may provide improved speech perception in quiet and noise and enhanced music perception compared to CI patients that lose residual audition. Despite conservation of residual hearing with more advanced surgical techniques and low trauma electrode designs, residual native auditory function continues to deteriorate years after surgery. Future trends of cochlear implantation will likely focus on drug-eluting electrodes and longer less-traumatic electrodes that can compensate for a loss of residual hearing many years post-implantation.