Evaluation of Hearing Loss after Electrode Insertion Trauma and Otoprotective Therapy

Problem: Electrode insertion trauma can cause loss of hearing due to the apoptosis of injured cochlear sensory cells. Methods: Hearing acuity was evaluated in rats before and after electrode insertion trauma both with and without scala tympani infusion of D-JNKI-1 peptide. Hearing was measured pre-trauma and for 7 days following trauma. Objective measurements were: distortion products of otoacoustic emissions (DPOAE), tone bursts (8–32kHz), and click-evoked auditory brain stem responses (ABRs) recorded using Intelligent Hearing Systems hardware and software. Results: Electrode insertion trauma consisted of insertion and withdrawal of a ball electrode through a round window membrane excision. Drug delivery consisted of infusion of D-JNKI-1 peptide through a micro-catheter inserted through the RWM. The otoprotective drug was a peptide inhibitor of c-Jun N-Terminal Kinase, an apoptosis signal molecule. The DPOAE threshold for pre-surgical rats was 25 dB SPL; ABR thresholds varied from 10 to 45 dB SPL depending on the frequency, and click-evoked thresholds varied from 30 to 40 dB SPL. There were progressive increases in thresholds and decreases in amplitudes of the ABRs following electrode insertion trauma. The amplitude of the DPOAEs in the electrode trauma cochleae also showed progressive decreases. For untreated, control cochleae there were no significant changes in either the DPOAE or ABR thresholds following electrode insertion into contra-lateral experimental cochleae. The efficacy of the otoprotective drug will be discussed. Conclusion: These results present an effective method for documenting progressive post-implantation trauma-generated hearing loss and suggest a novel therapeutic approach for preventing post-electrode insertion complications related to apoptosis. Significance: This study provides a better understanding of the hearing loss that occurs in response to cochlear implant electrode insertion trauma and may lead to the development of a novel therapy. Support: None reported.