ABR Threshold Shift and Mechanism Involved in Loss or Preservation of Residual Hearing in Implanted Cochlea, Exposed to Noise

Introduction: immediate macroscopic damage to the cochlea is followed by early and late molecular an cellular damage, following cochlear implantation. There is uncertainty regarding the mechanism for delayed loss and regarding the impact of noise trauma (NT) on the residual hearing following CI.

Method: this is a prospective animal study on pigmented guinea pigs (GP). in the ABR threshold shift study we had 3 groups of GP: EIT with dexamethasone eluting electrode (+dex.) + NT; EIT (-dex.) + NT; NT only (control). ABR were performed in order to analyse the threshold shift 1 and 30 days post NT. In the gene expression portion of study we had: EIT (+dex) + NT; EIT (-) + NT; EIT (-dex) only; NT only; no intervention (control). cochleae from all groups were harvested and analysed for expression of inflammation, apoptosis and fibrosis genes.

Results: ABR study: The threshold shift was significantly larger in controls compare to EIT+NT in day 1 and 30 post NT, in all the tested frequencies. Gene expression study: Proapoptotic (TNFα, TNFαR1a) and pro-fibrotic (TGFβ) genes were >X2 up-regulated following EIT and EIT+NT with the latter group to lesser extent. The use of dex. eluting electordes yielded much smaller up-regulation of these genes compare to non-eluting electrode.

Conclusion: The implanted cochlea tend to be less vulnerable to NT (lower threshold shift and lower expression of proapoptotic and profibrogenic genes). Dex. have shown promising results for hearing protection in the implanted GP exposed to NT