HYPOTHESIS: The progressive loss of hearing that develops after electrode insertion trauma (EIT) can be attenuated by local dexamethasone (DXM) therapy. BACKGROUND: Hearing loss (HL) that develops after cochlear implant EIT occurs in two stages in laboratory animals, that is, an immediate loss followed by a progressive loss. Direct infusion of DXM into the guinea pig cochlea can attenuate both ototoxin- and noise-induced HL. MATERIALS AND METHODS: Auditory-evoked brainstem responses (ABRs) of guinea pigs were measured for 4 frequencies (i.e., 0.5, 1, 4, and 16 kHz) before, immediately after, and more than 30 days post-EIT for experimental (EIT,EIT + artificial perilymph, and EIT + DXM) and for the contralateral unoperated cochleae of each group. An electrode analog of 0.14-mm diameter was inserted through a basal turn cochleostomy for a depth of 3 mm and withdrawn. DXM in artificial perilymph was delivered immediately post-EIT into the scala tympani via a miniosmotic pump for 8 days. RESULTS: The ABR thresholds of EIT animals increased progressively post-EIT. Contralateral unoperated cochleae had no significant changes in ABR thresholds. Immediately post-EIT, that is, Day 0, the DXM-treated animals exhibited a significant HL at 1, 4, and 16 kHz, but this HL was no longer significant by Day 30 compared with contralateral control ears. CONCLUSION: The results from immediate local treatment of the cochlea with DXM in an animal model of EIT-induced HL suggest a novel therapeutic strategy for hearing conservation by attenuating the progressive HL that can result from the process of electrode array insertion during cochlear implantation.
HYPOTHESIS: The progressive loss of hearing that develops after electrode insertion trauma (EIT) can be attenuated by local dexamethasone (DXM) therapy. BACKGROUND:Hearing loss (HL) that develops after cochlear implant EIT occurs in two stages in laboratory animals, that is, an immediate loss followed by a progressive loss. Direct infusion of DXM into the guinea pig cochlea can attenuate both ototoxin- and noise-induced HL. MATERIALS AND METHODS: Auditory-evoked brainstem responses (ABRs) of guinea pigs were measured for 4 frequencies (i.e., 0.5, 1, 4, and 16 kHz) before, immediately after, and more than 30 days post-EIT for experimental (EIT,EIT + artificial perilymph, and EIT + DXM) and for the contralateral unoperated cochleae of each group. An electrode analog of 0.14-mm diameter was inserted through a basal turn cochleostomy for a depth of 3 mm and withdrawn. DXM in artificial perilymph was delivered immediately post-EIT into the scala tympani via a miniosmotic pump for 8 days. RESULTS: The ABR thresholds of EIT animals increased progressively post-EIT. Contralateral unoperated cochleae had no significant changes in ABR thresholds. Immediately post-EIT, that is, Day 0, the DXM-treated animals exhibited a significant HL at 1, 4, and 16 kHz, but this HL was no longer significant by Day 30 compared with contralateral control ears. CONCLUSION: The results from immediate local treatment of the cochlea with DXM in an animal model of EIT-induced HL suggest a novel therapeutic strategy for hearing conservation by attenuating the progressive HL that can result from the process of electrode array insertion during cochlear implantation.
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