The Bionics Institute, 384-388 Albert Street, East Melbourne, Australia; The Department of Medical Bionics, University of Melbourne, Australia.
The Bionics Institute, 384-388 Albert Street, East Melbourne, Australia.
Hear Res. 2022 Dec;426:108635. doi: 10.1016/j.heares.2022.108635. Epub 2022 Oct 13.
There is an increasing trend to provide cochlear implants for people with useful residual hearing, typically in the low frequency range (<2 kHz). These recipients typically use both electrical stimulation from their implant and acoustic stimulation that has been amplified with a hearing aid to access their residual hearing, so called electro-acoustic stimulation (EAS). However, a significant problem is the loss of residual hearing following implantation that can occur immediately following surgery or delayed over many months. One potential cause of the loss of residual hearing is the over stimulation of remaining hair cells due to the combination of an amplified acoustic input and direct electrical activation. This paper aims to test this hypothesis. Here, we have used a neonatal aminoglycoside-induced partial hearing cat model that resulted in a high frequency hearing loss (>4 kHz). Two separate cohorts of animals were implanted and received unilateral chronic electrical stimulation using clinical stimulators and speech processors over 5 months. To simulate potential over stimulation via a hearing aid, one cohort of animals were also exposed to an enhanced acoustic environment consisting of 80 dB SPL 4-talker babble presented 14 h per day. Hearing thresholds for both stimulated and unstimulated ears were measured throughout the implantation period. Cochleae were collected for histology to measure spiral ganglion neuron survival, hair cell survival and tissue response to chronic implantation and electrical stimulation. Consistent with clinical observations, cochlear implantation and stimulation resulted in an increase in threshold across the population. There was no significant effect of the enhanced acoustic environment on auditory thresholds or histological measures (hair cell survival, neuronal survival) of hearing, indicating that hair cell overstimulation was not a significant driver of loss of residual hearing.
越来越多的人选择为具有有用残余听力（通常在低频范围<2 kHz）的人提供人工耳蜗植入。这些接受者通常同时使用人工耳蜗的电刺激和经过助听器放大的声学刺激来利用其残余听力，这种方法称为电声刺激（EAS）。然而，一个显著的问题是植入后残余听力的损失，这种损失可能在手术后立即发生，也可能在数月后延迟发生。残余听力损失的一个潜在原因是由于放大的声学输入和直接电激活的组合，对剩余毛细胞的过度刺激。本文旨在验证这一假说。在这里，我们使用了一种新生氨基糖苷诱导的部分听力猫模型，该模型导致高频听力损失（>4 kHz）。两组动物分别接受单侧慢性电刺激，使用临床刺激器和言语处理器进行刺激，时间超过 5 个月。为了模拟助听器潜在的过度刺激，一组动物还暴露在增强的声学环境中，该环境包括每天 14 小时 80 dB SPL 的 4 个说话者的 babble。在整个植入期间，测量了受刺激和未受刺激耳朵的听力阈值。收集耳蜗进行组织学测量，以测量螺旋神经节神经元存活、毛细胞存活以及组织对慢性植入和电刺激的反应。与临床观察一致，耳蜗植入和刺激导致整个群体的听力阈值增加。增强的声学环境对听觉阈值或听力的组织学测量（毛细胞存活、神经元存活）没有显著影响，表明毛细胞过度刺激不是残余听力丧失的主要原因。
