INTENSITY CODING IN ACOUSTIC AND ELECTRIC HEARING

拟议研究的长期目标是：(1)制定一项 听力正常时声强编码的统一理论， 听障和植入型听者，(2)区分功能性 听障和植入型听者可能由于 大脑外周兴奋模式改变的传递，以及(3) 设计能够最大限度地补偿 这些听力受损的听者存在功能缺陷。这 该方案解决了亮度编码的动态范围问题 在声学和电学听力方面。一方面，声学动力学 射程问题指的是大的心理物理之间的差异 响度范围和有限的生理范围 大多数独立的听觉神经元。另一方面，电力 动态范围问题是临床医生面临的一个现实而严峻的现实。 在安装语音处理器时：植入通常为6-20分贝的听者 音域必须适应正常语音和环境声音，包括 40-60分贝范围内的重要信息。具体目标是(1) 了解编码巨大数据的潜在神经机制 声学听力的动态范围，(2)量化响度增长和 电子听力中的辨别功能，以及(3)确定哪一个 电听力中是否缺少正常的机制？ 可以通过补偿这些来增加电动态范围 缺少正常的机械装置。我们的假设是，响度的增长和 辨别功能主要由外围设备决定 激励模式和中央系统以类似的方式响应 而不考虑外围设备输入的变化。我们的实验 设计是为了测量响度增长和辨别功能 改变中央系统外围输入的条件。 用于改变外围输入的方法包括声学高通 噪声、低通和带通噪声、前向掩蔽、幅度或相位- 调制刺激、前庭神经切断术、电刺激 听神经和耳蜗核。相应的生理学 要检查的机制是：兴奋沿基底动脉的传播 膜，抑制和兴奋掩蔽，适应和低- 自发性听觉神经元，神经放电的同步性， 传出神经元的贡献，基底的非线性振动 膜及其相关现象(如侧向抑制)。一个 这一方案的独特之处在于，它采用了人工耳蜗植入、听觉 脑干植入和前庭神经切除术患者更好地了解 大动态范围声音编码的神经机制 强度。从这项提议中获得的结果可能会导致更好的 听力假体和助听器的设计将补偿 由于两种电刺激导致的动态范围减小 听觉系统和听力损失。

The long-term objectives of the proposed study are to (1) develop a unified theory of the encoding of sound intensity in normal-hearing, hearing-impaired, and implant listeners, (2) differentiate the functional deficits that hearing-impaired and implant listeners may have due to the delivery of altered peripheral excitation patterns the brain, and (3) design rehabilitative devices that can maximally compensate for the functional deficits in these listeners with hearing impairment. This proposal addresses the dynamic range problem for the encoding of intensity in both acoustic and electric hearing. On one hand, the acoustic dynamic range problem refers to the discrepancy between the large psychophysical loudness range and the limited physiological range demonstrated by the majority of individual auditory neurons. On the other hand, the electric dynamic range problem is a practical and harsh reality facing clinicians in fitting speech processors: implant listeners who have typically 6-20 dB range must accommodate normal speech and environmental sounds containing important information over a 40-60 dB range. The specific aims are to (1) understand the underlying neural mechanisms of encoding the enormous dynamic range in acoustic hearing, (2) quantify loudness growth and discrimination functions in electric hearing, and (3) determine which normal mechanisms are missing in electric hearing and whether it is possible to increase the electric dynamic range by compensating for these missing normal mechanisms. Our hypothesis is that loudness growth and discrimination functions are primarily determined by the peripheral excitation pattern and the central system responds in a similar fashion regardless of the changes in the peripheral inputs. Our experimental design is to measure loudness growth and discrimination functions in conditions that alter the peripheral inputs to the central system. Methods used to alter the peripheral inputs include acoustic high-pass noise, low- and band-pass noise, forward masking, amplitude or phase- modulated stimuli, vestibular-nerve-section, electric stimulation of the auditory nerve and cochlear nucleus. Corresponding physiological mechanisms to be examined are: spread of excitation along the basilar membrane, suppressive and excitatory masking, adaptation and low- spontaneous rate auditory neurons, synchronization of neural firing, contributions of efferent neurons, nonlinear vibration of the basilar membrane and its associated phenomena (e.g. lateral suppression). A unique feature of this proposal is that it uses cochlear implant, auditory brainstem implant, and vestibular neurectomy patients to better understand the neural mechanisms of encoding the large dynamic range of sound intensity. The results obtained from this proposal could lead to better designs of auditory prostheses and hearing aids that will compensate for the reduced dynamic range that occurs with both electric stimulation of the auditory system and hearing loss.