Otoacoustic Emission Cochleography

描述（由申请人提供）：计划中的研究旨在更好地理解DPOAE生成的机制以及这种发射的大而复杂的响应空间的关键特征。这一总体目标是通过使用DPOAE水平/相位（L/P）图来实现的，该图将DPOAE幅度和相位视为f2/f1比和DPOAE频率的函数。根据普遍接受的DPOAE产生的2源模型，在这些图中，水平相位条带（浅相位斜率与fdp）表示来自f2位置的失真源发射，而垂直相位条带（陡相位斜率与fdp）表示来自DPOAE频率位置（fdp）的反射发射。最近，我们发现，干扰音（IT）在这些地图中放置在fdp附近无法删除所有的垂直相位带在较高的主色调水平在人类，或提取任何DPOAE反射成分的存在下，垂直相位带在兔子。目的#1调查的假设，垂直相带难治性ITs附近的fdp取决于主音水平，物种，和SFOAE。因此，DPOAE L/P地图从兔子，龙猫，和人类收集和没有IT附近fdp在不同的f1和f2水平将进行比较，并与SFOAE的存在，反射机制的签名。据推测，耳声发射难治性ITs附近FDP产生的分布式基础源的DPOAE，因此这些排放的发病lavian应短于失真排放相同的F2。目标#2的重点是假设，这取决于主色调水平和物种，DPOAE成分提取与IFFT方法可能不匹配的IT技术揭示的，因为，而人类和兔子表现出浅和陡峭的相位梯度DPOAE组件，他们不同的FDP附近的IT的响应。目的#3研究DPOAE的基础源在由高于f2的噪声音调或频带揭示的DPOAE残差中起重要作用的概念。该来源还起到“填充”传统DP图所揭示的功能障碍区域的作用。这个基础源的可能性将通过确定八度音阶范围来研究，在该范围内，不同的音调（f2-f1）可以产生不同水平的f1和f2。噪声频带与越来越高的低频截止相对于f2和IT放置在连续0.33倍频程增量以上f2将被用来揭示异常残差DPOAE L/P地图噪声损伤后，并帮助建立的基础源的DPOAE的存在和属性。最后，在听力图中有4 kHz噪声诱导切迹的人中，将在有和没有高于f2的IT0.33倍频程的情况下收集DP图，以确定相应DP图切迹的真实范围是否与兔子一样被基础DPOAE源部分掩盖。计划中的研究承诺修改公认的智慧DPOAE产生的机制，也可能导致DPOAE测试的发展，更有用的，允许准确的耳蜗损伤模式，以揭示在较高的主音水平的信噪比显着改善。我们对畸变产物耳声发射的大多数理论认识是基于低水平声刺激。拟议的研究将这些努力扩展到更临床相关的水平，其中基础发生器似乎掩盖了细胞损伤模式。了解这些机制可能最终允许更准确地描述耳蜗功能障碍的模式，改善临床患者表现出特定的听力障碍的信噪比。

DESCRIPTION (provided by applicant): The planned research is designed to provide an improved understanding of the mechanisms underlying both the generation of DPOAEs as well as the key features of this emission's large, complex response space. This general aim is being accomplished by using DPOAE level/phase (L/P) maps that consider both DPOAE magnitude and phase as a function of f2/f1 ratio and DPOAE frequency. According to the commonly accepted 2-source model of DPOAE generation, in these maps, horizontal-phase banding (shallow phase slope vs. fdp) is indicative of distortion-source emissions from the f2 place, while vertical-phase banding (steep phase slope vs. fdp) signifies reflection emissions from the DPOAE-frequency place (fdp). Recently, we discovered that interference tones (ITs) placed near fdp in these maps were unable to remove all vertical-phase banding at higher primary-tone levels in humans, or to extract any DPOAE-reflection components in the presence of vertical-phase banding in rabbits. Aim #1 investigates the hypothesis that vertical-phase banding refractory to ITs near fdp depends on primary-tone level, species, and SFOAEs. Thus, DPOAE L/P maps from rabbits, chinchillas, and humans collected with and without an IT near fdp at various f1 and f2 levels will be compared, and related to the presence of SFOAEs, a signature of the reflection mechanism. It is postulated that OAEs refractory to ITs near fdp arise from a distributed basal source of DPOAEs and therefore onset latencies of these emissions should be shorter than distortion emissions obtained for the same f2. Aim #2 focuses on the hypothesis that depending upon primary-tone levels and species, DPOAE components extracted with IFFT methods may not match those revealed by IT techniques because, while both humans and rabbits exhibit shallow and steep phase-gradient DPOAE components, they differ in their response to ITs near fdp. Aim #3 investigates the notion that a basal source of DPOAEs plays a substantial role in DPOAE residuals revealed by tones or bands of noise above f2. This source also acts to `fill in' regions of dysfunction as revealed by traditional DP-grams. The likelihood of this basal source will be investigated by determining the octave extent over which difference tones (f2-f1) can be produced for various levels of f1 and f2. Noisebands with increasingly higher low-frequency cutoffs with respect to f2 and ITs placed at successive 0.33-octave increments above f2 will be used to reveal abnormal residuals in DPOAE L/P maps following noise damage and help establish the presence and properties of a basal source of DPOAEs. Finally, DP-grams will be collected with and without an IT 0.33 octaves abovef2 in humans with 4-kHz noise-induced notches in their audiograms to determine if, as in rabbits, the true extent of the corresponding DP-gram notch is partially obscured by a basal DPOAE source. The planned studies promise to modify accepted wisdom regarding mechanisms of DPOAE generation, and may also lead to the development of DPOAE tests that are more useful by allowing accurate cochlear-damage patterns to be revealed at higher primary-tone levels where signal-to-noise ratios are notably improved. The majority of our theoretical understanding of distortion product otoacoustic emissions is based on low-level acoustic stimulation. The proposed studies extend these efforts to more clinically relevant levels where basal generators appear to obscure cellular damage patterns. Understanding these mechanisms may eventually permit a more accurate depiction of the pattern of cochlear dysfunction with improved signal-to-noise ratios for clinic patients exhibiting particular hearing impairments.