Avan Paul, Bonfils Pierre, Mom Thierry
Laboratory of Sensory Biophysics, School of Medicine, Clermont-Ferrand, France.
Noise Health. 2001;3(12):1-18.
Distortion product otoacoustic emissions (DPOAE) are increasingly used as an objective test for noninvasive hearing screening. When two pure tones with frequencies f1 and f2 are sent to the cochlea, the most prominent DPOAE is the cubic one produced at 2f1-f2, and this presentation will mainly emphasize its properties. DPOAEs are undoubtedly generated by cochlear nonlinearities. It is widely held that they arise from certain stages of sound processing by the outer hair cells (OHC) and that OHCs ensure normal cochlear sensitivity and tuning. Thus, DPOAEs should provide a privileged tool for monitoring the harmful effects of loud sound because OHCs are known to be one of the main targets of NIHL. Although DPOAEs provide the clinicians with a reliable screening limit of about 30 dB HL around f2, no reliable relationship has been found thus far between possible residual DPOAEs and either hearing loss or amount of impaired sensory cells. Furthermore, puzzling contradictory findings have been reported as to the presence of DPOAEs despite a large hearing loss (i.e. >30-40 dB) notably with high-level stimuli. These observations raise the following issues. What is the generation site of DPOAEs in a normal or pathological cochlea (OHCs, basilar membrane, place tuned to f2, 2f1-f2, places basal to f2.)? Is it necessary to account for interferences between several discrete sources, arising from different locations or different mechanisms and possibly exhibiting differential susceptibility to sensory cell damage? Do DPOAE changes depend on the nature of OHC pathology (NIHL, anoxia, ototoxic drugs, genetics.)? Once a source of DPOAE is characterized, is there any means of modelling the physiological process of its generation and deriving what might quantitatively relate DPOAE amount to sensory cell activity and thresholds? The goal of this presentation is to examine these issues, review the available data and propose a comparatively simple model.
畸变产物耳声发射（DPOAE）越来越多地被用作非侵入性听力筛查的客观测试方法。当将两个频率分别为f1和f2的纯音发送到耳蜗时，最突出的DPOAE是在2f1 - f2处产生的三次谐波，本报告将主要强调其特性。DPOAE无疑是由耳蜗的非线性产生的。人们普遍认为它们源于外毛细胞（OHC）对声音处理的某些阶段，并且OHC确保了正常的耳蜗敏感性和调谐。因此，DPOAE应该为监测强声的有害影响提供一个特殊的工具，因为已知OHC是噪声性听力损失（NIHL）的主要靶点之一。尽管DPOAE为临床医生提供了在f2附近约30 dB HL的可靠筛查阈值，但迄今为止，尚未发现可能存在的残余DPOAE与听力损失或感觉细胞受损数量之间存在可靠的关系。此外，尽管存在较大听力损失（即>30 - 40 dB），尤其是在高强度刺激下，关于DPOAE的存在仍有令人困惑的矛盾发现被报道。这些观察结果引发了以下问题。在正常或病理耳蜗中（OHC、基底膜、调谐到f2、2f1 - f2的部位、f2下方的部位），DPOAE的产生部位在哪里？是否有必要考虑几个离散源之间的干扰，这些干扰源于不同的位置或不同的机制，并且可能对感觉细胞损伤表现出不同的敏感性？DPOAE的变化是否取决于OHC病理的性质（NIHL、缺氧、耳毒性药物、遗传学……）？一旦确定了DPOAE的来源，是否有任何方法可以模拟其产生的生理过程，并推导可能将DPOAE量与感觉细胞活动和阈值定量相关的因素？本报告的目的是研究这些问题，回顾现有数据，并提出一个相对简单的模型。
