Effects of age on the distortion product otoacoustic emission growth functions

Effects of age on the distortion product otoacoustic emission growth functions
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DOI:
10.1016/s0378-5955(01)00377-x
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发表时间:
2002-01-01
期刊:
影响因子:
2.8
通讯作者:
Rubel, EW
Rubel, EW
中科院分区:
医学1区
文献类型:
--
作者:
Gates, GA;Mills, D;Rubel, EW

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老年性听力损失(老年性耳聋)被认为是由于与年龄相关的耳蜗变性(老化)加上外在损害(噪音和其他耳毒性物质)和内在疾病(如系统性疾病)的累积效应造成的。以前的研究表明,毛细胞功能障碍(感觉性老年性耳聋)是年龄相关性听力损失的主要机制。然而,最近来自安静饲养的沙土鼠的证据表明,耳蜗老化主要是由于血管纹的萎缩,这与耳蜗内电位(EP)降低、螺旋神经节萎缩和相对平坦的听力损失有关,称为代谢性老年性耳聋。由于目前还不可能在临床环境中直接测量EP,我们想知道是否可以从现有的临床测试中间接证明耳蜗代谢功能障碍,特别是失真产物(DP)耳声发射的输入-输出(10)增长函数与行为听力阈值(HTL)的关系。我们预计会发现HTL和10项功能之间的不一致性,如果年龄相关的耳蜗代谢功能障碍是可操作的,HTL的10项功能随年龄的下降比10项功能的下降更大,或者如果外毛细胞功能障碍是主要的病理,10项功能的丧失比HTL更大。为了解决这一假设,我们分析了一大群成年人的现有听觉数据,以确定DP10功能的三个方面随年龄的变化:曲线下面积、阈值和斜率。分析表明,年龄对HTL的影响大于对DP10测量的影响。这一效应支持了这一假说,即人工耳道功能障碍是耳蜗老化的一个实质性因素。目前对这种功能障碍的病因和机制尚无定论。(C)2002 Elsevier Science B.V.保留所有权利。
Age-related hearing loss (presbycusis) is thought to result from age-related degeneration (aging) of the cochlea plus the cumulative effects of extrinsic damage (noise and other ototoxic agents) and intrinsic disorders (e.g. systemic diseases). Previous studies have implicated dysfunction of the hair cells (sensory presbycusis) as the principal mechanism of age-related hearing loss. However, recent evidence from quiet-reared gerbils suggests that cochlear aging results primarily from atrophy of the stria vascularis, which is associated with diminished endocochlear potential (EP), spiral ganglion atrophy, and a relatively flat audiometric loss, termed metabolic presbycusis. Because it is not currently possible to measure EP directly in the clinical setting, we wondered if cochlear metabolic dysfunction might be evidenced indirectly from existing clinical tests, specifically, the input-output (10) growth function of the distortion product (DP) otoacoustic emissions in relation to behavioral hearing threshold levels (HTL). We anticipated finding discordance between the 10 functions and HTL with either a greater decline with age in HTL than in 10 functions if an age-related metabolic dysfunction of the cochlea was operant, or a greater loss of 10 function than HTL if outer hair cell dysfunction was the dominant pathology. To address this supposition we analyzed existing auditory data from a large cohort of adults to determine the change with age in three aspects of the DP 10 function: area under the curve, threshold, and slope. The analyses demonstrated a greater effect of age on HTL than on the DP 10 measures. This effect supports the hypothesis that strial dysfunction is a substantive factor in cochlear aging. The etiology and mechanisms for this dysfunction are conjectural at present. (C) 2002 Elsevier Science B.V. All rights reserved.