Harding Gary W, Bohne Barbara A, Ahmad Mueed
Department of Otolaryngology, Box 8115, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Hear Res. 2002 Dec;174(1-2):158-71. doi: 10.1016/s0378-5955(02)00653-6.
A detailed comparison of 2f(1)-f(2) distortion product otoacoustic emission (DPOAE) level shifts (LS) and auditory brainstem response (ABR) threshold shifts with noise-induced histopathology was conducted in chinchillas. DPOAE levels (i.e., L(1) and L(2)) at f(1) and f(2), respectively, ranged from 55-75 dB sound pressure level (SPL), with f(2)/f(1)=1.23, 6 points/octave, f(2)=0.41-20 kHz, and ABR thresholds at 0.5-20 kHz, 2 points/octave, were determined pre-exposure. The exposure was a 108 dB SPL octave band of noise centered at 4 kHz (1-1.75 h, n=6) or 80-86 dB SPL (24 h, n=5). DPOAE LSs (magnitude pre- minus post-exposure) and ABR threshold shifts (TS) were determined at 0 days and up to 28 days post-exposure. The cochleae were fixed, embedded in plastic and dissected into flat preparations. The length of the organ of Corti (OC) was measured; missing inner (IHC) and outer (OHC) hair cells counted; stereocilia damage rated; and regions of OC and nerve-fiber loss determined. Cytocochleograms were made showing functional loss and structural damage with the LS and TS overlaid. Some unexpected results were obtained. First, the best correlation of LS with histopathology required plotting the DPOAE data at f(1) with respect to the chinchilla-place map. The best correlation of TS was with IHC and nerve-fiber loss. Second, wide regions of up to 10% scattered OHC loss in the apical half of the OC showed little or no LS. Third, with the 108 dB SPL noise, there was 20-40 dB of recovery for DPOAEs at mid-high frequencies (3-10 kHz) in eight of 12 cochleae where there was 70-100% OHC loss in the basal half of the OC. The largest recovery at mid-high frequencies occurred in regions where the OC was entirely missing. Fourth, with the 80-86 dB SPL noise, there was no LS at small focal lesions (100% loss of OHCs over 0.4 mm) when the frequency place of either f(1) or f(2) was within the lesion but not both. There was no correlation of LS with OHC stereocilia loss, fusion or disarray. These results suggest that, after noise exposure, DPOAEs at mid-high frequencies can originate from or be augmented by generators located at someplace other than the frequency place of f(2), possibly the basal 20% of the OC when this region is intact. Also, noise-induced DPOAE LSs seemed to reflect differing mechanisms for temporary and permanent hearing loss.
在栗鼠身上进行了2f(1)-f(2)畸变产物耳声发射（DPOAE）水平偏移（LS）和听觉脑干反应（ABR）阈值偏移与噪声诱导的组织病理学的详细比较。分别在f(1)和f(2)处的DPOAE水平（即L(1)和L(2)），声压级（SPL）范围为55 - 75 dB，f(2)/f(1)=1.23，每倍频程6个点，f(2)=0.41 - 20 kHz，且在暴露前确定了0.5 - 20 kHz、每倍频程2个点的ABR阈值。暴露为以4 kHz为中心的108 dB SPL倍频程噪声带（1 - 1.75小时，n = 6）或80 - 86 dB SPL（24小时，n = 5）。在暴露后0天至28天确定DPOAE LSs（暴露前与暴露后幅度之差）和ABR阈值偏移（TS）。将耳蜗固定、包埋在塑料中并切成薄片标本。测量柯蒂氏器（OC）的长度；计数缺失的内毛细胞（IHC）和外毛细胞（OHC）；评定静纤毛损伤程度；确定OC和神经纤维损失区域。制作了细胞耳蜗图，显示功能损失和结构损伤，并叠加了LS和TS。获得了一些意外结果。首先，LS与组织病理学的最佳相关性要求根据栗鼠部位图绘制f(1)处的DPOAE数据。TS与IHC和神经纤维损失的相关性最佳。其次，OC顶端半部高达10%的散在OHC损失的广泛区域显示出很少或没有LS。第三，对于108 dB SPL噪声，在12个耳蜗中的8个中，OC基部半部有70 - 100%的OHC损失，中高频（3 - 10 kHz）的DPOAEs有20 - 40 dB的恢复。中高频的最大恢复发生在OC完全缺失的区域。第四，对于80 - 86 dB SPL噪声，当f(1)或f(2)的频率位置在病变内但不是两者都在时，小的局灶性病变（0.4 mm以上OHC 100%损失）处没有LS。LS与OHC静纤毛损失、融合或紊乱没有相关性。这些结果表明，噪声暴露后，中高频的DPOAEs可能源自f(2)频率位置以外的其他地方的发生器或由其增强，当该区域完整时可能是OC的基部20%。此外，噪声诱导的DPOAE LSs似乎反映了暂时性和永久性听力损失的不同机制。
