Harrison R V
Department of Otolaryngology, University of Toronto and The Hospital For Sick Children, Ontario, Canada.
Ear Hear. 1998 Oct;19(5):355-61. doi: 10.1097/00003446-199810000-00002.
We describe an animal model of auditory neuropathy in which subjects have extensive, scattered inner haircell loss but with a relatively intact outer haircell population.
Such a pattern of cochlear haircell damage can be produced in the chinchilla by treatment with the anticancer agent carboplatin.
In these subjects, otoacoustic emissions (OAEs) and cochlear microphonics remain normal while auditory brain stem evoked potential (ABR) thresholds are significantly elevated. However, in the same subjects, central auditory neurons (in the inferior colliculus) have response thresholds that are considerably lower (by up to 50 dB) than ABR thresholds. These findings parallel the characteristics of auditory neuropathy in humans, in which absent or abnormal ABRs are recorded in patients with only mild to moderate audiometric thresholds and preserved OAEs.
We suggest that scattered inner haircell lesions also can result from long-term cochlear hypoxia, and we propose that this is a likely candidate for the etiology of many types of auditory neuropathy in human subjects.
我们描述了一种听觉神经病动物模型,该模型的实验对象存在广泛、散在的内毛细胞丢失,但外毛细胞群体相对完整。
通过用抗癌药物卡铂治疗,可以在灰鼠身上产生这种耳蜗毛细胞损伤模式。
在这些实验对象中,耳声发射(OAE)和耳蜗微音电位保持正常,而听性脑干诱发电位(ABR)阈值显著升高。然而,在同一实验对象中,中枢听觉神经元(在下丘)的反应阈值比ABR阈值低得多(高达50分贝)。这些发现与人类听觉神经病的特征相似,在人类听觉神经病中,听力阈值仅为轻度至中度且耳声发射保留的患者记录到ABR缺失或异常。
我们认为散在的内毛细胞损伤也可能由长期耳蜗缺氧导致,并且我们提出这可能是人类多种类型听觉神经病病因的一个候选因素。