The pattern of vestibular nerve response to loud sound after total destruction of cochlea

本研究的目的是探讨前庭诱发肌源性电位(VEMP)的机制。首先，我们尝试用氨基糖苷类药物破坏耳蜗神经。肌肉注射阿米卡星450 mg/kg连续14d后1个月，仍可记录到动作电位。然后我们将剂量从450 mg/kg增加到900 mg/kg。1个月后耳蜗区完全破坏，但在最大声强下声刺激无反应。这表明阿米卡星不仅破坏了耳蜗区，也破坏了前庭。我们试图确定在不破坏前庭的情况下破坏耳蜗的合适剂量。虽然我们额外使用了450 mg/kg和700 mg/kg两种剂量，但未能确定合适的剂量。其次，我们试图通过大声音破坏耳蜗组织。动物暴露于115dB白噪声12h后，仍可记录到复合动作电位，提示耳蜗区未受到破坏。第三，我们评估了诱发耳鸣的药物(水杨酸盐和奎宁)对耳蜗皮层和听觉皮质的影响。静脉注射水杨酸盐或肌肉注射奎宁均未引起初级听觉皮质自发活动的显著改变。药物对耳蜗神经自发活动的影响尚未得到证实。我们报道了实验诱导的内淋巴积液中CAP适应性的变化。我们还进行了临床研究，并报告了患有Ramsay Hunt综合征、急性感音神经性耳聋、前庭神经炎和内耳道狭窄的患者的VEMP模式。此外，还报道了年龄对VEMP的影响。

The purpose of this study was to examine the underlying mechanisms of vestibular evoked myogenic potential(VEMP) by performing single unit recording from vestibular nerve in response to the loud sound after total destruction of cochlea Firstly, we tried to destruct cochlea by administration of aminoglycoside. One month after intramuscularly administration of amikacin at the dose 450 mg/kg for 14 days, action potential was still recorded. Then we increased dosage from 450 mg/kg to 900 mg/kg. The cochlea was completely destructed after 1 month, however acoustic stimuli induced no response at the maximum sound intensity. This suggests that the administration of amikacine induced destruction not only cochlea but also vestibule. We tried to determine the appropriate dosage which destruct cochlea without destruct vestibule. Although we applied two additional dosages of 450 mg/kg and 700 mg/kg, we failed to decide appropriate dosage.Secondary, we tried to destruct cochlea by loud sound. Animals were exposed to the white noise at the intensity of 115 dB for 12hours, compound action potential was still recorded and this suggests that the cochlea was not destructed. Thirdly, we evaluated the effects of tinnitus inducing drugs (salicylate and quinine) on both cochlea and auditory cortex. Either intra-venous administration of salicylate or intramuscular administration of quinine induced no marked change in spontaneous activity in the primary auditory cortex. The effects of drugs on the spontaneous activity in the cochlear nerve were not confirmed. We reported the changes in CAP adaptation in experimentally induced endolymphatic hydrops.We also performed clinical study and reported the VEMP pattern who suffered from Ramsay Hunt syndrome, acute sensorineural hearing loss, vestibular neuritis, and narrow internal auditory canal. In addition, the effect of age on VEMP was reported.