Noguchi Yoshihiro, Nishida Hiroaki, Tokano Hisashi, Kawashima Yoshiyuki, Kitamura Ken
Department of Otolaryngology, Tokyo Medical and Dental University Graduate School, Tokyo, Japan.
Ann Otol Rhinol Laryngol. 2004 Mar;113(3 Pt 1):194-9. doi: 10.1177/000348940411300304.
To clarify the pathogenesis of acute low-tone sensorineural hearing loss (ALHL), we retrospectively compared the electrocochleographic findings from 20 patients with ALHL with those from 58 patients with Meniere's disease (MD) classified into 4 groups (MD1 through MD4) according to their pure tone average. The mean summating potential-action potential ratio in the ALHL group was 0.35 +/- 0.13, which was significantly higher than the control ratio but similar to the ratio seen in the MD1 group (pure tone average < 25 dB hearing level). The mean detection threshold of the cochlear microphonics in the ALHL group was 32.0 +/- 9.4 dB normal hearing level, which was again similar to that seen in the MDI group. Moreover, more than 50% of patients with ALHL had normal cochlear microphonics input-output curves. We therefore conclude that the pathogenesis of ALHL arises from an endolymphatic hydrops with little or no impairment of hair cells that resembles early-stage MD.
为阐明急性低频感音神经性听力损失（ALHL）的发病机制，我们回顾性比较了20例ALHL患者与58例梅尼埃病（MD）患者的耳蜗电图结果。MD患者根据纯音平均听阈分为4组（MD1至MD4）。ALHL组的平均总和电位-动作电位比值为0.35±0.13，显著高于对照组，但与MD1组（纯音平均听阈<25dB听力级）的比值相似。ALHL组耳蜗微音器电位的平均检测阈值为32.0±9.4dB正常听力级，同样与MD1组相似。此外，超过50%的ALHL患者耳蜗微音器电位输入-输出曲线正常。因此，我们得出结论，ALHL的发病机制源于内淋巴积水，毛细胞几乎没有或没有损伤，类似于MD早期阶段。
