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耳硬化症出现感觉神经性聋的机理有各种学说:Siebnmann认为病灶产生毒性物质损伤螺旋器毛细胞。Causse等认为耳海绵症病灶中组织细胞内释放蛋白分解酶,为感觉神经性损伤的主要因素。Glorig比较耳硬化症患者与正常人骨导听阈,未发现有明显差异;Guild通过颞骨组织学研究发现耳硬化症耳螺旋器及耳蜗神经萎缩者并不比非耳硬化症耳发生率高,亦支持上述观点。本文报告自1964至1973年间,对25名手术证实单侧耳硬化症患者进行研究,男16名、女9名,年龄16～69岁,气-骨导差为25～45分贝,健耳气-骨寻差为10～20分贝。
There are various theories about the mechanism of otic deafness in otosclerosis: Siebnmann believes that the lesions produce toxic substances that damage the spiral hair cells. Causse, etc. that ear vernacular lesions in tissue cells release proteolytic enzymes, sensory neuropathy is the main factor. Glorig compared auditory threshold of otoconjunctival and normal subjects and found no significant difference; Guild found by temporal bone histology of otosclerosis and cochlear nerve atrophy is not as high as non-otus sclerotioris, and also supports the above View. This article reports from 1964 to 1973 on 25 patients with unilateral otosclerosis confirmed by surgery, 16 males and 9 females, aged 16 to 69 years, air-bone conduction difference of 25 to 45 dB, health ear gas - Bone difference is 10 to 20 dB.