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目的 :探讨听神经病的听功能状态及病损部位。方法 :分析 6 5例听神经病患者的临床资料、纯音测听、声导抗测试、听性脑干反应 (ABR)、4 0Hz听觉相关电位及OAE检查结果。结果 :听神经病的低频听力损失源于蜗后的传入、传出神经及听性脑干受损 ,表现为声反射、传出抑制、ABR异常及诱发性OAE与纯音听阈不呈平行关系 ,与之相对应 ,低频区的外毛细胞处于失抑制的超常活动状态 ,表现为低频区SOAE增强、TEOAE反应幅值及DPOAE幅值升高 ;听神经病的高频听力损失源于耳蜗的外毛细胞损害 ,表现为高频区DPOAE幅值与纯音听阈呈一致性下降 ;听神经病的中频听力损失最轻或接近正常 ,表现为 2kHz附近的纯音听阈和DPOAE幅值均接近于正常。结论 :听神经病的传入、传出系统及耳蜗水平均有不同程度的功能障碍 ,其病损部位主要在耳蜗传入、传出神经 ,向上可侵及脑干 ,向下可侵及耳蜗
Objective: To investigate the auditory function of auditory neuropathy and lesion site. Methods: Clinical data, pure tone audiometry, acoustic impedance test, auditory brainstem response (ABR), 40 Hz auditory related potentials and OAE findings of 65 patients with auditory neuropathy were analyzed. Results: The low frequency hearing loss of auditory neuropathy originated from afferent cochlea, the afferent nerve and auditory brainstem were damaged. The acoustic reflex, efferent inhibition, ABR abnormality and induced OAE were not parallel to pure tone threshold, Correspondingly, the outer hair cells in the low-frequency region are in a state of dyskinesia, showing enhanced SOAE in the low-frequency region, and increased TEOAE response amplitude and DPOAE amplitude. The high-frequency hearing loss in the auditory neuropathy originates from the outer hair of the cochlea Cell damage, manifested as high amplitude DPOAE amplitude and pure tone hearing threshold decreased; intermediate hearing loss of auditory neuropathy, the lightest or near normal hearing, performance 2kHz near the pure tone threshold and DPOAE amplitude are close to normal. CONCLUSIONS: The afferent and efferent systems of auditory neuropathy and the level of cochlea all have different degrees of dysfunction. The lesion sites are mainly in the cochlea, afferent nerve, invading the brainstem, invading the cochlea