人类声诱发短潜伏期负电位的研究

目的在极重度感音性聋耳的ABR检测中发现一个位于3～4ms潜伏期的"V"字形负向波形,称声诱发短潜伏期负电位(Acoustically Evoked Short Latency Negative Response,ASNR)。本研究通过大宗病例调查和临床实验来探讨ASNR的特点和起源。方法回顾性调查并分析3104例ABR检测结果,以详尽了解ASNR的出现率和特性。对20名双耳极重度感音性耳聋患者(6～62岁)和12名健康人(23～30岁)进行了ABR和前庭诱发肌源性电位(VEMP)测试。患者组包括了16名人工耳蜗植入术后的患者,植入耳在裸耳状态时可提供无功能耳蜗模型。结果判读侧重于:人工耳蜗植入耳能否诱发ASNR,以及对比在极重度感音性聋耳中ASNR组和非ASNR组的VEMP出现率及反应阈值。结果ASNR仅出现于极重度感音性聋耳,并且对强声刺激(80～120dBnHL)有依赖性。在653例极重度感音性聋患者(981耳)的ABR波形中,有80例(12.3%)117耳(11.9%)出现了ASNR。ASNR有良好的重复性,可排除伪迹干扰的可能性。ASNR具有神经电位的特征,表现在随着声刺激的增强,其潜伏期缩短而振幅增大。ASNR与ABR的波形完全不一样,无法将其解释为传统听觉神经通路产生的电位。临床实验中,3个人工耳蜗植入耳能诱发出ASNR,说明ASNR的发生与耳蜗无关。所有9个ASNR耳都诱发出VEMP,且阈值与正常对照组无统计学差异(P>0.05),提示ASNR耳具有正常的球囊功能。在非ASNR组中,三分之二没有引出VEMP,而另外三分之一虽然可以诱发出VEMP,但阈值明显较正常对照组高(P<0.01),分别提示球囊功能丧失或低下。此外,有一外半规管麻痹耳诱发出了ASNR和VEMP。结论ASNR并非伪迹,而是一种依赖强声刺激,且只出现于极重度感音性聋耳的神经电位。ASNR的出现完全依赖于正常的球囊功能,而不依赖于残余听力或者半规管功能。据此认为ASNR起源感觉器官为球囊,根据其潜伏期推测电位源自前庭神经核。

Study of acoustically evoked short latency negative response in human

Objective In our auditory brainstem responses(ABR) tests, a peculiar V-shaped negative wave at around 3-4 ms latency was observed. At present, this acoustically evoked short latency negative response(ASNR) is poorly understood. Retrospective investigation and prospective clinical tests were conducted to study the characteristics and origin of ASNR. Methods In order to study its appearance and characteristics, ABR data of 3104 tests during 1980-1998 were retrospectively reviewed and analyzed. Twenty bilateral profound hearing loss patients including 16 cochlear implant recipients and 20 healthy normal-hearing subjects, serving as the control group, were involved in the prospective clinical tests. ABR and vestibular evoked myogenic potential (VEMP) were recorded. We focused our interest on results of presence/absence of ASNR in cochlear implant ears, presence/absence and threshold of VEMP in ASNR ears vs. in non-ASNR ears. Results The ASNR was found only in profound hearing loss ears under intense stimuli(80-120 dB nHL). Out of the total 653 profound hearing loss patients(981 ears), the click evoked ASNRs were present in 80 patients (12.3%), 117 ears(11.9%). The ASNR was excluded from an artifact by its reproducibility over time, equipment and institutes. Moreover, it became absent after external auditory canal occlusion, which simply blocked the air conduction without any influence upon scalp potentials or equipment. It had neural response characteristics that the latency and amplitude shortened and increased respectively in response to the increase of stimulus intensity. Because the peculiar V-shaped waveform obviously differs from ABR, the ASNR was not interpreted as a potential generated from the conventional auditory pathway. In clinical tests, ASNR was recorded by sound stimulation from 3 unaided cochlear implant ears, a model of functionless cochlea. VEMP was evoked by sound stimulation to all the 9 ASNR ears without threshold difference from normal control(P > 0.05), implying normal saccular function for the ASNR ears. For the profound hearing loss ears with absent ASNR, about two thirds were considered as saccular afunction because of absent VEMP. The other one third displayed VEMPs with higher thresholds than normal control (P < 0.01) indicating saccular hypofunction. Furthermore, ASNR and VEMP were elicited from an ear diagnosed with semicircular canal hypofunction. Conclusions ASNR, other than an artifact, appears in only profound hearing loss ears under intense stimuli. It is clear that the presence of ASNR is not dependent on residual hearing or semicircular canal but on normal saccular function. Based on the results, we believe that ASNR is of saccular origin and originated from the vestibular nuclei.