Nong Dong X, Ura Masaharu, Kyuna Asanori, Owa Tatsuhito, Noda Yutaka
Department of Otorhinolaryngology, Faculty of Medicine, University of Ryukyus, Okinawa, Japan.
Otol Neurotol. 2002 Nov;23(6):953-7. doi: 10.1097/00129492-200211000-00024.
To determine the origin of the acoustically evoked short latency negative response (ASNR), a peculiar V-shaped response at about 3 to 4 milliseconds found during auditory brainstem response recordings. Previous reports demonstrated that the ASNR is present only in ears with profound hearing loss under intense stimulation. It has already been excluded as any kind of artifact. The individuals with ASNR had good vestibular function in spite of their poor hearing, suggesting a relation between the ASNR and the vestibular system. The saccule and vestibular nuclei are hypothesized to be the sense organ and the generator of the response, respectively. The current study tested the saccular function for ears with ASNR and searched for ASNR in ears with a functionless cochlea.
Prospective study.
Academic tertiary referral center.
Twenty patients with bilateral profound hearing loss, aged 6 to 62 years, including 16 cochlear implant recipients. Twelve healthy participants with normal hearing, aged 23 to 30 years, served as the control group.
Recordings of vestibular evoked myogenic potential (VEMP) and auditory brainstem responses.
The presence or absence of ASNR in ears with cochlear implants. The presence or absence and threshold of VEMP in ears with ASNR versus ears without ASNR.
ASNR was recorded by sound stimulation from three ears with unaided cochlear implants, a model of functionless cochlea. VEMP was evoked by sound stimulation to all the nine ASNR ears without threshold difference from normal control ( > 0.05), implying normal saccular function for the ASNR ears. For the ears with profound hearing loss and absence of ASNR, about two thirds were considered to have saccular afunction because of absence of VEMP. The other third displayed VEMPs with higher threshold than normal control ( < 0.01), indicating saccular hypofunction. Furthermore, ASNR and VEMP were elicited from an ear diagnosed with semicircular canal hypofunction.
It is clear that the presence of ASNR is dependent not on residual hearing but on normal saccular function. On the basis of these results, the authors believe ASNR to be saccular in origin.
确定听觉脑干反应记录过程中发现的一种特殊的V形反应——听觉诱发短潜伏期负反应（ASNR）的起源。先前的报告表明，ASNR仅在强烈刺激下的极重度听力损失耳中出现。它已被排除为任何类型的伪迹。尽管听力不佳，但有ASNR的个体前庭功能良好，这表明ASNR与前庭系统之间存在关联。推测球囊和前庭核分别是该反应的感觉器官和发生器。本研究测试了有ASNR耳的球囊功能，并在耳蜗无功能的耳中寻找ASNR。
前瞻性研究。
学术性三级转诊中心。
20例双侧极重度听力损失患者，年龄6至62岁，其中16例为人工耳蜗植入者。12名听力正常的健康参与者，年龄23至30岁，作为对照组。
记录前庭诱发肌源性电位（VEMP）和听觉脑干反应。
人工耳蜗植入耳中ASNR的有无。有ASNR耳与无ASNR耳中VEMP的有无及阈值。
通过声音刺激，在3只使用非辅助人工耳蜗的耳中记录到了ASNR，这是一种耳蜗无功能的模型。声音刺激诱发了所有9只出现ASNR耳的VEMP，与正常对照组相比阈值无差异（>0.05），这意味着有ASNR耳的球囊功能正常。对于极重度听力损失且无ASNR的耳，约三分之二因未引出VEMP而被认为球囊无功能。另外三分之一的耳引出的VEMP阈值高于正常对照组（<0.01），表明球囊功能减退。此外，在一只被诊断为半规管功能减退的耳中引出了ASNR和VEMP。
显然，ASNR的出现不依赖于残余听力，而是依赖于正常的球囊功能。基于这些结果，作者认为ASNR起源于球囊。
