Electrophysiological biomarkers for spatial hearing impairments resulting from ea

描述(由申请人提供)：传导性听力损失(CHL)--例如由中耳感染和其他耳朵疾病引起的--可以对听觉系统产生深远和有害的影响。由CHL引起的干扰通常是双耳听力任务的损害，需要整合来自两只耳朵的信息，例如声音的“过滤” 在嘈杂和混响的环境中。慢性语言障碍可能会导致长期的言语和语言障碍。时至今日，CHL长期影响中枢听觉系统的确切方式尚不完全清楚，但很明显，其影响可能是严重和持久的。由此产生的一系列症状被称为中枢性听觉处理障碍(或(C)apd)。目前，(C)动作障碍的诊断很困难，需要一系列的测试和数月的时间。这对S来说是有问题的，因为研究表明，尽早治疗(C)apd是有益的。听觉脑干反应(ABR)的双耳交互作用成分(BIC)是一种可用于评估双耳听力功能和诊断(C)动作电位的潜在指标。声诱发双耳交互作用成分(BIC)是从单耳诱发ABR的总和中减去双耳诱发ABR后剩余的ABR。B峰是BIC中的第一个负峰，与双耳处理有关。在人类和动物研究中的潜伏期表明，它在下丘及其输入水平上起源于脑干。下丘是所有脑干核团的汇聚部位，包括上橄榄复合体的核团，它计算位置的双耳听觉线索(耳间时间(ITD)和水平(ILD)差)。BIC可能具有重要的诊断价值；例如，儿童和成人的B峰潜伏期和波幅的改变与慢性CHL相关的双耳加工中相同的长期行为缺陷相关并预测。在这个方案中，我们研究了CHL对BIC？峰的影响，并将BIC与声音定位能力的行为测量--声学惊吓反应--相关联。在诱发单侧CHL的过程中，将在一系列ITD和ILD提示的位置上评估BIC？峰的幅度和潜伏期，并在相应的时间点评估声音定位行为。我们假设，CHL以一种可预测的方式改变了声音定位线索的整合，这将增强我们对CHL对双耳听力影响的理解。此外，我们预计行为和BIC都会随着时间的推移而恢复，BIC可以预测声音定位能力的水平。了解声音定位和BIC之间的相互作用有望为评估患有中耳炎的儿童的双耳听力和CHL提供一个临床有用的工具。这项建议是专门为提供听力研究的基础科学和临床方面的培训而设计的，以促进NIDCD的使命。

DESCRIPTION (provided by applicant): Conductive hearing loss (CHL)-such as is caused by middle ear infections and other ear conditions-can affect the auditory system in a profound and detrimental manner. The disruptions caused by CHL are often impairments of binaural hearing tasks that require the integration of information from both ears, such as the "filtering" of sounds in noisy and reverberant environments. Long-term speech and language impairments can result from CHL. Still today, the exact manner in which long-term CHL affects the central auditory system is not entirely known, but it is clear that the effects can be severe and long lasting. The cluster of symptoms that result are termed Central Auditory Processing Disorder (or (C)APD). Currently, diagnosis of (C)APD is difficult, requiring a battery of tests and months of time. This s problematic, since studies have shown that it is beneficial to treat (C)APD as early as possible. One potential metric that could be used to assess binaural hearing function and diagnose (C)APD is the binaural interaction component (BIC) of the auditory brainstem response (ABR). The sound-evoked binaural interaction component (BIC) is the residual auditory brainstem response (ABR) remaining after subtracting the binaurally evoked ABR from the sum of the monaurally evoked ABRs. The ß peak is the first negative peak in the BIC, which is related to binaural processing. Latencies of ß in both human and animal studies indicate it has a brainstem origin at the level of the inferior colliculus and its inputs. The inferior colliculus isa site of convergence of inputs from all brainstem nuclei, including nuclei of the superior olivary complex, which computes binaural acoustical cues to location (interaural time (ITD) and level (ILD) differences). The BIC may have important diagnostic value; for example, altered latencies and amplitudes of the ß peak in children and adults are correlated with and predictive of the same long-term behavioral deficits in binaural processing associated with chronic CHL. In this proposal, we investigate the effect of CHL on the BIC ß peak and correlate the BIC with a behavioral measure of sound localization ability, the acoustic startle response. The amplitude of and latency of the BIC ß peak will be assessed across a range of ITD and ILD cues to location during the course of an induced unilateral CHL, and sound localization behavior will be assessed at corresponding time points. We hypothesize that CHL alters the integration of sound localization cues in a predictable way, which will enhance our understanding of the effect of CHL on binaural hearing. Furthermore, we expect that both behavior and BIC will recover with time, with BIC predicting the level of sound localization ability. Understanding the interaction between sound localization and the BIC promises to yield a clinically useful tool for assessing binaural hearing ability and CHL in children with otitis media. This proposal is specifically designed to provide training in both basic science and clinical aspects of auditory research, furthering the mission of the NIDCD.