Lefler Shannon M, Duncan Robert K, Goodman Shawn S, Guinan John J, Lichtenhan Jeffery T
Department of Otolaryngology, Washington University School of Medicine in St. Louis, Saint Louis, MO, United States.
Department of Otolaryngology-Head and Neck Surgery, Kresge Hearing Research Institute, University of Michigan, Ann Arbor, MI, United States.
Front Surg. 2021 Oct 5;8:687490. doi: 10.3389/fsurg.2021.687490. eCollection 2021.
Loudness recruitment is commonly experienced by patients with putative endolymphatic hydrops. Loudness recruitment is abnormal loudness growth with high-level sounds being perceived as having normal loudness even though hearing thresholds are elevated. The traditional interpretation of recruitment is that cochlear amplification has been reduced. Since the cochlear amplifier acts primarily at low sound levels, an ear with elevated thresholds from reduced cochlear amplification can have normal processing at high sound levels. In humans, recruitment can be studied using perceptual loudness but in animals physiological measurements are used. Recruitment in animal responses has never been unequivocally demonstrated because the animals used had damage to sensory and neural cells, not solely a reduction of cochlear amplification. Investigators have thus looked for, and found, evidence of recruitment in the auditory central nervous system (CNS). While studies on CNS recruitment are informative, they cannot rule out the traditional interpretation of recruitment originating in the cochlea. We used techniques that could assess hearing function throughout entire frequency- and dynamic-range of hearing. Measurements were made from two animal models: guinea-pig ears with endolymphatic-sac-ablation surgery to produce endolymphatic hydrops, and naïve guinea-pig ears with cochlear perfusions of 13 mM 2-Hydroxypropyl-Beta-Cyclodextrin (HPBCD) in artificial perilymph. Endolymphatic sac ablation caused low-frequency loss. Animals treated with HPBCD had hearing loss at all frequencies. None of these animals had loss of hair cells or synapses on auditory nerve fibers. In ears with endolymphatic hydrops and those perfused with HPBCD, auditory-nerve based measurements at low frequencies showed recruitment compared to controls. Recruitment was not found at high frequencies (> 4 kHz) where hearing thresholds were normal in ears with endolymphatic hydrops and elevated in ears treated with HPBCD. We found compelling evidence of recruitment in auditory-nerve data. Such clear evidence has never been shown before. Our findings suggest that, in patients suspected of having endolymphatic hydrops, loudness recruitment may be a good indication that the associated low-frequency hearing loss originates from a reduction of cochlear amplification, and that measurements of recruitment could be used in differential diagnosis and treatment monitoring of Ménière's disease.
响度重振常见于疑似内淋巴积水的患者。响度重振是指响度异常增长，即尽管听力阈值升高，但高强度声音却被感知为具有正常响度。对重振的传统解释是耳蜗放大功能降低。由于耳蜗放大器主要在低声强水平起作用，因此耳蜗放大功能降低导致阈值升高的耳朵在高声强水平仍可进行正常处理。在人类中，可以使用感知响度来研究重振，但在动物中则使用生理测量方法。动物反应中的重振从未得到明确证实，因为所使用的动物的感觉和神经细胞均有损伤，而不仅仅是耳蜗放大功能降低。因此，研究人员一直在寻找并发现了听觉中枢神经系统（CNS）中重振的证据。虽然关于中枢神经系统重振的研究提供了很多信息，但它们无法排除起源于耳蜗的重振的传统解释。我们使用了能够在整个听力频率和动态范围内评估听力功能的技术。测量是在两种动物模型上进行的：通过内淋巴囊切除术产生内淋巴积水的豚鼠耳朵，以及在人工外淋巴中灌注13 mM2-羟丙基-β-环糊精（HPBCD）的未处理豚鼠耳朵。内淋巴囊切除导致低频听力损失。用HPBCD处理的动物在所有频率上均有听力损失。这些动物均未出现毛细胞损失或听神经纤维突触损失情况。在内淋巴积水的耳朵和灌注HPBCD的耳朵中，与对照组相比，低频的基于听神经测量显示出重振现象在高频（>4 kHz）未发现重振现象内淋巴积水耳朵的听力阈值正常而灌注HPBCD耳朵的听力阈值升高。我们在听神经数据中发现了令人信服的重振证据。如此明确的证据以前从未有过。我们研究结果表明，在疑似患有内淋巴积水的患者中响度重振可能是相关低频听力损失源自耳蜗放大功能降低的一个良好指标并且重振测量可用于梅尼埃病的鉴别诊断和治疗监测。
