The middle ear muscle reflex: Current and future role in assessing noise-induced cochlear damage.

The middle ear muscle reflex: Current and future role in assessing noise-induced cochlear damage.
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DOI:
10.1121/10.0016853
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发表时间:
2023-01
期刊:
The Journal of the Acoustical Society of America
影响因子:
--
通讯作者:
Monica Trevino;Andie Zang;E. Lobarinas
Monica Trevino;Andie Zang;E. Lobarinas
中科院分区:
其他
文献类型:
--
作者:
Monica Trevino;Andie Zang;E. Lobarinas

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人的中耳肌反射(MEMR)是中耳镫骨肌响应于中等到高强度的声学刺激而双侧收缩。临床上,MEMR阈值已用于耳病理学的鉴别诊断数十年。最近,MEMR幅度或阈值的变化已被提出作为噪声诱导的突触病的评估,这是一种亚临床形式的耳蜗损伤,其特征在于作为内毛细胞(IHC)突触丧失的函数而发生的阈上听力问题,包括噪声中听力缺陷、耳鸣和听觉过敏。在动物模型中,宽带MEMR导抗的变化与噪声诱导的突触病相关;然而,人类研究显示了更多不同的结果。在研究中观察到的差异可能反映了人类突触病的异质性,而不是参数差异或测量相对灵敏度的影响。虽然突触病的病因和程度可以在动物模型中仔细控制,但人类的突触病可能源于多种病因,因此在人群中可能差异很大。在这里,我们探讨了不断发展的研究证据MEMR反应与亚临床噪声引起的耳蜗损伤和MEMR作为一个早期相关的阈上赤字。
The middle ear muscle reflex (MEMR) in humans is a bilateral contraction of the middle ear stapedial muscle in response to moderate-to-high intensity acoustic stimuli. Clinically, MEMR thresholds have been used for differential diagnosis of otopathologies for decades. More recently, changes in MEMR amplitude or threshold have been proposed as an assessment for noise-induced synaptopathy, a subclinical form of cochlear damage characterized by suprathreshold hearing problems that occur as a function of inner hair cell (IHC) synaptic loss, including hearing-in-noise deficits, tinnitus, and hyperacusis. In animal models, changes in wideband MEMR immittance have been correlated with noise-induced synaptopathy; however, studies in humans have shown more varied results. The discrepancies observed across studies could reflect the heterogeneity of synaptopathy in humans more than the effects of parametric differences or relative sensitivity of the measurement. Whereas the etiology and degree of synaptopathy can be carefully controlled in animal models, synaptopathy in humans likely stems from multiple etiologies and thus can vary greatly across the population. Here, we explore the evolving research evidence of the MEMR response in relation to subclinical noise-induced cochlear damage and the MEMR as an early correlate of suprathreshold deficits.