Subclinical cochlear dysfunction in newly diagnosed relapsing-remitting multiple sclerosis
Subclinical cochlear dysfunction in newly diagnosed relapsing-remitting multiple sclerosis
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DOI：
10.1016/j.msard.2019.05.020
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发表时间：
2019-08-01
影响因子：
4
通讯作者：
Albanese, Maria
中科院分区：
文献类型：
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作者：
Di Mauro, Roberta;Di Girolamo, Stefano;Albanese, Maria
背景：多发性硬化的听力损害一直被认为是一个主要与中枢听觉系统有关的过程。然而，越来越多的证据也表明内耳的外周受累。本研究的目的是探讨亚临床耳蜗功能障碍和可能的相关性与疾病的严重程度在未经治疗的新诊断的多发性硬化症患者使用瞬态诱发和畸变产物otoacoustic emissions.Methods：40例新诊断的复发缓解型多发性硬化症，临床听力正常，没有脑干病变（研究组）和40个匹配的对照组（对照组）被纳入本研究。所有受试者均进行常规听力学评估，包括病史和临床检查、纯音测听、声导抗测试、听性脑干反应和耳声发射记录。结果：所有患者的听性脑干反应和纯音听阈均在正常范围内。瞬态诱发和失真产物耳声发射响应的幅度显着降低，在1000，1500，2000和3000 Hz的研究组相比，对照group.Conclusions：这项研究表明，未治疗的多发性硬化症患者的耳声发射幅度降低，临床听力正常，没有脑干脱髓鞘斑块，这表明亚临床耳蜗损害。这种改变可能是外周听力损伤的早期迹象，提示耳声发射在多发性硬化患者耳蜗功能障碍的早期诊断中的作用。然而，考虑到耳声发射主要反映耳蜗功能，并且听觉脑干反应的波I被保留，支持多发性硬化症引起的声通路外周受累的证据只能假设归因于外毛细胞的早期亚临床受累。
Background: Hearing impairment in multiple sclerosis has long been considered a process mainly related to the central auditory system. However, increasing evidence also suggests a peripheral involvement of the inner ear. The objective of this study was to investigate subclinical cochlear dysfunction and possible correlation with disease severity in untreated newly diagnosed multiple sclerosis patients using transient-evoked and distortion-product otoacoustic emissions.Methods: Forty patients with newly diagnosed relapsing-remitting multiple sclerosis, clinically normal hearing and no brainstem lesions (study group) and forty matched controls (control group) were included in the study. All subjects had a routine audiological evaluation including history and clinical examination, pure tone audiometry, acoustic immittance test, auditory brainstem response and otoacoustic emissions recording. Self-administered questionnaires were used to evaluate self-perception of hearing disability.Results: Auditory brainstem response and pure tone audiometry thresholds resulted within normal range in all patients. The amplitudes of transient-evoked and distortion-product otoacoustic emissions responses were significantly reduced at 1000, 1500, 2000 and 3000 Hz in the study group compared to the control group.Conclusions: This study shows decreased otoacoustic emission amplitudes in untreated multiple sclerosis patients with clinically normal hearing and no brainstem demyelinating plaques, suggesting a subclinical cochlear impairment. This alteration may represent an early sign of peripheral hearing damage, suggesting a role for otoacoustic emissions in the early diagnosis of cochlear dysfunction in multiple sclerosis patients. However, given that otoacoustic emissions primarily reflects cochlear function, and that the wave I of the auditory brainstem responses was spared, the evidence supporting a peripheral involvement of acoustic pathways due to multiple sclerosis can only be hypothetically attributed to an early subclinical involvement of outer hair cells.