新生儿声音剥夺对动物研究的影响

D. Webster
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引用次数: 4

摘要

在本期的其他地方提出了完整的文献综述,这些文献综述与以下假设一致,但没有证明:幼儿复发性或慢性中耳炎相关的轻度至中度听力损失可导致交流障碍。这一假设尚未得到证实,或许也无法得到证实,因为长期的回顾性人体研究固有地缺乏严谨性(Hanson and Ulvestad, 1979;Ventry, 1980;天堂,1981)。然而,有几项非人类研究与这一假设有关;本文将对它们进行回顾。虽然大多数研究都是为了探索听力发育的基本机制,但它们也可能有助于回答一个重要的临床问题:出生后传导性听力损失与听觉行为、生理和/或形态之间是否存在因果关系?首先,我们必须认识到,用非人类实验来回答有关人类问题的问题既有优点也有缺点。我们感兴趣的非人类研究通常是在啮齿动物身上进行的,通过去除听小骨或阻断外耳道来施加传导损失,这两种方法都会导致传导损失40至55 dB;这比患有中耳炎的儿童所遭受的15至30分贝损失要大得多。此外,这些传导性损失在啮齿类动物中是持续持续的,而在中耳炎儿童中,它们通常是波动的。此外,大多数啮齿动物的听力直到出生后8至12天才开始,直到16至24天才成熟,而新生的人类婴儿已经有成熟的听力(尽管没有成熟的加工)。最后,既然我们关注的是人类独有的语音和语言,我们也必须关注语音处理的中心机制是否为人类独有;如果是这样的话,将实验动物的数据应用于这个特殊的人类问题可能是不合适的。有利的一面是,非人体实验可以被严格控制,而人体研究却不能。导电损失可以在已知的时间产生,独立于任何病理。我们可以设计实验组和控制组。通过使用近交系,人们甚至可以接近遗传同质性。饮食、社会经济背景和病史都不是问题,受试者在实验前不会搬离城镇
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of Neonatal Sound Deprivation in Animal Research
Elsewhere in this issue are presented complete literature reviews that are consistent with, but do not prove, the hypothesis that the mild-to-moderate hearing losses associated with recurrent or chronic otitis media in young children can cause communicative disorders. The hypothesis has not been, and perhaps cannot be, proved, since lack of rigor is inherent in long-term retrospective human studies (Hanson and Ulvestad, 1979; Ventry, 1980; Paradise, 1981.) There have been several nonhuman studies, however, that are relevant to this hypothesis; this article will review them. Although most were undertaken to explore the basic mechanisms of the development of hearing, they may also help answer the important clinical question: Is there a causal relationship between postnatal conductive hearing loss and auditory behavior, physiology, and/or morphology? At the outset we must recognize that there are both advantages and disadvantages in using nonhuman experiments to answer questions about human problems. The nonhuman studies we are interested in have usually been performed on rodents, with the conductive losses imposed either by removing the auditory ossicles or by blocking the external auditory meatus, both of which result in a conductive loss of 40 to 55 dB; this is considerably greater than the 15 to 30 dB loss suffered by children with otitis media. Furthermore, these conductive losses have been of constant duration in the rodents, whereas in otitis media children they are usually fluctuating. Moreover, hearing does not begin in most rodents until 8 to 12 days after birth and is not mature until 16 to 24 days, whereas newborn human infants already have mature hearing (although not mature processing). Finally, since we are concerned with speech and language, which are unique to the human, we must also be concerned with whether the central mechanisms of speech processing are unique to the human; if so, it may be inappropriate to apply data from experimental animals to this particular human problem. On the plus side, nonhuman experimentation can be rigorously controlled, whereas human studies cannot be. Conductive losses can be created at known times, independent of any pathology. One can design experimental and control groups. By using inbred strains, one can even approach genetic homogeneity. Diet, socioeconomic background, and medical history are not a problem, and the subjects do not move out of town before the experi-
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