Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, Boston, 02114, USA.
J Assoc Res Otolaryngol. 2011 Oct;12(5):535-47. doi: 10.1007/s10162-011-0271-6. Epub 2011 May 24.
Decades of clinical and basic research in visual system development have shown that degraded or imbalanced visual inputs can induce a long-lasting visual impairment called amblyopia. In the auditory domain, it is well established that inducing a conductive hearing loss (CHL) in young laboratory animals is associated with a panoply of central auditory system irregularities, ranging from cellular morphology to behavior. Human auditory deprivation, in the form of otitis media (OM), is tremendously common in young children, yet the evidence linking a history of OM to long-lasting auditory processing impairments has been equivocal for decades. Here, we review the apparent discrepancies in the clinical and basic auditory literature and provide a meta-analysis to show that the evidence for human amblyaudia, the auditory analog of amblyopia, is considerably more compelling than is generally believed. We argue that a major cause for this discrepancy is the fact that most clinical studies attempt to link central auditory deficits to a history of middle ear pathology, when the primary risk factor for brain-based developmental impairments such as amblyopia and amblyaudia is whether the afferent sensory signal is degraded during critical periods of brain development. Accordingly, clinical studies that target the subset of children with a history of OM that is also accompanied by elevated hearing thresholds consistently identify perceptual and physiological deficits that can endure for years after peripheral hearing is audiometrically normal, in keeping with the animal studies on CHL. These studies suggest that infants with OM severe enough to cause degraded afferent signal transmission (e.g., CHL) are particularly at risk to develop lasting central auditory impairments. We propose some practical guidelines to identify at-risk infants and test for the positive expression of amblyaudia in older children.
几十年来,视觉系统发育的临床和基础研究表明,退化或不平衡的视觉输入会导致一种持久的视觉障碍,称为弱视。在听觉领域,已经证实,在年轻的实验动物中诱导传导性听力损失(CHL)与广泛的中枢听觉系统异常相关,从细胞形态到行为。人类听觉剥夺,以中耳炎(OM)的形式,在幼儿中非常常见,但几十年来,将 OM 病史与持久的听觉处理障碍联系起来的证据一直存在争议。在这里,我们回顾了临床和基础听觉文献中的明显差异,并进行了荟萃分析,以表明人类弱视的证据,即弱视的听觉类似物,比人们普遍认为的更有说服力。我们认为,造成这种差异的一个主要原因是,大多数临床研究试图将中枢听觉缺陷与中耳病史联系起来,而弱视和弱视等大脑发育性损伤的主要风险因素是传入感觉信号在大脑发育的关键时期是否退化。因此,针对 OM 病史且伴有听力阈值升高的儿童亚组进行的临床研究始终一致地确定了在听力正常后仍能持续多年的感知和生理缺陷,这与 CHL 的动物研究一致。这些研究表明,患有 OM 的婴儿,其传入信号传输严重受损(例如 CHL),特别容易发展为持久的中枢听觉障碍。我们提出了一些实用的指导方针,以识别高危婴儿并测试大龄儿童中弱视的阳性表达。