Thai-Van Hung, Cozma Sebastian, Boutitie Florent, Disant François, Truy Eric, Collet Lionel
Université de Lyon, Lyon, F-69003, France.
Clin Neurophysiol. 2007 Mar;118(3):676-89. doi: 10.1016/j.clinph.2006.11.010. Epub 2007 Jan 16.
Maturation of acoustically evoked brainstem responses (ABR) in hearing children is not complete at birth but rather continues over the first two years of life. In particular, it has been established that the decrease in ABR wave V latency can be modeled as the sum of two decaying exponential functions with respective time-constants of 4 and 50 weeks [Eggermont, J.J., Salamy, A., 1988a. Maturational time-course for the ABR in preterm and full term infants. Hear Res 33, 35-47; Eggermont, J.J., Salamy, A., 1988b. Development of ABR parameters in a preterm and a term born population. Ear Hear 9, 283-9]. Here, we investigated the maturation of electrically evoked auditory brainstem responses (EABR) in 55 deaf children who recovered hearing after cochlear implantation, and proposed a predictive model of EABR maturation depending on the onset of deafness. The pattern of EABR maturation over the first 2 years of cochlear implant use was compared with the normal pattern of ABR maturation in hearing children.
Changes in EABR wave V latency over the 2 years following cochlear implant connection were analyzed in two groups of children. The first group (n=41) consisted of children with early-onset of deafness (mostly congenital), and the second (n=14) of children who had become profoundly deaf after 1 year of age. The modeling of changes in EABR wave V latency with time was based on the mean values from each of the two groups, allowing comparison of the rates of EABR maturation between groups. Differences between EABRs elicited at the basal and apical ends of the implant electrode array were also tested.
There was no influence of age at implantation on the rate of wave V latency change. The main factor for EABR changes was the time in sound. Indeed, significant maturation was observed over the first 2 years of implant use only in the group with early-onset deafness. In this group maturation of wave V progressed as in the ABR model of [Eggermont, J.J., Salamy, A., 1988a. Maturational time-course for the ABR in preterm and full term infants. Hear Res 33, 35-47; Eggermont, J.J., Salamy, A., 1988b. Development of ABR parameters in a preterm and a term born population. Ear Hear 9, 283-9] of normal hearing children: a sum of two decaying exponential functions, one showing an early rapid decrease in latency and the other a slower decrease. Remarkably, the time-constants fell well within the ranges described by Eggermont and Salamy (i.e., 3.9 and 68 weeks), consistent with the time-course of the neurophysiological mechanisms presumably involved in auditory pathway maturation during the first 2 years of life: i.e., myelination and increased synaptic efficacy. In contrast, relatively little change in wave V was evident in children with late-onset deafness. In agreement with the notion that EABR maturation follows an apex-to-base gradient as described for ABR, we observed that wave V latencies were longer for the basal than the apical end of the implant electrode array and remained so throughout the study period, whatever the time of onset of deafness.
The findings in the early-onset of deafness group support the theory that auditory pathways remain "frozen" during the period of sensory deprivation until cochlear implant rehabilitation restores the normal chronology of maturational processes. In children with late-onset deafness, however, some maturational processes may occur before the onset of deafness, and thus less additional maturation is required during the first two years of implant use resulting in no significant EABR latency changes being observed in this period. The results suggest that the rehabilitation-induced plasticity of the auditory pathways is, in case of late auditory deprivation, unlikely to result in neurophysiological outcomes similar to those observed in children with early auditory deprivation.
Changes in EABR wave V latency over the first 2 years of cochlear implant use were found to be well fitted by the sum of two decaying exponential functions in children with early-onset deafness. This is in line with the maturation of ABR wave V latency in normal-hearing children over the first two years of life. Further studies are needed to assess whether the differences observed in terms of auditory pathways maturation are associated with consistent differences in terms of language development.
听力正常儿童的听觉脑干诱发电位（ABR）在出生时并未完全成熟，而是在生命的头两年持续发育。特别是，已经确定ABR波V潜伏期的缩短可以用两个衰减指数函数之和来模拟，其各自的时间常数分别为4周和50周[埃格蒙特，J.J.，萨拉米，A.，1988a。早产和足月婴儿ABR的成熟时间进程。听觉研究33，35 - 47；埃格蒙特，J.J.，萨拉米，A.，1988b。早产和足月出生人群ABR参数的发育。耳与听觉9，283 - 289]。在此，我们研究了55名接受人工耳蜗植入后恢复听力的聋儿的电诱发听觉脑干反应（EABR）的成熟情况，并提出了一个根据耳聋发病时间预测EABR成熟的模型。将人工耳蜗植入使用的头两年内EABR成熟模式与听力正常儿童ABR成熟的正常模式进行了比较。
分析了两组儿童人工耳蜗植入连接后两年内EABR波V潜伏期的变化。第一组（n = 41）由耳聋发病早（大多为先天性）的儿童组成，第二组（n = 14）由1岁后严重耳聋的儿童组成。EABR波V潜伏期随时间变化的建模基于两组各自的平均值，以便比较两组之间EABR成熟的速率。还测试了植入电极阵列基底端和顶端引出的EABR之间的差异。
植入时的年龄对波V潜伏期变化速率没有影响。EABR变化的主要因素是接触声音的时间。实际上，仅在耳聋发病早的组中，在人工耳蜗使用的头两年观察到了显著的成熟。在该组中，波V的成熟过程与[埃格蒙特，J.J.，萨拉米，A.，1988a。早产和足月婴儿ABR的成熟时间进程。听觉研究33，35 - 47；埃格蒙特，J.J.，萨拉米，A.，1988b。早产和足月出生人群ABR参数的发育。耳与听觉9，283 - 289]中听力正常儿童的ABR模型一样：两个衰减指数函数之和，一个显示潜伏期早期快速缩短，另一个较慢。值得注意的是，时间常数完全落在埃格蒙特和萨拉米描述的范围内（即3.9周和68周），这与生命头两年听觉通路成熟可能涉及的神经生理机制的时间进程一致：即髓鞘形成和突触效能增加。相比之下，耳聋发病晚的儿童波V变化相对较小。与EABR成熟如ABR那样遵循从顶端到基底端梯度的观点一致，我们观察到无论耳聋发病时间如何，植入电极阵列基底端的波V潜伏期比顶端更长，并且在整个研究期间一直如此。
耳聋发病早组的研究结果支持这样的理论，即在感觉剥夺期间听觉通路保持“冻结”状态，直到人工耳蜗康复恢复成熟过程的正常时间顺序。然而，在耳聋发病晚的儿童中，一些成熟过程可能在耳聋发病前就已发生，因此在人工耳蜗使用的头两年所需的额外成熟较少，导致在此期间未观察到EABR潜伏期有显著变化。结果表明，在晚期听觉剥夺情况下，康复诱导的听觉通路可塑性不太可能产生与早期听觉剥夺儿童中观察到的类似神经生理结果。
发现人工耳蜗植入使用的头两年内，耳聋发病早的儿童EABR波V潜伏期的变化可以很好地用两个衰减指数函数之和来拟合。这与听力正常儿童头两年内ABR波V潜伏期的成熟情况一致。需要进一步研究来评估在听觉通路成熟方面观察到的差异是否与语言发育方面的一致差异相关。
