人工耳蜗电极的新发展趋势

C. Jolly, J. Mueller, S. Helbig, S. Usami
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引用次数: 2

摘要

背景人工耳蜗电极是连接内耳可兴奋组织的神经接口。通过分布在鼓室内的电极驱动的小电流,能够根据电流强度同步地使小到大的传入神经元群去极化。最初,CI电极是为深度耳聋患者设计的,假设大部分神经细胞以螺旋神经节细胞和相关轴突的形式存在。在患者组中没有可测量的残余听力存在,并且通常假设树突缺失是因为耳聋的持续时间和相关的未受刺激的神经突缓慢逆行变性。神经元的逆行变性始于Corti器官的第一个突触,并向孔束和位于小梁上部和基底转罗森塔尔管的初级听传入神经元的胞体发展。无髓鞘螺旋神经节细胞体被广泛认为是电刺激下spike起始的部位。由于没有假设树突存活,也没有残余的听力存在,电极损伤的问题被减少到保护小舌内的感觉细胞体。
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New trends with cochlear implant electrodes
Background A cochlear implant (CI) electrode is a neural interface to the excitable tissue of the inner ear. Small currents, driven through electrodes distributed within scala tympani, are able to synchronously depolarize small to large groups of afferent neurons depending on current intensity. Originally, CI electrodes were designed for profoundly deaf patients assuming that a mostly depleted neural population was present in the form of spiral ganglion cells and associated axons. No measurable residual hearing was present in the patient group, and it was often assumed that the dendrites were absent because of the duration of deafness and associated slow retrograde degeneration of unstimulated neurites. Retrograde degeneration of neurons begins at the first synapse in the organ of Corti and progresses toward the habenula perforata and the soma of the primary auditory afferent neurons located in the superior portion of the modiolus and in the Rosenthal’s canal of the basal turn. The unmyelinated spiral ganglion cell soma was widely believed to be the site of spike initiation under electrical stimulation. Because no dendrite survival was assumed and no residual hearing was present, the issue of electrode trauma was reduced to protecting the soma of sensory cells within the modiolus.
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