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... "model" to explain what might be happening is shown in figure 20. Because there is an over-stimulation of a certain region of the cochlea, we suppose that these more active neurons win in the competition to form synapses on target cells. ...
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... from one experimental animal are shown in figure 22 (adapted from Harrison, Ibrahim and Mount 1998). In this chinchilla, as a neonate, we made a widespread cochlear lesion which started in the basal cochlear turn and extended apically. ...
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... at the mid brain level we have a different picture. Figure 23 shows results from two tonotopic mapping experiments in inferior colliculus Figure 23. Tonotopic mapping at level of inferior colliculus in chinchilla after basal cochlear lesion induced in the neonatal animal (left-hand panels) versus in the adult subject (right-hand panels). ...
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... at the mid brain level we have a different picture. Figure 23 shows results from two tonotopic mapping experiments in inferior colliculus Figure 23. Tonotopic mapping at level of inferior colliculus in chinchilla after basal cochlear lesion induced in the neonatal animal (left-hand panels) versus in the adult subject (right-hand panels). ...
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... point-to-point transmission system can be potentially degraded in many ways. Figures 26-29 show, diagrammatically, some of the possible ways in which the projection system from cochlea to cortex might be degraded. The lower panel of each figure represents the neural array of activity at the cochlear nerve level evoked by the speech signal "we play ball on summer days" (adapted from figure 24). ...
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... 26-29 show, diagrammatically, some of the possible ways in which the projection system from cochlea to cortex might be degraded. The lower panel of each figure represents the neural array of activity at the cochlear nerve level evoked by the speech signal "we play ball on summer days" (adapted from figure 24). The upper panels show (two) stages of pro- gressive degradation of the signal. ...
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... figure 26 the small degradation is a "blur" in the clarity of representation of frequency across the neural array. This degradation in spectral frequency Figure 26. Schematic diagrams of the spatio-temporal patterns of neural activity representing a speech signal at three levels within the auditory system. ...
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... of abnormal noise levels. Figure 28. Schematic diagrams of the spatio-temporal patterns of neural activity representing a speech signal at three levels within the auditory system. ...
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... way in which we can degrade information reaching cortex from the cochlea is by adding noise, as illustrated in figure 27. Physiologically, such noise may result from a lack of inhibition in the neural systems involved. ...
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... next example of a potential source of degradation is depicted in figure 28, and relates to reducing the number of channels of information, which can carry neural representations of sound to cortex. This is the situation, for example, in sub- jects having a cochlear implant device in which the channel numbers are consider- ably reduced (down to the number of implanted electrodes). ...
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Citations
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The term "auditory neuropathy" is being used in a rapidly increasing number of papers in the audiology/otolaryngology literature for a variety of individuals (mostly children) who fulfill the following criteria: (1) understanding of speech worse than predicted from the degree of hearing loss on their behavioral audiograms; (2) recordable otoacoustic emissions and/or cochlear microphonic; together with (3) absent or atypical auditory brain stem responses. Because of the general lack of anatomic foundation for the label "auditory neuropathy" as currently used, we review the anatomy of the auditory pathway, the definition of neuropathy and its demyelinating, axonal, and mixed variants. We submit that the diagnostic term "auditory neuropathy" is anatomically inappropriate unless patients have documented evidence for selective involvement of either the spiral ganglion cells or their axons, or of the 8th nerve as a whole. In view of biologic differences between peripheral nerves and white matter tracts in the brain, the term "auditory neuropathy" is inappropriate for pathologies affecting the central auditory pathway in the brainstem and brain selectively. Published reports of patients with "auditory neuropathy" indicate that they are extremely heterogeneous in underlying medical diagnosis, age, severity, test results, and that only a small number have undergone the detailed investigations that would enable a more precise diagnosis of the locus of their pathologies. The electrophysiology of peripheral neuropathies and the deficits expected with pathologies affecting the hair cells, spiral ganglion cells and their axons (auditory neuropathy sensu stricto), and brain stem relays are reviewed. In order to serve patients adequately, including potential candidates for cochlear implants, and to increase knowledge of auditory pathologies, we make a plea for more comprehensive evaluation of patients who fulfill the currently used audiologic criteria for "auditory neuropathy" in an effort to pinpoint the site of their pathologies. We suggest that the term auditory neuropathy be limited to cases in which the locus of pathology is limited to the spiral ganglion cells, their processes, or the 8th nerve, and that the term neural hearing loss be considered for pathologies that affect all higher levels of the auditory pathway, from the brainstem to the auditory cortex.