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... of this maturation is paralleled by anatomical developments of cere- bral cortex. Figure 11 illustrates schemat- ically the projections from the cochlea to auditory cortex. During early development it is known that the projections from one level to the next are not direct point-to- point connections, but rather there is considerable divergence of the connections at all levels. ...
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... in the adult animal as modeled in figure 12, we see that the divergent connections have become much more direct. Now, with a precise point-to-point projection system, neural activity pat- terns that represent sound frequencies at the level of the cochlea are faithfully transmitted to the cortex. ...
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... are various mechanisms whereby the organization of the pathways becomes more ordered, i.e. changes from that in figure 11 to that of figure 12. For example, some lateral (divergent) connections die out, by mechanisms not clearly understood. ...
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... 1984; Harrison, Nagasawa, Smith, Stanton and Mount 1991; Har- rison, Smith, Nagasawa, Stanton and Mount 1992; Harrison, Ibra- him, Stanton and Mount 1996a; Harrison 1996, 2000). Figure 13 shows the general protocol for a typical develop- mental plasticity experiment. It depicts the time course of the sub- ject from birth to maturity. ...
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... first experiments that I review here were made in the cat. If we do nothing to the newborn kitten, i.e. if it matures normally, then we will record a normal fre- quency map in primary auditory cortex as is illustrated in figure 14. We can suppose that in this subject there has been a good development of point to point projections such that in auditory cortex there is a very accurate rep- resentation of what is happening at the level of the cochlea (as de- picted in the "model" of figure 12). Figure 15 shows the results from an experimental animal in which we induced a basal cochlear lesion within a few days of birth. ...
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... we do nothing to the newborn kitten, i.e. if it matures normally, then we will record a normal fre- quency map in primary auditory cortex as is illustrated in figure 14. We can suppose that in this subject there has been a good development of point to point projections such that in auditory cortex there is a very accurate rep- resentation of what is happening at the level of the cochlea (as de- picted in the "model" of figure 12). Figure 15 shows the results from an experimental animal in which we induced a basal cochlear lesion within a few days of birth. ...
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... can suppose that in this subject there has been a good development of point to point projections such that in auditory cortex there is a very accurate rep- resentation of what is happening at the level of the cochlea (as de- picted in the "model" of figure 12). Figure 15 shows the results from an experimental animal in which we induced a basal cochlear lesion within a few days of birth. This cochlear damage results in a high frequency cochlear hearing loss as shown in the audiogram (derived from ABR thresholds to tone pips). ...
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... simple interpretation of these experimental findings is depicted in figure 16. We have damaged the base of the coch- lea, and the associated cochlear afferent neurons have degenerated. ...
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... could imagine this process occurring at all levels in the auditory system such that we end up with a large iso-frequency region of auditory cortex where all the neurons are essentially connected up from one point along the cochlear length, at the bor- der of the experimental lesion. Figure 17 shows data from another experiment. In this case, the lesion that we have made to the coch- lea during early development is much more extensive, as reflected in the sloping ABR audiogram. ...
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... to nine months later, the mature cats were used in cortical mapping experiments. Figure 18 shows the tonotopic map in cortex of a normal control animal (upper panel) compared with an experimental "augmented" animal (lower panel). On these maps, iso-frequency contours are spaced at one octave intervals. ...
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... map from the subject which was reared in the environ- ment containing that 8 kHz signal shows a significant increase in the amount of cortex which is coding, or representing frequencies at 8 kHz and above. Figure 19 shows pooled results from 3 experimental animals, versus 3 age-matched controls. The graph shows the percentage of auditory cortex that is devoted to par- ticular sound stimulus frequencies. ...
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... the following set of experiments we have looked at changes to tonotopic maps at the level of the mid-brain, i.e. the cen- tral nucleus of inferior colliculus. The experimental protocol is similar to that outlined in figure 13. The animal (in this case the chinchilla) is born and then we immediately induce a lesion to the cochlea taking advantage of the ototoxic effects of the aminoglycoside amikacin. ...
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... allow the animal to mature (3 months) and then we investigate tonotopic mapping in inferior colliculus. Figure 21 shows the tonotopic map in the inferior colliculus (central nucleus) of a normal chinchilla. As depicted in the lower left panel, an electrode intro- duced into the dorsal region will record from neurons responding best to low frequencies. ...
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... many ways, the mid-brain tonotopic map changes are rather similar to what we found at the level of auditory cortex in our other experiments. In this chinchilla we also note that the tono- topic map for lower frequency regions is abnormal (compare with control animal of figure 21). We suppose that this is related to abnormal activity pat- terns arising from the damaged sens- ory epithelium of apical regions of the cochlea. ...
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... importantly, it could result from a failure to establish good point-to-point projections during early development. In other words it could represent a failure of the projection system to change from its early divergent innervation pattern depicted in figure 11 to the more direct pattern shown in figure 12. ...
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... importantly, it could result from a failure to establish good point-to-point projections during early development. In other words it could represent a failure of the projection system to change from its early divergent innervation pattern depicted in figure 11 to the more direct pattern shown in figure 12. ...
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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.
