Brain Advance Access originally published online on July 7, 2003
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Brain, Vol. 126, No. 10, 2235-2245,
October 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg228
Enhanced frequency discrimination near the hearing loss cut-off: a consequence of central auditory plasticity induced by cochlear damage?
1 Unité CNRS UMR 5020 Laboratoire ‘Neurosciences et Systèmes Sensoriels’, CNRS GDR 2213 ‘Prothèses auditives’, Université Claude Bernard Lyon I, Lyon, 2 Service d’Audiologie et d’Explorations Orofaciales, Hôpital Edouard Herriot, Lyon, France and 3 Department of Experimental Psychology, University of Cambridge, Cambridge, UK
Correspondence to: Dr Hung Thai-Van, Service d’Audiologie et d’Explorations Orofaciales, Pavillon U, CHU Edouard Herriot, Place d’Arsonval, 69437 Lyon Cedex 03, France E-mail: hung.thaivan{at}chu-lyon.fr
Patients with steeply sloping hearing losses of cochlear origin may exhibit enhanced difference limens for frequency (DLFs) near the cut-off frequency (Fc) of their hearing loss. This effect has been related to observations in deafened animals of an over-representation of Fc in the primary auditory cortex. However, alternative interpretations in terms of peripheral mechanisms have not been eliminated. In the present study, we assessed the possible role of two peripheral mechanisms [loudness cues and spontaneous otoacoustic emissions (SOAEs)] in a group of patients with high-frequency hearing loss. We tested first whether the DLF enhancement effect was still observed under conditions where subjects could not rely on loudness cues to perform the frequency discrimination task. To achieve this, we adjusted the nominal level of each stimulus so that it fell on an equal loudness contour measured at very fine (1/8 octave) frequency intervals, and we roved the level of each stimulus over a large range (12 dB). Under these conditions, the DLF enhancement was still observed in all patients; this demonstrates that the effect cannot be explained simply by loudness cues. We then screened the patients for SOAEs to test whether the DLF enhancement effect could be explained by the presence of such emissions in the vicinity of the Fc. None of the patients exhibited SOAEs. Finally, we tested whether the patients had cochlear dead regions, i.e. regions lacking functional inner hair cells and/or auditory nerve fibres. Using a refined version of a non-invasive clinical test for the identification of dead regions, we assessed the presence of such regions in fine frequency steps (1/4 octave) up to very high frequencies. All of the patients had cochlear dead regions. The first two findings support the hypothesis that DLF enhancement is due to injury-induced central reorganization in the auditory system. The last one is consistent with neurophysiological data in animals, which suggest that complete deprivation from auditory input at certain cochlear sites may be a necessary condition for the occurrence of injury-induced cortical reorganization.
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