The prevalence of hearing problems in the Western world has, due to aging of the population, doubled over the past 30 years. Thereby, noise-induced hearing loss is an important factor that worsens over time in addition to age-related hearing loss. Hearing loss is usually measured as an elevation of a person's hearing thresholds, expressed in decibel (dB). However, recent animal studies have unraveled a type of permanent cochlear damage, without an elevation of hearing thresholds. This subtle damage is linked to a permanent and progressive degeneration of auditory fibers that occurs in association with damage of the inner hair cell synapse. Afferent neuronal degeneration has been suggested to be involved in hyperacusis (over sensitivity to sound) and tinnitus (a phantom sound percept). Hyperacusis and tinnitus are potentially devastating conditions that are still incurable. The main risk factors to develop tinnitus or hyperacusis are hearing loss, social stress and age. Both tinnitus and hyperacusis have been discussed in the context of a pathological increased response gain in subcortical brain regions as a reaction to deprivation of sensory input. Novel studies confirm the involvement of peripheral deafferentation for tinnitus and hyperacusis, but suggest that the disorder results from different brain responses to different degrees of deafferentation: while tinnitus may arise as a failure of the brain to adapt to deprived peripheral input, hyperacusis may result from an 'over-adaptive' increase in response gain. Moreover, moderate and high stress levels at the time of acoustic trauma have been suggested to play a pivotal role in the vulnerability of the cochlea to acoustic damage and therefore for the development of tinnitus and hyperacusis.

The pathophysiology underlying tinnitus, a hearing disorder characterized by the chronic perception of phantom sound, has been related to aberrant plastic reorganization of the central auditory system. More specifically, tinnitus is thought to involve changes in the tonotopic representation of sound. In the present study we used high-resolution functional magnetic resonance imaging to determine tonotopic maps in the auditory cortex of 20 patients with tinnitus but otherwise near-normal hearing, and compared these to equivalent outcomes from 20 healthy controls with matched hearing thresholds. Using a dedicated experimental paradigm and data-driven analysis techniques, multiple tonotopic gradients could be robustly distinguished in both hemispheres, arranged in a pattern consistent with previous findings. Yet, maps were not found to significantly differ between the two groups in any way. In particular, we found no evidence for an overrepresentation of high sound frequencies, matching the tinnitus pitch. A significant difference in evoked response magnitude was found near the low-frequency tonotopic endpoint on the lateral extreme of left Heschl’s gyrus. Our results suggest that macroscopic tonotopic reorganization in the auditory cortex is not required for the emergence of tinnitus, and is not typical for tinnitus that accompanies normal hearing to mild hearing loss.

When stimulated by tones, the ear appears to emit tones of its own, stimulus-frequency otoacoustic emissions (SFOAEs). SFOAEs were measured in 17 chinchillas and their group delays were compared with a place map of basilar-membrane vibration group delays measured at the characteristic frequency. The map is based on Wiener-kernel analysis of responses to noise of auditory-nerve fibers corroborated by measurements of vibrations at several basilar-membrane sites. SFOAE group delays were similar to, or shorter than, basilar-membrane group delays for frequencies $>4\mathrm{kHz}$ and $<4\mathrm{kHz}$ , respectively. Such short delays contradict the generally accepted “theory of coherent reflection filtering” [Zweig and Shera, J. Acoust. Soc. Am. 98, 2018–2047 (1995)], which predicts that the group delays of SFOAEs evoked by low-level tones approximately equal twice the basilar-membrane group delays. The results for frequencies higher than $4\mathrm{kHz}$ are compatible with hypotheses of SFOAE propagation to the stapes via acoustic waves or fluid coupling, or via reverse basilar membrane traveling waves with speeds corresponding to the signal-front delays, rather than the group delays, of the forward waves. The results for frequencies lower than $4\mathrm{kHz}$ cannot be explained by hypotheses based on waves propagating to and from their characteristic places in the cochlea.