Neuroscience
-
Noise-induced hidden hearing loss (NIHHL) has attracted great attention in hearing research and clinical audiology since the discovery of significant noise-induced synaptic damage in the absence of permanent threshold shifts (PTS) in animal models. Although the extant evidence for this damage is based on animal models, NIHHL likely occurs in humans as well. This review focuses on three issues concerning NIHHL that are somewhat controversial: (1) whether disrupted synapses can be re-established; (2) whether synaptic damage and repair are responsible for the initial temporal threshold shifts (TTS) and subsequent recovery; and (3) the relationship between the synaptic damage and repair processes and neural coding deficits. We conclude that, after a single, brief noise exposure, (1) the damaged and the totally destroyed synapses can be partially repaired, but the repaired synapses are functionally abnormal; (2) While deficits are observed in some aspects of neural responses related to temporal and intensity coding in the auditory nerve, we did not find strong evidence for hypothesized coding-in-noise deficits; (3) the sensitivity and the usefulness of the envelope following responses to amplitude modulation signals in detecting cochlear synaptopathy is questionable.
-
The effects of traumatic noise-exposure and deafening on auditory system function have received a great deal of attention. However, lower levels of noise as well as temporary conductive hearing loss also have consequences on auditory physiology and hearing. Here we review how abnormal acoustic experience at early ages affects the ascending and descending auditory pathways, as well as hearing behavior.
-
Many, or most, tinnitus models rely on increased central gain in the auditory pathway as all or part of the explanation, in that central auditory neurones deprived of their usual sensory input maintain homeostasis by increasing the rate at which they fire in response to any given strength of input, including amplifying spontaneous firing which forms the basis of tinnitus. However, dramatic gain changes occur in response to damage to the auditory periphery, irrespective of whether tinnitus occurs. This article considers gain in its broadest sense, summarizes its contributory processes, neural manifestations, behavioral effects, techniques for its measurement, pitfalls in attributing gain changes to tinnitus, a discussion of the minimum evidential requirements to implicate gain as a necessary and/or sufficient basis to explain tinnitus, and the extent of existing evidence in this regard. ⋯ A few studies show changes specifically attributable to tinnitus at group level, but the limited attempts so far to classify individual subjects based on gain metrics have not proven successful. If gain turns out to be unnecessary or insufficient to cause tinnitus, candidate additional mechanisms include focused attention, resetting of sensory predictions, failure of sensory gating, altered sensory predictions, formation of pervasive memory traces and/or entry into global perceptual networks. This article is part of a Special Issue entitled: Hearing Loss, Tinnitus, Hyperacusis, Central Gain.
-
Primary Neural Degeneration in the Human Cochlea: Evidence for Hidden Hearing Loss in the Aging Ear.
The noise-induced and age-related loss of synaptic connections between auditory-nerve fibers and cochlear hair cells is well-established from histopathology in several mammalian species; however, its prevalence in humans, as inferred from electrophysiological measures, remains controversial. Here we look for cochlear neuropathy in a temporal-bone study of "normal-aging" humans, using autopsy material from 20 subjects aged 0-89 yrs, with no history of otologic disease. Cochleas were immunostained to allow accurate quantification of surviving hair cells in the organ Corti and peripheral axons of auditory-nerve fibers. ⋯ The results suggest that a large number of auditory neurons in the aging ear are disconnected from their hair cell targets. This primary neural degeneration would not affect the audiogram, but likely contributes to age-related hearing impairment, especially in noisy environments. Thus, therapies designed to regrow peripheral axons could provide clinically meaningful improvement in the aged ear.
-
Sound therapies are a common component of treatments for tinnitus and hyperacusis. The original idea was to partially or completely mask tinnitus with broadband noise delivered by sound generators or hearing aids, for a few hours each day. Over several months, many patients reported that their tinnitus became quieter or easier to bear, and that loud sounds became less aversive. ⋯ However, studies of sound treatments in animals with putative tinnitus or hyperacusis have been rare. Clinical sound therapy trials are emerging, but outcomes typically remain modest, and few patients achieve complete remission of tinnitus or hyperacusis, unless the underlying hearing loss is treated with hearing aids or implants, in which case success rates are higher. More studies are needed, on both animal models and human subjects, to further explore the rationales for the various sound therapy options reviewed here, and to optimally tailor sounds and treatment approaches to individual patients, so that maximum benefits can be obtained.