Neuroscience
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Review
Age-related Changes in Neural Coding of Envelope Cues: Peripheral Declines and Central Compensation.
Aging listeners often experience difficulties in perceiving temporally complex acoustic cues in noisy environments. These difficulties likely have neurophysiological contributors from various levels of auditory processing. Cochlear synapses between inner hair cells and auditory nerve fibers exhibit a progressive decline with age which is not reflected in the threshold audiogram. ⋯ This results in a modulation frequency selective increase in the representation of envelope cues at the level of the auditory midbrain and cortex. These changes may be shaped by mechanisms such as decreased inhibitory neurotransmission occurring with age across various central auditory nuclei. Altered representations of the differing temporal components of speech due to these interactions between multiple levels of the auditory pathway may contribute to the age-related difficulties hearing speech in noisy environments.
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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.
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Attention may be an important factor in tinnitus. Individuals most disturbed by their tinnitus differ from those who are not in terms of attention allocation. This study used an operant-conditioning animal model to examine the interaction between tinnitus and auditory vigilant attention as well as auditory selective attention. ⋯ A brief free-field sound cue, consisting of either a short train of identical noise pulses (standard stimulus), or a noise train with one substituted tone pulse (oddball stimulus), cued a left or right nose poke for food. On this selective attention task, Tinnitus animals performed consistently worse than Non-tinnitus or Unexposed control animals regardless of stimulus features. As predicted, animals with behavioral evidence of tinnitus showed tinnitus-related attentional changes, including impaired selective attention but increased vigilance to sounds approximating their tinnitus.
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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.
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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.