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      On the Etiology of Listening Difficulties in Noise Despite Clinically Normal Audiograms

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          Abstract

          Many people with difficulties following conversations in noisy settings have “clinically normal” audiograms, that is, tone thresholds better than 20 dB HL from 0.1 to 8 kHz. This review summarizes the possible causes of such difficulties, and examines established as well as promising new psychoacoustic and electrophysiologic approaches to differentiate between them. Deficits at the level of the auditory periphery are possible even if thresholds remain around 0 dB HL, and become probable when they reach 10 to 20 dB HL. Extending the audiogram beyond 8 kHz can identify early signs of noise-induced trauma to the vulnerable basal turn of the cochlea, and might point to “hidden” losses at lower frequencies that could compromise speech reception in noise. Listening difficulties can also be a consequence of impaired central auditory processing, resulting from lesions affecting the auditory brainstem or cortex, or from abnormal patterns of sound input during developmental sensitive periods and even in adulthood. Such auditory processing disorders should be distinguished from (cognitive) linguistic deficits, and from problems with attention or working memory that may not be specific to the auditory modality. Improved diagnosis of the causes of listening difficulties in noise should lead to better treatment outcomes, by optimizing auditory training procedures to the specific deficits of individual patients, for example.

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          Tinnitus with a normal audiogram: physiological evidence for hidden hearing loss and computational model.

          Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.
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            Age-related cochlear synaptopathy: an early-onset contributor to auditory functional decline.

            Aging listeners experience greater difficulty understanding speech in adverse listening conditions and exhibit degraded temporal resolution, even when audiometric thresholds are normal. When threshold evidence for peripheral involvement is lacking, central and cognitive factors are often cited as underlying performance declines. However, previous work has uncovered widespread loss of cochlear afferent synapses and progressive cochlear nerve degeneration in noise-exposed ears with recovered thresholds and no hair cell loss (Kujawa and Liberman 2009). Here, we characterize age-related cochlear synaptic and neural degeneration in CBA/CaJ mice never exposed to high-level noise. Cochlear hair cell and neuronal function was assessed via distortion product otoacoustic emissions and auditory brainstem responses, respectively. Immunostained cochlear whole mounts and plastic-embedded sections were studied by confocal and conventional light microscopy to quantify hair cells, cochlear neurons, and synaptic structures, i.e., presynaptic ribbons and postsynaptic glutamate receptors. Cochlear synaptic loss progresses from youth (4 weeks) to old age (144 weeks) and is seen throughout the cochlea long before age-related changes in thresholds or hair cell counts. Cochlear nerve loss parallels the synaptic loss, after a delay of several months. Key functional clues to the synaptopathy are available in the neural response; these can be accessed noninvasively, enhancing the possibilities for translation to human clinical characterization.
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              Rapid task-related plasticity of spectrotemporal receptive fields in primary auditory cortex.

              We investigated the hypothesis that task performance can rapidly and adaptively reshape cortical receptive field properties in accord with specific task demands and salient sensory cues. We recorded neuronal responses in the primary auditory cortex of behaving ferrets that were trained to detect a target tone of any frequency. Cortical plasticity was quantified by measuring focal changes in each cell's spectrotemporal response field (STRF) in a series of passive and active behavioral conditions. STRF measurements were made simultaneously with task performance, providing multiple snapshots of the dynamic STRF during ongoing behavior. Attending to a specific target frequency during the detection task consistently induced localized facilitative changes in STRF shape, which were swift in onset. Such modulatory changes may enhance overall cortical responsiveness to the target tone and increase the likelihood of 'capturing' the attended target during the detection task. Some receptive field changes persisted for hours after the task was over and hence may contribute to long-term sensory memory.
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                Author and article information

                Journal
                Ear Hear
                Ear Hear
                AUD
                Ear and Hearing
                Williams And Wilkins
                0196-0202
                1538-4667
                March 2017
                24 February 2017
                : 38
                : 2
                : 135-148
                Affiliations
                George S. Osborne College of Audiology, Salus University, Elkins Park, Pennsylvania, USA.
                Author notes
                Address for correspondence: Martin Pienkowski, George S. Osborne College of Audiology, Salus University, 8360 Old York Road, Elkins Park, PA 19027, USA. E-mail: mpienkowski@ 123456salus.edu
                Article
                00002
                10.1097/AUD.0000000000000388
                5325255
                28002080
                1053df76-01b1-40f2-b2fe-ab2c92ae7714
                Copyright © 2016 The Author. Ear & Hearing is published on behalf of the American Auditory Society, by Wolters Kluwer Health, Inc.

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

                History
                : 19 April 2016
                : 30 September 2016
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                auditory development and plasticity,auditory processing disorder,hidden hearing loss,speech intelligibility in noise

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