Hearing research

Publisher: Elsevier

Journal description

Current impact factor: 2.85

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.848
2012 Impact Factor 2.537
2011 Impact Factor 2.696
2010 Impact Factor 2.428
2009 Impact Factor 2.177
2008 Impact Factor 2.333
2007 Impact Factor 2.062
2006 Impact Factor 1.584
2005 Impact Factor 1.674
2004 Impact Factor 1.578
2003 Impact Factor 1.502
2002 Impact Factor 1.969
2001 Impact Factor 1.586
2000 Impact Factor 1.753
1999 Impact Factor 1.804
1998 Impact Factor 1.598
1997 Impact Factor 1.915
1996 Impact Factor 1.641
1995 Impact Factor 1.908
1994 Impact Factor 1.744
1993 Impact Factor 1.853
1992 Impact Factor 1.792

Impact factor over time

Impact factor

Additional details

5-year impact 2.06
Cited half-life 9.90
Immediacy index 0.34
Eigenfactor 0.01
Article influence 0.75
ISSN 1878-5891

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • Hearing research 09/2015; 327:58-68.
  • Jafri Kuthubutheen, Harvey Coates, Corwyn Rowsell, Julian Nedzelski, Joseph M Chen, Vincent Lin
    [Show abstract] [Hide abstract]
    ABSTRACT: Steroids have been shown to reduce the hearing threshold shifts associated with cochlear implantation. Previous studies have examined only the administration of steroids just prior to surgery. The aim of this study is to examine the role of extended preoperative systemic steroids in hearing preservation cochlear implantation. An animal model of cochlear implantation was used. 24 Hartley strain guinea pigs with a mean weight of 768 g and normal hearing were randomised into a control group, a second group receiving a single dose of systemic dexamethasone one day prior to surgery, and a third group receiving a daily dose of systemic dexamethasone for 5 days prior to surgery. A specially designed cochlear implant electrode by Med-EL (Innsbruck) was inserted through a dorsolateral approach to an insertion depth of 5mm and left in-situ. Auditory brain stem responses at 8kHz, 16kHz and 32 kHz were measured preoperatively, and 1 week, 1 month and 2 months postoperatively. Cochlear histopathology was examined at the conclusion of the study. At 1-week post operative, both groups receiving dexamethasone prior to implantation had smaller threshold shifts across all frequencies and which was significant at 32kHz (p<0.05). There were no differences among the three groups in the area of electrode related fibrosis. Spiral ganglion neuron (SGN) density was significantly higher in the group receiving steroids for 5 days, but only in the basal cochlear turn. This is study demonstrates the benefits of extended preoperative systemic steroids on hearing outcomes and SGN density in an animal model of cochlear implantation surgery. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.010
  • Sophie Vanvooren, Michael Hofmann, Hanne Poelmans, Pol Ghesquière, Jan Wouters
    [Show abstract] [Hide abstract]
    ABSTRACT: In the brain, the temporal analysis of many important auditory features relies on the synchronized firing of neurons to the auditory input rhythm. These so-called neural oscillations play a crucial role in sensory and cognitive processing and deviances in oscillatory activity have shown to be associated with neurodevelopmental disorders. Given the importance of neural auditory oscillations in normal and impaired sensory and cognitive functioning, there has been growing interest in their developmental trajectory from early childhood on.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.011
  • Michel R Benard, Deniz Başkent
    [Show abstract] [Hide abstract]
    ABSTRACT: In complex listening situations, cognitive restoration mechanisms are commonly used to enhance perception of degraded speech with inaudible segments. Profoundly hearing-impaired people revalidated with a cochlear implant (CI) show less benefit from such mechanisms. However, both normal hearing (NH) listeners and CI users do benefit from visual speech cues in these listening situations. In this study we investigated if an accompanying video of the speaker can enhance the intelligibility of interrupted sentences, and the phonemic restoration benefit, measured by an increase in intelligibility when the silent intervals are filled with noise. Similar to previous studies, restoration benefit was observed with interrupted speech without spectral degradations (experiment 1), but was absent in acoustic simulations of CIs (experiment 2) and was present again in simulations of Electric Acoustic Stimulation (experiment 3). In all experiments, the additional speech information provided by the complementary visual cues lead to overall higher intelligibility, however, these cues did not influence the occurrence or extent of the phonemic restoration benefit of filler noise. Results imply that visual cues do not show a synergistic effect with the filler noise, as adding them equally increased the intelligibility of interrupted sentences with or without the filler noise. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.013
  • Travis White-Schwoch, Evan C Davies, Elaine C Thompson, Kali Woodruff Carr, Trent Nicol, Ann R Bradlow, Nina Kraus
    [Show abstract] [Hide abstract]
    ABSTRACT: Early childhood is a critical period of auditory learning, during which children are constantly mapping sounds to meaning. But learning rarely occurs under ideal listening conditions-children are forced to listen against a relentless din. This background noise degrades the neural coding of these critical sounds, in turn interfering with auditory learning. Despite the importance of robust and reliable auditory processing during early childhood, little is known about the neurophysiology underlying speech processing in children so young. To better understand the physiological constraints these adverse listening scenarios impose on speech sound coding during early childhood, auditory-neurophysiological responses were elicited to a consonant-vowel syllable in quiet and background noise in a cohort of typically-developing preschoolers (ages 3-5 yr). Overall, responses were degraded in noise: they were smaller, less stable across trials, slower, and there was poorer coding of spectral content and the temporal envelope. These effects were exacerbated in response to the consonant transition relative to the vowel, suggesting that the neural coding of spectrotemporally-dynamic speech features is more tenuous in noise than the coding of static features-even in children this young. Neural coding of speech temporal fine structure, however, was more resilient to the addition of background noise than coding of temporal envelope information. Taken together, these results demonstrate that noise places a neurophysiological constraint on speech processing during early childhood by causing a breakdown in neural processing of speech acoustics. These results may explain why some listeners have inordinate difficulties understanding speech in noise. Speech-elicited auditory-neurophysiological responses offer objective insight into listening skills during early childhood by reflecting the integrity of neural coding in quiet and noise; this paper documents typical response properties in this age group. These normative metrics may be useful clinically to evaluate auditory processing difficulties during early childhood. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.009
  • [Show abstract] [Hide abstract]
    ABSTRACT: This article describes the creation and accomplishments of the Tinnitus Research Consortium (TRC), founded and supported through philanthropy and intended to enrich the field of tinnitus research. Bringing together a group of distinguished auditory researchers, most of whom were not involved in tinnitus research, over the fifteen years of its life it developed novel research approaches and recruited a number of new investigators into the field. The purpose of this special issue is to highlight some of the significant accomplishments of the investigators supported by the TRC. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.008
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hybrid or electro-acoustic stimulation (EAS) cochlear implants (CIs) are designed to provide high-frequency electric hearing together with residual low-frequency acoustic hearing. However, 30-50% of EAS CI recipients lose residual hearing after implantation. The objective of this study was to determine the mechanisms of EAS-induced hearing loss in an animal model with high-frequency hearing loss. Guinea pigs were exposed to 24 hours of noise (12-24 kHz at 116 dB) to induce a high-frequency hearing loss. After recovery, two groups of animals were implanted (n=6 per group), with one group receiving chronic acoustic and electric stimulation for 10 weeks, and the other group receiving no stimulation during this time frame. A third group (n=6) was not implanted, but received chronic acoustic stimulation. Auditory brainstem responses were recorded biweekly to monitor changes in hearing. The organ of Corti was immunolabeled with phalloidin, anti-CtBP2, and anti-GluR2 to quantify hair cells, ribbons and post-synaptic receptors. The lateral wall was immunolabeled with phalloidin and lectin to quantify stria vascularis capillary diameters. Bimodal or trimodal diameter distributions were observed; the number and location of peaks were objectively determined using the Aikake Information Criterion and Expectation Maximization algorithm. Noise exposure led to immediate hearing loss at 16-32 kHz for all groups. Cochlear implantation led to additional hearing loss at 4-8 kHz; this hearing loss was negatively and positively correlated with minimum and maximum peaks of the bimodal or trimodal distributions of stria vascularis capillary diameters, respectively. After chronic stimulation, no significant group changes in thresholds were seen; however, elevated thresholds at 1 kHz in implanted, stimulated animals were significantly correlated with decreased presynaptic ribbon and postsynaptic receptor counts. Inner and outer hair cell counts did not differ between groups and were not correlated with threshold shifts at any frequency. As in the previous study in a normal-hearing model, stria vascularis capillary changes were associated with immediate hearing loss after implantation, while little to no hair cell loss was observed even in cochlear regions with threshold shifts as large as 40-50 dB. These findings again support a role of lateral wall blood flow changes, rather than hair cell loss, in hearing loss after surgical trauma, and implicate the endocochlear potential as a factor in implantation-induced hearing loss. Further, the analysis of the hair cell ribbons and post-synaptic receptors suggest that delayed hearing loss may be linked to synapse or peripheral nerve loss due to stimulation excitotoxicity or inflammation. Further research is needed to separate these potential mechanisms of delayed hearing loss. Copyright © 2015 Elsevier B.V. All rights reserved.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.007
  • [Show abstract] [Hide abstract]
    ABSTRACT: Tinnitus, the phantom perception of sound, is physiologically characterized by an increase in spontaneous neural activity in the central auditory system. However, as tinnitus is often associated with hearing impairment, it is unclear how a decrease of afferent drive can result in central hyperactivity. In this review, we first assess methods for tinnitus induction and objective measures of the tinnitus percept in animal models. From animal studies, we discuss evidence that tinnitus originates in the cochlear nucleus (CN), and hypothesize mechanisms whereby hyperactivity may develop in the CN after peripheral auditory nerve damage. We elaborate how this process is likely mediated by plasticity of auditory-somatosensory integration in the CN: the circuitry in normal circumstances maintains a balance of auditory and somatosensory activities, and loss of auditory inputs alters the balance of auditory somatosensory integration in a stimulus timing dependent manner, which propels the circuit towards hyperactivity. Understanding the mechanisms underlying tinnitus generation is essential for its prevention and treatment. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.005
  • [Show abstract] [Hide abstract]
    ABSTRACT: Human sound source localization relies on acoustical cues, most importantly, the interaural differences in time and level (ITD and ILD). For reaching a unified representation of auditory space the auditory nervous system needs to combine the information provided by these two cues. In search for such a unified representation, we conducted a magnetoencephalography (MEG) experiment that took advantage of the location-specific adaptation of the auditory cortical N1 response. In general, the attenuation caused by a preceding adaptor sound to the response elicited by a probe depends on their spatial arrangement: if the two sounds coincide, adaptation is stronger than when the locations differ. Here, we presented adaptor-probe pairs that contained different localization cues, for instance, adaptors with ITD and probes with ILD. We found that the adaptation of the N1 amplitude was location-specific across localization cues. This result can be explained by the existence of auditory cortical neurons that are sensitive to sound source location independent on which cue, ITD or ILD, provides the location information. Such neurons would form a cue-independent, unified representation of auditory space in human auditory cortex. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.006
  • [Show abstract] [Hide abstract]
    ABSTRACT: The Tinnitus Research Consortium (TRC) issued a Request for Proposals in 2003 to develop a new tinnitus outcome measure that would: (1) be highly sensitive to treatment effects (validated for "responsiveness"); (2) address all major dimensions of tinnitus impact; and (3) be validated for scaling the negative impact of tinnitus. A grant was received by M. Meikle to conduct the study. In that observational study, all of the TRC objectives were met, with the final 25-item Tinnitus Functional Index (TFI) containing eight subscales. The study was published in 2012, and since then the TFI has received increasing international use and is being translated into at least 14 languages. The present study utilized data from a randomized controlled trial (RCT) that involved testing the efficacy of "tinnitus telephone education" as intervention for bothersome tinnitus. These data were used to confirm results from the original TFI study. Overall, the TFI performed well in the RCT with Cohen's d being 1.23. There were large differences between the eight different subscales, ranging from a mean 13.2-point reduction (for the Auditory subscale) to a mean 26.7-point reduction (for the Relaxation subscale). Comparison of TFI performance was made with the Tinnitus Handicap Inventory. All of the results confirmed sensitivity of the TFI along with its subscales. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.004
  • [Show abstract] [Hide abstract]
    ABSTRACT: The resistivity of bone is the most variable of all the tissues in the human body, ranging from 312 Ω.cm to 84 745 Ω.cm. Volume conduction models of cochlear implants have generally used a resistivity value of 641 Ω.cm for the bone surrounding the cochlea. This study investigated the effect that bone resistivity has on modelled neural thresholds and intracochlear potentials using user-specific volume conduction models of implanted cochleae applying monopolar stimulation. The complexity of the description of the head volume enveloping the cochlea was varied between a simple infinite bone volume and a detailed skull containing a brain volume, scalp and accurate return electrode position. It was found that, depending on the structure of the head model and implementation of the return electrode, different bone resistivity values are necessary to match model predictions to data from literature. Modelled forward-masked spatial tuning curve (fmSTC) widths and slopes and intracochlear electric field profile length constants were obtained for a range of bone resistivity values for the various head models. The predictions were compared to measurements found in literature. It was concluded that, depending on the head model, a bone resistivity value between 3 500 Ω.cm and 10 500 Ω.cm allows prediction of neural and electrical responses that match measured data. A general recommendation is made to use a resistivity value of approximately 10 000 Ω.cm for bone volumes in conduction models of the implanted cochlea when neural excitation is predicted and a value of approximately 6 500 Ω.cm when predicting electric fields inside the cochlear duct. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.003
  • [Show abstract] [Hide abstract]
    ABSTRACT: The basilar membrane velocity of gerbil cochlea showed discrepancy between theoretical model and experimental measurements. We hypothesize that the reasons of such discrepancies are due to the arch towards the scala tympani and radial tension present in the basilar membrane of the gerbil cochlea. The arch changes the bending stiffness in the basilar membrane, reduces the effective fluid force on the membrane and increases the basilar membrane's inertia. The existence of the radial tension also dampens the acoustic travelling wave. In this paper, the wave number functions along the gerbil basilar membrane are calculated from experimentally measured physical parameters with the theoretical model as well as extracted from experimentally measured basilar membrane velocity with the wave number inversion formula. The two wave number functions are compared and the effects of the tension and membrane arch on the wave number are studied based on various parameters of the model. We found that the bending stiffness across the gerbil basilar membrane varies (1-2 orders along the cochlea in the section 2.2 mm to 3 mm from base) more than the calculated value in the flat basilar membrane model and the radial tension increases the damping of the travelling wave in gerbil cochlea significantly (5 times more than that without radial tension). These effects of arch and radial tension in the basilar membrane elucidate the discrepancy between previous theoretical model and experimental measurements in gerbil cochlea. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.002
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cortical development is dependent to a large extent on stimulus-driven input. Auditory Neuropathy Spectrum Disorder (ANSD) is a recently described form of hearing impairment where neural dys-synchrony is the predominant characteristic. Children with ANSD provide a unique platform to examine the effects of asynchronous and degraded afferent stimulation on cortical auditory neuroplasticity and behavioral processing of sound. In this review, we describe patterns of auditory cortical maturation in children with ANSD. The disruption of cortical maturation that leads to these various patterns includes high levels of intra-individual cortical variability and deficits in cortical phase synchronization of oscillatory neural responses. These neurodevelopmental changes, which are constrained by sensitive periods for central auditory maturation, are correlated with behavioral outcomes for children with ANSD. Overall, we hypothesize that patterns of cortical development in children with ANSD appear to be markers of the severity of the underlying neural dys-synchrony, providing prognostic indicators of success of clinical intervention with amplification and/or electrical stimulation. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.06.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: From histopathological specimens, endolymphatic hydrops has been demonstrated in association with inner ear disorders. Recent studies have observed findings suggestive of hydrops using MRI in humans. Previous studies suggest that vasopressin may play a critical role in endolymph homeostasis and may be involved in the development of Ménière's disease. In this study we evaluate the effect of vasopressin administration in vivo in longitudinal studies using two mouse strains. High resolution MRI at 9.4 T in combination with intraperitoneally delivered Gadolinium contrast, was performed before and after chronic subcutaneous administration of vasopressin via mini-osmotic pumps in the same mouse. A development of endolymphatic hydrops over time could be demonstrated in C57BL6 mice (5 mice, 2 and 4 weeks of administration) as well as in CBA/J mice (4 mice, 2 weeks of administration; 6 mice, 3 and 4 weeks of administration). In most C57BL6 mice hydrops developed first after more than 2 weeks while CBA/J mice had an earlier response. These results may suggest an in vivo model for studying endolymphatic hydrops and corroborates the future use of MRI as a tool in the diagnosis and treatment of inner ear diseases, such as Ménière's disease. MRI may also be developed as a critical tool in evaluating inner ear homeostasis in genetically modified mice, to augment the understanding of human disease. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.05.008
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sound waves are converted into electrical signals by a process of mechano-electrical transduction (MET), which takes place in the hair bundle of cochlear hair cells. In response to the mechanical stimulus of the hair bundle, the tip-links, key components of the MET machinery, are tensioned and the MET channels open, which results in the generation of the cell receptor potential. Tip-links are composed of cadherin-23 (Cdh23) and protocadherin-15 (Pcdh15), both non-conventional cadherins, that form the upper and the lower part of these links, respectively. Here, we review the various Pcdh15 isoforms present in the organ of Corti, their localization in the auditory hair bundles, their involvement in the molecular complex forming the tip-link, and their interactions with transmembrane molecules that are components of the lower MET machinery. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 06/2015; DOI:10.1016/j.heares.2015.05.005
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scalp-recorded evoked potentials (EP) provide researchers and clinicians with irreplaceable means for recording stimulus-related neural activities in the human brain, due to its high temporal resolution, handiness, and, perhaps more importantly, non-invasiveness. This work recorded the scalp cortical auditory EP (CAEP) in unanesthetized monkeys by using methods that are essentially identical to those applied to humans. Young adult rhesus monkeys (Macaca mulatta, 5-7 years old) were seated in a monkey chair, and their head movements were partially restricted by polystyrene blocks and tension poles placed around their head. Individual electrodes were fixated on their scalp using collodion according to the 10-20 system. Pure tone stimuli were presented while electroencephalograms were recorded from up to nineteen channels, including an electrooculogram channel. In all monkeys (n = 3), the recorded CAEP comprised a series of positive and negative deflections, labeled here as macaque P1 (mP1), macaque N1 (mN1), macaque P2 (mP2), and macaque N2 (mN2), and these transient responses to sound onset were followed by a sustained potential that continued for the duration of the sound, labeled the macaque sustained potential (mSP). mP1, mN2 and mSP were the prominent responses, and they had maximal amplitudes over frontal/central midline electrode sites, consistent with generators in auditory cortices. The study represents the first noninvasive scalp recording of CAEP in alert rhesus monkeys, to our knowledge. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 05/2015; DOI:10.1016/j.heares.2015.05.007
  • [Show abstract] [Hide abstract]
    ABSTRACT: Individual variation in the susceptibility of the auditory system to acoustic overstimulation has been well-documented at both the functional and structural levels. However, the molecular mechanism responsible for this variation is unclear. The current investigation was designed to examine the variation patterns of cochlear gene expression using RNA-seq data and to identify the genes with expression variation that increased following acoustic trauma. This study revealed that the constitutive expressions of cochlear genes displayed diverse levels of gene-specific variation. These variation patterns were altered by acoustic trauma; approximately one-third of the examined genes displayed marked increases in their expression variation. Bioinformatics analyses revealed that the genes that exhibited increased variation were functionally related to cell death, biomolecule metabolism, and membrane function. In contrast, the stable genes were primarily related to basic cellular processes, including protein and macromolecular syntheses and transport. There was no functional overlap between the stable and variable genes. Importantly, we demonstrated that glutamate metabolism is related to the variation in the functional response of the cochlea to acoustic overstimulation. Taken together, the results indicate that our analyses of the individual variations in transcriptome changes of cochlear genes provide important information for the identification of genes that potentially contribute to the generation of individual variation in cochlear responses to acoustic overstimulation. Copyright © 2015 Elsevier B.V. All rights reserved.
    Hearing research 05/2015; DOI:10.1016/j.heares.2015.04.010
  • [Show abstract] [Hide abstract]
    ABSTRACT: DBA/2J mice are characterized by early onset hearing loss at about 3 to 4 weeks of age. Mutations in cadherin 23 (Cdh23) and fascin-2 (Fscn2) are responsible for the phenotypes, but the underlying mechanism is unknown. In the present study, DBA/2J mice displayed progressive hair cell loss and degeneration of spiral ganglion neurons (SGNs) after 2 weeks of age; however, the mRNA level of Caspase-3 in the inner ears was much higher at 2 weeks of age than that at 4 or 8 weeks of age. Moreover, transcriptional levels of Caspase-3 and Caspase-9 in the inner ears of DBA/2J mice were significantly higher than those of C57BL/6J mice at 2 or 8 weeks of age. Immunohistochemistry localized Caspase-3 and Caspase-9 mainly to the hair cells, SGNs and stria vascularis of the cochleae. To determine the significance of caspase-dependent apoptosis in the hearing loss, the pan-caspase inhibitor Z-VAD-FMK was given intraperitoneally to DBA/J2 mice over an 8-week period starting at one week of age. Blockage of caspases preserved hearing in the mice by more than 10 decibels (dB) sound pressure level (SPL) of the ABR thresholds and significantly reduced outer hair cell loss at the basal turns of the cochleae. These results demonstrate that apoptosis in the cochleae of DBA/J2 mice contributes to the early onset of hearing loss, which can be attenuated by anti-apoptotic treatment. Copyright © 2015. Published by Elsevier B.V.
    Hearing research 05/2015; 327. DOI:10.1016/j.heares.2015.05.006