LATEST HEARING & BALANCE RESEARCH
Here you can find some of the latest published articles or papers in hearing and balance research. If you'd like to share a peer-reviewed research article or publication with us, please email Tara Guastella at firstname.lastname@example.org
for more information.
By: Ruili Xie, Paul B. Manis
Published: July 25, 2013
Summary: Glycine is the essential inhibitory neurotransmitter in the mammalian cochlear nucleus. Unfortunately, in the process of age-related hearing loss, glycinergic inhibition weakens in the cochlear nucleus. The conditions responsible for the weakening process are still unknown. Researchers from The University of North Carolina investigated glycinergic transmission in the cells of the cochlear nucleus in normal hearing CBA/Caj mice and in DBA/2j mice. The DBA/2j mice contain a strain that results with an early occurrence of age-related hearing loss. Mice brain slices were analyzed for gylcinergic postsynaptic transmission. The amplitudes of inhibitory postsynaptics current evoked (eIPSC) in the dorsal cochlear nucleus were much small and the failure rate was higher with increasing age. Evidence shows that glycinergic inhibition onto bushy cells result with impairment with age.
By Dane J. Genther, MD; Kevin D. Frick, PhD; David Chen, BS; Joshua Betz, MS; Frank R. Lin, MD, PhD
Published: June 12, 2013
Summary: A team of researchers at Johns Hopkins School of Medicine recently found that older adults with hearing loss are more likely than peers with normal hearing to require hospitalization and suffer from periods of inactivity and depression. “Hearing loss may have a profoundly detrimental effect on older people’s physical and mental well-being, and even health care resources,” says senior study investigator and Johns Hopkins Otologist and epidemiologist Frank Lin, M.D., Ph.D. Lin says social isolation resulting from hearing loss may explain the physical and mental declines — as well as the cognitive deficits — that afflict older adults. This has the possibility of leading to more illness and hospitalization, he says. The analysis included health survey data from 1,140 men and women aged 70 and older with hearing loss found that those with hearing deficits were 32 percent more likely to have been admitted to a hospital than 529 older men and women with normal hearing.
By Frank R. Lin, MD, PhD; Kristine Yaffe, MD; Jin Xia, MS; Qian-Li Xue, PhD; Tamara B. Harris, MD, MS; Elizabeth Purchase-Helzner, PhD; Suzanne Satterfield, MD, DrPH; Hilsa N. Ayonayon, PhD; Luigi Ferrucci, MD, PhD; Eleanor M. Simonsick, PhD; for the Health ABC Study Group
Published: January 21, 2013
Summary: Compared to those with normal hearing, individuals with hearing loss at baseline had a 24% increased risk for incident cognitive impairment. Rates of cognitive decline and the risk for incident cognitive impairment were linearly associated with the severity of an individual's baseline hearing loss. Hearing loss is independently associated with accelerated cognitive decline and incident cognitive impairment in community-dwelling older adults. Further studies are needed to investigate what the mechanistic basis of this association is and whether hearing rehabilitative interventions could affect cognitive decline.
Auditory Processing Disorders
By Amineh Koravand, Benoit Jutras
Published: November 2012
Summary: Forty children 9 to 12 years old participated in the study: 12 with sensory hearing loss (HL), 12 with central auditory processing disorder (CAPD), and 16 with normal hearing. They performed an ASO task in which they were asked to recall two, three, and five verbal and nonverbal stimuli with an inter-stimulus interval (ISI) of 425 ms as well as sequences of two elements with an ISI of 20 or 1000 ms. There was no significant difference found between the group of children with HL and the two other groups on non-verbal stimuli in all testing conditions. Results suggest that hearing loss can induce a specific signature when processing these verbal stimuli.
Summary: A team of researchers at the University of Washington developed a strategy allowing for hearing-impaired individuals to hear music with the advancement of their cochlear implants. The investigators altered the signals in cochlear implants. This allowed for users to ultimately hear music at a higher quality. Jay Rubinstein, a University of Washington professor of Otolaryngology and of biomedical engineering, believes music aides individuals to allow them to express themselves emotionally and can increase the quality of life. The research project involved cochlear-implant users that used the new coding strategy. Results showed they were able to differentiate between musical instruments. Users were tested by melodies such as “Twinkle, Twinkle, Little Star,” in which the rhythms were removed. Timbre recognition increased although it was still difficult for people to observe melodies.
By: Carina Pals, Anastasios Sarampalls, Deniz Baskent
Published: December 28, 2012
Summary: Nineteen normal-hearing participants listened to CI simulations with varying numbers of spectral channels. A dual-task paradigm combining an intelligibility task with either linguistic or non-linguistic visual response-time (RT) task measured intelligibility and listening efforts. The simultaneously-performed tasks competed for limited cognitive resources; changes in effort associated with the intelligibility task were reflected in changes in RT on the visual task. All measures showed significant improvements with increasing spectral resolution up to 6 channels. In contrast, only the RT measure of listening effort continued improving up to 8 channels. The effects were stronger for RTs recorded during listening than for RTs recorded between listening. The results suggest that listening effort decreases with increased spectral resolution. Moreover, these improvements are best reflected in objective measures of listening effort such as RTs on a secondary task, rather than intelligibility scores or subjective effort measures.
By Diane S. Lazard, Christophe Vincent, Frederic Venail, Paul Van de Heyning, Eric Truy, Oliver Sterkers, Piotr H. Skarzynski, Karen Schauwers, Stephen O’Leary, Deborah Mawman, Bert Maat, Andrea Kleine-Punte, Alexander M. Huber, Kevin Green, Paul J. Govaerts, Bernard Fraysse, Richard Dowell, Norbert Dillier, Elaine Burke, Andy Beynon, Francois Bergeron, Deniz Baskent, Francoise Artieres, Peter J. Blamey
Published: November 9, 2012
Summary: Several new statistical analyses were conducted on the dataset described in Blamey et al (in press). The dataset consisted of retrospective information for 2251 CI recipients evaluated with various speech tests and conditions (quiet and noise) from 15 international centres. All centres provided the core information on implant performance (on an open-set speech perception test in quiet and in noise without lip-reading), duration of s/p HL, age at onset of s/p HL, etiology, and cochlear implant experience. Speech scores in quiet and in noise at two postoperative times for each recipient were requested from the clinics: one score collected early after activation of the CI (T1) and one score collected later on (T2). The choice of the date of the tests was free and varied between and within centres. The influence of 15 pre-, per- and postoperative factors, such as the duration of moderate hearing loss (mHL), the surgical approach (cochleostomy or round window approach), the angle of insertion, the percentage of active electrodes, and the brand of device were tested. The significant factors were: the pure tone average threshold of the better ear, the brand of device, the percentage of active electrodes, the use of hearing aids (HAs) during the period of pHL, and the duration of mHL.
By Ann E. Geers, Johanna G. Nicholas
Published: November 2012
Summary: Sixty children participated in a prospective longitudinal study of outcomes at 4.5 and 10.5 years of age. Twenty-nine children received a sequential second CI. Test scores were compared to normative samples of hearing age-mates and predictors of outcomes identified. As a result, standard scores on language tests at 10.5 years of age remained significantly correlated with age of first cochlear implantation. Scores were not associated with receipt of a second, sequentially-acquired CI. Significantly higher scores were achieved for vocabulary as compared with overall language, a finding not evident when the children were tested at younger ages.
Genetics and Hearing Loss
By: Bifeng Pan, Gwenaelle S. Geleoc, Yukako Asai, Geoffrey C. Horwitz, Kiyoto Kurima, Kotaro Ishikawa, Yoshiyuki Kawashima, Andrew J. Griffith, Jeffrey R. Holt
Published: July 18, 2013
Summary: A team of researchers at National Institute on Deafness and Communication Disorders (NIDCD) who were working with scientists at the Boston Children’s Hospital found two inner ear proteins. These proteins are crucial for hearing. Genetic mutations are known to delay or even harm these proteins causing hearing loss. Proteins that are encoded byTMC1/TMC2 genes are components of channels that convert mechanical sound waves into electrical signals. These signals are then processed in the brain. Any mutation in the gene sequence will result with a variance in the aspects of the channels causing deafness.
By: Xiangming Li, Joel D. Sanneman, Donald G. Habidge, Fei Zhou, Taku Ito, Raoul Nelson, Nicolas Picard, Regine Chambrey, Dominique Eladari, Tracy Miesner, Andrew J. Griffith, Daniel C. Marcus, Philine Wangermann
Published: July 11, 2013
Summary: At Kansas State University, a group of researchers investigated a project that would conceivably lead to the treatment of human deafness and loss of balance. This project was funded by the National Institute on Deafness and Other Communicative Disorders (NIDCD) as well as other organizations. A mutation of the SLC26A4 gene often leads to hearing loss in children. This gene is located in the cochlea, vestibular organs of the inner ear and in the endolymphatic sac. Studies found that when mutant mice lacked SLC26A4 expression, their inner ears swelled during embryonic development. As a result, the mice became deaf and suffered from imbalance. The researchers proposed if they could restore proper expression in the endolymphatic sac, which would prevent swelling, they would also inhibit the swelling in other areas of the inner ear. Results showed the mice did not suffer from hearing or imbalance and it lasted for the duration of the testing period. “Our study provides the proof-of-concept that a therapy aimed at repairing the endolymphatic sac during embryonic development is sufficient to restore a lifetime of normal hearing and balance,” Wangermann, Kansas State University distinguishes professor of Anatomy and Physiology.
By: Stefan Volkenstein, Kazuo Oshima, Saku T. Sinkkonen, C. Eduardo Corrales, Sam P. most, Renjie Chai, Taha A. Jan, Alan G. Cheng, and Stefan Heller
Published: August 12, 2013
Summary: Within the first few weeks of birth, neuronal survival in the cochlear nucleus (CN) is determined by the afferent innervation from the cochlea. Ironically, neurogenesis was not surveyed as a mechanism of postnatal plasticity even though it has been analyzed thoroughly within the CN. In this study, neurons were created in a pivotal time period of postnatal plasticity. Data showed detailed networking of Wnt, Notch, and TGFβ/BMP signaling which were shown to regulate a culture of precursor cells. The removal of the cochlear yielded a decrease in the amount of precursor and Wnt/ β-catenin-active cells.
Summary: A team of researchers from Harvard determined a leucine-rich repeat, a structural motif in amino acids with a repetitive sequencing pattern rich in leucines, which has the ability to hair cell differentiate in vitro. This protein contains G-protein-coupled receptor 5 (Lgr5)- expressing cochlear supporting cells which can also facilitate self-renewal. These cells were receptive to Wnt signaling. In neonatal mice, the balance of β –catenin in supporting cells yielded proliferation of supporting cells and the formation of hair cells. Results showed that Wnt/ β-catenin can initiate Lgr5-positive cells to act as hair cell progenitors.
By: Kindsey A. May, Inga I. Kramarenko, Carlene S. Brandon, Christina Voelkel-Johnson, Soumen Roy, Kristy truong, Shimon P. Francis, Elyssa L. Monzacki, Fu-Shing Lee, and Lisa L. Cunningham
Published: July 25, 2013
Summary: A team of researchers have discovered that supporting cells in the inner ear of mice can laboriously aid in repairing damaged sensory hair cells. These sensory cells turn vibrations into electrical signals. In the study, supporting cells and heat shock protein 70 (HSP70), a chemical the supporting cells generate, both act in part in protecting damaged hair cells. Dr. Lisa Cunningham, Ph.D., did previous work that promoted the theory of HSP70, a protein that is secreted in the inner ear after contact with stress (such as toxins and noise), can ultimately conserve hair cells. “Our study indicates that when the inner ear is under stress, the cell that responds by generating protective proteins is not a hair cell, but a supporting cell,” says Dr. Cunningham. During the project, the researchers initiated contact between mice utricles and heat but then rapidly secured them. As a result, HSP70 was expressed. The microscopy techniques demonstrated the protein was discovered in the supporting cells and not in the hair cells.
By: Karl R. Koehler, Andrew M. Mikosz, Andrei I. Molosh, Dharmeshkumar Patel, and Eri Hashino
Published: July 10, 2013
Summary: A team of researchers at Indiana University have found a way to use embryonic mice stem cells in order to grow tissues of the inner ear. This novel approach will provide new insight of ways on how to restore hearing. These 3D aggregates of tissues are sensory epithelia. It consists of hair cells, supporting cells and neurons which are all vital for efficient hearing. A person can identify sound waves, react to head movements as well as gravity with these hair cells. Leading researchers, Eri Hashino and Karl Koehler stated they concocted the necessary amount of chemicals and proteins in order to make these delicate tissues. As a team, they mirrored the body’s natural environment during stages of fetal development. This allowed the tissues to grow in their ‘natural habitat’. Hair cells form a network with neurons. This allows for the brain to process the information. “Now we can study the hair cell-neuron connection, which is very important. It shows us how the ear forms and how things go wrong,” Koehler said.
By: Artur A. Indzhykulian, Ruben Stepanyan, Anastasiia Nelina, Kateri J. Spinelli, Zubair M. Ahmed, Inna A. Belyantseva, Thomas B. Friedman, Peter G. Barr-Gillespie, Gregory I. Frolenkov
Summary: Tip links are extracellular tethers that link stereo-cilia, the tiny sensory projections on inner ear hair cells that convert sound into electrical signals, and play a key role in hearing. This study highlights an unexpected two-step process that happens during the growth and regeneration of inner ear tip links. The discovery offers a possible mechanism for potential interventions that could preserve hearing in people whose hearing loss is caused by genetic disorders related to tip link dysfunction. Tip links break easily with exposure to noise. But unlike hair cells, which do not regenerate in humans, tip links repair themselves, mostly within a matter of hours. The breaking of tip links, and their regeneration, has been known for many years, and is seen as one of the causes of the temporary hearing loss you might experience after a loud blast of sound (or a loud concert). Once the tip links regenerate, hair cell function returns, usually to normal levels. This study sheds light on how the tip link reassembles.
By Kunio Mizutari, Masato Fujioka, Makoto Hosoya, Naomi Bramhall, Hirotaka James Okano, Hideyuki Okano, Albert S.B. Edge
Published: January 9, 2013
Summary: Hearing loss due to damage to auditory hair cells is normally irreversible because mammalian hair cells do not regenerate. Here, we show that new hair cells can be induced and can cause partial recovery of hearing in ears damaged by noise trauma, when Notch signaling is inhibited by a γ-secretase inhibitor selected for potency in stimulating hair cell differentiation from inner ear stem cells in vitro. Hair cell generation resulted from an increase in the level of bHLH transcription factor Atoh1 in response to inhibition of Notch signaling. In vivo prospective labeling of Sox2-expressing cells with a Cre-lox system unambiguously demonstrated that hair cell generation resulted from transdifferentiation of supporting cells. Manipulating cell fate of cochlear sensory cells in vivo by pharmacological inhibition of Notch signaling is thus a potential therapeutic approach to the treatment of deafness.
By Jin Liang, Dongmei Wang, Gabriel Renaud, Tyra G. Wolfsberg, Alexander F. Wilson, Shawn M. Burgess
Published: October 3, 2012
Summary: The sensory epithelium of the inner ear is mainly composed of two types of cells: hair cells and supporting cells. Inner ear hair cells are the basic mechanosensory receptors for hearing and balance, while supporting cells provide a variety of functions including being the stem cells for replacing hair cells in most vertebrates. In mammals, loss of inner ear hair cells caused by acoustic over-exposure or aging is the major cause of permanent auditory and vestibular deficiencies because mammals lose regenerative ability after birth. A powerful profiling technique digital gene expression (DGE) was used to study the hair cell regeneration in zebrafish at high resolution to get a more comprehensive view of the process. In zebrafish, spontaneous and damage-induced hair cell production has been demonstrated in both the inner ear and the a mechanosensory structure highly similar to the sensory epithelia of the inner ear.
Moreover, the stat3/socs3a pathway is involved in hair cell production in zebrafish development. In addition to the hair cells in their inner ears, zebrafish, like other fishes and amphibians, also possess the mechanosensory lateral line organ for detecting water movement over the body. The neuromasts in the lateral line are composed of hair cells and supporting cells that are highly similar to those in the inner ear sensory epithelium. In addition, the hair cell regeneration in the lateral line neuromasts shares a similar molecular mechanism to that in the inner ear. To further clarify the function of stat3, we compared the hair cell regeneration processes with and without the presence of a stat3 inhibitor. The majority of the chemical inhibitors were ototoxic and could not be used for regeneration studies. One published inhibitor, S3I-201, was not toxic on its own and was used to test the role of stat3 in hair cell regeneration. S3I-201 is a cell-permeable chemical that binds to the SH2 domain of mammalian stat3 protein and reportedly blocks the dimerization of phosphorylated (activated) stat3 molecules.
By Shi-Ming Yang, Wei Chen, Wei-Wei Guo, Shuping Jia, Jian-He Sun, Hui-Zhan Liu, Wie-Yen Young, David Z. Z. He
Published: September 27, 2012
Summary: Noise-induced hearing loss (NIHL) is a major health problem. Acoustic trauma causes NIHL when permanent cochlear damage results from exposure to high-intensity sounds, such as explosions, gunfire, and firecrackers. NIHL is usually due to destruction of cochlear hair cells and/or damage to their hair bundles. Cochlear hair cells transduce mechanical stimuli into electrical activity. The hair bundle, a staircase array of stereocilia of different heights, is the site of mechanoelectrical transduction. The delicate hair bundle is susceptile to both acoustic trauma and ototoxic drugs. The inability of stereocilia to self-repair can subsequently lead to hair cell death and permanent hearing loss.
Moreover, adult guinea pigs were exposed to 200 rounds of simulated gunfire. The CM was measured to monitor the damage of the hair cells in some animals. The CM, an electrical potential generated in the cochlear hair cells in response to acoustic stimulation, primarily reflects mechanotransduction in the stereocilia of outer hair cells. The CM response before and after 1, 10, and 200 rounds of gunfire was recorded. After exposures to 10 and 200 rounds of gunfire, the magnitude decreased by 66% and 97%, respectively. The reduction represents a significant disruption of outer hair cell (OHC) mechanotransduction after noise exposure. ABRs, frequently used to monitor hearing loss, are electrical signals evoked from the brainstem during presentation of an acoustic signal. ABR thresholds were obtained from both ears of 19 animals at 4, 8, 16, and 20 Hz using tone pips.
Hearing Impairment & Disability Over Time
Summary: Spatial hearing can be affected by an alteration in binaural experience. In the mouse primary auditory cortex (A1), a versatile unilateral conductive hearing loss (CHL) will be achieved experimentally at various discoveries. The effects were characterized approximately a week after hearing was reestablished. Prior to P16, conductive hearing loss disturbs normal interaural frequency tuning in contrast to CHL at P16. Results suggest a resilience in the maturing auditory cortex that shows similarities to Amblyaudia, a hearing impairment resulting with otitis media in infants.
By Anil K. Lalwani, Karin Katz, Ying-Hua Liu, Sarah Kim, Michael Weitzman
Published: June 17, 2013
Summary: Compared to normal weight counterparts, obese adolescents are more likely to have hearing loss. This study found that obesity in adolescents is associated with sensorineural hearing loss, caused by damage to inner ear hair cells, across all frequencies (the frequency range that can be heard by humans). The highest rates were for low-frequency hearing loss -- 15.16 percent of obese adolescents compared with 7.89 percent of non-obese adolescents. Although the overall hearing loss among obese adolescents was relatively mild, the almost 2-fold increase in the odds of unilateral low-frequency hearing loss is particularly worrisome. It suggests early, and possibly ongoing, injury to the inner ear that could progress as the obese adolescent becomes an obese adult. Obesity also may contribute indirectly to hearing loss as a result of its comorbidities, including type II diabetes, cardiovascular disease, and high cholesterol -- all of which have been reported to be associated with loss of peripheral hearing (relating to the outer, middle, and inner ear).
By Robert A. Dobie
Published: November/December 2011
Summary: This study supports the continued use of the 1979 AMA* method (“hearing handicap” or “binaural hearing impairment” in which air-conduction thresholds at 500, 1000, 2000, and 3000 Hz; assumes a “low fence” of 25 dB HL and a “high fence” of 92 dB HL; and gives five times more weight to the better ear than to the worse ear. BHI** is calculated from these eight thresholds). Incorporation of WRSs(word recognition scores)***, as typically measured clinically, into methods of estimating hearing disability is not supported because of negligible improvement in accuracy and inability to control exaggeration for speech tests in medical-legal settings.
*- American Medical Association
**- Binaural Hearing Impairment
By Howard J. Hoffman, Robert A. Dobie, Chia-Wen Ko, Christa L. Themann, and William J. Murphy
Published: December 2010
Summary: Across age and sex groups, median thresholds were lower (better) in the 1999–2004 survey at 500, 3000, 4000, and 6000 Hz (8000 Hz was not tested in the 1959–1962 survey). For both men and women, the prevalence of hearing impairment was significantly lower in 1999–2004 at 500, 2000, and 4000 Hz, but not at 1000 Hz. For men and women of a specific age, high-frequency hearing thresholds were lower (better) in 1999–2004 than in 1959– 1962. The prevalences of hearing impairment were also lower in the recent survey. Differences seen at 500 Hz may be attributable at least in part to changes in standards for ambient noise in audiometry. The National Health and Nutrition Examination Survey 1999–2004 distributions are offered as a possible replacement for Annex B in ISO-1999 and ANSI S3.44.
Noise-Induced Hearing Loss and Tinnitus
By: Mingqian Huang, Albena Kantardhieva, Deborah Scheffer, M. Charles Liberman, and Zheng-Yi Chen
Published: September 18, 2013
Summary: A team of researchers from the Massachusetts Eye and Ear and Harvard Medical School have designed a new mouse model. They expressed genes in the inner ear hair cells that aid in the protection of age-related hearing loss (ARHL) and noise-induced hearing loss (NIHL). In their project, they proposed new mechanisms for hearing loss as well as other therapies including gene therapy or medicine. The researchers set forth investigating the different mechanisms in both types of hearing losses which may have a common pathway. They examined the overexpression of Islet1 (precursor gene located in the inner ear that assists with differentiation and development). Results showed that Islet1 expression aided in the protection of the hair cells and support hair cell survival. When mice were exposed to acoustic trauma, their hearing was more intact compared to their kin who did not have the gene. “The Islet1 gene further preserved the connections between hair cells and neurons, which is necessary for hearing,” said senior author Zheng-Yi Chen, Ph.D, Massachusetts Eye and Ear researcher.
By: Kevin W. Christie, Elena Sivan-Loukianova, Wesley C. Smith, Benjamin T. Aldrich, Michael A. Schon, Madhuparna Roy, Bridget C. Lear, and Daniel F. Eberl.
Published: September 3, 2012
Summary: A team of researchers proposed the first noise induced hearing loss (NIHL) study in the fruit fly, Drosophila melanogaster. The auditory function was investigated after the flies were exposed to acoustic trauma. Results showed that acoustic trauma changed the neural mitochondria size as well as the auditory system function. As a result, metabolic stress can occur. Some mutant flies are not successful in handling these stresses. The damage would be more impaired. Sound-evoked potentials (SEP) were greatly reduced by the acoustic trauma endured. Seven days after the trauma, mitochondrial cross-sectional area reduced in size. These effects by the Drosophila display traits resembling those found in vertebrates. Using the Drosophila melanogaster as a model structure for further research on NIHL will provide as an economical and influential tool.
By: John S. Oghalai, Sung-Il Cho, Simon S. Gao, Jongmin Baek, David Jacobs, Anping Xia, Rosalie Wang, Felipe T. Salles, Patrick D. Raphael, and Homer Abaya, Jacqueline Wachtel, and Matthew N. Rasband.
Published: July 1, 2013
Summary: Researchers at Stanford University have found that loud blasts cause hair-cell and nerve damage as opposed to structural damage to the cochlea. “It means we could potentially try to reduce this damage” says John Oghalai, MD. If the cochlea was severely damaged structurally by the blasts, such as shredding, the damage would be permanent. A mouse model was used to investigate what causes permanent hearing loss. Anesthetized mice were exposed to loud blasts. The cochlea was then examined day one through three months with the use of a micro-CT scanner. Oghalai stated that after blast damage, the resulting hearing loss is caused by the body’s immune response to these injured cells with the creation of scar tissue. Scar tissue inhibits the organ to vibrate which would allow the hearing mechanism to work.
By: Fei Zhang, Min Dai, Lingling Neng, Jin Hui Zhang, Zhongwei Zhi, Anders Fridberger, and Xiaorui Shi.
Published: May 31, 2013
Summary: The Endocochlear potential (EP) is vital for hearing properly. A team of researchers found that tissue perivascular resident macrophages (PVM/Ms) are fundamental for maintaining this EP. These cells display traits of both macrophages and melanocytes. These PVM/Ms cells regulate expression of tight/adherens- junction proteins by secreting a signaling molecule, pigment epithelium growth factor (PEDF). The researchers observed a notable connection between abnormalties in PVM/Ms and the endothelial barrier disruption from acoustic trauma in the mouse ear. As a result of acoustic trauma, PVM/Ms are activated and detachments from capillary walls are visible.
By Shuang Li, Veronica Choi, and Thanos Tzounopoulos
Published: May 2013
Summary: Tinnitus, the perception of phantom sound, is often a debilitating condition that affects many millions of people. Little is known, however, about the molecules that participate in the induction of tinnitus. In brain slices containing the dorsal cochlear nucleus, we reveal a tinnitus-specific increase in the spontaneous firing rate of principal neurons (hyperactivity). This hyperactivity is observed only in noise-exposed mice that develop tinnitus and only in the dorsal cochlear nucleus regions that are sensitive to high frequency sounds. We show that a reduction in Kv7.2/3 channel activity is essential for tinnitus induction and for the tinnitus-specific hyperactivity. This reduction is due to a shift in the voltage dependence of Kv7 channel activation to more positive voltages. Our in vivo studies demonstrate that a pharmacological manipulation that shifts the voltage dependence of Kv7 to more negative voltages prevents the development of tinnitus. Together, our studies provide an important link between the biophysical properties of the Kv7 channel and the generation of tinnitus. Moreover, our findings point to previously unknown biological targets for designing therapeutic drugs that may prevent the development of tinnitus in humans.
By: Jae-Jin Song, Andrea Kleine Punte, Dirk De Ridder, Sven Vanneste, Paul Van de Heyning
Published: May 2013
Summary: A collection of quantitative electroencephalography (qEEG) data from nine SSD patients who underwent CI for tinnitus management was done. By correlating the degree of improvement in tinnitus intensity and tinnitus-related distress with preoperative source-localized qEEG findings and comparing qEEG findings of patients with marked improvement after CI with those with relatively slight improvement with regard to source-localized activity complimented by connectivity analysis, we attempted to find preoperative predictors of tinnitus improvement. Hence, there were increased activities of the auditory cortex (AC), posterior cingulate cortex (PCC) and increased functional connectivity between the AC and PCC as negative prognostic factors for the reduction of tinnitus intensity after CI in patients with SSD.
By Yuguang Niu, Anand Kumaraguru, Rongguang Wang, Wei Sun
Published: November 14, 2012
Summary: The effects of narrow‐band noise exposure on the firing properties of neurons in the inferior colliculus (IC) were studied, which has complex neural circuits and plays an important role in sound processing. It was found that noise exposure (20 kHz, 105 dB SPL, 30 min) caused a dramatic decrease of the characteristic frequency in about two‐thirds of high‐frequency neurons with/without causing a significant threshold shift. The noise exposure also caused an increase in firing rate of the low‐frequency neurons at suprathreshold levels, whereas it dramatically decreased the firing rate of the high‐frequency neurons.
By Robert A. Dobie
Published: July 2012
Summary: The population burden of hearing loss, or any other disorder, can be measured using disease-specific metrics (e.g., audiometry and hearing disability questionnaires). Occupational noise probably causes 5- 10% of the adult hearing loss burden in wealthy countries. Occupational noise is greater in developing countries for 2 reasons: (1) manufacturing jobs have been relocating to these countries; (2) the average lifespan is shorter in the developing world, reducing the burden of age- related hearing loss. Non-occupational noise has a similar impact and should be reduced through education and clinical counseling.
By Robert A. Dobie
Published: August 2008
Summary: Occupational noise exposure probably accounts for less than 10% of the burden of adult hearing loss in the United States; most of the rest is age-related. Most of the occupational noise burden is attributable to unprotected exposures above 95 dBA, and becomes apparent in middle age, when occupational noise exposure has ceased but age-related threshold shifts are added to prior noise-induced shifts, resulting in clinically significant impairment.
Moreover, in the current state of knowledge, noise-induced hearing loss is still the most important preventable cause of hearing loss in the United States. The burden of occupational noise-induced hearing loss could probably be reduced by stricter enforcement of existing regulations. Longer lifespans in developed countries and migration of manufacturing jobs to developing countries will continue to reduce the relative contribution of occupational hearing loss in countries like the United States. Preventive interventions for age-related hearing loss, even if only partially effective, could potentially reduce the burden of adult hearing loss more than elimination of occupational noise.
Are We Facing an Epidemic of Noise- Induced Hearing Loss?
By Robert A. Dobie
Published: September/October 2008
Summary: NIHL is not increasing in the USA since there is no national representative way to count cases of NIHL. Is Noise exposure increasing? Since 1983, American employers provided hearing protection devices for the noise- exposed workers. Over time, the number of manufacturing jobs decreased by 50%. As some Americans like to use guns, shooting requires hearing protection devices. Also, the numbers of hunting licenses have been stable for decades. Thus it is hard to argue that hazardous noise exposure is increasing.
Moreover, What about iPods, etc.? For iPods, it is possible to play music loud enough and long enough to cause NIHL; but very few people do that. There is no substantial evidence that iPods have had an effect on hearing of the population. What about the ‘noise of everyday life’? There is no evidence that people who live in busy big cities suffer from hearing loose than those who live in tranquil. Do people hear worse now than in previous years? Dobie’s research indicates that hearing thresholds as a function of age, sex have been stable in the US for the past 40 years.
Lastly, And the developing world? Manufacturing jobs have been moving to developing countries for decades. Unfortunately, in these conditions, developing countries do not have the ability or will to implement effect hearing conservation programs. Hence, the most cost-effective interventions are those directed at the most underserved groups.
By Cac T. Nguyen, Sarah R. Robinson, Woonggyu Jung, Michael A. Novak, Stephen A. Boppart, Jont B. Allen
Published: July 2013
Summary: In recent studies, clinical evidence was provided in which confirmed a parallel connection between chronic Otitis Media (OM) and the presence of a bacterial biofilm (behind the tympanic membrane). The acoustic effects of bacterial biofilms were investigated and confirmed using a process called Optical Coherence Tomography (OCT), in adult ears. Images were collected to visualize the cross- sectional structure of the middle ear, which verified the presence of biofilm behind the tympanic membrane. Measurements of acoustic reflectance and impedance were used to study the acoustic properties of ears with confirmed bacteria biofilms. In comparison to known acoustic properties of normal middle ears, the ears which contained the bacteria biofilm had elevated power of reflectance. This corresponded to an abnormally small resistance. This provided assistance for clinical diagnosis of bacterial biofilm which may lead to improved treatment of chronic middle ear infection.
By Jessica Bondy, MHA; Stephen Berman, MD; Judith Glazner, MS; and Dennis Lezotte, PhD
Published: June 2000
Summary: Twenty-eight percent of children experienced at least 1 episode of diagnosed otitis media. The proportion of children with a diagnosis of otitis media was highest (42%–60%) in the 7-month to 36-month age range. The proportion was also higher among white(34.5%) and Hispanic (25.3%) children than among black children (18.5%), as well as among rural (34.5%) compared with urban children (27.2%). Children 19 to 24 months of age incurred the highest total annual expenditures per child with otitis media ($239.68). Expenditures for drugs, visits, and procedures were all highest for this group. The per-patient cost to Medicaid was greater for visits than for drugs or procedures across all age groups.
Moreover, total per-patient expenditures were higher for males ($174.67) than for females ($154.47) and higher for white children ($176.59) than for Hispanic ($154.12) or black children ($134.44). The differences among the ethnic groups can be attributed almost entirely to differences in expenditures for procedures and drugs. Although mean expenditures per patient varied substantially by some patient characteristics (eg, race), these differences accounted for only a small fraction of the enormous variation in costs per patient.
In addition, because 40% of expenditures to treat otitis media are incurred between 1 and 3 years of age, vaccines designed to reduce the incidence of otitis media are most likely to be cost-effective if they can be administered before the child’s first birthday. Because visits are the most costly category of service for all payers, otitis media case management guidelines should emphasize reducing unnecessary visits, for instance, by improving physician training in pneumatic otoscopy, which has been shown to be critical to an accurate diagnosis of otitis media, and by scheduling follow-up visits for children who have become asymptomatic 3 to 4 weeks after diagnosis rather than after 10 to 14 days, allowing time for resolution of the middle ear effusion.
By Sofia Waissbluth, Sam J. Daniel
Published: May 2013
Summary: Cisplatin is a potent antineoplastic agent widely used for a variety of cancer types. Unfortunately, its use leads to dose limiting side effects such as ototoxicity. Up to 93% of patients receiving cisplatin chemotherapy will develop progressive and irreversible sensorineural hearing loss which leads to a decreased quality of life in cancer survivors. No treatment is currently available for cisplatin-induced ototoxicity. It appears that cisplatin causes apoptosis by binding DNA, activating the inflammatory cascade as well as generating oxidative stress in the cell. There were some key highlights: (1) Increase in ctr1 and decrease in ctr2 causes an increase in intracellular cisplatin, (2) Organic cation transporter OCT2 is an important transporter for cisplatin, not OCT1, (3) TRPA1 and TRPV1 expression is increased when cells are exposed to cisplatin, (4) Roles of TRPA1 and TRPV1 in cisplatin toxicity are poorly understood, (5) There is no evidence to suggest cisplatin may enter cells through calcium channels.
By Jennifer J. Lentz, Francine M Jodelka, Anthony J Hinrich, Kate E McCaffrey, Hamilton E Farris, Matthew J Spalitta, Nicolas G Bazan, Dominik M Duelli, Frank Rigo & Michelle L Hastings.
Published: February 4, 2013
Summary: Researchers are reporting that hearing and balance can be rescued by a new therapy in a mouse model of Usher syndrome (Usher) that contains the mutation responsible for type 1C Usher. The results provide the first evidence that congenital deafness can be effectively overcome by treatment early in development to correct gene expression.
By Louise H. Williams, Kerry A. Miller, Hans- Henrik M. Dahl, Shehnaaz S.M. Manji
Published: May 2013
Summary: Myosin VI (Myo6) is known to play an important role in the mammalian auditory and vestibular systems. A novel N-ethyl-N-nitrosourea mutagenized mouse strain, Charlie was identified. It carries an intronic Myo6 splice site mutation. This mutation causes the skipping of exon 5 and may cause a frame shift as well as premature termination of the protein. There was no trace of Myo6 transcript in tissue from Charlie homozygous mutant mice. These mice exhibited vestibular dysfunction and profound hearing impairment when it was first tested at four weeks of age. Under electron microscopy and immunohistochemistry, highly disorganized hair bundles with irregular orientation at postnatal stage were visible. After a few weeks, the majority of hair cell stereocillia were missing, fused or elongated and degeneration of the sensory epithelium occurred.