Music-Induced Hearing Loss: What Do College Students Know?

By Frankie Huang

Music-induced hearing loss (MIHL) is a result from listening to music that exceeds 85 decibels for prolonged periods of time. A decibel, or dB, is a unit to measure sound intensity, and 85 dB is roughly equivalent to the sound of heavy city traffic. Our listening devices and preferred listening levels are the leading cause for MIHL. For example, when you’re working out at the gym and you up the volume of your music to 100% to drown out the music the gym is broadcasting, you are putting yourself at risk for permanent hearing loss.

The frequent use of these devices to listen to music and watch videos typically requires the use of headphones, increasing the risk of MIHL. Portnuff, Figor, and Arehart (2011) found that a person should only use their listening devices for no more than 4 hours per day at 70% volume, or 90 minutes per day at 80% volume.

In a recent study, researchers measured college students’ knowledge on the proper use of listening devices and the effects of listening to music at high volumes. It was found that prolonged use of these devices coupled with loud preferred listening levels is higher in males than in females, with males being less aware of safe listening habits and were more likely to exceed the recommended daily limit. The study also found that female students were more conscious of these limits and more knowledgeable about the maximum listening levels per day, compared with their male counterparts. Furthermore, younger students (freshmen) were less aware of safe listening levels compared with older students who were sophomores.

The use of certain headphones can also increase the risk of MIHL. Among college students, in-ear headphones (e.g., earbuds) are more commonly used than over-the-ear, noise-canceling headphones, and in-ear headphones are associated with a higher risk of MIHL. The biggest difference between in-ear and over-the-ear headphone users was the individual’s listening levels: The study found that in-ear headphone users preferred to listen at a higher volume, while over-the-ear headphone users favored a lower volume because the noise-canceling features meant ambient noise was less of an issue.

Headphone users tend to increase the volume if they can’t block out environmental noises. New York City, for example, is usually noisy so individuals are more likely to listen to their music at a higher volume, which is putting individuals at a greater risk of MIHL. There’s also a greater preference for in-ear headphones between males and females. According to the studies, 52.8% of males believed that in-ear headphones delivered better sound than over-the-ear headphones, compared with 46.4% of females.

Overall, the study suggested that individuals should refrain from listening to music and watching videos at the maximum volume for an extensive amount of time. However, if there’s too much background noise, and it's a distraction, the individual should only increase the volume to 80% of the maximum for no more than 90 minutes daily. In addition, education about the risks of hearing loss and how to prevent it is important, including how noise-canceling headphones drown out environmental noises so the wearer can enjoy music on their personal devices at safer levels.

Hearing loss is irreversible, so investing in a quality headphone that can reduce the risk of MIHL is priceless.

References

Berg, Abbey L. et al. Music-Induced Hearing Loss:What Do College Students Know?. 43rd ed. 2016. Web. 12 Dec. 2016.

http://www.asha.org/uploadedFiles/ASHA/Publications/cicsd/2016F-Music-Induced-Hearing-Loss.pdf

Your Support Is Needed!

Hair cell regeneration is a plausible goal for eventual treatment of hearing and balance disorders.

The question is not if we will regenerate hair cells in humans, but when.  

However, we need your support to continue this vital research and find a cure!

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The HRP Shifts Gears for Greater Impact

By Peter Barr-Gillespie, Ph.D.

It’s remarkable to me that the Hearing Restoration Project (HRP) is five years old! While the past five years revealed that regeneration of sensory hair cells is more complex than anticipated, our scientists have nonetheless made significant progress. Several notable HRP research projects supported by Hearing Health Foundation (HHF) were published in 2016, and more are on the way.

Financial investment in the HRP is crucial for our success. Through the HRP, HHF supports promising innovative research areas that due to the lack of available funds are not adequately financed by other agencies. We continue to acquire large-scale genomics datasets, and the more we generate the more valuable they all are—comparing the results from different types of experiments is a key approach of the HRP.

In 2017 we will see a change in the way the HRP conducts its research. At our HRP meeting this past November, the consortium updated its research methods for the upcoming year, choosing to focus and devote more resources on two promising, major experimental strategies. This is a shift from the approach over the past five years, when the HRP followed various independent paths to understanding hair cell regeneration.

The first project will use “single-cell sequencing” experiments, which will reveal the molecular processes of hair cell regeneration in chicks and fish with unprecedented resolution. Single-cell methods allow us to examine thousands of genes in hundreds of individually isolated supporting cells, some of which are responding to hair cell damage.

With these voluminous datasets, we will then describe the succession of molecular changes needed to regenerate hair cells. Results from these experiments will be compared with similar experiments examining hair cell damage in mice, which like all mammals, including humans, do not regenerate hair cells.

The second project will examine whether epigenetic DNA modification (the inactivation of genes by chemical changes to the DNA) is why mice supporting cells are unable to transform into hair cells after damage to the ear. Our existing data suggests this is the case, and so a strategy for hearing restoration may involve the reversal of these epigenetic modifications.

The first project will allow us to identify the genes involved, and the second project will help us understand how to effectively manipulate those genes despite their DNA modifications—and to biologically restore hearing.

The consortium approach funded by HHF provides a unique opportunity; the collaboration of 15 outstanding hearing investigators will lead to results far more quickly than traditional projects that rely on a single investigator. All HRP investigators plan projects and interpret data arising from them, allowing us to collectively utilize our 200-plus years of experience we have studying the ear.

HHF has been able to increase HRP funding for 2017 compared with 2016—for this I am grateful. However, there are several research needs unmet. Increased funding levels would speed our deeper understanding of hair cell regeneration, which will ultimately lead us to find therapies to treat human hearing loss and tinnitus.

Most of all, we are looking to add additional scientists to HRP labs to increase productivity and significantly accelerate research progress. There is also an urgent need for more “bioinformatics” scientists to thoroughly examine our data and identify common threads buried deep within our results. In addition, the HRP has research projects that have been placed on hold until funding is found for them.

We are excited about the coming year’s planned research, and eagerly await the results. On behalf of myself and the other scientists who make up the HRP, I thank you for your investment and interest in our work. I look forward to giving you further updates.

HRP scientific director Peter Barr-Gillespie, Ph.D., is the associate vice president for Basic Research and a professor of otolaryngology at the Oregon Hearing Research Center, and a senior scientist at the Vollum Institute, all at Oregon Health & Science University. 

We need your help in funding the exciting work of hearing and balance scientists.

To donate today to support HHF's groundbreaking research,

please visit hhf.org/donate.

New Insights Into Age-Related Hearing Loss

By Ruili Xie, Ph.D.

Age-related hearing loss (ARHL), also known as presbycusis, is one of the most prevalent health conditions affecting older adults. The leading cause of ARHL is generally attributed to damage in the ear during aging, which include the loss of the inner ear’s sensory hair cells and spiral ganglion cells (SGCs).  

Hair cells act like antennae for the auditory system to receive sound information from the environment. SGCs are the nerve cells that connect the ear and the brain, with their peripheral branches receiving sound information from hair cells, and their central branches forming the auditory nerve to pass information to the brain. Recent studies showed that the terminals (endpoints) of SGC peripheral branches are vulnerable and can be damaged during aging, which are thought to be the primary cause of ARHL.    

However, the majority (over 70 percent) of SGC peripheral terminals survive normal aging. It is unclear whether, with age, sound information is reliably transmitted through the surviving SGCs to the brain; and if not, how this may contribute to ARHL.

One particular point of interest lies in the terminals of the SGC central branches (the auditory nerve synapses) that activate their target neurons in the brain. Deterioration in the information flow at these synapses with age would reduce sensory input to the brain and lead to ARHL.

For the first time, Dr. Paul B. Manis and I have found that the transmission of information from SGCs to their target neurons in the cochlear nucleus (the first auditory station in the brain) is compromised in aged mice with ARHL. The transmission process deteriorates due to abnormal calcium signaling at the central terminals of the SGCs. The study not only proposes a novel brain mechanism that underlies ARHL, but also provides new strategies in developing future clinical treatments.

Ruili Xie, Ph.D., a 2009 and 2010 Emerging Research Grants recipient, is an assistant professor in the Department of Neuroscience at the University of Toledo, in Ohio.The study “Synaptic Transmission at the Endbulb of Held Deteriorates During Age-Related Hearing Loss” appeared in The Journal of Physiology on Sept. 13, 2016.

We need your help supporting innovative hearing and balance science through our Emerging Research Grants program. Please make a contribution today.

Educators Must Address Diabetes-Related Hearing Loss

By Susan Weiner, MS, RDN, CDE, CDN and Joanne Rinker, MS, RD, CDE, LDN

Hearing loss may not be commonly thought of as a complication of diabetes. How did you become interested in the condition?

As a diabetes educator, when I think of diabetes complications, I think of kidney, eye, heart and nerve damage. What I don’t think about is hearing loss. In 2012, a colleague asked me what screenings I do for my patients to determine if they have hearing loss. I realized I did nothing because hearing loss really was never on my radar. Then she asked me to think about how a patient who has diabetes might feel if they also had trouble hearing. I started to think about how hearing loss can not only make life more difficult, but could also lead to depression. For a diabetes patient who is already dealing with the pressures of a complicated disease, adding hearing impairment to the list of stressors would be devastating. So, I decided that this was something worth discussing with other diabetes educators.

How common is hearing loss among people with diabetes?

I did some research, and it turns out that nearly 26 million people in the United States have diabetes, and an estimated 36 million people have some type of hearing loss (17%). NIH has found that hearing loss is twice as common among people with diabetes as among those who don’t have the disease. Also, of the 79 million adults thought to have prediabetes, the rate of hearing loss is 30% higher than in those with normal blood sugar levels.

Research suggests that diabetes may lead to hearing loss by damaging the nerves and blood vessels of the inner ear. Autopsy studies of patients with diabetes have shown evidence of such damage.

A recent study from Handzo and colleagues found that women between the ages of 60 and 75 years with well-controlled diabetes had better hearing than women with poorly controlled diabetes, with hearing levels similar to those of women of the same age without diabetes. The study also showed significantly worse hearing in all women younger than 60 years with diabetes, even when the disease is well controlled.

Additionally, a study by Bainbridge and colleagues showed that 54% of people with diabetes had at least mild hearing loss in their ability to hear high-frequency tones, compared with 32% of those with no history of diabetes. And 21% of participants with diabetes had at least mild hearing loss in their ability to hear low- to mid-frequency tones, compared with 9% of those without diabetes.

People with diabetes are 2.3 times more likely to have mild hearing loss, defined as having trouble hearing words spoken in a normal voice from more than 3 feet away. But the effects of hearing loss go beyond the ability to detect sound. Hearing loss is shown to lead to sadness and depression increasing with severity of hearing loss; worry and anxiety, including periods of a month or longer when the patient reports feeling worried, tense or anxious; paranoia (“people get angry at me for no reason”); less social activity; and emotional turmoil and insecurity.

What can diabetes educators do to help patients with hearing loss?

Encourage diabetes patients to be screened routinely for hearing loss, just as they are for eye and kidney problems. Those with mild to severe impairment should be referred to an audiologist for more intense screening and treatment.

Treatment for hearing loss will typically start with a hearing aid. Often this will alleviate the problem. In about 10% of the population, medication may also be necessary, but most hearing loss is corrected with the introduction of a hearing aid. With improved hearing, patients will also likely experience increased alertness; improved job performance, memory and mood; less loneliness, fatigue, tension, stress, negativism and anger; better relationships and feelings about themselves; and greater independence and security — improved overall quality of life.

The bottom line is that diabetes educators must remember to add this to their diabetes education curriculum. They should know the resources in their area and have a process for referring patients to an audiologist who can do more extensive screenings as well as order and fit patients for hearing aids. Lastly, they should follow up with patients with hearing loss about overall quality of life. I am sure they will surprised how much adding this one aspect of care can benefit the lives of their patients.

References:

• Bainbridge KE, et al. Ann Intern Med. 2008;149(1):1-10.

• Handzo D, et al. Effect of diabetes on hearing loss. Presented at: Triological Society 2012 Combined Sections Meeting. Miami Beach, Fla.; Jan. 26-28, 2012.

• National Academy on an Aging Society. Hearing loss: a growing problem that affects quality of life. 1999. Available at: http://ihcrp.georgetown.edu/agingsociety/pdfs/hearing.pdf

This blog post orginally appeared on Healio.com on March 1, 2016. 

Joanne Rinker, MS, RD, CDE, LDN, is Senior Director for Community Health Improvement at Population Health Improvement Partners and the 2013 American Association of Diabetes Educators (AADE) Diabetes Educator of the Year. She has been elected to the AADE Board of Directors 2015-2018. She can be reached at jorinker@gmail.com.

Susan Weiner, MS, RDN, CDE, CDN, is the 2015 AADE Diabetes Educator of the Year and author of The Complete Diabetes Organizer and Diabetes 365 Tips For Living Well. She is the owner of Susan Weiner Nutrition PLLC and is the Endocrine Today Diabetes in Real Life column editor. She can be reached at susan@susanweinernutrition.com.

Can a Mutation Predict Ear Infections?

By Regie Lyn P. Santos-Cortez, M.D., Ph.D.

Otitis media or middle ear infection is a common disease in childhood; in the United States, it is the most frequent reason for antibiotic use in children and pediatric office visits. Typically when children have otitis media it is usually acute. This means the duration of infection since the start of symptoms is under two weeks, and there is inflammation such as redness of the eardrum and pus in the middle ear, with or without the perforation of the eardrum (a hole in the eardrum).

In such cases, what causes the infection is usually a common bacterium such as Streptococcus pneumoniae (“strep”) or Haemophilus influenzae (including type B, or Hib). The infection can become chronic, so there is a persistent perforation that may not heal and a chronic or recurrent ear discharge.

Otitis media is typically treated with antibiotics and may require surgery. If left untreated, it can lead to complications, the most common of which is hearing loss. Today, there is a preventative vaccination available for bacteria (strep and some Hib) that cause acute otitis media.

Aside from young age, there are many risk factors that contribute to otitis media, such as lack of breastfeeding, allergies, upper respiratory infection, daycare attendance or overcrowding, exposure to tobacco smoke, low socioeconomic status, and family history. Over the past few years, the availability of new sequencing technologies has sped up the identification of novel genes associated with disease including infections and immune states.

Through funding from Hearing Health Foundation, our group studied an indigenous Filipino community that is relatively homogeneous, highly intermarried, and has about a 50 percent prevalence of otitis media. In this population quantitative age, sex, body mass index, breastfeeding, tobacco exposure or swimming in deep seawater were not associated with otitis media. All members of the indigenous community have poor access to health care and low socioeconomic status.

By using next-generation sequencing in two indigenous second cousins who have chronic otitis media, we identified a mutation in the A2ML1 gene that is shared by the two cousins. This gene encodes a protease inhibitor localized to the middle ear epithelium. (An inhibitor is a compound that traps protease—an enzyme that breaks up protein—and brings it to other cell structures for clearance.)

In this study, we reconstructed a large pedigree of 37 indigenous relatives with different forms of otitis media, and showed that each relative with the mutation has an 80 percent chance of having any form of otitis media. When the study was expanded to 85 community members, the A2ML1 mutation was the only significant predictor of otitis media within the community, and carriage of the mutation increases the risk of otitis media almost four-fold. Our study was published in American Academy of Otolaryngology–Head and Neck Surgery Foundation's journal on August 2, 2016.

Among A2ML1 mutation carriers, otitis media may be diagnosed within the first months of life, with chronic otitis media occurring in later childhood and persisting well into adulthood, suggesting that the mutation affects otitis media onset and recovery. Furthermore, mutation carriers with chronic otitis media have higher relative abundance of the bacteria Fusobacterium and Porphyromonas, which are relatively uncommon for the disease.

Taken together, these findings are consistent with the role of A2ML1 protein as a protective factor in the middle ear; defective A2ML1 protein makes the middle ear mucosa susceptible to damage from proteases produced by both bacteria and inflammatory cells. The mutation of the gene means its protease inhibitor action fails to trap and clear damaging enzymes.

Remarkably the same A2ML1 mutation that was found in the indigenous Filipinos was also identified in three European and Hispanic-American children, indicating that this mutation is not limited to the Filipinos. (It’s possible the same ancestor from Spain, estimated to be 1,800 years ago, introduced the variation to these populations.) The three U.S. children who carried the mutation also had early-onset otitis media that required surgery by six months. Additionally we also identified rare A2ML1 mutations in six other otitis-prone children in the U.S.

We have established A2ML1’s involvement in otitis media susceptibility and can use this knowledge to predict otitis media occurrence in mutation carriers. Now we are expanding our research by studying DNA and/or microbial samples from additional U.S. and Filipino families, and RNA and additional microbial samples from the indigenous Filipino population. Our goal is to identify additional genes and pathways that play a role in otitis media susceptibility and that may be targeted to develop novel treatments of chronic otitis media.

Regie Lyn P. Santos-Cortez, M.D., Ph.D., is an associate professor in the Department of Otolaryngology, University of Colorado Denver, Anschutz Medical Campus. A 2011 and 2012 Emerging Research Grants scientist, she also received the 2012 Collette Ramsey Baker Research Award (in memory of Collette Ramsey Baker, HHF’s founder).

The study “Genetic and Environmental Determinants of Otitis Media in an Indigenous Filipino Population” was published in the journal of Otolaryngology–Head & Neck Surgery online on August 2, 2016.

Hearing Beyond the Hair Cell

By Yehoash Raphael, Ph.D.

Recently, it became clear that loud signals can also damage the connecting interface between the hair cell and the auditory nerve. This interface is the synapse. When the synapse is disrupted, hearing is impaired even without the loss of hair cells, leading to a condition called synaptopathy.

Experiments using transgenic mice showed that elevating levels of a specific molecule called NT3 in the area of the synapse can heal synaptopathy caused by exposure to loud noise. Since transgenic technology is a research tool not applicable for clinical use on humans, it is now necessary to design methods for elevating NT3 in human ears, leading to repair of synaptopathy. This is an important task, because if left untreated, synaptopathy progresses to include nerve cell death and permanent hearing deficits.

One potential way to increase NT3 concentration in the cochlea is by the use of gene transfer technology, which is based on infecting cochlear cells with viruses that are engineered to secrete NT3 and not cause infections. A potential risk of this method is that the site of NT3 is not restricted to the area of the synapses affected by the synaptopathy; NT3 can influence other types of cells.

In my lab at the University of Michigan, we tested the outcome of injecting such viruses on the structure and function of normal (intact) ears. We determined that the procedure resulted in the deterioration of hearing thresholds, and the auditory nerve and its connectivity to the hair cells were also negatively affected.

This negative outcome indicates that treatment of synaptopathy should be based on a more specific way to provide NT3 in an area restricted to the synaptic region. My work with the Hearing Restoration Project is dedicated to optimization of gene transfer technology in the cochlea, and may assist in finding more detailed methods for NT3 gene transfer that better target affected cells.

More information on Dr. Raphael’s research can be found in his report, “Viral-mediated Ntf3 overexpression disrupts innervation and hearing in nondeafened guinea pig cochleae,” published in the journal Molecular Therapy—Methods & Clinical Development on August 3, 2016.

Yehoash Raphael, Ph.D., is the The R. Jamison and Betty Williams Professor at the Kresge Hearing Research Institute, in the Department of Otolaryngology–Head and Neck Surgery at the University of Michigan.

New Player Identified in Hair Cell Development

By Betty Zou, Sunnybrook Research Institute

Sensory hair cells (red) and supporting cells (green) are intricately organized in the developed cochlea. Supporting cells have high levels of the Kremen1 protein, which is stained with a green fluorescent marker here. [Image courtesy of Dr. Alain Dabdoub]

There are roughly 37.2 trillion cells in the human body, each of which can be categorized into one of about 200 different types. What’s remarkable about this immense number and diversity of cells is that they all came from a microscopic cluster that comprises the embryo. Many of these early progenitor cells start out the same, but they receive different programming instructions along the way that enable them to replicate and differentiate to form various tissues and organs.

Signalling pathways are cellular communication systems that govern whether a cell keeps dividing or stops, where it goes and, ultimately, what it becomes. One such pathway is Wnt (pronounced “wint”) signalling, a group of signal transmission networks that play a critical role in embryonic development. Dr. Alain Dabdoub, a scientist in Biological Sciences at Sunnybrook Research Institute, is studying how Wnt signalling affects inner ear development and hearing. A new study by his team has shown for the first time that Kremen1, a poorly understood member of the Wnt network, plays a direct role in the formation of the cochlea, a spiral-shaped auditory sensory organ in the inner ear.

“We know that initially at the very early stages [of development], Wnt signalling pushes cells to proliferate,” says Dabdoub. “Then division stops and cell differentiation occurs. We’re trying to find out what promotes this high level of Wnt and also what decreases it.”

Kremen1 is a protein that sits on the cell surface where it receives and transmits signals to the cellular machinery inside. Previous studies have shown that it blocks Wnt signalling, so Dabdoub and his team decided to investigate whether Kremen1 is involved in cell differentiation in the cochlea.

The researchers found that at an early embryonic stage Kremen1 was present in the precursor cells that give rise to hair cells and supporting cells. Shortly thereafter, Kremen1 was only found in the supporting cells that surround hair cells. When the researchers forced the precursor cells to overproduce Kremen1, fewer of them went on to become hair cells and more became supporting cells. In contrast, knocking down levels of Kremen1 resulted in more hair cells. The results were published in August 2016 in the journal Scientific Reports.

The cochlea contains tens of thousands of hair cells, which have hair bundles on their surface to detect and amplify sound. In mammals, when these cells are damaged or destroyed, they are not replaced and hearing loss results. Supporting cells, on the other hand, remain abundant during an individual’s lifetime and do not appear to be affected by the insults that batter hair cells.

Dabdoub’s research seeks to understand how the cochlea and hair cells form, as well as how these sensory cells can be replenished to restore hearing. “If you think about regeneration, where are the cells that you’re going to regenerate coming from?” he says.

The survival of supporting cells makes them excellent candidates from which to regrow hair cells, but they must first replicate to ensure there are enough to maintain a stable number of supporting cells and form new hair cells. Dabdoub thinks that exploiting the proliferation-enhancing properties of Wnt signalling will help achieve this. His finding that Kremen1 plays an important role in cell fate decisions in the cochlea will be critical to future efforts to regenerate hair cells. “This is a molecule that we should keep an eye on as we work towards regeneration,” he says.

Funding for this study came from the Hearing Health Foundation’s Hearing Restoration Project, Koerner Foundation and Sunnybrook Hearing Regeneration Initiative.

This blog was reposted with the permission of Sunnybrook Research Institute.
 

We need your help in funding the exciting work of hearing and balance scientists.

To donate today to support HHF's groundbreaking research,

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A Balancing Act

By Morgan Leppla

Balancing is pretty great. Not needing to think about how to stand upright is something I yield great benefit from, but is something that occurs without conscious effort or thought. I am fortunate, but many are not. This week is Balance Awareness Week, and HHF is highlighting the the inner ear and its mechanics!

The inner ear is a tiny but notable body part; not only is it important to hearing, but it is also where the balance organs and nerves are located.

The basic components of the inner ear include semicircular canals, the cochlea, the utricle, the saccule, and the vestibulocochlear nerve. The cochlea and one half of the vestibulocochlear nerve (the cochlear nerve) are in charge of hearing. The remaining semicircular canals, utricle, saccule, and vestibular nerve are responsible for balance.

There are three semicircular canals that contain fluid to activate sensory hair cells, which are arranged at ninety degree angles and detect different kinds of movement: up and down, side to side, and tilting. The utricle connects the semicircular canals to the saccule, which also detect motion. They are located in the vestibule inside of the labyrinth, which is the bony outer wall of the inner ear. All of this is the vestibular system.

But it is not only the vestibular system that assists with balance. Vision and sensory receptors (muscles, joints, skin, etc.) all transmit messages to the brain that work together and voila! balance.

Vestibular disorders can have a big effect on one’s equilibrium. People might experience dizziness, vertigo, or imbalance, as well as other inner ear-related issues. A commonly diagnosed  balance disorder is Meniere’s disease, which is one focus areas for our Emerging Research Grant (ERG) recipients.

Balance disorders can disrupt everyday life for those who experience them. It is also fairly common - in fact, about 69 million Americans or 35% of adults aged 40 and up have experiences vestibular dysfunction at some point in their life!

While it might be hard to believe something as tiny as the inner ear can affect a person’s ability to participate fully in daily life, HHF is fully committed to funding research that explores hearing and balance health.

Donate today to support groundbreaking research! 

We need your help in funding the exciting work of hearing and balance scientists.

Emerging Research Grants: 2017 Application Period is Now Open

Noise-Induced Brain Inflammation May Result in Painful Hearing

By Drs. Senthilvelan Manohar, Kelly Radziwon, and Richard Salvi

What do jet engines, sirens, and rock bands have in common? The sounds they emit are so intense that they are not only loud, but also painful, sometimes evoking a painful sensation around the external ear. The acoustic threshold for pain, 130-140 dB SPL, is intense enough to destroy or damage the delicate sensory hair cells, supporting cells and auditory nerve fibers in the inner ear. The axons from the auditory nerve deliver their messages to neurons located in the cochlear nuclei in the brainstem. 

In a recent paper published in Molecular and Cellular Neuroscience, Drs. Baizer and Manohar at the University at Buffalo were surprised to find that intense noise exposures that destroyed the sensory hair cells in the rat inner ear led to a prolonged period of auditory nerve fiber degeneration in the cochlear nucleus in the brainstem (Bazier et al., Neuroscience 303 (2015) 299–311). Nerve fiber degeneration was still occurring 6-9 months post-exposure, nearly a third of the rat’s lifespan. In brain regions where the fibers were degenerating, there was robust upregulation of brain immune cells (microglia), indicative of long-term neuro-inflammation triggered by the release of inflammatory molecules in the brain. Since sensory nerve fibers (e.g., pain, touch) from the face, head, neck and shoulders (facial, trigeminal and spinal nerves) enter the cochlear nucleus, the long-term neuro-inflammation occurring in this region could lower pain thresholds (hyperalgesia). If this were to occur, much lower, moderate-intensity sounds (60-80 dB) might be sufficient to cause hyperacusis (loudness intolerance) with ear pain.

With funding from the Hearing Health Foundation obtained by Drs. Radziwon* and Manohar to identify pain-related molecules in the auditory pathway as a result of noise exposure, Drs. Manohar, Adler, and Salvi carried out a second study in which they measured noise-induced changes in the expression (amount) of genes involved in the synthesis of proteins known to be involved in neuropathic pain and neuro- inflammation. Interestingly, the researchers found that intense noise exposure significantly altered the expression of six genes (Ccl12, Tlr2, Oprd1, II1b, Ntrk1 & Kcnq3) in the cochlear nucleus (Manohar et al., Molecular and Cellular Neuroscience 75 (2016) 101–112). These results suggest that noise-induced inflammation in the parts of the central auditory pathway that also processes sensory information related to pain might, in turn, activate the central pain pathway thus producing ear pain. Determining whether neuro-inflammation is directly responsible for ear pain will open the door for novel interventions to treat hearing loss and hyperacusis.

*Kelly Radziwon, Ph.D., is a 2015 Emerging Research Grants recipient. Her grant was generously funded by Hyperacusis Research Ltd. Learn more about Radziwon and her work in “Meet the Researcher.”
 

We need your help in funding the exciting work of hearing and balance scientists. Donate today to Hearing Health Foundation and support groundbreaking research: hhf.org/donate.