by Neil Bauman, Ph.D.
February 8, 2017
Perhaps you have heard the relatively-new term “hidden hearing loss” (coined in 2009) and wondered, “What in the world is hidden hearing loss?” After all, aren’t all hearing losses hidden? Since you can’t see a hearing loss, of course it’s hidden. So why are researchers finally getting concerned about hidden hearing loss?
Introduction
The hidden hearing loss that researchers are talking about is not about how to help us (hard of hearing people) better cope with our invisible hearing losses. Rather, hidden hearing loss is the new term researchers are using to describe hearing losses that do not show up on conventional audiograms, but are nevertheless very real.
Traditionally, audiologists have diagnosed hearing loss based on the increase in the sound level required in order to hear a series of tones produced by an audiometer. These results are plotted on an audiogram. This is the gold standard test used to determine hearing loss. (1) If your hearing loss does not show up on a standard audiogram, you have a hidden hearing loss.
Your first response is likely, “How can that be? How can you have a hearing loss that doesn’t show up on an audiogram?” That’s what audiograms are for—to show your degree of hearing loss—right?
You are correct—most of the time—but there are exceptions that do not show up on an audiogram. You see, there are a number of kinds of hidden hearing losses including auditory neuropathy and central auditory processing disorders for two. As Dr. Zeng explains, “At least some people with either of these disorders can have normal audiograms, yet still have impaired hearing function, especially those related to temporal processing [the timing of speech] and speech recognition [understanding what was said].” (2)
A third kind of hidden hearing loss is the current audiometric practice of only testing hearing up to 8,000 Hz. For example, you could have your hearing tested and show perfectly-normal hearing in the conventional testing frequencies between 125 Hz and 8,000 Hz, yet still have a severe hearing problem.
This is because your audiologist did not test your hearing between 8,000 Hz and the upper limit of human hearing (around 20,000 Hz). If you have a hearing loss in these higher frequencies and it’s not tested, it is essentially hidden.
Fortunately, it is easy to “unhide” this kind of hidden hearing loss. All your audiologist needs to do is test your hearing to the highest frequency you can hear. I’ve been advocating testing these high frequencies for almost two decades, but audiologists seem to be totally set in their ways and choose not to see the value of such high-frequency testing, or have been brainwashed into thinking such high-frequency testing is not necessary.
I think it is vital to test your high-frequency hearing because high-frequency testing often provides an early warning of impending hearing loss in the conventionally-tested frequencies below 8,000 Hz. You see, hearing loss very often starts in the highest frequencies you can hear and works its way down the frequency spectrum. A good example of this in action is progressive hearing loss resulting from taking ototoxic drugs, from excessive noise exposure and from the effects of aging.
Noise-Induced Hidden Hearing Loss
Recently, a fourth kind of hidden hearing loss has come to light. This hearing loss goes by the name of “Noise-Induced Hidden Hearing Loss” (NIHHL).
Noise-induced hidden hearing loss may be a bit of a misnomer because it refers to any functional impairment seen in people who have exposed their ears to louder noise, but have not had a resulting permanent hearing loss (what doctors call a permanent threshold shift [PTS]).
Unlike audiograms that disclose the degree of hearing loss from exposing your ears to loud sounds that results in a permanent threshold shift, this hearing loss hides behind normal audiograms. (1, 3)
Since there is no change in hearing sensitivity (no permanent threshold shift), these functional deficits cannot be detected using routine audiological evaluations and may be unknown to the people who have them—thus the moniker “hidden hearing loss”. (4)
This is different from the conventional definition of noise-induced hearing loss (NIHL), which is based on changes in hearing sensitivity resulting in a permanent threshold shift and is thus visible on an audiogram. (4)
A typical scenario might be where you go to an audiologist complaining that you can’t hear speech well when there is background noise present. You may even bring a family member with you who confirms that this is true. Or you may have a child whose school teacher is concerned that she isn’t hearing well in the classroom.
After pure tone and word recognition testing, the audiologist explains that your hearing thresholds (or your child’s) are within normal limits. In other words, as far as they are concerned, you have normal hearing.
If you are elderly, you might have a slightly different scenario. Your audiogram may show that you have some degree of high-frequency hearing loss—but that your degree of hearing loss is not consistent with the severity of your hearing complaints.
Based on the results of your hearing testing, your audiologist may confidently tell you, “your hearing testing shows that you have normal hearing”.
Audiologist Dr. Hall explains, “In most such cases, this statement is inaccurate, misleading, and of no comfort to people and their families who are convinced that they have a real and serious hearing problem.” (5)
He adds, “A more appropriate response would be: ‘The results of your simple hearing test were within normal limits. Now, we’ll conduct a comprehensive evaluation of your hearing, including tests that measure how your ears and your brain process sound’.” (5)
The truth is, complaints of difficulty understanding speech in the presence of background noise are not uncommon in people with normal audiograms. (2) This is why people who have normal audiograms, but who also have noise-induced hidden hearing loss can hear just fine in quiet situations, but have difficulty understanding speech in noisy situations as compared to people with normal audiograms who do not have noise-induced hidden hearing loss.
Noise-induced hidden hearing loss can start at a young age. It is more likely to affect young people who attend loud music concerts, who frequent loud nightclubs or who spend time listening to loud music through headphones. (6) Note this well—every time you go to loud concerts or use loud power tools without ear protection, you may be losing cochlear nerve fibers and increasing your degree of hearing impairment. (7)
Once you have noise-induced hidden hearing loss, you’ll find it adversely affects your ability to detect high-frequency sounds and to hear in noisy settings. You won’t notice this hearing loss in quiet places, but you’ll struggle when you’re in bars or restaurants where there’s a lot of background noise present. (6)
Another insidious characteristic of noise-induced hidden hearing loss is that if you have noise-induced hidden hearing loss earlier in life, it leaves you more vulnerable to more severe permanent hearing problems as you get older. (8) For example, it accelerates the further loss of hair cells and cochlear neurons as you age, even in the absence of further ear abuse. (3)
In addition, it also leaves you vulnerable to auditory processing disorders in the future. (9) This is predicated on animal studies that have shown inner ear damage caused by loud noises can predict worsening hearing loss as you age, even without the death of hair cells. (10)
Hidden Hearing Loss Basics
In order to understand noise-induced hidden hearing loss, you need to learn some lesser-known facts about how your inner ears work.
Auditory Nerve Fibers
The auditory nerve goes from the cochlea in your inner ear to the auditory circuits in your brain. Your auditory nerve consists of two kinds of nerve fibers—afferent and efferent fibers. Afferent auditory nerve fibers send sound signals from your inner ears to your brain where your brain processes them as sound. When your brain want to tell your inner ears to focus on certain sounds, it sends messages to your inner ears via efferent auditory nerve fibers. The easy way to remember this is that the “A” in Afferent means “Away from” the ears and to your brain.
There are two kinds of afferent auditory nerve fibers—high-spontaneous-rate and low-spontaneous-rate nerve fibers.
High-spontaneous-rate nerve fibers activate in quiet situations. They are responsible for your hearing sensitivity to quiet sounds, and are saturated by high-level background noise. (4)
Low-spontaneous-rate nerve fibers activate in noisy situations and are critical for hearing in noisy environments due to their larger dynamic range, higher thresholds and their ability to follow the fast-changing amplitude of sound signals. (4)
Unfortunately, low spontaneous rate auditory nerve fibers are more vulnerable to noise damage than are the high spontaneous rate fibers. (4)
Knowing this is critical to understanding noise-induced hidden hearing loss.
Collectively, all the nerve fibers in the cochlea are called the spiral ganglion. Think of the spiral ganglion as underlying the hair cells and connecting them to the auditory nerve.
Synapses and Synaptopathy
Individual nerve fibers consist of a series of cells called neurons. Between each neuron there is a synapse. Synapses are tiny “gaps” between adjacent neurons, or between neurons and others sensory cells such as hair cells, that “fire” to transmit their sound signals across these gaps. This is how your body moves messages up and down your nerves and around in your brain—from neuron to neuron via the synapses between them.
Each synapse has a presynaptic dense body called a ribbon on the one side, and a postsynaptic nerve terminal on the other side. (4) When either of these structures is damaged, the synapse won’t work.
The synapses between the inner hair cells and the primary spiral ganglion neurons are very sensitive to noise. Noise exposure causes damage to both the presynaptic ribbons and postsynaptic nerve terminals of the ribbon synapses. The damaged synapses exhibit various degrees of swelling of the terminals. This results in disruption of the synaptic connections between the inner hair cells and the spiral ganglion neurons. (4)
The fancy medical term for synapses that do not work properly is synaptopathy [sih-NAP-toe-path-ee]. It should be no surprise then, that cochlear synaptopathy is the medical term that tells you there is damage to the auditory nerve fibers (neurons) where they connect to the sensory “hair cells” inside the cochlea. Sometimes doctors refer to this condition as cochlear neuropathy, which is a more general term than cochlear synaptopathy.
With synaptopathy, the synapse is damaged such that it won’t fire and transmit sound signals. When a neuron fails to transmit a sound signal via a synapse from its corresponding hair cell, this sound signal is lost as it is not transmitted to the brain.
Fortunately for us, our bodies can often repair these damaged synapses. For example, in one study, the average number of ribbon synapses per inner hair cell was 16.7. One day after exposure to noise that did not cause permanent hearing loss, the average number of working ribbon synapses per hair cell dropped to 9.2, a reduction of 45%. At the end of one week, some synapses had recovered such that the number of working ribbon synapses per hair cell had climbed to 12.8. At the end of the first month, the number of working ribbon synapses per hair cell reached 13.8. This was still 17.3% below normal, even though no inner hair cells had died at this point. (11)
The fact that hearing thresholds can drop and then recover within hours or days after you expose your ears to loud sounds doesn’t mean that all components in your inner ears have completely recovered. (7)
In this study, click-evoked compound action potential (CAP) testing (measured in microvolts) revealed a reduction in voltage corresponding to the reduction in ribbon counts. For example, one day after noise exposure, the compound action potential had dropped by a whopping 87.2%. Fortunately, one month later, the compound action potential values had recovered so they were only down 22.6%. This indicates that many, but not all, of the disrupted synapses re-established their connections. (11)
“The change in the amplitude of the compound action potential corresponded to the changes in ribbon counts: a large initial reduction in CAP amplitude and synapse counts were followed by a significant recovery after the noise exposure.” (4)
These data show that after loud noise exposure, your body attempts to repair any resulting damage to the synapses. Many of the damaged synapses are re-established, and begin working again. That’s the good news. The bad news is that unfortunately, these repairs are not always completely functional, and thus the synapses no longer work normally. Part of the synaptopathy in noise-induced hidden hearing loss is likely related to this faulty synaptic repair after initial damage by noise, rather than just from the initial loss (breaks) in the synapses. (4)
Sound Processing
Anything that interferes with the processing of sound signals in your cochlea or the auditory parts of your brain results in difficulty in hearing and understanding speech and other sounds.
Louder sounds primarily damage or destroy the synapses to the slow-response-rate afferent auditory nerve fibers which are known to be vital for signal coding in noisy backgrounds. (4) This results in two kinds of impaired sound processing.
Sound Intensity Coding: Your body’s ability to encode sound intensity and to follow quick changes in the amplitude of sounds is called intensity coding. Exposing your ears to louder sounds damages the ability of the low-spontaneous-rate auditory nerve fibers to encode sound intensities accurately. (4)
Temporal Coding: In addition to incorrectly coding the amplitude of sounds, damaged synapses may also delay the timing when encoding sound signals in people with noise-induced hidden hearing loss. This is because damaged synapses have less efficient neurotransmitter release. (4)
These temporal processing difficulties are the result of functionally abnormal synaptic repair after the initial damage. (4) This means that if the low-spontaneous-rate auditory nerve fibers are damaged, you will not hear as well as you used to in noisy environments. And since the high-spontaneous-rate auditory nerve fibers are not as sensitive to louder sounds, they are not damaged much or at all. The result is that you hear normally in quiet situations, but have difficulty understanding speech in noise. This is noise-induced hidden hearing loss in action.
Plastic Reorganization in Your Brain: When synapses are destroyed, whether or not you have hearing loss, your auditory nerve sends fewer auditory signals to your brain. In fact, noise-induced hidden hearing loss first manifests itself as reduced output of the auditory nerve at high sound levels, without affecting the hearing threshold. (4) This means your brain is not receiving all the sound signals in normally would.
This lack of input to your brain, in turn, results in your brain reorganizing itself (plastic reorganization of the brain). (4) In this case, this is not a good thing. For more information on the detrimental effects of plastic reorganization of your brain, see my article “Constraint-Induced Sound Therapy for Sudden Sensorineural Hearing Loss”.
The Insidious Nature of Noise-Induced Hidden Hearing Loss
Research over the past few decades has shown that when we overexpose our ears to loud sounds, this loud noise can destroy the delicate hair cells and nerve fibers in our inner ears without causing us any pain or providing us with any other obvious warning signs apart from sometimes causing tinnitus (making our ears ring). (7) When hair cells die, they can no longer convert the mechanical wave motion in the cochlea into electrical impulses. Thus, those sounds are not transmitted to our brains. When this happens, we have noise-induced hearing loss.
Unfortunately, in our modern society, our ears are constantly bombarded by loud noises capable of doing permanent damage to our inner ears. Listening to extremely-loud sounds can instantaneously cause permanent hearing loss due to the death of some hair cells. Most people know this.
What many people do not realize is that exposing our ears to sounds greater than 80 – 85 dB, but not so loud that they cause instant hearing loss, can also cause permanent hearing loss over time. Whether it be days, weeks, months, years or decades, the result is still the same. These louder sounds result in hair cells eventually dying. When they die, we no longer hear the frequency of sounds they used to transmit to our brains. These kinds of hearing losses also show up on our audiograms if they occur in the frequencies below 8,000 Hz. They are not hidden.
However, exposing our ears to loud sounds that do not result in death to hair cells can still cause hearing problems. For example, say you go to a loud concert, night club, ball game or other sports event. When you come out you notice your ears are ringing and everything sounds muffled. This is because you now have a temporary hearing loss (what doctors call a temporary threshold shift). In a few hours, the muffled feeling goes away (and hopefully the tinnitus) and your hearing returns to normal.
For decades, doctors thought that as long as a conventional audiogram showed your hearing had returned to normal, everything was “hunky-dory” (6)—that there wasn’t any permanent damage. Now, researchers are realizing this is just not true. Everything isn’t ok. Some hidden hearing loss has indeed occurred.
You see, in the past, the dogma was that the hair cells in our inner ears are the most vulnerable cells to noise damage, and when the hair cells die, we have noise-induced hearing loss. Then, sometime after the hair cells have died, since they don’t have “jobs” anymore, the corresponding neurons in the underlying spiral ganglion also begin to die. (3)
However, researchers have now discovered that the nerve fibers in the spiral ganglion are even more vulnerable to noise damage than are the hair cells themselves. (7) More specifically, when noise damage occurs, it is the synapses between the hair cells and the cochlear nerve terminals in the spiral ganglion that degenerate first.
The reason that researchers previously had thought that hair cells were the most sensitive to noise damage was because they could detect hair cell loss just hours after ears were exposed to loud sounds. In contrast, they could not detect any loss of spiral ganglion neurons until months or even years later. (3)
Because of this, researchers assumed sounds that caused a temporary threshold shift weren’t anything to worry about since these sounds seemingly didn’t result in any permanent hearing loss.
What researchers didn’t know up to this point is that sounds that aren’t so loud that they cause permanent hearing loss can, and do, damage our ears. Doctors Sharon Kujawa and Charles Liberman of the Massachusetts Eye and Ear Infirmary discovered that brief noise exposure that causes a temporary threshold shift can indeed cause dramatic and permanent physical damage to our inner ear structures, even when our hair cells recover and our hearing returns to normal. (3)
It appears that the fundamental cause of noise-induced hidden hearing loss is related to the destruction or malfunction of the synapses between the hair cells and underlying spiral ganglion neurons in the inner ear (cochlear synaptopathy).
Theoretically, you can have a normal audiogram and normal hair cell function despite a profound loss of the neural infrastructure that is critical for auditory processing in noise. (9)
One of the insidious things about noise-induced hidden hearing loss is that this synaptic damage actually starts long before your hair cells themselves die from the results of any loud noise. (1) First, there is damage to the synapses in the auditory-nerve neurons that connect to hair cells and help you hear in noisy environments—hence the “hidden” in hidden hearing loss. (6)
Although no hair cells may have died, what happens next is even more insidious. The loud sounds destroy many of the synapses between your hair cells and your auditory nerve fibers. When the synapses don’t work, you can’t get the messages from your inner ear hair cells to your auditory nerve fibers—and thus your brain can’t process those sounds.
I can hear you asking, “If the synapses are destroyed so the sound signals can’t jump across the synaptic gaps, how come this doesn’t show up on a conventional audiogram, and why can I still seem to hear perfectly?”
This is where the insidious nature of this hearing loss comes in. Here’s what actually happens—as far as researchers know at this point.
There are two kinds of nerve fibers—ones that transmit sounds generated in quiet situations, and ones that transmit sounds generated under noisy conditions.
The most vulnerable cochlear neurons to both noise and aging are those in the high-threshold, low-spontaneous-rate nerve fibers. These low-spontaneous-rate fibers do not contribute to threshold detection in quiet, but, by virtue of their high thresholds, are key to the coding of speech sounds in the presence of continuous background noise. Thus, low-spontaneous-rate fiber loss appears to be a major factor to the classic problem in people with sensorineural hearing losses, namely, difficulty understanding speech in noisy environments.(3) When noise damages or destroys synapses on these nerve fibers, your brain receives lesser and poorer information from your ears. Therefore it struggles to interpret the information correctly. (8)
Thus, when you try to hear in situations where there is a lot of background noise, you can’t understand what people are saying. Everyone else can understand, but not you, because the synapses that carry sound signals in noise are now largely destroyed. That’s when your noise-induced hidden hearing loss finally comes to light.
In contrast, the synapses in the low-threshold, high-spontaneous-rate nerve fibers that transmit sounds to your brain in quiet situations typically are not damaged or just a few are damaged. That is why, when your audiologist tests your pure tone hearing in the acoustically-quiet sound booth, you get a “perfect” score.
How Did Noise-Induced Hearing Loss Remain Hidden for So Long?
How did noise-induced hidden hearing loss remain “hidden” for so long? According to Dr. Liberman, there are two key reasons.
First, this phenomenon remained obscure for so long because, until recently, no one realized that you can lose up to 90% of the afferent nerve fibers in your cochlea without a change in your ability to detect a tone in quiet. This is because a hearing test administered in a quiet room does not activate the low-response-rate auditory nerve fibers that are often damaged by noise.
Rather, such hearing tests only test the high-response-rate auditory nerve fibers that are activated in quiet situations. This is because hearing tests are looking for the softest sound intensity you can hear—a tone in quiet—as the basis for determining your degree of hearing loss. (7) Thus, they do not pick up on this damage. The result is that people can easily pass a hearing test, even though many of the synapses on these slow-response-rate auditory nerve fibers have been damaged or destroyed. (6)
Second, the loss of synapses remained “hidden” because, although the loss of synapses is immediate, the synapses between the nerve terminals and the hair cells, up to now, have been very difficult to see. To overcome this, researchers now use a special stain to stain the synapses. This way, they can see and easily count the synapses using a light microscope. “This enabled them to view a large number of synapses on hair cells in a normal ear, as well as the greatly reduced numbers of synapses on hair cells following noise exposure that caused only a transient elevation of thresholds [temporary hearing loss].” (7)
Each missing synapse represents a cochlear nerve fiber that has been disconnected from the nervous system. Researchers now know that in noise-exposed ears showing no hair cell loss, the cochlear nerve no longer responds to sounds like it did before (12) because these louder sounds have decimated the number of synapses in the spiral ganglion. (4) The truth is that up to 50% of the synapses between the inner hair cells and the primary afferent auditory nerve fibers can be lost. (3) When these synapses can no longer function, not only do their signals not get sent to our brains, but also, within a few months or years, the rest of the neuron will slowly degenerate and disappear (7) if the synaptic connections are not reestablished. (4)
Furthermore, this synaptic damage is insidious because the degeneration of these cochlear neurons does not cause changes in behavior or in electrophysiological thresholds until it becomes extreme. (3)
Noise-Induced Hidden Hearing Loss Is Both Common and Widespread
By the very nature of it being “hidden”, noise-induced hidden hearing loss very likely is grossly under-diagnosed. It affects both people with supposedly normal hearing and also hard of hearing people.
Noise-induced hidden hearing loss is especially widespread among young people who regularly abuse their ears in spite of their having normal audiograms. (3)
In one study to prove how common this is among young adults (college age students), researchers divided 34 college volunteers into two groups: a low-risk group composed of students studying “quiet subjects” (such as communication science) and a high-risk group mostly consisting of music students exposed to loud sounds for four to six hours per day.” (6)
Those who did not protect their ears during their noisy activities had the same level of hearing sensitivity and the same ability to understand speech in quiet environments as those who routinely protected their ears. In other words, both groups passed their basic audiograms with flying colors.
“While hearing sensitivity was the same across all subjects, there was reduced responses from the auditory nerve in participants exposed to noise on a regular basis and, as expected, that loss was matched with difficulties understanding speech in noisy and reverberating environments.” (1)
However, when the researchers measured the high-frequency thresholds (from 8–16 kHz), because that is where the first signs of noise-induced hair cell damage show up, the high-risk students showed significant hearing loss at all test frequencies above 8 kHz, (a hearing loss averaging 20 dB at 16 kHz). This high-frequency hearing loss is consistent with early noise damage. (3)
This is another good reason why hearing testing should be conducted in the high frequencies above 8,000 Hz and up to the highest frequency the person can hear. Otherwise, you and your audiologist are missing the incipient warnings of hearing loss.
Furthermore, high-frequency hearing testing might inspire young people to regularly use ear protectors to prevent future hearing loss from louder sounds, especially since other studies have shown that noise exposure causes accelerated age-related hearing loss in the future. (3) So not only will young people have more trouble hearing and understanding speech now, but they are setting themselves up for even more hearing loss as they get older.
Not only that, the high-risk young adults with substantial noise exposure history showed significantly poorer performance on word recognition in noise or with time compression and reverberation. In short, the high-risk group, on average, reported more difficulty hearing and understanding speech in noisy backgrounds (3) and at lower volumes. (6)
Incidentally, the researchers determined that the high-risk group’s difficulty in understanding speech in noise was not due to their loss of hearing in the higher frequencies, but was related to the damage done to their synapses. (3)
Hyperacusis and Tinnitus
Noise-induced hidden hearing loss (the loss of neurons and synapses) may also cause you to become overly sensitive to normal sounds (hyperacusis) and may cause tinnitus (ringing in your ears). (3. 10)
When asked to rate the loudness and annoyance of 12 everyday sounds, students in the high-risk group (in the above-mentioned study) demonstrated significantly heightened sound annoyance and avoidance symptoms. (12) For example, they indicated they were more ‘bothered’ by everyday sounds like a dog barking or a baby crying than the low-risk group was. (6) Thus, they rated these sounds as louder, and more annoying, and tended to avoid noisy environments. (3) In other words, they had developed hyperacusis to some degree. (12)
This is because when numbers of synapses are lost (cochlear synaptopathy), fewer signals are sent to your brain. One of the things that then happens is an imbalance between excitation and inhibition—in other words, the auditory circuits in your brain become hyperactive and/or hyper-responsive. The result is that there is an increase in central gain (you now hear things louder) and thus may begin hearing tinnitus sounds as well as hearing everything too loud (hyperacusis). (1, 3, 4, 12)
For example, one study reported that an increase in central gain was responsible for tinnitus in people with typical damage seen in noise-induced hidden hearing loss (i.e., reduced auditory nerve input to the brain as measured by a smaller auditory brainstem response [ABR] wave I and an increase in the wave V/I ratio) but normal hearing. (4)
In another study using rats, researchers found tinnitus six months after they exposed the rats to noise that caused minimal permanent hearing loss but significant loss of auditory nerve fibers (and thus synapses). (4)
How Can You Tell If You Have Noise-Induced Hidden Hearing Loss?
Diagnosing noise-induced hidden hearing loss requires new “tools”. One way to diagnose this kind of hidden hearing loss is to closely examine Wave I in Auditory Brainstem Response (ABR) testing.
As Dr. Zeng explains, “When all other tests are normal, including the audiogram, otoacoustic emissions, and even Wave V of the ABR, a missing or diminished Wave I would suggest a reduced number of auditory nerve fibers in the human ear.
Reliable and accurate ABR recording also will help differentiate the condition from other forms of hidden hearing loss, such as auditory neuropathy, which usually affects both Waves I and V.” (2)
Researchers found that people with tinnitus and normal hearing had reduced wave I amplitudes on their auditory brainstem response (ABR) tests. This reduced wave 1 amplitude represented the sum of the reduced activity of the cochlear nerve. (12)
“Present data suggest that a combination of ear-canal electrocochleography, high-frequency audiometry and word recognition tasks can possibly identify the earliest signs of noise damage to hair cells and neurons [noise-induced hidden hearing loss], neither of which is detected by standard audiometry.” (3) To this I’d add, if you have normal hearing, yet have tinnitus and/or hyperacusis, these are two more symptoms indicating that you likely have noise-induced hidden hearing loss.
Treating Noise-Induced Hidden Hearing Loss
What can we do about noise-induced hidden hearing loss? First we need to teach young people (and adults too for that matter) that exposing themselves to noise levels that they don’t think of as being extreme can impact their hearing for the rest of their lives. (6) The truth is, noise exposure causing noise-induced hidden hearing loss occurs frequently in daily life and impacts much of the general population. (4) Thus, each person needs to protect himself from noise-induced hidden hearing loss by limiting his exposure to louder sounds and wearing ear protection when this is not possible. (6)
Furthermore, we need to revise our current standards regulating noise in the workplace. (6) This is necessary because all of our federal safe noise exposure levels are based on the likelihood that noise exposure above a given level will result in permanent hearing loss. Thus, they assumed that all noise exposure below that level would not cause permanent hearing loss and consequently would be safe. (3, 4) We now know that this is incorrect—hence the need to revise noise exposure regulations and base them on this new knowledge. (7)
“Fortunately, even after noise-induced hidden hearing loss has occurred, the picture is not entirely bleak.” (6) It appears there is a long therapeutic window within which the sensory cells and sensory neurons could be reconnected. (3)
“Since the ultimate death of neural cell bodies and axonal projections to the brain is so slow, it appears there may be enough time to “elicit sprouting of the nerve terminals to reestablish synaptic connections between neuron and hair cell,” according to Dr. Liberman. (7)
For example, the evidence indicates that, to some degree, our bodies can repair the resulting damage to the connections between the sensory cells and the auditory nerve (ribbon synapses) caused by noise that did not result in permanent hearing loss, although the repairs may not be complete. (4)
Under some conditions, certain growth factors can help our bodies repair the damage to the ribbon synapses. Research has shown that a class of secreted growth-factor proteins called neurotrophins plays a key role in the survival of cochlear nerve fibers. (1, 7) For example, treating “the ears of mice exposed to loud sounds with Neurotrophin 3 helped reverse noise-induced hidden hearing loss by repairing some of the damage to auditory nerve fibers.” (6)
Researchers “described a significant attenuation of the impact of noise trauma to ABR wave I amplitudes and cochlear synaptic populations with round-window delivery of neurotrophins.” This could provide neurotrophic support to the spiral ganglia. (12)
Indeed, recent animal research has reported regeneration of cochlear nerve synaptic connections with inner hair cells after noise exposure, along with corresponding functional recovery, using neurotrophin-based therapies. (3)
As it turns out, Neurotrophin 3 (NT3) helps establish ribbon synapses that link the hair cells in our inner ears to nerve cells in our brains. (13) When exposed to loud noise, these ribbon synapses break, resulting in loss of hearing clarity in noise.
Incidentally, normal aging can also damage our ribbon synapses, so NT3 therapy may help counteract normal age-related hearing loss as well. (13)
While researchers are looking for a drug solution to raise NT3 levels, a Chinese study suggests astaxanthin could be used for this purpose. Astaxanthin is believed to be one of the most potent antioxidants nature has to offer, and exhibits very strong free-radical scavenging activity that protects your cells, organs and body tissues from oxidative damage. (13)
According to Dr. Mercola, “there are only two main sources of natural astaxanthin—the microalgae that produce it (Haematococcus pluvialis), and the sea creatures that consume the algae, such as salmon, shellfish and krill.” He advises, “If you decide to give astaxanthin a try, I recommend starting with 2 mg per day.” (13)
Research has also shown that, “in addition to NT3, brain-derived neurotrophic factor (BDNF) also plays an important role in the development and survival of auditory neurons in your brain. One 1996 study found that loss of auditory hair cells and auditory neurons can be prevented by therapies that boost either NT3 or BDNF.” (13)
Interestingly, one lifestyle factor that naturally boosts BDNF is exercise. Dr. Mercola wonders, “It’s intriguing to speculate whether exercise may also help prevent hearing loss through this mechanism.” (13)
Rather than wondering or worrying whether some treatment or other will help restore your damaged auditory neurons, just do the smart thing and protect your ears from sounds louder than 80 – 85 dB. Then you won’t have any problems in this regard.
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(1) Massachusetts Eye and Ear Infirmary. Evidence of “Hidden Hearing Loss” in College-Age Human Subjects. ScienceDaily. ScienceDaily, 12 September 2016.
(2) Zeng, Fan-Gang. 2015. Uncovering Hidden Hearing Loss. The Hearing Journal.
(3) Liberman, Charles, et. al. 2016. Towards a Differential Diagnosis of Hidden Hearing Loss in Humans.
(4) Shi, Lijuan, et. al. 2016. Cochlear Synaptopathy and Noise-Induced Hidden Hearing Loss.
(5) Hall, James. Hidden Hearing Loss: An Audiologist’s Perspective. The Hearing Journal. Volume 1, Number 1, January, 2017.
(6) Caruso, Catherine. 2016. Can You Hear Me Now? Detecting Hidden Hearing Loss in Young People. Scientific American.
(7) Acoustical Society of America (ASA). Noise-Induced “Hidden Hearing Loss” Mechanism Discovered. ScienceDaily. ScienceDaily, 7 May 2014.
(8) Hidden Hearing Loss. 2015.
(9) Kraus, Nina & Travis White-Schwoch. 2016. Not-So-Hidden Hearing Loss. Hearing Journal May 2016 – Volume 69 – Issue 5 – pp 38, 40.
(10) Cara, Ed. 2016. What Is ‘Hidden Hearing Loss’? Scientists Detect Symptoms in Young Adults.
(11) Song, Quang, et. al. 2016. Coding Deficits in Hidden Hearing Loss Induced by Noise. Scientific Reports 6, Article number: 25200 (2016).
(12) Lin, Harrison. 2016. Hidden Hearing Loss: A Clinician’s Perspective. The Hearing Journal.
(13) Mercola, Joseph. 2016. How to Prevent Hearing Loss and Improve Your Hearing with Nutrition.
Nuala Leong says
Hi, I am looking for a clinic that tests for hidden hearing loss in MA or NH is there a database for this?
Neil Bauman, Ph.D. says
Hi Nuala:
Sorry, I can’t help you there. I’m not aware of any database of clinics that test for hidden hearing loss.
Cordially,
Neil
Chris says
Neil,
With the advent of OTO-413 and other similar medications do you feel excited that hidden hearing loss may now in fact be cured and therefore for some tinnitus, hyperacusis and other sdynromes may have a possible cure?
Cheers,
Chris
Neil Bauman, Ph.D. says
Hi Chris:
I’m at the most cautiously optimistic. From what I know about drug trials, they put a overly-positive spin on their results. So far, the trials of OTO-413 haven’t shown much improvement–just “clinically significant” which could be just a 10% improvement or even less. If the results had been great–such as a 80% absolute (not relative) improvement they would have touted this to the skies. Since they haven’t, I wouldn’t expect a “cure”, but there may be some degree of improvement in some people. But the people will still be left with significant hearing losses and thus tinnitus. Every improvement is a step in the right direction to be sure, but it is far from a “cure”. That’s my opinion.
Cordially,
Neil