Member- Aug 24, 2014
- 179
- Tinnitus Since
- 07/2009
- Cause of Tinnitus
- Loud Music and being dumb
10 Hz Amplitude Modulated Sounds Induce Short-Term Tinnitus Suppression
- Thread starter EatMoTacos
- Start date
- Apr 18, 2013
- 1,633
- Tinnitus Since
- 2003
- Cause of Tinnitus
- Flu, Noise-induced, Jaw trauma
Yes it's relatively easy to do. Just take the tone and modulate the amplitude - basically so it pulses on and off at a rate of 10Hz (10 times per second).
TinnitusPro is a piece of software that let's you listen to music of your choosing that is passed through a notch filter. To be fair, their software conditions the signal with a few more bells and whistles than just a simple notch, but, in a nutshell this is notch software that anyone can try for a reasonable cost. TinnitusPro has been tested in legit, peer-reviewed studies (have a look for Tinnitus studies published by C. Pantev). I usually encourage people to try it as a first line of defense because it is low-risk and backed by a least some science. The results aren't fantastic but they can help get you through a rough patch. It will work best if you have tonal tinnitus and not whirring, clicking, noise etc. The main issues with all passive listening therapies are: 1) they don't work for a lot of people, 2) For most people, the residual inhibition lasts for minutes-hours after the sound is turned off, 3) the kicker is that once the residual inhibition tapers off, the tinnitus is often experienced at a greater ferocity than before the sound therapy.
With all that said, TinnitusPro is worth a look if you are curious about the benefits of notched masking. Pound-for-pound, probably a better investment than 10Hz AM. At a minimum, most people would prefer to listen to sounds that are enjoyable (music or nature) than meaningless synthetic noise.
The mechanism is tied into the central gain theory of tinnitus. The typical explanation is that most tinnitus is triggered by pathology in the middle or inner ear that has the effect of reducing the quality and strength of the signal transmitted from the inner ear to the brain. The loss of input from the ear triggers a compensatory response in auditory processing centers of the brain. The neurons increase their "gain" (i.e., amplification) on the weakened inputs coming in from the ears so as to restore their overall excitability back to their natural set point. For some individuals, the increased amplification destabilizes patterns of electrical activity within these networks of inter-connected neurons that leads to the false perception of sounds that do not exist in the environment (tinnitus) or the perception that sounds are louder than they actually are (some types of hyperacusis).
Logically, the tinnitus could go away if only the pathologically over-powered amplification was turned down a little bit. If the loss of input from the ear was the reason it was turned up too high, than increasing the activity transmitted through the damaged auditory nerve might coax the amplifier back down. This is where maskers come in (as well as hearing aids or other personal listening devices). By increasing the signal traveling down the damaged auditory nerve, they briefly coax the central gain down and most people get relief from their tinnitus during the sound or for a little while afterward. This is residual inhibition. It doesn't last because the damage is still there and the system will once again start cranking up the gain within minutes or hours after the passive listening is ended.
You are technically correct, but I think you are presenting it in an unnecessary negative light: no tinnitus therapy works for a lot of people (unless I missed a major announcement). What I mean is that it's not an issue that is specific to sound therapies: it's the unfortunate realities of all tinnitus therapies (except for the rare cases that can address root causes such as stapedotomies for otosclerosis patients, which has a really good success rate to restore hearing (~90%) and a not too bad success rate for addressing T (~50%)).
Do you have sources for assertions #2 and #3?
I'm particularly interested in it because I've perused quite a few studies on sound therapy (I write code that builds Tinnitus sound therapy files so I've tried to target things that had both reasonable success rates and fairly detailed specifications) and I've never come across a study that looked at residual inhibition as primary or secondary outcomes.
Residual inhibition is a well documented phenomenon and I've never come across it as a goal for long term relief of this condition.
I did come across anecdotal reports of people "getting worse" when listening to some sound therapy (mostly in this forum), but it didn't strike as any worse than other T therapies (people get worse with rTMS, tDCS, hi-focus ultrasound, or anything else you throw at them) - perhaps I didn't come across a legit report.
This makes sense to me. What I can't make sense of is the success rate reported with Linear Octave Frequency Transposition hearing aids, since they seem to move energy from the spectral area where the patient doesn't hear down to the area where the patient hears, thus not amplifying at all in the former area. That baffles me and I wonder what's at play there.
For someone with notched or steeply sloping hearing loss, signals essential for communication (e.g., speech reception) might overlap with regions of the cochlea with reduced or absent sensitivity to sound. These transposition aids shift those signals into a cochlear region where thresholds or normal. The immediate effect, I am told, is that everything sounds incredibly weird. But, overtime, your brain sorts it out and your neurons are able to take advantage of speech signals that would have otherwise been lost.
How can this help with tinnitus? The argument follows the same logic as notched music. The basilar membrane is arranged like a piano keyboard, with low frequencies activating one end and high frequencies the other. This 'tonotopic organization' is preserved in many auditory processing centers of the brain. The neurons are organized into a tonotopic map that mirrors the organization of the cochlea. When a bunch of the keys on the actual keyboard are smashed (e.g., hearing loss), neurons in the corresponding region of the map lose their primary input and the amplification in that region of the brain maps gets turned way up. Like I mentioned earlier, this can destabilize the electrical activity patterns in this region of the map, leading to hyper-excitability. Many have argued that this is why the subjective pitch of the tinnitus tone is often within or close to regions of hearing loss.
With that said, let's turn to your main question. The goal is to turn down the over-powered amplification in these narrowly defined zones of the tonotopic maps in hopes of extinguishing the tinnitus percept. If someone has mild-moderate hearing loss, you can still drive neurons in those parts of the map by programming the masking sound to include frequencies in the hearing loss zone. Another approach is to direct the stimuli at spared frequency regions that border the hearing loss zone because activating these keys to quiet the activity in noisy zone of the maps through a process called lateral inhibition. This is the basis for notched maskers focus the signal into frequency ranges that bookend the tinnitus frequency. If you have serious/profound hearing loss, focusing the acoustic frequencies into the 'dead' zone isn't going to do much good. So, if you move transpose that frequency band to a neighboring, intact region you can hear those frequencies again and you can also reap the benefits of lateral inhibition. But, critically, these sounds aren't just passively experienced. The brain is actively processing them to extract meaning and support speech perception. This can engage a competitive plasticity process that recruits neurons that were formally mapped onto the dead zone in the keyboard into this new frequency representation. This remapping can last longer than residual inhibition through notched listening.
The punch line is that tinnitus inhibition can last much longer for sounds that are not just passively experienced. Passive listening doesn't engage a plasticity in adult brains but actively listening through a transposition HA could.
Yes, I agree with you 100%. Thanks for bringing this up. In fact, masking therapies are probably the most reliable form of tinnitus suppression. They don't introduce a lot of negative side effects, so there isn't a major cost in people firing out what works for them. Beyond the tinnitus suppression, learning about what maskers work can yield some insight into the underlying pathology as well. So, I didn't mean to be too negative. Anything that can provide some relief, that is non-invasive and helps people get through bad days is a great asset. The biggest issue with the maskers is the duration of benefit, and that is what I was getting at with that comment. Maskers are quite literally life savers for a lot of people with tinnitus and I think it is great that people are findings ways to make them more potent and long-lasting. However, I am always thinking about therapies that can provide tinnitus relief on the scale of days, weeks or years. I think maskers are inherently limited on these time scales so it is worth thinking of adjuvant therapies that can be used in combination of maskers. Alas, as you know all too well, these have yet to deliver on their promise.
Thanks for correcting me on that. What I wrote came off as too dismissive (again...hand slap to forehead).
Thanks for the detailed prose.
Ah, this is the key part that contains the "meat" I was looking for - thanks. Do you know if this is a theory or if there has been some studies that confirm this process?
During my consultation with a T expert at UCSF, he did mention that he recommended that I kept playing music (since I am a musician) and stayed engaged in it, offering that there would be a better success at dealing with T if there was some kind of emotional connection between me and the music I would be listening to.
He did make a point about having that "emotional connection" vs plain colored noises, and perhaps that is linked to neuronal plasticity.
Very interesting stuff! Again, thank you for taking the time.
Ah, this is the key part that contains the "meat" I was looking for - thanks. Do you know if this is a theory or if there has been some studies that confirm this process?
During my consultation with a T expert at UCSF, he did mention that he recommended that I kept playing music (since I am a musician) and stayed engaged in it, offering that there would be a better success at dealing with T if there was some kind of emotional connection between me and the music I would be listening to.
He did make a point about having that "emotional connection" vs plain colored noises, and perhaps that is linked to neuronal plasticity.
Very interesting stuff! Again, thank you for taking the time.
No, this is anecdotal. It has been relayed to me by clinicians and patients. There may be research papers on it but I cannot name them. The problem is that tinnitus severity is subjective and communicated through self-report. Many researchers are put off by the perceived problem that the act of self-report, in and of itself, will affect the outcome. This problem plagues many studies that seek to track shifts in subjective tinnitus magnitude over time. If anyone knows of studies that have done a convincing job tracking residual inhibition over time, I would be interested in reading more about this.
It's always on my mind too...
There was an ATA video published last summer (maybe july 2016?) where they describe experiments with current stimulation (I think it's AC), with electrodes in forehead+ear (in one of the experiments) and then surgically inserted in the middle ear (for one of them) and in the ear canal (for the other) in the other experiment. They reported residual inhibition in the order of hours (8h if I recall correctly, after a few minutes of stimulation), and if it can be automated safely (much like pacemakers are) it could lead to an interesting option - at least for those who are receptive to this type of treatment. The idea was to stimulate regularly to keep the RI active "forever".
However, not unlike other "great T findings", I haven't heard much in that therapy avenue unfortunately.
Personally, I'd be interested in trying electro magnetic fields, but I wonder whether my titanium prosthesis (from my stapedotomy) is going to throw a wrench into this plan. My surgeon tells me "it should be ok", but obviously it's not his ear that will be getting a bunch of Teslas, or some current running through it. Gotta love induction!
No worries. It's all good.
Yes, there are hundreds of studies in animal models that look at 'plasticity' in the tonotopic arrangement of sound frequencies that accompany hearing loss and/or actively discriminating sounds in a narrow frequency region. In fact, many of the most important studies on this topic were done at UCSF. Fewer studies have looked into this in human subjects, mostly because you need MRI scanners with high field strength to clearly resolve the 'keyboard' in the human brain. However, there is a researcher in Switzerland who has published some nice papers both on the hyper excitability and 'filling in' in subjects with tinnitus as well as the map plasticity that accompanies active use of restricted frequency ranges.
Brain Topogr. 2017 Feb 6. doi: 10.1007/s10548-017-0547-1. [Epub ahead of print]
High-Resolution fMRI of Auditory Cortical Map Changes in Unilateral Hearing Loss and Tinnitus.
Ghazaleh N1,2, Zwaag WV3,4, Clarke S5, Ville DV6,7, Maire R8, Saenz M6,9.
J Neurosci. 2013 Jan 30;33(5):1858-63. doi: 10.1523/JNEUROSCI.4405-12.2013.
Tuning in to sound: frequency-selective attentional filter in human primary auditory cortex.
Da Costa S1, van der Zwaag W, Miller LM, Clarke S, Saenz M.
Maybe you will indulge me in a little experiment. I was wondering if you could play scales (or another melody) where all/most of the notes are focused on frequencies close the border of your hearing loss. As a musician, I am sure you can do this with few errors. Since you are an audio geek (like me), try finding an audio file that has multiple simultaneous speakers and filter the sound (if necessary) so that it has plenty of energy in the frequency range that borders your tinnitus and the musical scale/melody you are playing. Adjust the level of the filtered speech sound so that it is hard, but not impossible, to hear the notes you are producing. Keep producing scales or melodies in this frequency range, as fast as you can with no errors. As you are getting better at it, turn up the volume of the interfering speech sound until it becomes more difficult (and try not to "cheat" by using visual or proprioceptive cues to tell you what notes you are/should be playing). I bet you get stronger residual inhibition from this exercise then you get from an equivalent period of listening to masking noise...
By the way, was the clinician you saw at UCSF Dr. Cheung?
OK, give me a bit of time to reread this a few times. I didn't get it the first couple of times. I'll get back to you on it. I may need some clarifications.
BTW, I've never experienced RI, but I've also never really focused on triggering it. I've always been leery (perhaps for no good reason) of trying to focus energy on the area of my cochlea that is damaged.
Ugh, no sorry - my brain screwed up my recollection: I went to UCSF for a hearing test, but the T expert I saw was at the Kaiser facility in SF. I think it was Robert Miley.
Could this imply that when research is able to turn these overexcited neurons down again (reduce the gain in these areas) this may influence hearing threshold negatively?
Nice catch. Yes, this is one implication of studies that would seek to dial down the central gain. Ideally, the "knob" could be turned down just enough to silence the T without causing audibility to take too much of a hit. But this is pie in the sky at this point. The central gain knob has only been adjusted in the auditory cortex of animal models.
Thank you for that.
Just one more thought I would like to share (just sideways related to this thread) (-:
This trying to dial down central gain could be counter-productive for tinnitus? When indeed hearing threshold for this already damaged area increases even further, it could "increase" the tinnitus sensation. (Like plugging your ears or be in a quit place). After all there is even less input from the outside world to distract from tinnitus.
But like you wrote: at the moment it is pie in the sky.
- Aug 24, 2014
- 179
- Tinnitus Since
- 07/2009
- Cause of Tinnitus
- Loud Music and being dumb
It does make sense in a way. I was playing several tonse above and below an octave what I think is my T and I did get a moment of silence (maybe roughly about several minutes. At one instance I did get about two hours of no T one night went to bed and woke up right before T came back stronger than ever.
@HomeoHebbian are you suggesting to play Tones closer to what our hearing loss or T tone? I have made several notched sounds and have used the TinnitusPro app for some time but only for white noise and not for music. As of now I feel like my T is around the 2.6kHz tone but my hearing loss mainly is in my right ear above the 11.5kHz (I have to play it at almost 60% volume to hear it)
@HomeoHebbian are you suggesting to play Tones closer to what our hearing loss or T tone? I have made several notched sounds and have used the TinnitusPro app for some time but only for white noise and not for music. As of now I feel like my T is around the 2.6kHz tone but my hearing loss mainly is in my right ear above the 11.5kHz (I have to play it at almost 60% volume to hear it)
- Apr 18, 2013
- 1,633
- Tinnitus Since
- 2003
- Cause of Tinnitus
- Flu, Noise-induced, Jaw trauma
@HomeoHebbian In your opinion could we potentially keep the recruitment of neurons that create the gain increase and give us tinnitus, but encourage them to selectively increase gain so that they only improve hearing?
It feels feasible that the brain could be trained to turn the gain on/off rather than a constant on. After all the phenomenon of "reactive tinnitus" is like a gain increase based on specific circumstances.
It feels feasible that the brain could be trained to turn the gain on/off rather than a constant on. After all the phenomenon of "reactive tinnitus" is like a gain increase based on specific circumstances.
To clarify, think of central gain as a u-shaped curve.
-Prolonged periods in very quiet environments are associated with low levels of electrical signaling flowing into the brain from the auditory nerve. The brain's amplifier compensates by turning up central gain. This is why people who don't have chronic subjective tinnitus can experience it by putting in earplugs (Reversible induction of phantom auditory sensations through simulated unilateral hearing loss R Schaette, C Turtle, KJ Munro - PLoS One, 2012 - journals.plos.org)
-Prolonged periods in very loud environments damage auditory nerve synapses and hair cells. This also reduces signaling through the auditory nerve and causes the brain's amplifier compensates by turning up central gain.
- The "Goldilocks" zone where central gain is low is somewhere in between. According to central gain theory, most people with tinnitus are on the right side of that curve. If the gain could be turned down into the Goldilocks zone, the tinnitus would go away.
So, I'm not sure I understand your point, Reinier. According to this logic it would be helpful to turn the gain down.
One school of thought it to turn the gain down by increasing the level of activity in the auditory nerve. This can either be done with masking, but the effects are usually temporary and masking sound interferes with your ability to process other environmental sounds). Or perhaps someday it could be achieved on a more permanent basis via inner ear therapies such as cochlear synapse repair, hair cell regeneration etc. The other school of thought is that central gain could be turned down by directly manipulating the brain's amplifier itself, not by changing activity levels in the auditory nerve. This has been done in animal models and people are thinking about how to move this towards clinical research studies. But that is a topic for a different thread.
I'm less familiar with the relationship you described. Most people with high-frequency hearing loss experience the tinnitus pitch to be slightly higher than the steepest slope of the audibility loss, as described here:
Course of hearing loss and occurrence of tinnitus
O König, R Schaette, R Kempter, M Gross - Hearing research, 2006 - Elsevier
Without seeing your audiogram, I would say I don't know. But if I were forced to make a suggestion, it would be to focus the notch on your perceived tinnitus pitch, not the hearing loss (if for no other reason than you won't be able to hear the higher frequency band anyway [or it would be so loud you would damage whatever is left in the high-frequency cochlear base]). Also, try the music feature on Tinnitus Pro. Listening to flat noise for extended periods of time probably isn't a great idea. It turns the inhibition down further.
Most people in the central gain camp think it is a heterosynaptic plasticity process. That means that all synaptic inputs impinging on a neuron with increased gain will get amplified, whether the input is conveying an acoustic signal from the environment or the spontaneous firing of nearby neurons. Either input will be converted into the perception of sound (the former as a sound from the environment, the latter the internal 'noise' of the brain that is perceived as tinnitus). So, I think most people in the central gain camp would say no. At this point, there is no reason to think you separably adjust the gain for external vs internal signals.
But central gain isn't the only game in town. Others argue that the perception of the phantom sound arises from a separate process than neurons in the "bottom-up" auditory pathway that encode sound features and shape our perception of the environment. They argue that the core pathology underlying tinnitus lies in the improper regulation of brain circuits that normally cancel out predicted inputs. In their view, the two could be independently adjusted.
At the end of the day, these things could be very non-linear. A tiny adjustment in gain could be enough to get rid of tinnitus without causing a perceptible effect on detection thresholds. I know I would gladly give up a few dB of sensitivity to get rid of my tinnitus!
My point is that if you turn down the gain you also turn down sound from the outside world.
Than the signal to noise ratio is worse, when I think in audio engineering terms (-;
It al depends on how much the tinnitus sensation is turned down at the same time I think.
So, I think I can understand this "goldilocks" zone.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035238
I wonder if there could have been a possibility that one of the people in this research could have ended up with permanent tinnitus.
After all even now there is no full understanding why we get tinnitus.
Also there is talk about these people having healthy hearing. Now we find that it is still not possible to know if hearing is not damaged (perfect audiogram is perfect hearing/hidden hearing loss?).
So if one of the participants was not "aware" of tinnitus it could have been "triggered" by this research.
I wonder if there could have been a possibility that one of the people in this research could have ended up with permanent tinnitus.
After all even now there is no full understanding why we get tinnitus.
Also there is talk about these people having healthy hearing. Now we find that it is still not possible to know if hearing is not damaged (perfect audiogram is perfect hearing/hidden hearing loss?).
So if one of the participants was not "aware" of tinnitus it could have been "triggered" by this research.
Well, let's not get too dismayed about the sum total of what we don't know. I think we do know what constitutes normal, healthy hearing. If audiologists would loosen their grip on the 0.5-8k audiogram and begin including a few additional measures such as speech in noise testing, otoacoustic emissions, Wideband elicitors of the middle ear reflex and perhaps an electrophysiology measure based on one of the frequency following response measures, I think their patients would leave the office with a far more complete picture of hearing health.
As for tinnitus, I think we have a good handle on the risk factors. I don't see an ethical issue with having them wear an earplug for a short period of time. On the other hand, I agree that the "ghost in the machine" is still at large when it comes to tinnitus; we have yet to define a reliable and sensitive tinnitus test that would direct measure the source of the pathophysiology. Until we have this measure, I see your point, Reinier, that we are still in the dark to some degree when it comes to identifying the basis for tinnitus.
Sometimes I wonder about this. I have personal experience that an ENT told nothing was wrong with the hearing of a person after tinnitus complaints following a loud explosion. He concluded that no damage was done after having checked the audiogram. (8kHz max.)
Also, I have read this many times here on the forum. People have tinnitus complaints and nothing is wrong according to a specialist (ENT).
But I do think you are correct when you say "we know what constitutes normal, healthy hearing".
I can understand that there needs to be much more than the standard 8kHz audiogram.
Especially after my own experience regarding this issue.
But that is a completely different discussion
I don't want to sound too negative. That is not how I feel about al the research that is happening at the moment.
Sometimes I wonder about this. I have personal experience that an ENT told nothing was wrong with the hearing of a person after tinnitus complaints following a loud explosion. He concluded that no damage was done after having checked the audiogram. (8kHz max.)
Also, I have read this many times here on the forum. People have tinnitus complaints and nothing is wrong according to a specialist (ENT).
But I do think you are correct when you say "we know what constitutes normal, healthy hearing".
I can understand that there needs to be much more than the standard 8kHz audiogram.
Especially after my own experience regarding this issue.
But that is a completely different discussion
I don't want to sound too negative. That is not how I feel about al the research that is happening at the moment.
I know, it seems crazy. The root of the problem comes down to the sociology of medicine. Tinnitus and hidden hearing loss fall at the intersection of neurology, otolaryngology, and audiology. It should be on all of their radars, but in fact it ends up on none. The pathology is not the result of a stroke/seizure (the focus of neurology), nor is there a medication or surgical option (the focus of ENT), nor can it be reliably corrected with a hearing aid (the focus of audiology).
The massive shortcomings of the audiogram for diagnosing hearing health is very well understood among hearing scientists. When I said "we", I was referring to researchers. I really feel your frustration when it comes to the audiologists and the ENT docs. A lot of the problems underlying hidden hearing loss and tinnitus are neural and most audiology/ENT training programs don't go beyond the hair cell so, in my experience, many (but not all) know less about these issues than a well-informed participant on this website. Of course, they don't know what they don't know and the clinical culture (at least in the US) places a premium on confidence and efficiency over deep thinking. If your doc doesn't go to international meetings or read the best journals otolaryngology or hearing research journals, chances are they are totally in the dark about this stuff.
I think the hearing research community will have to develop the tests for them. Mass. Eye and Ear just received a large award from the NIH this month to pursue this very issue. It will fund four laboratories (one project per laboratory) as they try to nail down new types of measurements that would shed light on the pathology underlying hearing in noise and tinnitus.
Project Number: 1P50DC015857-01A1 Contact PI / Project Leader: KUJAWA, SHARON G
Title: COCHLEAR SYNAPTOPATHY: PREVALENCE, DIAGNOSIS AND FUNCTIONAL CONSEQUENCES Awardee Organization: MASSACHUSETTS EYE AND EAR INFIRMARY
Project Start Date: 2-AUG-2017 Project End Date: 31-JUL-2022
Cochlear synaptopathy is the loss of nerve connections between the sensory cells and the brain, which occurs in noise-damaged and aging ears. Although not detected by the threshold audiogram, this nerve damage is likely a major contributor to difficulties understanding speech in a noisy environment and may also instigate changes resulting in tinnitus and hyperacusis. Our Research Center aims to understand the prevalence of cochlear synaptopathy, measure/infer its consequences to suprathreshold sound processing, and to identify diagnostic markers. Therapies to reconnect nerves and sensory cells are on the horizon, and proper diagnostics are key to the design of clinical trials. The results are important to the public health, because noise- and ototoxic drug exposures may be damaging the ear well before the effects are seen in the threshold audiogram.
Abstract Text:
Overall Project Summary New insights from animal studies of noise-induced and age-related hearing loss suggest that the most vulnerable elements in the inner ear are the synaptic connections between hair cells and sensory neurons. This primary neural degeneration, also called cochlear synaptopathy, does not elevate thresholds. Thus, it can be widespread in ears with intact hair cell populations and normal audiograms, where it has been called "hidden" hearing loss. It likely contributes to difficulties understanding speech in a noisy environment and may be an instigating factor in the generation of tinnitus and hyperacusis. Cochlear synaptopathy may also be widespread in acquired sensorineural hearing loss of other etiologies and degrees of hair cell damage. Thus, it may be a major contributor to the well-known differences in auditory performance among people with identical audiometric patterns of "overt" hearing loss. Our Research Center aims to take these paradigm-shifting ideas from animal models to human subjects. Based on the synthesis of many research threads from the study of overt and hidden hearing loss, we have devised a set of physiological, electrophysiological and psychophysical tests of hearing and cochlear function that we believe are most powerful in the diagnosis and understanding of cochlear synaptopathy in human subjects. In Project 1, we apply this test battery to gerbils exposed to noise or ototoxic drugs and test their diagnostic power by directly measuring the underlying cochlear histopathology in cases of overt or hidden hearing loss. In Project 2, we use immunostaining to directly assess the prevalence of cochlear synaptopathy in human temporal bones from subjects with overt or hidden hearing loss with a range of etiologies. In Project 3, we study hidden hearing loss in college students by applying the test battery to subjects with normal audiograms but a broad range of reported and measured sound exposures. In Project 4, we assess older adults with overt hearing loss by applying the tests to a subject pool with carefully matched down-sloping audiograms and by characterizing training-based improvements in speech-in-noise performance as reflected at different peripheral, brainstem, midbrain and cortical levels. Our preliminary studies of young adults show clear signs of hidden hearing loss in a group with repeated exposure to high-level music, suggesting the importance of this phenomenon to the public health. The success of neurotrophin-based approaches to the treatment of cochlear synaptopathy in animal models suggests that therapies may be on the horizon. Thus, the need for better understanding of the prevalence, diagnosis and functional consequences of cochlear synaptopathy is clear.
ManagerThis is interesting. Because I have had this idea for some time now that binaural fusion, or a disrupted binaural fusion, perhaps as a result of a unilateral cochlear damage, may be instigating chronic tinnitus. Has binaural fusion been studied in relation to tinnitus?
Hi Samir, you'll have to give me a little more context for what you mean by "binaural fusion". The inputs from the two ear are fused at a very early stage of processing in the auditory brainstem. Our perception of where sounds occur in space arises directly from precise computations of tiny differences in the amplitude and timing differences of sound pressure waveform at each ear. The ability to spatially separate the sound of your conversation partner across the table from the loud speech babble of people seated nearby is essential to tracking a conversation in noise. When there is hearing loss, these brainstem circuits cannot do their job, which can cause problems with speech communication. But I have not made a connection between these processes and tinnitus.
Now, you may be referring to I-dosing. I-dosing is advertised as "digital drugs" that let people get high off sound. They really are audio files that take advantage of binaural processing to induce binaural beats at certain frequencies in your central auditory system. This thread started with a description of a 10 Hz sound file. If neurons synchronize to a 10 Hz modulation frequency, it should induce an alpha rhythm (relaxation, drowsiness). I have wondered whether an audio engineering aficionado like @Steve has played with binaural beats in the context of tinnitus. I haven't read much about this but I think it could have some interesting implications.
- Aug 24, 2014
- 179
- Tinnitus Since
- 07/2009
- Cause of Tinnitus
- Loud Music and being dumb
I'm curious as well. I have tried making different tones using not just sine waves but I've created "Notched" noise with 10Hz AM on top, makes it sound like a old style steam train passing by if you generate it with white noise.
