I wanted to share all the scientific understanding I have collected in the last 6 months from spending countless hours looking for an answer and reading about a potential path to a true cure.
For the first few weeks after having T I had a blocked sensation which felt like hearing loss. During the first few months the ringing was quite loud and sharp, and it would exacerbate with normal volume environments like restaurants or the music at the gym. Lately it seemed to have quieted down a bit and the sound itself is more dull although it is a high frequency tone, kind of a hissing type. I have performed audiometry testing up to 16kHz. The only thing they noticed was a 15 dB difference at 16kHz in my T ear compared to my non-T ear (which hears at 0 dB at 16kHz to this day!) I believe this is enough damage to explain the T.
The months went by and I was eager to learn about a cure and how this all happens. And I read and read and read and it's not until I undestood what happens at a cellular level that it all became clear to me. It has even helped me understand my own T.
Importantly, I want to clearly mention this : T is primarily a NERVE defect rather than a hair cell defect.
- synapses between hair cells and nerve endings are the first area to get permanent damage. I believe this is EXACTLY where T prone people are having a problem. They are more likely to have damage to these synapses than most people.
-this damage is cumulative over a lifetime and cannot fully regenerate (yes, every night out at the club adds up)
-when these synapses are defective, the cell bodies of these nerves start to die very slowly within months to years, and less and less nerve fibers send signals to the brain.
-these vulnerable parts of the nerve account for high thresholds of sound and also for background noise recognition
-Low threshhold fibers can remain attached to hair cells after acoustic trauma and THAT'S why hearing SEEMS normal on the audiogram. In other words you can keep most or all your hair cells but they aren't innevated as much
-When this loss of nerve connections happens, the brainstem senses the decrease of input and this is where T begins: The input of the nerves from the head and the neck comes in the equation and COMPENSATES for the loss of input from the ear. BUT the mechanism unfortunately tends to OVERCOMPENSATE and this overexcitation is relayed all the way to the brain where there is overexpression of some specific frequencies.
-Important to note the difference between outer hair cells (OHC) and inner hair cells (IHC). The OHC work as sound amplifiers and work in groups of 3 cells, and 1 IHC works in conjunction with these 3 OHC. These OHC don't carry much innervation to the brain. The IHC on the other hand are highly innervated and receive the amplifications sent from the OHC and transmit the information to the brain making us able to hear sounds. I believe that when OHC damage occurs, hearing loss occurs, but when IHC damage occurs in addition to OHC damage (OHC damage happens first usually because they work actively, wheras IHC damage less often because they are more passive in function), then T occurs, so T indicates a more extensive damage to a region of the cochlea. This in my opinion may explain why some people have hearing loss but no T : They haven't affected their IHC but OHC are damaged. This also explains temporary T after a loud concert for example. The IHC have damaged synapses that are getting repaired and while this is happening, there is temporary loss of input to the brain.
That's how it happens, in a nutshell.
- If you are "lucky" and your damage is minimal, your continuous T can disappear or become intermittent, like what happened to some T cases I read about. Otherwise more damage is unlikely to completely disappear, until the treatemts are out!
Now the cure is basically giving back the lost input to the auditory nerve so that the head and neck input gets more suppressed like it used to and the percep of T will disappear completely. I personally believe that fixing the problem within the cochlea will fix the problem in the brain, regardless of how long noise-induced T has been present.
There are few approaches under way.
The drug Autifony is in its trial phases but looks very promising at reducing T or maybe eliminating it. It is a Kv3 potassium-channel modulator in the auditory pathways, and has proven to abolish chronic tinnitus in mice. It looks like it will need another 3-4 years to be available since they need to complete Phase IIa, and Phase III on a larger sample scale, and then get it approved for the public.
(http://www.autifonytherapeutics.com/publications/Turneretal2013-TRI_final.pdf)
Also there is regeneration of the synapses shortly after acoustic trauma that cured partial hearing loss in mice within 2 weeks. This could be a cure within the weeks to months after damage, when minimal or no hair cell loss has occurred.
The limitation with this treatment is that there is a time window. Once the cell bodies of the affected nerves die after months to years, there cannot be regeneration of more synapses.
(http://www.sciencedaily.com/releases/2014/10/141020212308.htm)
http://www.medicalnewstoday.com/articles/284159.php
Last but not least gene therapy and stem cell therapy for hair cell and nerve cell regeneration. Basically regenerating the lost hair cells and connecting them to their nerve fibers. The holy grail and true cure.
They have transplanted new nerve cells which reconnected with hair cells.
http://www.cbsnews.com/news/gerbils-regain-hearing-thanks-to-stem-cell-therapy/
This article discusses the promising role of endogenous stem cells to regenerate the lost auditory nerve fibers in the inner ear.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048968/
They have also induced cells in the inner ear to become new hair cells.
http://www.sciencedaily.com/releases/2014/12/141222165437.htm
Basically they now have discovered how to make new hair cells and connect them to a nerve. Great stuff.
I also read about a case of a man with 3 year history of constant T, which was caused by some form of impigement on his cervical nerves in the neck area. This man was treated and his T was cured. This case, to me, shows that even long standing T (more than 1.5 years) can be cured as long as the source of damage is cured.
(http://www.ncbi.nlm.nih.gov/pubmed/24452662)
My impression from this research is that we will first be able to suppress the sound of T with medication, and a few years later we will reverse the damage altogether with hair cell/nerve cell regeneration. Both are good news. So let's not forget that the sound of silence IS on it's way back...I would guess that in 5-7 years a great change will come!
http://hearinghealthfoundation.org/cure_for_tinnitus
For the first few weeks after having T I had a blocked sensation which felt like hearing loss. During the first few months the ringing was quite loud and sharp, and it would exacerbate with normal volume environments like restaurants or the music at the gym. Lately it seemed to have quieted down a bit and the sound itself is more dull although it is a high frequency tone, kind of a hissing type. I have performed audiometry testing up to 16kHz. The only thing they noticed was a 15 dB difference at 16kHz in my T ear compared to my non-T ear (which hears at 0 dB at 16kHz to this day!) I believe this is enough damage to explain the T.
The months went by and I was eager to learn about a cure and how this all happens. And I read and read and read and it's not until I undestood what happens at a cellular level that it all became clear to me. It has even helped me understand my own T.
Importantly, I want to clearly mention this : T is primarily a NERVE defect rather than a hair cell defect.
- synapses between hair cells and nerve endings are the first area to get permanent damage. I believe this is EXACTLY where T prone people are having a problem. They are more likely to have damage to these synapses than most people.
-this damage is cumulative over a lifetime and cannot fully regenerate (yes, every night out at the club adds up)
-when these synapses are defective, the cell bodies of these nerves start to die very slowly within months to years, and less and less nerve fibers send signals to the brain.
-these vulnerable parts of the nerve account for high thresholds of sound and also for background noise recognition
-Low threshhold fibers can remain attached to hair cells after acoustic trauma and THAT'S why hearing SEEMS normal on the audiogram. In other words you can keep most or all your hair cells but they aren't innevated as much
-When this loss of nerve connections happens, the brainstem senses the decrease of input and this is where T begins: The input of the nerves from the head and the neck comes in the equation and COMPENSATES for the loss of input from the ear. BUT the mechanism unfortunately tends to OVERCOMPENSATE and this overexcitation is relayed all the way to the brain where there is overexpression of some specific frequencies.
-Important to note the difference between outer hair cells (OHC) and inner hair cells (IHC). The OHC work as sound amplifiers and work in groups of 3 cells, and 1 IHC works in conjunction with these 3 OHC. These OHC don't carry much innervation to the brain. The IHC on the other hand are highly innervated and receive the amplifications sent from the OHC and transmit the information to the brain making us able to hear sounds. I believe that when OHC damage occurs, hearing loss occurs, but when IHC damage occurs in addition to OHC damage (OHC damage happens first usually because they work actively, wheras IHC damage less often because they are more passive in function), then T occurs, so T indicates a more extensive damage to a region of the cochlea. This in my opinion may explain why some people have hearing loss but no T : They haven't affected their IHC but OHC are damaged. This also explains temporary T after a loud concert for example. The IHC have damaged synapses that are getting repaired and while this is happening, there is temporary loss of input to the brain.
That's how it happens, in a nutshell.
- If you are "lucky" and your damage is minimal, your continuous T can disappear or become intermittent, like what happened to some T cases I read about. Otherwise more damage is unlikely to completely disappear, until the treatemts are out!
Now the cure is basically giving back the lost input to the auditory nerve so that the head and neck input gets more suppressed like it used to and the percep of T will disappear completely. I personally believe that fixing the problem within the cochlea will fix the problem in the brain, regardless of how long noise-induced T has been present.
There are few approaches under way.
The drug Autifony is in its trial phases but looks very promising at reducing T or maybe eliminating it. It is a Kv3 potassium-channel modulator in the auditory pathways, and has proven to abolish chronic tinnitus in mice. It looks like it will need another 3-4 years to be available since they need to complete Phase IIa, and Phase III on a larger sample scale, and then get it approved for the public.
(http://www.autifonytherapeutics.com/publications/Turneretal2013-TRI_final.pdf)
Also there is regeneration of the synapses shortly after acoustic trauma that cured partial hearing loss in mice within 2 weeks. This could be a cure within the weeks to months after damage, when minimal or no hair cell loss has occurred.
The limitation with this treatment is that there is a time window. Once the cell bodies of the affected nerves die after months to years, there cannot be regeneration of more synapses.
(http://www.sciencedaily.com/releases/2014/10/141020212308.htm)
http://www.medicalnewstoday.com/articles/284159.php
Last but not least gene therapy and stem cell therapy for hair cell and nerve cell regeneration. Basically regenerating the lost hair cells and connecting them to their nerve fibers. The holy grail and true cure.
They have transplanted new nerve cells which reconnected with hair cells.
http://www.cbsnews.com/news/gerbils-regain-hearing-thanks-to-stem-cell-therapy/
This article discusses the promising role of endogenous stem cells to regenerate the lost auditory nerve fibers in the inner ear.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048968/
They have also induced cells in the inner ear to become new hair cells.
http://www.sciencedaily.com/releases/2014/12/141222165437.htm
Basically they now have discovered how to make new hair cells and connect them to a nerve. Great stuff.
I also read about a case of a man with 3 year history of constant T, which was caused by some form of impigement on his cervical nerves in the neck area. This man was treated and his T was cured. This case, to me, shows that even long standing T (more than 1.5 years) can be cured as long as the source of damage is cured.
(http://www.ncbi.nlm.nih.gov/pubmed/24452662)
My impression from this research is that we will first be able to suppress the sound of T with medication, and a few years later we will reverse the damage altogether with hair cell/nerve cell regeneration. Both are good news. So let's not forget that the sound of silence IS on it's way back...I would guess that in 5-7 years a great change will come!
http://hearinghealthfoundation.org/cure_for_tinnitus
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