Can someone ask on Twitter if the presentation will be made public?
Can someone ask on Twitter if the presentation will be made public?
I think it's for the same reason nerve pain fluctuates and that is... we don't know.Kinda. The fact that it fluctuates for some people leads me to believe that it is not as simple as "tinnitus is in the brain". It makes me think that it is a nerve dysfunction, likely at the synapses in the cochlea, they are healing a little, then getting worn out on a cycle. Me thinks.
That's probably 100% correct.Maybe as a person ages the cilia in their ears die off naturally. Unlike acoustic hearing loss where the hairs are shocked to death.
I bet that happens because micro blood vessels in the capillaries break down with age. With noise there is something called the glutamate storm.Maybe as a person ages the cilia in their ears die off naturally.
Usually it changes during sleep. What a mystery!Kinda. The fact that it fluctuates for some people leads me to believe that it is not as simple as "tinnitus is in the brain". It makes me think that it is a nerve dysfunction, likely at the synapses in the cochlea, they are healing a little, then getting worn out on a cycle. Me thinks.
No mystery. Your cochlea has a circadian clock. It is doing different things at different times of the day. This probably explains why so people get different types of damage, because of the time(s) of day it occurs.Usually it changes during sleep. What a mystery!
I was thinking mitochondrial aging may have more to do with this but it's probably multi factorial.I bet that happens because micro blood vessels in the capillaries break down with age. With noise there is something called the glutamate storm.
I don't think they ever answer on Twitter.Can someone ask on Twitter if the presentation will be made public?
fMRI's are loud. If you're looking at the auditory cortex while undergoing fMRI, of course it's going to show activity, that doesn't mean that's where the sound is originating. The only way to see that would be to have a perfectly silent MRI machine and show that the auditory cortex is active and the auditory nerve is not.I've said it before but it's pretty much proven it's in the brain. fMRIs have been done to show this. All the main researchers, the ones specifically targeting tinnitus, working on treatments are targeting the brain and have shown this reduces tinnitus (like Dr. Shore).
The brain makes it in response to damage in the cochlea. The hope is fixing that damage would also stop the brain's response of said damage (tinnitus).
But can't they compare it to a normal person's MRI? Yes, and they do.fMRI's are loud. If you're looking at the auditory cortex while undergoing fMRI, of course it's going to show activity, that doesn't mean that's where the sound is originating. The only way to see that would be to have a perfectly silent MRI machine and show that the auditory cortex is active and the auditory nerve is not.
Also, the tinnitus is in the brain hypothesis falls apart knowing that it goes away sometimes for some people and that OTO-313 showed reduction of tinnitus and that stuff get's nowhere near the brain, it goes into the cochlea, and stops the cochlea itself from being hyperactive. The cochlear fluids are separated from the brain by the BBB, the systemic blood flow, and the BLB. OTO-313 isn't restoring hair cells, or hearing function, it is an NMDA antagonist, acting on the NMDA receptors on the nerves in the cochlea, which means that the tinnitus signal, at least in many cases, originates in the cochlea.
A likely scenario is where we end up with a classification of subtypes of tinnitus. I do agree a large amount of patients will probably be helped with some sort of hearing restoration. That doesn't mean those patients will be cured with hearing restoration, but at least their tinnitus will be quietened.fMRI's are loud. If you're looking at the auditory cortex while undergoing fMRI, of course it's going to show activity, that doesn't mean that's where the sound is originating. The only way to see that would be to have a perfectly silent MRI machine and show that the auditory cortex is active and the auditory nerve is not.
Also, the tinnitus is in the brain hypothesis falls apart knowing that it goes away sometimes for some people and that OTO-313 showed reduction of tinnitus and that stuff get's nowhere near the brain, it goes into the cochlea, and stops the cochlea itself from being hyperactive. The cochlear fluids are separated from the brain by the BBB, the systemic blood flow, and the BLB. OTO-313 isn't restoring hair cells, or hearing function, it is an NMDA antagonist, acting on the NMDA receptors on the nerves in the cochlea, which means that the tinnitus signal, at least in many cases, originates in the cochlea.
Your trial?And yet the doctor in charge of my OTO-313 trial knows that tinnitus is in the brain.
That may or may not be true but fMRIs on the whole are much more problematic than most people realize:I've said it before but it's pretty much proven it's in the brain. fMRIs have been done to show this. All the main researchers, the ones specifically targeting tinnitus, working on treatments are targeting the brain and have shown this reduces tinnitus (like Dr. Shore).
The brain makes it in response to damage in the cochlea. The hope is fixing that damage would also stop the brain's response of said damage (tinnitus).
So then why is my tinnitus basically gone, right this instant? Because my cochlea is on the border between normal and malfunctioning and depending on my current status I can hear and then not hear and then my tinnitus comes back?But can't they compare it to a normal person's MRI? Yes, and they do.
And yet the doctor in charge of my OTO-313 trial knows that tinnitus is in the brain.
Did you end up getting the shot yet?But can't they compare it to a normal person's MRI? Yes, and they do.
And yet the doctor in charge of my OTO-313 trial knows that tinnitus is in the brain.
@Lucifer I'm gonna get the shot in less than two weeks.So then why is my tinnitus basically gone, right this instant? Because my cochlea is on the border between normal and malfunctioning and depending on my current status I can hear and then not hear and then my tinnitus comes back?
The tinnitus is in muh brain theory is based on something called the gating mechanism. They use that to say that the gating is broken and that's why some people have tinnitus and others don't that even have more hearing loss.
But if the gating mechanism thing is true, then how come some people get tinnitus immediately following acoustic shock? Because their gate is disrupted? Well then how come these some people don't get tinnitus every single time they are in silence? That doesn't make sense. Rauschecker is a goofball with tunnel vision. A better theory is that tinnitus is actually originating in the part of the auditory system before it reaches the brain.
Also, several of us get relief from curcumin. So is the curcumin adjusting the gating mechanism? Or is it reducing inflammation and possibly acting on BDNF levels in the auditory nerve? That makes more sense.
When people say brain, I automatically think of the auditory cortex. The brainstem makes more sense bexause it can be modulated by jaw movements. Im calling bullshit on the origins being in the auditory cortex.The research that looks very much undoubtedly true is the hyperactivity of fusiform cells in the dorsal cochlea nucleus, part of the brainstem.
The auditory cortex research is newer, it could be that what is happening there is what causing it to happen in the brainstem. They were able to cure it mice by eliminating the inflammation, then verified it by inducing tinnitus in the mice by introducing the inflammation. It is still newer, but it's the cure if it works in humans. They are going to keep researching the pill's safety before trying it in humans.When people say brain, I automatically think of the auditory cortex. The brainstem makes more sense bexause it can be modulated by jaw movements. Im calling bullshit on the origins being in the auditory cortex.
Not to be a Debby downer but I don't believe anybody "knows" anything about tinnitus's exact mechanism. If they did we could just target that specifically and be done with it.@Lucifer I'm gonna get the shot in less than two weeks.
Tinnitus being in the brain is not the gating theory. Rauschecker is a goofball, agreed there, his gating theory is massively flawed.
The research that looks very much undoubtedly true is the hyperactivity of fusiform cells in the dorsal cochlea nucleus, part of the brainstem. That's what Dr. Shore of the University of Michigan is targeting. That's how she has been able to quiet tinnitus in her ongoing trials built on over 15 years of research.
University of Arizona has actually recently found that tinnitus' root cause is that the cells in the auditory cortex are firing spontaneously (in line with Dr. Shore's research) because of inflammation in that region of the brain in response to acoustic trauma. They have found specifically, it is an abundance of the protein TNF-ALPHA and cytokines.
You're not downing me. I'll take Dr. Susan Shore's word over yours any day.Not to be a Debby downer but I don't believe anybody "knows" anything about tinnitus's exact mechanism. If they did we could just target that specifically and be done with it.
I'm not a fan of the calming down neuro excitation method as it seems like a band-aid that will have to be re-administered continuously. I mean if it works "yay". BUT I'd much rather cure damage.
Again. All speculations. Nobody "knows" until we really truly know.
How exactly would inflammation in the auditory cortex cause the DCN to be inflammed?The auditory cortex research is newer, it could be that what is happening there is what causing it to happen in the brainstem. They were able to cure it mice by eliminating the inflammation, then verified it by inducing tinnitus in the mice by introducing the inflammation. It is still newer, but it's the cure if it works in humans. They are going to keep researching the pill's safety before trying it in humans.
It's awesome that you make that connection, that's actually a criteria Dr. Shore looks for in her trial. She calls it somatic tinnitus as not all people can do it. It's being able to change the tinnitus with body movements (like clenching your teeth or opening your jaw), she says this modulates the activity of the fusiform cells.
Hey, if people are really getting silence now due to Lenire's bimodal stimulation treatment then that's news to me - and that's awesome. But I haven't seen too many glowing reviews of it here.You're not downing me. I'll take Dr. Susan Shore's word over yours any day.
Have you even really looked into her research yet? You realize she's gotten people to silence right? Over 15 years of research to the point where she does have a mechanism to "target specifically"?
I believe that there are people out there that get it. There's really only a handful of prevailing theories. There is a Galileo out there somewhere.Not to be a Debby downer but I don't believe anybody "knows" anything about tinnitus's exact mechanism.
Her device is the original, Lenire is basically a knock off by a private Irish start up company.Hey, if people are really getting silence now due to Lenire's bimodal stimulation treatment then that's news to me - and that's awesome. But I haven't seen too many glowing reviews of it here.
That's more of my theory, but I think it's the same principle in that the brain is very interconnected. I'm thinking these same inflammatory proteins are ending up in the DCN causing all the misfires, or if not it could be that the electrical misfires in the auditory cortex are also causing the misfires in the DCN. Ultimately, I think it is likely that it's all connected. Our biology always relies on its different parts working in unity, and problems in one area often cause problems in another.How exactly would inflammation in the auditory cortex cause the DCN to be inflammed?