Your graph clearly points to how that nerve reaches the DCN. All nerves eventually reach the brain. That's basics of the CNS.
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- Thread starter threefirefour
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Not the drug itself, but the neurotransmitters from the drug.
Your theory still offers no explanation of how it would spread to my other ear that wasn't injected without going through my brain first.
There are no neurotransmitters from the drug. The drug is the drug. Your body makes neurotransmitters.
The drug didn't touch your brain. I can tell you that with near certainty.
You need to be calling up the clinic and demanding answers and asking them about how much was detected in your blood and even ask them if it got into your brain.
@ChrisBoyMonkey
did you read this thread?
https://www.tinnitustalk.com/threads/update-on-am-101-aka-keyzilen.15942/
Keyzilen was another NMDA receptor antagonist that failed to treat tinnitus.
did you read this thread?
https://www.tinnitustalk.com/threads/update-on-am-101-aka-keyzilen.15942/
Keyzilen was another NMDA receptor antagonist that failed to treat tinnitus.
I already know it got in my brain, that's how the drug works. The drug activates neurotransmitters. Or rather sends signals to supposedly calm over stimulation of them. Glutamate in specific. In my case it clearly did not work how it was supposed.
You need to learn more about the brain and the CNS. It simply isn't true that tinnitus is solely in ear thing. That's what the old guard had been saying for years and what good came of it? TRT? Instead of just saying that they could've been researching the brain aspects further, getting us closer to treatments. Instead we had to wait all these wasted years for them to finally start getting treatments. The first one to do it was a private startup. What does that say about the old guard? Wrong. Completely and utterly wrong.
But now even they are finally starting to see the light. The brain is largely responsible for this and the science community is finally starting to do something about it using this knowledge. I'll be giving this science a try myself very soon.
Sadly I did, but I was thinking that perhaps Otonomy's formulation was better. I was going off the information they provided me that no one got worse and some people were getting better. I'm betting now that it was all bullshit.
I really hope mine goes back to baseline. At least on my left, it feels even worse than my right in a quiet room even though the right is still louder. What I'm scared of is knowing about this "sustained release" crap. I don't know how long this junk will be in me. Thank you for checking into that too though my friend.
I think now we can say for sure now that NDMA antagonists do not work for tinnitus.
what if silence is when neurotransmitters are flowing and and sounds are actually the interruption of those? like an inverse?
nerve on = silence
nerve off = sound
that sure as hell would perfectly explain tinnitus.
think about a binary wave. we want to think of the 1 as the signal but sometimes it is actually the 0.
what if the silent state is the 1 and the 0 is what is carrying the sound information, the lack of signal rather. this would explain why tinnitus can start immediately, it's not depriving the brain of sound, it's depriving it of an active state which is itself silence. what if the little hair cells vibrating don't trigger the nerve impulse, but actually stop it and that's what sound perception is? Like your brain is always ringing (whoops there I go flip flopping again) and silence and sound are your nerves stopping it.
does that make sense to anyone else?
nerve on = silence
nerve off = sound
that sure as hell would perfectly explain tinnitus.
think about a binary wave. we want to think of the 1 as the signal but sometimes it is actually the 0.
what if the silent state is the 1 and the 0 is what is carrying the sound information, the lack of signal rather. this would explain why tinnitus can start immediately, it's not depriving the brain of sound, it's depriving it of an active state which is itself silence. what if the little hair cells vibrating don't trigger the nerve impulse, but actually stop it and that's what sound perception is? Like your brain is always ringing (whoops there I go flip flopping again) and silence and sound are your nerves stopping it.
does that make sense to anyone else?
Wrong.
Buster. I have a Bachelor's degree in Bio-medical Engineering Technology. I studied the entire human body extensively and made A's in all my A&P classes and took exams pointing out structures in real human brains.
I think:
Our brains are always trying to ring. When we here the outside world, we are actually hearing our brains. When you hear a sound that is your brain ringing, at the frequency that matches the pitch of the stimulus. Silence is your nerves in an active state silencing the auditory cortex. It's backwards. We want to think of our ears as microphones sending a signal to the brain. Your auditory cortex is a sound generator. It has to be deactivated, not activated.
Our brains are always trying to ring. When we here the outside world, we are actually hearing our brains. When you hear a sound that is your brain ringing, at the frequency that matches the pitch of the stimulus. Silence is your nerves in an active state silencing the auditory cortex. It's backwards. We want to think of our ears as microphones sending a signal to the brain. Your auditory cortex is a sound generator. It has to be deactivated, not activated.
I'm stupid as duck, but the lack of signal theory, could explain why cochlear implants can help in silencing Tinnitus, but not cure it completely. I mean, these implants are not perfect, and don't provide as much signals as a healthy ear. Also, hearing aids provide some kind of signals to the ear, and they help people in silencing Tinnitus, too.
It would be good, to see what kind of people are born with Tinnitus. Do they have hidden hearing loss, or some other health problems, that would cause lack of signal in the auditory system.
I don't know.. It just seems, that we are getting closer and closer to curing Tinnitus. I keep thinking about Lidocaine, and I'm sure that the current studies on its effect on Tinnitus, will help us understand things more.
To be clear, I wasn't saying it directly affects the brain. I do think the fact that both ears reacted makes me wonder if the receptor blockage causes an increase in glutamate release. Similar to, for instance, when you have abnormal stimulation of thyroid receptors and your brain responds by increasing TSH. Does that make sense?
- Jan 25, 2013
- 3,576
- Tinnitus Since
- 2008
- Cause of Tinnitus
- TMJ disorder, airplane barotrauma, noise exposure.
I read a while back that the precuneus may be involved in how tinnitus is perceived. There have been imaging studies that show it acts differently in tinnitus brains compared to non-tinnitus brains.
The precuneus is connected to the dorsal attention network and the default mode network which both do completely opposite jobs. The dorsal attention network is active when we are engaged and concentrating on something whereas the default mode network is active when our mind is at rest. When one network is active the other is switched off. From what I remember, it seems the precuneus may be a possible marker.
I believe the idea they had was that some tinnitus brains may struggle to switch off and are always at attention. I'm sure this was also correlated to tinnitus patients' lack of concentration and inability to sleep.
Our brains are mostly the same at the low level sensory perception level. Anyone can get tinnitus.
A study can't be conducted without a control group. In tinnitus cases where imaging comparisons are used, the control group are always people who don't have tinnitus. This is what is meant by tinnitus brains.
Medical imaging technology generates loud sounds. ALL data coming from these studies are in one way or another contaminated with "noise".
Our brains are synthesizers.
You can read more about it here:
https://www.sciencedirect.com/science/article/pii/S2213158217301808?via=ihub
In fact, I've read various studies that indicate similar things. Here's another example:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6078076/
Fatima Husain is well known in tinnitus research and she believes there could be a link between tinnitus (possibly severity), the precuneus, and the default mode network.
In that study, we compared a group of patients with mild tinnitus who had developed tinnitus recently, having had their percept for > 6 months but less than one year, to another group of patients with mild tinnitus that had their tinnitus for > one year. We examined three resting state networks (the DMN, dorsal attention, and auditory networks) and the only significant result was found in the DMN; patients with long-term tinnitus had decreased connectivity between seed regions and the precuneus when compared to the recent-onset group. This finding echoes the results found by Schmidt et al. (2013), which compared the same long-term group from Carpenter-Thompson et al. (2015) to control groups without tinnitus, and suggests that this disruption to the DMN is not immediate but occurs over time in patients.
In the current study, we examined an additional tinnitus characteristic's effect on resting state connectivity: tinnitus severity. Tinnitus severity in resting state studies has been variable, ranging from mild to catastrophic (Husain and Schmidt, 2014); it could therefore help to explain the differing results. The existing literature seems to suggest that tinnitus severity has a significant impact on the resting state.
I actually hypothesized something like what I just hypothesized exactly 13 months ago.
Our study begins the work of identifying invariant neural correlates of tinnitus across different subgroups, as well as determining measures that are unique to particular subgroups, using resting state functional connectivity. We propose that DMN-precuneus decoupling is a potential marker of long-term tinnitus, though increased tinnitus severity exaggerates this disruption. Further, coupling of the precuneus and DAN at rest is associated with bothersome tinnitus and is not always observed in those with mild tinnitus, possibly due to differences in habituation or more specific facets of tinnitus severity. Mild, recent-onset tinnitus appears to be a unique subgroup of tinnitus patients where resting state functional connectivity patterns have not yet changed from those seen in controls. The results of our study suggest that the efficacy of intervention studies can be investigated by noting changes in the pattern of DMN-precuneus and the DAN-precuneus connectivity; we hypothesize improvement in measures of tinnitus severity would be correlated with increased DMN-precuneus connectivity.
ajc
Member
- Feb 6, 2018
- 1,170
- Tinnitus Since
- 11/2002; spike 2009; worse 2017-18
- Cause of Tinnitus
- Loud music - noise damage
I guess you think this study is bullshit then?
https://www.bbc.com/news/science-environment-32414876
Then why aren't you grasping what the PhD researchers are saying while they quiet people's tinnitus?
The nerves always firing thing is true, it's just that they are overexcited when you have tinnitus from being exposed to loud sounds are caused from bearing damage. Dr. Shore has been looking into this thoroughly. Read more of her work.
"Tinnitus, sound perception in the absence of physical stimuli, occurs in 15% of the population and is the top-reported disability for soldiers after combat. Noise overexposure is a major factor associated with tinnitus but does not always lead to tinnitus. Furthermore, people with normal audiograms can get tinnitus. In animal models, equivalent cochlear damage occurs in animals with and without behavioral evidence of tinnitus. But cochlear-nerve-recipient neurons in the brainstem demonstrate distinct, synchronized spontaneous firing patterns only in animals that develop tinnitus, driving activity in central brain regions and ultimately giving rise to phantom perception. Examining tinnitus-specific changes in single-cell populations enables us to begin to distinguish neural changes due to tinnitus from those that are due to hearing loss."
https://www.cell.com/neuron/fulltext/S0896-6273(19)30433-7?_returnURL=https://linkinghub.elsevier.com/retrieve/pii/S0896627319304337?showall=true
The whole paper isn't released yet but that's from the abstract. I'm sure it will give us a lot more insight once it's fully available.
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