Tinnitus as the Phantom Limb Syndrome of the Brain — Tinnitus Spikes & Fluctuations

[Kriszti]

I am aware that tinnitus can be interpreted as the phantom limb syndrome of the brain. Brain loses auditory input and due to maladaptive plasticity neurons get hyperactive and create these phantom sounds: "when you disrupt the signal along the auditory pathway, the brain interprets the lack of signal as tinnitus." (Quote from @FGG).

What I don't understand is how we can insert temporary spikes or daily fluctuations in tinnitus volume into the picture? One of my tinnitus sounds is always elevated for hours after certain moderately loud things (blowdrying my hair with Peltor X5A muffs on, etc), and fortunately I don't have relentlessly the same volume all the time.

Can this mean that the hair cells are not totally dead, but damaged and during spikes they are holding to their dear life? Or is it more likely a synapse problem? Or the hyperactivity of the brain is not always on the same level?

Also, what's the difference in this case between unilateral and bilateral tinnitus? Can they have the same root cause or are they completely different? If damage is detectable on an audiogram only in one ear, but the tinnitus is bilateral and it's frequency matches where there is the drop in hearing, what does that mean? If we go back to the phantom limb analogy, it's like if the missing limb caused pain in the other leg as well, right? And similarly so, can hair cell damage cause only unilateral tinnitus? (I'm not sure if I'm making sense here...)

I apologize for the very laic approach to the problem.

 

[FGG]

I am aware that tinnitus can be interpreted as the phantom limb syndrome of the brain. Brain loses auditory input and due to maladaptive plasticity neurons get hyperactive and create these phantom sounds: "when you disrupt the signal along the auditory pathway, the brain interprets the lack of signal as tinnitus." (Quote from @FGG).

What I don't understand is how we can insert temporary spikes or daily fluctuations in tinnitus volume into the picture? One of my tinnitus sounds is always elevated for hours after certain moderately loud things (blowdrying my hair with Peltor X5A muffs on, etc), and fortunately I don't have relentlessly the same volume all the time.

Can this mean that the hair cells are not totally dead, but damaged and during spikes they are holding to their dear life? Or is it more likely a synapse problem? Or the hyperactivity of the brain is not always on the same level?

Also, what's the difference in this case between unilateral and bilateral tinnitus? Can they have the same root cause or are they completely different? If damage is detectable on an audiogram only in one ear, but the tinnitus is bilateral and it's frequency matches where there is the drop in hearing, what does that mean? If we go back to the phantom limb analogy, it's like if the missing limb caused pain in the other leg as well, right? And similarly so, can hair cell damage cause only unilateral tinnitus? (I'm not sure if I'm making sense here...)

I apologize for the very laic approach to the problem.

In regards to your first question, my understanding is that if you never have reactive tinnitus or spikes or fluctuations yours is just structural without cofactors.

However, inflammation in the cochlea can produce fluctuations. There seems to be a unique type of cochlear inflammation mediated by dynorphins released during chronic stress that perpetuates excess glutamate release and NMDA receptor sensitivity (it's directly pro-inflammatory cytokines, too)

Endogenous dynorphins, glutamate and N-methyl-D-aspartate (NMDA) receptors may participate in a stress-mediated Type-I auditory neural exacerbation of tinnitus

So people under chronic stress are not only going to have an unfavorable neuroimmune profile in terms of Glutamate ratio, but they are also going to have their cochlear NMDA receptors be more primed for overstimulation in response to noise.

So it seems that if there isn't a somatic cause to fluctuations, anxiety really can make you prone to noise setbacks and spikes.

 

[AliasM]

These are all questions I have wondered too Kriszti.

 

[AliasM]

I read the link you posted @FGG. I barely understood a word of it. It said 'treatment options are discussed' at the end of the abstract, but I can't see the full article.

Tinnitus is mainly in my brain, all over my brain. My brain is going OFF. Neurons are firing all over the place and I hear it and feel it.

 

[FGG]

I read the link you posted @FGG. I barely understood a word of it. It said 'treatment options are discussed' at the end of the abstract, but I can't see the full article.

Tinnitus is mainly in my brain, all over my brain. My brain is going OFF. Neurons are firing all over the place and I hear it and feel it.

I don't have access to the full article, either.

I'm not sure what treatment options they would discuss other than stress reduction treatments since stress' direct local effect on the cochlea were the focus of the article.

I posted it not for the treatment options part but more to show the link between chronic stress and local cochlear inflammation through the release of peptides in the body called dynorphins. This was mostly to explain fluctuations due to stress.

Fluctuations can happen due to somatic things, too, in the neck, jaw and also from middle ear muscle spasms. Do you know the cause of your tinnitus?

 

[annV]

I can't see the full article.

I don't have access to the full article, either.

 

[FGG]

I take it back. There is way more to this article.

I need to read it more carefully soon but the article was actually much more interesting than I suspected and was even suggesting a fully novel treatment for stress induced tinnitus fluctuations: opioid blockers.

The thinking is that, since dynorphins act on a subtype of opioid receptor, you can possibly block it with opioid receptor blocking. Seems like it could make pain potentially worse if you had noxacusis, though...

They also talked about NMDA receptor treatments like the one Otonomy has currently in clinical trials.

The theory that loudness hyperacusis is perpetuated by dynorphins' effects on the NMDA receptor is one I hadn't heard, either.

 

[FGG]

@Aaron91, @Zugzug:

You both might find the article @annV posted above interesting.

 

[Greg Sacramento]

@AliasM, go back to the thread - I Don't Know What to Do Anymore: We had a discussion there. Read my last message and then review our conversation. Consider to continue using a moist warm compress on center on neck and on neck under head.

 

[Greg Sacramento]

@FGG, there's nothing in that article that has any real treatment benefit. I read it before and researched all treatments. Not sure if I posted this article before.

 

[FGG]

@FGG, there's nothing in that article that has any real treatment benefit. I read it before and researched all treatments. Not sure if I posted this article before.

I disagree for a very specific subtype of people who have chronic (especially uncoping stress) as a severity co-factor. I'm not sure opioid blockers are the answer or not but I am glad the question is being asked.

The premise of the effects of dynorphins on the NMDA receptor is a specific kind of hyperactivity. It may explain why people under severe and prolonged stress can get tinnitus from a relatively low level noise exposure.

I think it's just part of an extremely multi factorial picture.

 

[AliasM]

@AliasM, go back to the thread - I Don't Know What to Do Anymore: We had a discussion there. Read my last message and then review our conversation. Consider to continue using a moist warm compress on center on neck and on neck under head.

Thanks Greg. I just read back over the notes and the MRA of my neck appears normal. It mentions nothing about the occipital nerves though. I had a professional massage a few days ago on my neck and have been getting my husband to do it also. Since then, no back of head chirping. I have been using the warm compress. The rest of my brain though is still absolutely going off. I see a neurologist on Wednesday. I have to travel 600km to see them, which I am incredibly anxious about. I have been getting panic attacks travelling just 5 minutes in the car. There is no way I will fly though at the moment so car it is. My father is going to take me. My goodness I hope the neuro is good.

 

[Jcmc]

The premise of the effects of dynorphins on the NMDA receptor is a specific kind of hyperactivity. It may explain why people under severe and prolonged stress can get tinnitus from a relatively low level noise exposure.

That's the point.

I want to add that stress in short term is like a boost to your body, for example your senses are heightened (like superhuman)!

When I was young a friend had an accident where he injured his leg. He had normal pain but he had a stressful situation where we had to leave running from school and he practically ran better than anyone else. However after that he had so much pain from his injury, much more intense than before.

So in stress we have heightened sense of hearing and if you have hearing loss at that point or have a noise exposure maybe this a good combination to get tinnitus and hyperacusis.

 

[Greg Sacramento]

I had a professional massage a few days ago on my neck and have been getting my husband to do it also. Since then, no back of head chirping. I have been using the warm compress.

I was pretty sure that warm compresses would help with head chirping. Did not want to mention massage as you didn't have a CT angiogram and with that not sure if something else besides inflamed occipital(s) is happening - including panic attacks - brief periods of hypertension blood pressure. Hopefully your neurologist is good and hope that all will go away in time. Be positive.

 

[Aaron91]

You both might find the article @annV posted above interesting.

I somehow missed this but thankfully saw your reply to @Zugzug on the other thread. I'm about to go to sleep but I've just had a brief scroll through on my phone and all I can say is that I don't think I've come across an article over the last 6 months that has piqued my interest as much as this one. I can't speak for ZugZug and I must caveat that I need to read and analyze this carefully, but on first impressions I think the mechanisms described here could be highly relevant to my case of hyperacusis, as I developed my symptoms while going through the most stressful time of my life (and to an extent, still am). I'll read more over the next day or two and get back to you. Thank you so much @FGG for bringing this to my attention.

 

[kuromi]

In regards to your first question, my understanding is that if you never have reactive tinnitus or spikes or fluctuations yours is just structural without cofactors.

This is the first time I've read anything like this! My tinnitus began with an ear infection and I'm 6 months in. I've never experienced any spikes at all, no reactivity or fluctuations (beyond some fading).

Could this point towards anything in particular in terms of structural damage?