Dr. Robert Aaron Levine's Tinnitus Tutorial

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Dr. Robert Aaron Levine's Tinnitus...

Sorry, just noticed right now this forum is considered "off-topic", but there is no "General" forum to post in the tinnitus subject, so I posted it here..

 

This is an interesting different theory about tinnitus sources and some of you might like it

 

I didn't find the medication Clonazepam in the medication catalogue for my Country, is it distributed under another name as well? Could it be Rivotril? I observe that Rivotril has some Clonazepam in it. When I read the list of side effects for Clonazepam it looks like a poison! Really horrific side effects. Perhaps it is removed from my domestic market of that reason. It happens.

 

I don't know about this theory: A decrease in stimulation from the cochlear nerves due to hearing loss, causes an increase in stimulus from other nerves connecting to the dorsal cochlear nucleus (DCN)?

I'm not sure if I buy into this theory. I've also thought that the DCN plays a role in certain types of tinnitus - somatic tinnitus - but not the normal variety. Seems plausible that signals from somasensory nerves (like from the spine and face) can get mixed up with auditory nerves at the DCN, causing somatic tinnitus. But this theory seems to place blame on the DCN for all types of tinnitus.

 

@Karl

Yes, DCN involvement in tinnitus is popular among researchers. Most studies, moreover, examine the DCN's role in noise exposure. In these studies, chronic tinnitus results from a breakdown in the DCN's gatekeeping function. If the DCN can't contain the tinnitus precept, it becomes chronic.

The DCN's breakdown of its gating function is why drugs like AM 101 will be pivotal in preventing chronic tinnitus. AM 101 calms the damaged nerves and thus the tinnitus precept will be reduced or eliminated. The drug might work for chronic tinnitus, but Auris Medical (the makers of AM 101) believe the best chances are while the tinnitus is new. As they note on their website (I'm paraphrasing), undoing tinnitus may be difficult once the brain memorizes the precept.

For more information, you can do a pubmed search on "dcn" and "tinnitus." I believe there's 16 articles that include full, free text.

Here's the abstract to one of those articles:

Proc Natl Acad Sci U S A. 2012 May 22;109(21):8292-7. doi: 10.1073/pnas.1116981109. Epub 2012 May 7.

Mechanisms contributing to central excitability changes during hearing loss.

Pilati N, Ison MJ, Barker M, Mulheran M, Large CH, Forsythe ID, Matthias J, Hamann M.

Abstract

Exposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of hyperactivity, remain poorly explored. Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal cells that is overcome when additional multisensory fibers are recruited. Furthermore, gain modulation by inhibitory synaptic transmission is disabled in both auditory and multisensory pathways. These cellular mechanisms that contribute to decreased cellular excitability in the central auditory pathway are likely to represent early neurobiological markers of hearing loss and may suggest interventions to delay or stop the development of hyperactivity that has been associated with tinnitus.

Source: http://www.ncbi.nlm.nih.gov/pubmed/22566618

You might start with this PDF that explains the various functions the DCN plays in tinnitus. It's interesting reading:

http://stuff.mit.edu/afs/athena/course/other/hst.722/www/Topics/DCN/Kaltenbach2006.pdf

Have fun!

 

I think that the key question here is whether you prefer tinnitus or prefer other side effects. Many people would prefer the other side-effects rather than to be left with tinnitus. It also says something interesting at the end of the video : If you try several GABA enhancing drugs, then some combination of them would shut down the tinnitus completely for more than 7% percentage of the population. The usage of this medication is considered "Chronic" which means once you stop taking these, the tinnitus will get back at even more intensity (but will always return to normal volume)

 

Yes. Clonazepam is distributed under the name Rivotril in some countries. See first paragraph in link below.

http://en.wikipedia.org/wiki/Clonazepam

 

I saw this thread earlier and funnily enought I came upon this thread while browsing for something else:

http://www.bluelight.ru/vb/archive/index.php/t-662532.html

Some really interesting discussion in this thread, they mention Levin's ideas, long-term treatment with benzo's, gabapentin, etc.

 

It's not like it's a choice between tinnitus and side effects, the drug is not that effective . If that was the case Clonazepam/Rivotril would be a sensational progress in T treatment, but it's not. It's just a psykofarmaka that can have some beneficial effects in context of T. The only guarantee here is side effects. Believe me, if this medication could CURE tinnitus everyone would take it.

 

Thank you, Jazz. I will peruse through these.

Last year I was reading a neurology book, and I remember reading about the DNC, and all the types of neurons that come together there. It's amazing how much knowledge brilliant medical researchers have amassed about the human brain.

My gut feeling is that tinnitus is due to a neurological circuit which is compensating for an imbalance in hearing. I view the brain like a radio with components. Whereas a radio has amplifiers, tuners and rectifiers, the auditory system has the DNC, and other "olive" size structures that are wired together, eventually delivering information to the higher brain. All of this stuff is very primitive, which is why our higher conscious thoughts have little control over some of these aspects of tinnitus.

I've never accepted Jastreboff's theory about the cause of tinnitus being due to "spontaneous neurological emissions". This study of the DNC seems promising. I hope that someday we can see an electrical schematic that will explain what is going wrong with the auditory circuit that causes tinnitus.

 

Hi, Is that the theory that ear imbalance (left ear hears 50%, right ear 100%) causes the tinnitus?
If so, then this doesn't explain why when the auditory nerve is cut then for some patients the tinnitus disappears. You would expect for ear imbalance that when the nerve is cut, then the tinnitus in the cut ear would be insane.
The theory here is the first I've seen to explain this phenomena.
Although, I don't really believe myself too much that such phenomena exists for large percentage of the tinnitus patients, even when I see studies point it out - just doesn't makes sense, because people who have gone deaf 80% of them have tinnitus. So why when the auditory nerve is cut the tinnitus disappears?

In other slide, Professor Levin says that the perception of tinnitus is when frequencies from the ear signals do not fire randomly. If the ear is firing randomly for all of it's 30,000 frequencies, then there will be no tinnitus sound. But if the ear is firing synchronously or do not fire at all for some of the frequencies, then there will be tinnitus.
In this case, when the ear seize to fire at 100% of it's frequencies, I wonder what will happen - will there be no tinnitus sound? unless the tinnitus is remembered at the neural regions. I wonder if there is a research paper telling the time-to-cut from the onset of tinnitus. If what Robert Levine says is true, then cutting the auditory nerve in <6 months should cure most of the hearing loss induced tinnituses. I wonder if there's a paper to verify that.

 

@Karl I like your radio analogy! Tinnitus is a two-part problem, initiated by the auditory periphery but maintained by the interactions among the auditory periphery and the auditory and non-auditory cortical structures and limbic system. I've read a few articles--which I need to locate--that suggest curing tinnitus will require treatment to the peripheral auditory system as well as the brain. This, of course, is after the tinnitus precept becomes chronic. While still acute, treating the ear alone should suffice.

You're right, the DCN and its related structures are why we struggle to consciously control our tinnitus. It's also obvious the "bottom up" approach alone holds the power to cure tinnitus. The "top down" approach of TRT and CBT may--at best--succeed in surpressing the tinnitus sound from our consciousness. What does Jastreboff say about the "habitation of perception?" I know he says it follows the "habituation of reaction," but does he argue that the former means you no longer hear the tinnitus at all? And why doesn't everyone achieve a "habitation of perception?" I, for example, very rarely react to my tinnitus--but I've not achieved a "habituation of perception." Several habituated people I know, moreoever, are all able to call up their tinnitus at will. But, in general, they are not aware of their noise.

About tinnitus' auditory circuitry, I believe it will be mapped within a few years, given all the imaging studies recently conducted and currently planned. How resting states between normal and tinnitus brains differ is usually the focus of most studies. Of course, other areas of interest include the interconnectedness of tinnitus circuits (or hubs), which is a favorite of De Ridder; and some scientists are exploring changes in gray matter between normal and tinnitus subjects.

Regarding Jastreboff's "spontaneous neurological emissions" concept, it does sound nebulous. Viewing these "emissions" as an effect--rather than a cause--is more logical. Of course, Jastreboff's contributions to tinnitus theory are immeasurable. Among them, he developed the first animal model of tinnitus, noted in his profile at Emory. From this model, I'm presuming, he developed his neurophysiological model tinnitus. That model's postulate of the limbic system's role in tinnitus is still relevant today, even if the exact details remain debatable.

I need to ask a quick question on hearing aid amplifiers. Where did you locate this information? I couldn't find any online manuals with technical specifications. I don't have Widex's hearing aids; I have Starkey's and, though designed for tinnitus, I wonder if it has too few amplifiers. (I also wonder about about the different compression algorithms.) Specifically, I wonder if more amplifiers might prevent or alleviate my recruitment. Unfortunately, I can't ask my audiologist as she's no longer available, and her former office will not tell me what happened to her. I've checked online and with licensure officials but she's apparently gone. (I suspect she'll turn up somewhere eventually.)

Of course, my hearing aids could just need an adjustment. But I'm not comfortable with another audiologist from her (former) office adjusting them, given the circumstances.

 

This is also an interesting talk on Tinnitus:

http://research.microsoft.com/apps/video/default.aspx?id=141026

 

Unfortunely, I do not know of ANY existing method to reverse hearing loss after noise exposure.
The only thing that comes to mind is hyperbaric chamber, but that is used for sudden deafness and in low agreement between experimental results too. I do not know of any hyperbaric chamber that was used for hearing loss after noise exposure.