Increased Pyramidal and VIP Neuronal Excitability in Auditory Cortex Correlates with Tinnitus

A study on rats looking at different pathways in tinnitus and similarities with neuropathic pain.

Increased Pyramidal and VIP Neuronal Excitability in Primary Auditory Cortex Directly Correlates with Tinnitus Behavior

This links in with Professor Dirk De Ridder's models and how he prescribes his medicine cocktails.

Episode #6: Part 1/2: "Medication for...

I hope some find it useful.

 

I think this research is promising.

 

Onset-offset cortical auditory evoked potential amplitude differences indicate auditory cortical hyperactivity and reduced inhibition in people with tinnitus

Conclusions: Hypothesized reduced central inhibition and/or increased excitation in tinnitus participants was partially supported by a group difference in ΔP2 amplitude.

Significance: This was the first study to evaluate CAEP onset minus offset differences to investigate changes in central excitation/inhibition in individuals with tinnitus versus controls in matched groups.

 

That was a great find. I like this kind of study a lot because they seem to be building on that upstream gating hypothesis proposed by Rauschecker, which they mention as well. I hope these researchers continue to build momentum in that direction as I genuinely feel that's where the most effective treatment, and perhaps even a cure, lies.

 

@UKBloke, the upstream gating I presume is the generation in the cochlear nucleus that spreads through the inferior colliculus, the thalamus, the auditory cortex and then to areas that react with emotion and cognition? I need to look into this more.

It's interesting as if you listen to Dr. Shore, she says the root is in the cochlear nucleus and if you can turn it off there, then tinnitus is treated. She seems certain and set in this, almost to the point that looking to treat elsewhere is unnecessary.

If you are interested in the gating mechanism, Min Chul Park from NZ has some presentations on this. You can open the PDF files through here:

Gating mechanism in tinnitus : explored in surgery-induced unilateral deafness in adult humans

 

@Nick47, you are a powerhouse with keeping the community updated. Thank you for your time and energy.

 

@Dam, driven by despair more like lol.

 

The Park study opening statement is absolutely key and a real golden-nugget:



I'm vaguely familiar with how gating/filtering works in the electronic circuit design sense, having studied this stuff at college level many years ago. That's probably why when I learned that Rauschecker in his 2011 tinnitus study had mentioned something else going on upstream from the cochlear, likely related to gating, it seemed to me to be an absolutely rational explanation for why some people with cochlear damage suffer tinnitus whilst others don't.

It's not to say that I disagree with Dr. Shore, (I'm not a research scientist at the end of the day), however I do see the UMich invention as more of a dampening device than a cure. In other words, I do think it can mitigate the tinnitus signal, which will be an absolute breakthrough for so many of us, but I don't believe the device will treat the underlying cause.

My gut feeling regarding that is that we sufferers are born with a genetic defect that affects the build-standard of our neural gating systems leading to errant control voltages and failure of those gates to keep neural sub-conscious noise separate from the conscious. I think the physical fix to tinnitus will eventually reside in treating those gating circuits so that they function correctly.

 

So are there people with noise/acoustic trauma induced hearing loss that do not have tinnitus?

I think the theory about sudden vs. gradual hearing loss makes more sense. When gradual, the brain manages to adapt, when sudden, it does not, and goes haywire. The "gating mechanism" to me sounds like baloney. I think the theory about DCN imbalance and cross-wired inputs from somatic nerves makes more sense. That's why I can create/modulate sound with my jaw now after my acoustic trauma induced hearing loss - the neurons in DCN went haywire. Before it was imperceptible. I do not have/never had any jaw issues. None whatsoever.

So Dr. Shore's device is on-point perhaps, even if it does not work perfectly.

 

No one knows for sure, but what you're saying makes sense. There is certainly something mysterious going on about the fact that some people don't ever get tinnitus despite smashing their ears with sound all their life, while others get it with just one small event.

My usual argument is what happens with the diseases that have tinnitus as a forced symptom (Meniere's, otosclerosis etc). You would think that some people, out of those affected, had a strong gating system that would negate the tinnitus caused by those diseases. But that doesn't happen, as far as I know. So it follows your logic: these diseases cause sudden losses, the brain goes haywire, tinnitus comes through.

It still remains unexplained how some people never get acoustic traumas or hearing loss (and subsequent tinnitus), no matter how loud lives they live. Genetics? Gating systems? Big strong cochleas?

 

Who knows. It could be a combination of factors. My acoustic trauma was aggravated by sinus infection I had at the time. It fooled me into thinking the noise is not as loud as it was and likely contributed to the damage/lack of recovery.