Tinnitus Mapped Inside Human Brain
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I really don't, Mark. Sorry to disappoint you. I just don't. I donate all the profits from my clinic to tinnitus research, and I encourage others to donate as they see fit. But that is currently the entire extent of my involvement.
When I'm not seeing patients or trying to address issues of concern on this board (from which I derive considerable pleasure), I work on my photography, participate in community volunteer efforts, attend theater and opera, read books, travel, and hang out with my wife ... whom I have totally adored for some forty years now. But during those times, tinnitus research is about the farthest thing from my mind.
MemberHave to agree with you there Doctor in lifestyle terms anyway. While I think research should be guided by sufferers as the undisputed "experts" in the field, The daily slog is better performed by those who don't have it (or at least not in a severe form) simply for objectivity and research bias purposes if nothing else.
How can you tell? So I might hear 'acoustic sounds' with my sensorimotor or limbic cortex?
I wrote something here about it,
https://www.tinnitustalk.com/threads/is-tinnitus-caused-by-damage.9365/#post-113721
And there you lost me. That all sounds like someone wants to sell more masking devices.
Yeah, the louder the better. It's called masking. Nothing new under the sun!
If two people talk and a third one yells like crazy those two having a hard time with their conversation, I suppose.
I get that you're cynical about this, and it's hard not to be if you're still struggling with your tinnitus.
However, if we ever want researchers to get serious about curing tinnitus, we need to stop belittling their efforts. And I think Gander's work here is nothing short of phenomenal - he's disproven 40 years of thinking about how tinnitus works in the brain.
Gander is just a researcher who works at a University - he doesn't sell anything, and he doesn't have a tinnitus-specific practice. If you read both the WBUR news release, and the underlying study in detail, you'll see that:
- The method of suppressing tinnitus through the use of sound is not masking; for decades, researchers know that a loud tone amplified through the ears suppresses the brain activities that generate the phantom sound. Masking doesn't suppress the brain activity involved in tinnitus, it just covers it up with something else that you focus on. The distinction is important.
- Mapping tinnitus in this way (showing that tinnitus requires large segments of the brain to participate in generating the phantom phenomenon, and not just the auditory cortex) has been successfully reproduced in animals by inducing tinnitus in them and observing how much of the brain is required to actually trigger the sounds we all hear.
I do not understand. Do you mean that research in tinnitus should be guided by "experts" in suffering?
Heracles slayed the hydra, it just took a lot of thinking and trial and error before he found a way.
Sorry you read it that way, I just fear that some research is driven by imperatives that aren't necessarily in the best interests of patients, and I think the experience of sufferers should be the first consideration, not say...the intellectual property needs of a drug company for example, or the publishing needs of yet another Lit searcher.
It look likes T is invading the whole brain. IT is like a brain tumor which is not going to kill you directly but inderctly(you will commit suicide).
Ahaaaa now researchers start digging into the brain they were asleep for so many years. Now they have figured it out aha it is even outside the auditory cortex. Same think could have been done long time ago why they have waited so long to see where is it. What, there were not a guinea pig?
But this is a good finding in the end of the day. Any finding about tinnitus is a good finding. But much more need to be done so our dream comes true one day.
Reproduced below was my comment on a scientific study entitled Intracranial Mapping of a Cortical Tinnitus System using Residual Inhibition (http://www.cell.com/current-biology/fulltext/S0960-9822(15)00278-X) which I read in Current Biology on the cell.com website. However, before I received a definite answer as to whether the comment would be appropriate for publication online by Cell Press Editors, I decided to go ahead and publish it immediately as a post on LinkedIn with a brief additional reflection included at the end of the comment.
'Tinnitus and the prefrontal cortex
I propose that residual inhibition (RI) in this study transiently brings about general aural alertness which would involve some of the impulses giving rise to tinnitus—such impulses being putatively associated with a proportion of sensory impulses from hair cells in the organ of Corti ascending via the non-specific projection nuclei of the thalamus (http://what-when-how.com/neuroscience/the-thalamus-and-cerebral-cortex-integrative-systems-part-2/) and diverted to control sensory input over the suprageniculate/limitans complex via the S1/M1. The result is desynchronization of delta/theta and alpha waves during tinnitus suppression observed as delta/theta and alpha oscillatory power decreases.
The hyperactivity noted in the division of the ascending fibres implicated in tinnitus I would interpret not to originate in the suprageniculate/limitans complex itself but actually to be as a result of afferent impulses from the damaged or faulty part of the peripheral auditory system being employed in the control of auditory sensory input and memory after being amplified by associated prefrontal cortex interneurones and reflected back as a constant din or echo emanating from the organ of Corti and ear-drum in conjunction with Wernicke's area (Wernicke's area, along with the A1, forming part of the superior temporal gyrus, STG).
Concerning such an elusive topic, substantially the same thing can, with benefit, be viewed from a slightly different angle:-
The 'underlying' heightened activity 'in the ascending auditory pathway' which is said to be the basis of tinnitus perception stems, in my view, from part of the damaged or faulty peripheral auditory system of the subject in the study which would have an adverse effect on a proportion of sensory impulses from hair cells in the organ of Corti putatively ascending via the non-specific projection nuclei of the thalamus and involved in the control of auditory memory and cognition. The hyperactivity stemming from the peripheral aural damage or fault is thus proposed to leak, as superfluous auditory input, into the non-specific projection nuclei of the thalamus and echo, in the form of beta2 and gamma power increases, in the organ of Corti and ear-drum in conjunction with Wernicke's area (which forms part of the superior temporal gyrus). The wide propagation within the auditory cortex of these beta2 and gamma oscillatory power increases, during tinnitus suppression, is proposed to be greatly aided and abetted by excitatory interneurones in the prefrontal cortex and paralleled by pathological delta oscillatory power decreases which, in the same manner, would also leak into the cerebral cortex via the non-specific projection nuclei of the thalamus and as a result of being employed to control input over the suprageniculate/limitans complex via the S1/M1.
Crucially, as is clear from my book (http://www.amazon.com/Human-Nervous-System-Programming-Behavioural/dp/1494917831/) overactive prefrontal cortex interneurones are well established to be a source of chronic physical and psychological disorders and tinnitus, in my view, is no exception in this regard. My recommendation as a mental health expert would be to desensitize those overactive parts of the prefrontal cortex which putatively amplify the tinnitus arising from the damaged or faulty part of the peripheral auditory system. The desensitization—possibly in the form of hypnosis, meditation or neurobiofeedback—may result in a beneficial disinhibition of the pathological delta frequency waves observed in this study in addition to a reduction in the level of tinnitus perceived by the individual affected.
For those who happen to have a copy of my aforementioned book, 'conflictive "interpretations" ' on pages 27, 31 and 32 give rise to emotional tension which in turn impels sustained cortical activities as an incentive in the individual to find semantically appropriate vocabulary to assuage such tension. 'Conflictive "interpretations" ' would directly correspond to 'prediction errors' in the present study that would give rise to high-end gamma oscillatory activity as an impetus in the subject concerned to assuage emotional tension (positive covariance)—apparently magnified by limbic structures—between various memory regions, for example auditory and visual memory centres involving association cortices and association fibres.
There is one apparently final puzzle to solve which is: What transiently causes the tinnitus suppression following the tonal stimulus (5 kHz) in the study? In my view, prefrontal cortex interneurones associated with sensory impulses arising from the non-specific projection nuclei of the thalamus and the S1/M1 and involved in controlling auditory input to A1 transiently inhibit reciprocal prefrontal cortex interneurones associated with impulses controlling auditory input to the non-A1 cortex, which latter impulses, as I have already emphasized, receive leaked superfluous ones from the damaged or faulty part of the peripheral auditory system—thereby producing tinnitus as an echo reverberating from the organ of Corti and ear-drum.
Readers of my book should be able to recognize, in the series of hypothetical diagrams of cortical activities, the prefrontal cortex interneurones associated with sensory impulses arising from the non-specific projection nuclei of the thalamus.
'Tinnitus and the prefrontal cortex
I propose that residual inhibition (RI) in this study transiently brings about general aural alertness which would involve some of the impulses giving rise to tinnitus—such impulses being putatively associated with a proportion of sensory impulses from hair cells in the organ of Corti ascending via the non-specific projection nuclei of the thalamus (http://what-when-how.com/neuroscience/the-thalamus-and-cerebral-cortex-integrative-systems-part-2/) and diverted to control sensory input over the suprageniculate/limitans complex via the S1/M1. The result is desynchronization of delta/theta and alpha waves during tinnitus suppression observed as delta/theta and alpha oscillatory power decreases.
The hyperactivity noted in the division of the ascending fibres implicated in tinnitus I would interpret not to originate in the suprageniculate/limitans complex itself but actually to be as a result of afferent impulses from the damaged or faulty part of the peripheral auditory system being employed in the control of auditory sensory input and memory after being amplified by associated prefrontal cortex interneurones and reflected back as a constant din or echo emanating from the organ of Corti and ear-drum in conjunction with Wernicke's area (Wernicke's area, along with the A1, forming part of the superior temporal gyrus, STG).
Concerning such an elusive topic, substantially the same thing can, with benefit, be viewed from a slightly different angle:-
The 'underlying' heightened activity 'in the ascending auditory pathway' which is said to be the basis of tinnitus perception stems, in my view, from part of the damaged or faulty peripheral auditory system of the subject in the study which would have an adverse effect on a proportion of sensory impulses from hair cells in the organ of Corti putatively ascending via the non-specific projection nuclei of the thalamus and involved in the control of auditory memory and cognition. The hyperactivity stemming from the peripheral aural damage or fault is thus proposed to leak, as superfluous auditory input, into the non-specific projection nuclei of the thalamus and echo, in the form of beta2 and gamma power increases, in the organ of Corti and ear-drum in conjunction with Wernicke's area (which forms part of the superior temporal gyrus). The wide propagation within the auditory cortex of these beta2 and gamma oscillatory power increases, during tinnitus suppression, is proposed to be greatly aided and abetted by excitatory interneurones in the prefrontal cortex and paralleled by pathological delta oscillatory power decreases which, in the same manner, would also leak into the cerebral cortex via the non-specific projection nuclei of the thalamus and as a result of being employed to control input over the suprageniculate/limitans complex via the S1/M1.
Crucially, as is clear from my book (http://www.amazon.com/Human-Nervous-System-Programming-Behavioural/dp/1494917831/) overactive prefrontal cortex interneurones are well established to be a source of chronic physical and psychological disorders and tinnitus, in my view, is no exception in this regard. My recommendation as a mental health expert would be to desensitize those overactive parts of the prefrontal cortex which putatively amplify the tinnitus arising from the damaged or faulty part of the peripheral auditory system. The desensitization—possibly in the form of hypnosis, meditation or neurobiofeedback—may result in a beneficial disinhibition of the pathological delta frequency waves observed in this study in addition to a reduction in the level of tinnitus perceived by the individual affected.
For those who happen to have a copy of my aforementioned book, 'conflictive "interpretations" ' on pages 27, 31 and 32 give rise to emotional tension which in turn impels sustained cortical activities as an incentive in the individual to find semantically appropriate vocabulary to assuage such tension. 'Conflictive "interpretations" ' would directly correspond to 'prediction errors' in the present study that would give rise to high-end gamma oscillatory activity as an impetus in the subject concerned to assuage emotional tension (positive covariance)—apparently magnified by limbic structures—between various memory regions, for example auditory and visual memory centres involving association cortices and association fibres.
There is one apparently final puzzle to solve which is: What transiently causes the tinnitus suppression following the tonal stimulus (5 kHz) in the study? In my view, prefrontal cortex interneurones associated with sensory impulses arising from the non-specific projection nuclei of the thalamus and the S1/M1 and involved in controlling auditory input to A1 transiently inhibit reciprocal prefrontal cortex interneurones associated with impulses controlling auditory input to the non-A1 cortex, which latter impulses, as I have already emphasized, receive leaked superfluous ones from the damaged or faulty part of the peripheral auditory system—thereby producing tinnitus as an echo reverberating from the organ of Corti and ear-drum.
Readers of my book should be able to recognize, in the series of hypothetical diagrams of cortical activities, the prefrontal cortex interneurones associated with sensory impulses arising from the non-specific projection nuclei of the thalamus.
http://www.sciencedaily.com/releases/2015/05/150512152646.htm
Though it's not known yet exactly where and how tinnitus occurs in the brain, Salvi says their functional MRI studies show the abnormal activity underlying tinnitus and hyperacusis isn't confined to a specific brain location, but actually involves a neural network.
Though it's not known yet exactly where and how tinnitus occurs in the brain, Salvi says their functional MRI studies show the abnormal activity underlying tinnitus and hyperacusis isn't confined to a specific brain location, but actually involves a neural network.
Please can you explain that in laymans language cos I am really sorry but i have not understood it at all and would really like to understand this...........i am sure that i am not the only one here who has not understood this.................please can you try to make it simple for us who are not medically trained - thanks ever so much.....
So, chicken or egg? Are they observing a cause or a result of tinnitus.
