Hyperacusis

[frozenborderline]

I have severe hyperacusis. It may be one of my worst symptoms. In past few days it had gotten worse so I'm extra motivated to research it ... but have low energy.

Anyway in the past I connected my hyperacusis to brainstem , especially bc I have cci. And brainstem is known to control sensory input (naviaux says this) . And specifically I found one paper that said high glutamate in brainstem is responsible for sound sensitivity.

Makes sense bc gabaergics and nmda antagonists, along with traction to some extent, were what relieved hyperacusis.

Anyway to treat hyperacusis I'm not sure I can just ask a palliative care doctor bc the treatment depends on the cause, even to justnpalliate the symptoms. There arent across the board broad hyperacusis drugs like there are forpain, it's even more heterogeneous.

So I am desperately trying to pinpoint cause. It does seem like medical establishment agrees that brainstem could be involved, heres a quote

What causes hyperacusis ?

• Inner ear -- e.g. Menieres's disease, Superior canal dehiscence
• 8th nerve -- e.g. microvascular compression, after surgery on the 8th nerve.
• Brainstem
• Brain -- migraine
• Psychological -- highly vigilant or obsessive people; Asperger's syndrome

There are many causes of hyperacusis (Katznell and Siegel, 2001). There is not a single mechanism, and furthermore there is not a single "magic bullet" for hyperacusis.



Anyway , later in that same article baclofen is listed as something that could help. Opioid agonists have also helped me some.

 

[Judee]

I think a lot of us deal with this type of sensory overload. I've often thought that autism and ME/CFS have some slight overlap because I've read of it in children with autism.

The Sound of a Miracle by Annabel Stehli talks about how they figured this out and had her daughter Georgie go through auditory retraining to correct the problem.

I don't know what to suggest though for you now. Hope someone can offer some good ideas.

 

[Hip]

I found very low dose amisulpride noticeably improves my hyperacusis (sound sensitivity). Does not eliminate it, but it helps.

My theory (see also here) is that sound sensitivity may be due to a sensory gating dysfunction in the brain (sensory gating is the brain's "computer firewall" that is supposed to prevent irrelevant sensory stimuli from reaching consciousness).

I've noticed that any drug which modulates dopamine D2 receptors (as amisulpride does) has an effect on my sound sensitivity. D2 receptors are thought to be involved in the "firewall" process of filtering out of irrelevant information.

According to this post I wrote in 2013, I also found vinpocetine, piracetam and Bacopa monnieri helpful, although I don't remember testing those for sound sensitivity.


There is an hyperacusis forum, though I did not find many useful treatments the last time I looked on it.

 

[frozenborderline]

I found very low dose amisulpride noticeably improves my hyperacusis (sound sensitivity). Does not eliminate it, but it helps.

My theory (see also here) is that sound sensitivity may be due to a sensory gating dysfunction in the brain (sensory gating is the brain's "computer firewall" that is supposed to prevent irrelevant sensory stimuli from reaching consciousness).

I've noticed that any drug which modulates dopamine D2 receptors (as amisulpride does) has an effect on my sound sensitivity. D2 receptors are thought to be involved in the "firewall" process of filtering out of irrelevant information.

According to this post I wrote in 2013, I also found vinpocetine, piracetam and Bacopa monnieri helpful, although I don't remember testing those for sound sensitivity.


There is an hyperacusis forum, though I did not find many useful treatments the last time I looked on it.

I remember your post on amisulpride , but do you think that the brainstem compression induced hyperacusis is treatable by amisulpride or do we have two separate types of hyperacusis/theories?

I also think its possible that neural strain/compression has same effects as viral or toxin induced inflammation/glutamate in the same area however.

Additionally, one of my doctors seemed to think it could be migraine related or work on a similar mechanism even if not a full blown migraine. However , the brainstem thing seems more likely to me based on my cci. Pretty sure @jeff_w and jen brea had their sensory sensitivity resolve after surgery

 

[Hip]

do you think that the brainstem compression induced hyperacusis is treatable by amisulpride or do we have two separate types of hyperacusis/theories?

I believe sensory gating (the firewall of consciousness) occurs in the brainstem, so I think these theories would be one in the same.

When the firewall is broken, lots of irrelevant stimuli enter into conscious awareness, rather than being suppressed before they reach consciousness. So consciousness gets overloaded with too much sensory info.


Years ago on another forum, someone with a PhD in biochemistry read a lot of papers on the dopamine receptors, and concluded that roughly speaking:

Dopamine D1 activation = task reward (the satisfaction you get from completing a task)

Dopamine D2 activation = firewall (filtering out irrelevant stimuli) and task focus (concentration on a specific task).

 

[Pyrrhus]

I believe sensory gating (the firewall of consciousness) occurs in the brainstem

I would think sensory gating occurs primarily in the thalamus, although there might be contributions from other regions of the brain, such as the prefrontal cortex or the basal ganglia.

The thalamus in this system acts as both the gate for sensory input to the cortex as well as the site for feedback from cortical pyramidal cells, implying a processing role in sensory perception in addition to its function in directing information flow. The state of the brain, whether it be conscious, in REM sleep, or non-rapid eye movement sleep, changes how sensory information is gated through the thalamus.

Source: https://en.wikipedia.org/wiki/Recurrent_thalamo-cortical_resonance

 

[Hip]

I would think sensory gating occurs primarily in the thalamus, although there might be contributions from other regions of the brain, such as the prefrontal cortex or the basal ganglia.

Interesting, I don't know too much about sensory gating; I have not looked into in any great length.

My suspicion that D2 receptors may be involved in sound sensitivity comes from the observation that very low dose amisulpride (acts on D2, D3 and D4) helps reduce my sound sensitivity, and when I take low doses of amantadine (acts on D2), my sound sensitivity always gets worse for a few days when I start amantadine, but then returns to baseline.

 

[Hip]

Just looking at my old notes on the subject of sound sensitivity and brain sensory filters (firewalls). I think the reason I assumed the brainstem may be involved is because the reticular formation is located in the brainstem, and one of the reticular formation's functions is filtering out irrelevant or repetitive stimuli.



It's interesting that in post-polio patients, post-mortem studies showed severe lesions within the reticular activating system, which is part of the reticular formation.

 

[Pyrrhus]

Just looking at my old notes on the subject of sound sensitivity and brain sensory filters (firewalls). I think the reason I assumed the brainstem may be involved is because the reticular formation is located in the brainstem, and one of the reticular formation's functions is filtering out irrelevant or repetitive stimuli

Yes, parts of the reticular activating system are in the brainstem and parts are in the thalamus.

If I remember correctly, pain gating is handled mostly by the parts in the brainstem. I suppose it's possible that there may be some low-level sound gating in the brainstem as well, but I would think that most sound gating occurs in the thalamus. Note that the optic nerve bypasses the brainstem entirely, so visual gating is likely to be confined to the thalamus.

But the whole thing is like trying to unravel spaghetti, and we have to remember that at the end of the day it's the pathways/circuits that count much more than the anatomical structures that the pathways happen to run through...

 

[Pyrrhus]

Related discussions:

Hyperacusis specialist?
https://forums.phoenixrising.me/threads/hyperacusis-specialist.27544/

Is wearing sunglasses and ear protection a helpful form of rest?
https://forums.phoenixrising.me/thr...-ear-protection-a-helpful-form-of-rest.75542/

 

[Pyrrhus]

And here's what the Wikipedia page on Sensory Gating says:

Information from sensory receptors make their way to the brain through neurons and synapse at the thalamus. The pulvinar nuclei of the thalamus plays a major role in attention, and has a major role in filtering out unnecessary information in regards to sensory gating.
[...]
The pulvinar nuclei in the thalamus function as the gatekeeper, deciding which information should be inhibited, and which should be sent to further cortical areas.[3] The CNS (Central Nervous System), after the pulvinar nuclei deems the information to be irrelevant, acts as an essential inhibitory mechanism that prevents the information from flowing into higher cortical centers.
[...]
Other areas of the brain associated with sensory gating include the amygdala, striatum, medial prefrontal cortex, and mid-brain dopamine cell region (GABAergic neurons only).
[...]
Studies on rats also show the brainstem, thalamus, and primary auditory cortex play a role in sensory gating for auditory stimuli.[4]

Source: https://en.wikipedia.org/wiki/Sensory_gating

 

[Pyrrhus]

Oh, and here's a related post that I had completely forgotten about!

I think you're describing how the thalamus serves as a "relay station" that connects all sensory information from the body to the cortical brain. (with the sole exception of the sense of smell) Each type of sensory information is relayed through its own "nucleus" in the thalamus:

But the thalamus is more than just a relay station that provides all the body's sensory information to the cortical brain. As you mention, the cortical brain provides "feedback" nerves to the thalamus, allowing the thalamus to suppress certain sensory information. It is thought that this cortical "feedback" is how the conscious brain decides which sensory information to pay attention to, and which sensory information to ignore. If there is a problem with this "feedback", then the conscious brain may be inundated with too much sensory information. (photophobia, hyperacusis?)

There is another important aspect to the connections between the thalamus and the cortical brain- the aspect of alert consciousness. There is recurring stimulation from the thalamus to the cortical brain and then back to the thalamus, forming a loop. This recurring stimulation through the loop leads to "thalamo-cortical oscillations". These oscillations can be roughly recorded using an electroencephalogram (EEG) as "alpha frequency waves". These alpha frequency waves in EEG typically represent a state of alert consciousness. If there is a problem with the thalamo-cortical oscillations, it may be hard to maintain a state of alert consciousness. (brain fog?)

EEG studies in ME have had a hard time documenting specific abnormalities. But one study noted that "In the eyes closed condition, peak alpha (the frequency between 8 to 13 Hz at which the greatest amount of energy was observed) correlated negatively with the 'fatigue today' rating." This means that patients who reported more fatigue had slower alpha-frequency waves.[1]

Reference
[1] https://www.tandfonline.com/doi/abs/10.1300/J184v02n02_04

 

[Dufresne]

At the risk of offering medical advice I'd suggest singing.

I know this isn't a broad panacea for anyone with hyperacusis but, based on what it's done for me, I'm pretty sure it would work for at least a few people out there. And who knows, my case seems to be brought on with certain kinds of immune stimulation, so this may really be worth a try for anyone with hyperacusis who's also suffering from Lyme, mold, ME/CFS, etc.

Although I've always had some degree of hearing sensitivity this became much worse a few years ago when i began implementing certain treatments. Once triggered it could then be made worse with noise exposure or from listening intently, but mostly noise. And it would remain problematic for 4-6 weeks before settling back down to baseline.

This cycle occurred perhaps four times before I stumbled upon the fix. 15 minutes of solfege exercises and the hyperacusis was gone, though there's always about a 12 hour delay from the time of singing before it lifts. I'm sure this all sounds dubious but I've repeated it at least a dozen times, and it always works.

 

[Pyrrhus]

Here is a study being conducted in the U.K., and funded by ME Research UK (MERUK), using non-invasive ElectroEncephaloGraphy (EEG):

Investigating sensory processing and cognitive function in people with ME: a pilot study
https://www.meresearch.org.uk/research/sensory-processing/

Excerpt:

Volunteers
Dr Kumar is currently looking for people with ME to take part in this study. If you live in the Oxford area and would like more information, please contact Alfred Veldhuis at aveldhuis@brookes.ac.uk, who is the researcher working on the project.

Funding
This research is being funded by ME Research UK, supported by a generous donation from the Sophie Miles Bequest.

Background and aim
Our senses are constantly being bombarded with information from our surroundings – the sights, sounds, sensations and smells around us, as well as the tastes in our mouths.

The brain has to work hard to process all this information simultaneously, and filter out what’s irrelevant so we can concentrate on what’s important at any given moment. But this ability can be impaired in people with certain clinical conditions, leading to a disabling hypersensitivity to the stimuli around them.

The resulting physical and mental overload can lead to poor coordination, dizziness, clumsiness, numbness, tingling and nausea, and may affect individuals’ ability to take in information and make decisions.

Dr Sanjay Kumar, Dr Farzaneh Yazdani and colleagues at Oxford Brookes University have previously looked at this phenomenon in people with post-concussion syndrome following head injury. And we recently awarded funding to the team to investigate the problem in ME/CFS.