Search results for query: *

This reminds me of something that Liberman remarked upon from an interview in 2019. "A challenge in pursuing these ideas is to develop an animal model of pain hyperacusis. I believe that pain hyperacusis, which can be very long-lasting, is fundamentally different from annoyance hyperacusis...

There's been some speculation on here as to whether the synapse drugs could help since in the same ears that saw an increase in type 2 afferent fibers as a result of acoustic trauma, there was a decrease/loss in type 1 afferent fibers. One of the things I was wondering is whether restoring the...

I don't think it should be regarded as a cure because ultimately it's not a drug that's actually aimed at repairing the cochlea. But there's probably a good amount of cochlear inflammation from noxacusis that would be well served by this drug.

Misophonia is thought to be a neurological condition, so no, it wouldn't treat misophonia.

I wonder if there are any other conditions we could look to that could possibly shed light on this - conditions where some type of peripheral sensitisation occurs following trauma/injury and what the prognosis is - I'm no scientist by any means though so not sure where to begin lol.

In this paper, the only reference I could find to a particular type of supporting cell is under the 'Discussion' heading, mentioning Hensen's cells: "Experimental ablation of OHCs was shown to initiate ATP-dependent calcium waves in nearby Hensen’s cells that further triggers release of ATP...

Yes, the 2015 Johns Hopkins paper states that "...type II afferents are activated when outer hair cells are damaged. This response depends on both ionotropic (P2X) and metabotropic (P2Y) purinergic receptors, binding ATP released from nearby supporting cells in response to hair cell damage."...

My first bout of hyperacusis also came on fairly gradually - initially, I noticed that cutlery sounded jarring and emptying the dishwasher was unpleasant.

Just to tag on to your second paragraph - my hyperacusis has improved significantly over the best part of the year - to the extent that the sensitivity I had to artificial audio, in particular, has now started to subside significantly in the past few months - I wouldn't say it's completely gone...

Yeah - I'm inclined to agree and I reckon that even if you picked the brains of the top researchers like Charles Liberman, even they probably couldn't give us a definitive answer at this point in time. But it's reassuring to know that it's being actively worked on.

I think our lack of knowledge on this really owes more to the fact that this is, ultimately, a super niche and rare disorder. It was only 5 years ago that they determined that the type 2 fibres behave like pain fibres so it's all very new. The Fuchs lab at Johns Hopkins are studying the role of...

This makes sense to me - from my own experience, even though I have achieved what could be called 'recovery' before, I always knew I was susceptible to a setback versus someone with healthy ears. The key question to me is whether repairing the underlying cause/damage of hair-cell death could...

Incidentally, Paul Fuchs has spoken about using magnetic nanoparticles for drug delivery to the inner ear in order to avoid systemic effects, so it seems implied that his lab are focusing on developing channel blockers that could be locally delivered although I'm not too sure. I assume they're...

@Diesel - speaking from my own experience, I noticed that when my facial symptoms started to improve, my head and ears felt like they were 'clearing' - this clearing feeling was accompanied by significant reduction in my facial/trigeminal symptoms.

In one of the conference summaries from Hyperacusis Research, it was stated that there are projections from the trigeminal ganglion to the cochlea and blood vessels, so this wouldn't at all surprise me.

I think this is a very reasonable possibility.

Honestly this could be a godsend for hyperacusis and even noxacusis - the Johns Hopkins lab are exploring the role of cochlear inflammation (in addition to the Type 2s) on noxacusis. I can imagine setbacks also stemming from a chronically inflamed cochlea. Perhaps inflammation could also be why...

I'd be very interested whether this could also potentially reduce hyperacusis-related inflammation.