I've had a good read of all that
@serendipity1996, thanks, very interesting and it goes into a lot of detail on cochlear pathology. I can see where you're coming from and think you're absolutely correct, it would be wrong to assume that it is all down to the mid ear only, mainly due to the frequency specific sensitivity and pain side of noxacusis which now suggests cochlea damage to me as well.
I don't know if you've noticed this too, but what I find so strange now after reading about it from both angles (cochlea vs. mid ear) is that neither research is particularly acknowledging of the other, there's a glaring lack of joined up thinking. Most of what I read about cochlea Type II sensitization does not seem to address the possible relationship with acoustic shock mid ear damage (even seems to dismiss it yet repeatedly refer to aching facial pain), and the only reference to Type II sensitization in the acoustic shock paper is that mid ear inflammation can diffuse through the round window and possibly cause Type II sensitization that way. There's no direct mention that it is also caused directly by noxious noise (that could well be responsible for the acoustic shock). But I'm starting to really see a connection between the 2 of them on how they may possibly trigger and interrelate with each other.
I would like to one day see a universal acknowledgment as well that there are evidently 2 main specific types of pain related to noxacusis and each one appears to be the result of a very different pathology. To simply say 'noxacusis or pain hyperacusis' I think is too broad now and to actually separate the pain types helps to understand the different possible underlying pathology in more detail. The models and hypotheses for example on central gain etc., how the cochlea nociceptors are communicating with the brain etc., and how the parts of the CNS are adjusting to pain / noise signals etc. seems to be related strictly to the cochlea and is directly related to the actual response to noise by the cochlea, i.e. the instant sharp specific frequency pain / sensitivity. But the delayed facial pain and even modulated tinnitus would suggest a secondary pain/symptom, and something completely different such as the theory on mid ear inflammation and TGN sensitization as a result of physical acoustic shock.
'Allan applied his expert knowledge of neuropathic pain to pain in hyperacusis. Based on hyperacusics' descriptions of their pain—burning, stabbing.' Notice the way that 'burning and stabbing' are grouped together. I think this is too broad. When you for example setback hearing a dog bark as a noxacusis sufferer it is instantly too loud and sensitive but doesn't last (at first), I think this is where the 'stabbing' occurs, whether it is in the cochlea itself or more likely triggered in the mid ear
by the cochlea response, the very instance of the sound, is what's causing this stabbing. The burning aching however is typically delayed, long lasting and facial and in my view is the result of secondary mid ear inflammation. I just see 2 very different types of pain and pathology regularly being bundled together as one.
You mention, '
Also, Ulf Baumgaertner's presentation again brings up middle ear pathology but it seems there's not much conclusive evidence for it as afferents of the trigeminal nerve are not excited by sound frequency'. The trouble with this statement is that it is suggesting that sound could be triggering facial neuralgia
directly which doesn't make much sense in itself. It doesn't take into account the full chain of events of sound triggering an acoustic shock that then leads to the mid ear inflammation and TGN sensitization which
could then easily explain facial neuralgia. Ongoing non-noxious sound then continues to excite and further inflame an already inflamed mid ear and a damaged TTN that cannot rest and recover (this could explain why people still suffer facial pain in particular from even non-noxious noise. Of course a highly inflamed cochlea could also possibly react to non-noxious noise, I don't know, but I doubt it would cause this kind of facial pain
directly, especially in silence where perhaps the mid ear still might do. Also would the stabbing sensation not be ongoing?). In addition, ongoing non-noxious noise also continues to possibly stimulate nociceptors in the cochlear where although the sound may be non-noxious in volume, the specific frequency
is noxious (I completely agree with you on this part now, I also think it could be one of the best explanations for a trigger for acoustic shock and setbacks as well. In essence this could be THE permanent damage that I believe repeatedly keeps causing setbacks no matter how well we recover and FX-322 would in theory be great for it). If it is all initiated by the cochlea however (the acoustic shock, the frequency specific pain, and the delayed facial pain) then its also a very positive sign for FX-322 and maybe SPI-1005.
This one also, '
He also states that it is unlikely that the TTM and the stapedius could be causing hyperacusis pain as TTM spasm results in pulsing tinnitus and since the stapedius contracts during speech, we would feel pain when talking. But some people report TMJ-like pain so the muscles controlling the jaw and TMJ could also be playing a role here.' This seems to be trying to hypothesize that a healthy, normally functioning middle ear is generating facial pain and not taking into account that it's not the movement of these muscles and nerves that cause the pain but the fact they've been sensitized and inflamed as a result of the acoustic shock
secondary to the cochlear damage / Type II sensitization. In a case where there was only cochlea damage, indeed causing its own type of pain, I'd guess these symptoms are more likely to be only instantaneous frequency specific sensitivity and pain with no delayed facial pain anyway (TGN not yet sensitized plus no middle ear inflammation). It's this kind of thing that makes me think the types of pain really need separating now for research to become more detailed.
In short I'd say that the lingering facial pain is more likely down to
any stimulation of the damaged mid ear, even non-noxious noise (this could explain why silence is sometimes all that will help. Also it could explain why it only gets worse if you try and 'push through the pain'). Even non-noise stimulation may still excite the middle ear (this could explain why sometimes even silence doesn't help). Setbacks however I think are more likely to be the result of repeat stimulation of sensitized Type II afferents because from my own experience and from what I read of a lot of others, setbacks usually follow noxious or frequency noxious noise exposure that causes the initial pin prick sensations in the ear (the stabbing?), and again whether this stabbing actually occurs inside the cochlea or is more likely the mid ears response to the cochlea nociceptor stimulation, this does appear to be as a direct instant reaction to actual noise (as opposed to a delayed secondary inflammatory pain). This bodes really well for fx322
as long as the mid ear pathology hasn't become a self sustaining problem in its own right.
With regard to the projections from the trigeminal ganglion to the cochlea, this is interesting because it puts a direct link between the two and it could in theory turn all the above upside down as well. I've read about this before and I'm open minded about it although I'm still slightly more steered to the possibility that this is a one way inflammation street
into the cochlea that is responsible for symptoms such as tinnitus modulation etc. (tinnitus fluctuating with facial pain). For this theory to be the sole cause of the facial pain would seem to rule out a lot of the acoustic shock symptoms cluster theory. I think the acoustic shock theory is more likely and conclusive though given that extensive paper on it. Of course however, if the single lingering action of the acoustic shock was to simply sensitize the TGN (but not stimulate it from within the mid ear, again doubtful due to apparent mid ear inflammation), then who knows, maybe cochlea inflammation could then affect the whole TGN via the cochlea TGN nerve endings. Another possible win for FX-322 and SPI-1005 if this is the case anyway.
The main thing that I'm still having trouble with in regards to the Type II sensitization causing noxacusis, is again how few noxacusis sufferers there appear to be in relation to the surely larger amount of people who must have OHC damage but simply just go deaf without pain. I'm starting to buy into the possibility it's down to genetics / predisposition based on this because so much else seems to be stacking up in favour of this theory for it to be ignored.
I've been working on some models based on the more feasible possible relationships between these 2 different angles, I'll post them soon once they're finished.
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