Just wondered if anyone else has read this acoustic shock model paper?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156190/
@grate_biff posted it several months ago (thanks) and I've read it a few times now. Each time I read it, I understand it and research the content a bit better and I'm starting to think that the mechanics behind acoustic shock induced noxacusis pain, including repeat injury (setbacks), TTTS, and possibly acoustic shock induced tinnitus are staring us in the face in this paper. I'm leaning more and more to a middle ear problem as a primary cause for acoustic shock induced noxacusis re-injury, pain and setbacks. And also whatever nerve blocker this paper talks about as the primary possible treatment (it doesn't actually say what it is though, maybe stellate ganglion block?). It seems the tensor tympani muscle can get very badly damaged during an acoustic shock and produce a lot of inflammation and nerve sensitization in the facial area, and most importantly become primed for constant re-injury.
The main thing I'm still trying to work out with regard to the referred pain this paper talks about (i.e. the delayed facial, jaw, neck pain), is the way the nerve pathways work between the middle ear and the cochlea. It's well noted that during acoustic shock ATP can possibly diffuse from the middle ear through the round window to the cochlea, but I can't find a direct nerve link between the middle ear and the cochlea for the cochlea to send pain signals back the other way (although this paper says that there is one, anyone know?). It seems that the only nerve links between the inner ear and the cochlea are via higher up parts of the nerve system. (trigeminocervical complex and cochlear nucleus). I think it's less likely anyway that the pain signal is being produced by the cochlea for acoustic shock noxacusis. I think it's more likely that the previously damaged tensor tympani muscle is being re-injured either because its having trouble healing (due to a noisy environment and hence why it's impossible to 'push through the pain barrier' with noxacusis) or because of some kind of lowered nervous system threshold that's making it so unnecessarily active that it cannot rest and heal even in relative quiet. According to this paper the tensor tympani muscle injury can cause sensitization that occurs in the trigeminal nerve mandibular branch which makes sense because that branch seems to connect to every crucial area or muscle where either noxacusis referred pain is associated, or areas that are related to the acoustic trauma injury. In particular the tensor tympani muscle itself, the middle ear mucosa, the outer ear drum, and these muscles; masseter, temporalis, lateral and medial pterygoid, the tensor veli palatini, the mylohyoid muscle, and anterior belly of the digastric muscle. (Basically the muscles just under/in front of the ear, cheek and jaw). The way I read it is that every time the vulnerable tensor tympani muscle get over exposed to noise it causes middle ear inflammation and triggers pain throughout the mandibular nerve and those muscles. I seriously cannot see how my cochlea can be receiving enough noise exposure to even be vunerable to any noise damage these days anyway even though I still get setbacks.