Fournier and Noreña recently released an interesting paper that somewhat follows up their 2018 acoustic shock study.
In the study, one of the patients reported getting a botox injection into their tensor tympani muscle (TTM) which they described as a "complete success":
"The patient recently received a treatment consisting of a botulinum toxin injection in the tensor and levator veli palatini muscles. One month later the patient reports that the intervention was a complete success: he doesn't experience pain in the ear after exposition to impulsive sound anymore. Following the intervention, he is not able to voluntarily contract his MEM. These results suggest that some muscle activity in the oro-facial area was responsible for the pain and was deactivated by the toxin." (p. 13)
This is obviously a fantastic result, and it seems to support that TTM hyperactivity (and subsequent inflammation) is a crucial part of pain hyperacusis. The question is whether that leads to sustained improvements. Botox injections don't last forever, so they would likely have to be repeated. I wonder if the injections can either 1) let the TTM rest more deeply, hopefully making it more resilient to injury, or 2) stop the TTM from triggering inflammation altogether, which could prevent setbacks from happening. We don't really know the extent/mechanisms involved in the centralization of pain that likely occur in chronic hyperacusis patients, but it could also give the brain a chance to recalibrate and hopefully drive down central sensitization. I have no idea if that would actually happen. I would happily be a guinea pig, if my circumstances allowed for it.
I'm thinking of contacting Noreña to ask if he has any more insights into potential treatments. If I get a response, I'll let you all know.
In the study, one of the patients reported getting a botox injection into their tensor tympani muscle (TTM) which they described as a "complete success":
"The patient recently received a treatment consisting of a botulinum toxin injection in the tensor and levator veli palatini muscles. One month later the patient reports that the intervention was a complete success: he doesn't experience pain in the ear after exposition to impulsive sound anymore. Following the intervention, he is not able to voluntarily contract his MEM. These results suggest that some muscle activity in the oro-facial area was responsible for the pain and was deactivated by the toxin." (p. 13)
This is obviously a fantastic result, and it seems to support that TTM hyperactivity (and subsequent inflammation) is a crucial part of pain hyperacusis. The question is whether that leads to sustained improvements. Botox injections don't last forever, so they would likely have to be repeated. I wonder if the injections can either 1) let the TTM rest more deeply, hopefully making it more resilient to injury, or 2) stop the TTM from triggering inflammation altogether, which could prevent setbacks from happening. We don't really know the extent/mechanisms involved in the centralization of pain that likely occur in chronic hyperacusis patients, but it could also give the brain a chance to recalibrate and hopefully drive down central sensitization. I have no idea if that would actually happen. I would happily be a guinea pig, if my circumstances allowed for it.
I'm thinking of contacting Noreña to ask if he has any more insights into potential treatments. If I get a response, I'll let you all know.