As I'm a compulsive problem solver, cursed by a mind that searches out challenging puzzles and won't let go of them until a reasonable solution is found ....
It has been brought to my attention by Dan Segal of the Hyperacusis Network (SASE to: 444 Edgewood Drive, Green Bay, WI 54302) that my book has very little on the subject. I realize now that when I was researching and writing the book, hyperacusis did not seem to be widespread. Although it still seems to be less prevalent than tinnitus, it is a major problem for many, and therefore an important challenge to my hypotheses and an interesting academic exercise for me.
I haven't seen surveys with quantitative measures, which would give a better clue as to the precise problem. The anecdotes I've heard indicate that often, a broad frequency range of very low amplitues (less than 50 dB) can actually be painful. I see three basic research approaches:
(1) What, where, how of pain in the ear.
Is the pain perceived at the middle ear tissues, the eardrum, or actually the inner ear? I suspect the inner ear -- the basilar membrane or hair cells -- assuming that all hyperacusis sufferers do have sound perception. That is, if there is total inner ear deafness, there is no pain. I suggest studying the latest research in chronic pain of all types. Surely someone has studied the latest on Transcutaneous Electrical Nerve Stimulation, or TENS, as a possible quick and dirty solution.
Assuming my basic tinnitus hypotheses are correct, hyperacusis would seem to be a lack of physiological excess-noise protection, or damping, at the outer hair cells. The outer hair cell body has been shown to contract due to outside stimulus (which can actually be chemical, electrical, contact, or vibration). It has been assumed that this is a dynamic amplifier, amplifying each cycle of a vibration, but I propose that it can also be a protective retraction to avoid destructive high amplitudes and/or pain.
Failure could be due to either a lack of signal from the efferent nerve fibers which stiffen the cells in response to any sound greater than 20, 40, or 60 dB, or a loss of "muscle tone" in the cells themselves. Some older references to this "motility" or stiffening of the outer hair cells can be found in Hearing Research: (Zenner 1986 p. 83 and Evans 1990, p. 265 and Carlon 1991 p. 7). Someone should search later info, using the keywords "motil* outer hair cell."
Assuming the above, there are two other possible approaches:
(2) Determine the difference between efferent-fiber synapse innervation of the OHC, and the better documented afferent-fiber innervation, in terms of the different neurotransmitters involved. This would indicate which neurotransmitters might be missing, and therefore a potential chemical treatment. Segal mentions that the pain may be delayed, and may be associated with inner ear pressure, supporting the idea of excess neurotransmitter buildup, especially in the scala media.
(3) More likely, especially after traumatic causes, are weakening or destruction of the actin, or "musculature" of the OHC, much the same as a sprain in any other weakened muscle in the body. This would indicate treatment in terms of either rest from sounds of similar frequency and amplitude to allow natural healing, or finding some way to either increase muscle tone or stiffen these flabby hair cells so that they couldn't be deflected enough to cause pain. If it were a permanent stiffening, however, this would theoretically lead to a loss of sound perception or deafness, although it's possible that inner hair cells might still provide some hearing in this range. Better would be temporary stiffening using microelectrodes as in stimulation of muscle fibers to maintain muscle tone in paralytics. This could also be shut off for brief periods so that low level sounds could be perceived when the pain could be tolerated. In fact, perhaps this sort of stimulation could be used to exercise the cells enough to return some muscle tone. If this isn't possible, a more drastic solution might be intentional selective total destruction of the hair cells involved, again leading to hearing loss.
If NONE of the above turn out to be practical, then we'll just have to think of something else, won't we?
I won't be able to stop ruminating over this (one more) puzzle. However, I can't afford much more volunteer involvement, since my oldest son is starting college, and I'm looking for ways to supplement my income -- ideally associated with medical research at some university to qualify for reseach grants in this area.
pvanvalken@aol.com