Subject: Re: sounds too loud From: Jont Allen <jba(at)RESEARCH.ATT.COM> Date: Mon, 22 Jan 2001 10:14:41 -0500Martin Braun wrote: > Jont Allen wrote: > > > Does anybody know of a condition where a person complains that sounds= are > too loud. > > Does this condition have a name? > > Is it a physiological condition, with a known cause? > > There is a large clinical survey on this issue: > > Hallpike and Hood (1959) measured recruitment and over-recruitment in 2= 00 > patients with unilateral Meni=E8re's disease. The applied audiological > technique was the "alternate binaural loudness balance" (Fouler test). = All > 200 patients showed recruitment in the affected ear, no matter if this = ear > had any significant hearing loss or not. Most importantly, two-thirds o= f > these ears also showed over-recruitment. Over-recruitment means (as > correctly reported to this list on Jan 19 by Brent Edwards) that above = a > certain sound level, say 80 dB, the affected ear hears louder than the > healthy ear. > > Hallpike, C.S. and Hood, J.D. (1959) Observations upon the neurological > mechanism of the loudness recruitment phenomenon. Acta Otolaryngol. > (Stockh.) 50, 472-486. Another one is Hallpike and Hood, JASA May 1951 vol 23(3) page 270-4 > [The discussion of possible causes is no longer useful today, but the > empirical data are classical.] > > Because Meni=E8re's disease is a cochlear-vestibular disease, hyperacus= is in > these patients is assumed to have cochlear origins. Hair cell damages c= an > not be a necessary element, because even affected ears without hearing = loss > often have hyperacusis. The only plausible hypothesis is a mechanical o= ne. > Expansion of the inner ear endolymph (called "endolymphatic hydrops"), = which > is present in all cases of Meni=E8re's disease, displaces various cochl= ear > components and reduces the normal cochlea's capacity of absorbing high-= level > acoustic energy. I agree with this 100%, up to the very last point. How does it follow tha= t hydrops reduces acoustic energy absorbtion? > The loss of inner-ear dampening leads to an increased hair > cell excitation, and thus increased loudness sensation, at medium and = high > sound levels. The loss of loudness compression is the source of recruitment. This was = first articulated by Steinberg and Gardner in 1938. They were right in my opini= on. Thus it seems that the hydrops (variation in cochlear pressure) is changi= ng the compression caused by the OHCs. According to the laws of fluid mechanics (at least as far as I understand= them) viscous damping does not depend on static pressure. So, in my opinion, th= e hydrops must play some other role in changing the OHC compression curve. I quote = from the 1951 Hallpike and Hood article (p 274): "As is well known, loudness recruitment manifests itself as a nonlineaity= of the loudness function. A necessary corollary of this nonlinearity is the comp= ression of the loudness scale over the intensity range concerned, ...." I would guess that the daily fluxuations (i.e., reversible hearing loss) = are an important clue. I would guess this change in cochlear pressure is modifyi= ng the active properties of the OHC, which lie in the OHC lipid membrane (Adachi= and Iwasa, PNAS, 1999). > A large amount a experimental and clinical evidence on the > relation of hyperacusis and inner ear mechanics was reviewed by Braun > (1996). > > Braun, M. (1996) Impediment of basilar membrane motion reduces overload > protection but not threshold sensitivity: evidence from clinical and > experimental hydrops. Hear Res 97, 1-10. > > Martin > > Martin Braun > Neuroscience of Music > Gansbyn 14 > S-671 95 Kl=E4ssbol > Sweden > nombraun(at)post.netlink.se Martin, Thanks for drawing the Hallpike and Hood paper to my attention. I had nev= er actually read it before, and it seems interesting. Given its publication = date it may be in a class with the Steinberg and Gardner JASA paper (1938), were they first identi= fy recruitment as a loss of compression. Jont -- Jont B. Allen AT&T Labs-Research, Shannon Laboratory, E161 180 Park Ave., Florham Park NJ, 07932-0971 973/360-8545voice, x7111fax, http://www.research.att.com/~jba