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Re: sounds too loud
Martin 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 200
> patients with unilateral Menière'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 of
> 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 Menière's disease is a cochlear-vestibular disease, hyperacusis in
> these patients is assumed to have cochlear origins. Hair cell damages can
> not be a necessary element, because even affected ears without hearing loss
> often have hyperacusis. The only plausible hypothesis is a mechanical one.
> Expansion of the inner ear endolymph (called "endolymphatic hydrops"), which
> is present in all cases of Menière's disease, displaces various cochlear
> 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 that 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 opinion.
Thus it seems that the hydrops (variation in cochlear pressure) is changing
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, the 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 compression
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 modifying the
active properties of the OHC, which lie in the OHC lipid membrane (Adachi and Iwasa,
> A large amount a experimental and clinical evidence on the
> relation of hyperacusis and inner ear mechanics was reviewed by Braun
> 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 Braun
> Neuroscience of Music
> Gansbyn 14
> S-671 95 Klässbol
Thanks for drawing the Hallpike and Hood paper to my attention. I had never
actually read it before, and it seems interesting. Given its publication date it may be in
with the Steinberg and Gardner JASA paper (1938), were they first identify recruitment
as a loss of compression.
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