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How does a hearing aid help?

Jerry Larson jlarson at op.net
Thu May 15 16:41:32 EST 1997

Stephen Black said:

>I want to apologize for taking so long to reply to Jerry Larson's
>interesting and detailed response. Also, I want to mention (although I
>expect no one remembers) that the version Jerry responded to had (as he
>guessed) some of Ron Blue's insights mixed in. If a post contains the
>words "wavelets" or "opponent-process", that's Ron, never me. 

interesting that it's Black and Blue discussing this.  Well, I guess you
can argue yourself Blue in the face......

>.  The basis of my question was that a
>hearing aid can help in SHL but I couldn't understand why. This is because
>the most likely cause of SHL is the loss of hair cells, the neural 
>elements which transduce the signal from vibration to neural activity. 
>Either the hair cells work or they don't, and if they don't, no amount of 
>amplification is going to bring them back to life. So what does the 
>hearing aid do?

See,I can't understand why you have any trouble understanding this.
Look at it this way:
The sound isn't loud enough.  You make it louder.  Voila, the person can
hear.  The mechanism of the hearing loss doesn't matter; the sound is not
loud enough for them, you make it louder.  Notice that, instead of using a
hearing aid, if the hearing-impaired person can simply get the speaker to
talk louder, that also helps (and not always, for the reasons I've

Now, as I explained, it it's far from being  that simple; there are issues
of dynamic range, distortion, speech discrimination, phase relationships; a
damaged ear isn't ONLY less sensitive.  And all these issues apply mainly
to sensory losses.  But the basic concept is as I have just explained it: a
damaged ear isn't entirely nonfunctional, it's just functioning poorly, in
particular with decreased sensitivity.  There is a limit to what can be
done for decreased dynamic range, speech comprehension, etc., but for
decreased sensitivity, amplifying the sound works to a very useful degree,
depending on the individual hearing loss.

I want to emphasize again that the vast majority of hearing losses are, at
least in part, sensory.  Significant conductive loss is uncommon now that
there is good middle ear surgery, and in any case the maximum conductive
loss is something like 35dB, which is mild to moderate.  If hearing aids
did not help sensorineural losses, there wouldn't be much of a market for
>Although Jerry provided useful information, he didn't touch on the
>underlying mechanism. A clue may be the observation he cited that
>frequencies are often not entirely missing in SHL, but can only be
>detected at higher sound level. But what is the physiological basis of
>this phenomenon? 

There isn't just one hair cell, or one per octave, or one for every 10Hz,
or anything like that; there are thousands, millions, I don't know.  You
lose some of the population, you lose some of your hearing.  Lose them all,
you lose all your hearing.  A partially depopulated ear has partial
When you say,
>Either the hair cells work or they don't, and if they don't, no amount of 
>amplification is going to bring them back to life

Do you have evidence for that?  I don't see why even an individual hair
cell, damaged but not yet dead, can't function at diminished efficiency. 
But in any case, it's only part of the population that's damaged.  The
remaining hair cells are responsible for the residual hearing.

>My conclusion is that probably no one really knows why a hearing aid helps
>in SHL. 

You could look it up.  There is a ton of literature on normal and abnormal
cochlear function, as well as on hearing aids.  Try the speech and hearing
journals, JSHD and JSHR.   As for material directly on the question you're
asking, I don't know, there might not be, because it would seem to be a
non-question.  The hearing aid helps by making the sound louder, thereby
overcoming decreased sensitivity.  There is no reason to expect that
amplifying sound wouldn't help, and acoustic hearing aids ("ear trumpets")
predate the differential diagnosis of conductive and sensorineural losses.

This is analogous (or possibly even directly relevant) to the
>puzzle of tinnitus. Tinnitus (an often-distressing noise heard within the
>ear) is caused by hair cell damage, but why the absence of input should
>give rise to the perception of sound is unknown (although there are
>speculations, of course). I find it interesting that it seems to parallel
>the equally unusual phenomenon of phantom limb pain (the sufferer feels
>pain in a body part that's no longer there, having been amputated). 

Something to do with the afferent control system, I'm sure.  You might look
up spontaneous (as opposed to evoked) oto-acoustic emissions.  The hair
cells are motile, and in response to sound they tune themselves up to  be
more responsive.  When that process goes haywire, you can actually get
spontaneous acoustic emission from them.  Generally, sensory systems are to
a considerable degree active (interactive) interpretive systems, not purely
passive, and look for the signal against a background.  Take away or
disturb the background, and the sensory system tends to make bizarre and
false interpretations.


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