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Re: Tinnitus and a dip in the audiogram

Your second point here is one I like. However it may also be the same as your first point :)

Our mixed-mode Cochlear amplifier supports your hypothesis.

The general idea is that certain types of Cochlea damage enhance the peripheral hearing circuit.

For example, consider this thought experiment based on our mixed-mode Cochlear amplifier model :

Imagine that your stereocillia are lopped off in a small region of inner hair cells - the same can be said for outer hair cells. This may happen due to ageing or damage. In this case assume that the stereocillia resistance is reduced - due to gaping open ion channels - and ionic currents into the cell (potassium) and our from the cell (sodium) are enhanced ... the hair cell now experience a depolarisation. This depolarisation generates more spontaneous neurotransmitter release. The neurotransmitters generate more synaptic transmission in the cochlear nerve. The cochlear nerve excites the superior olive and this not only generates perception of the tone, but sends signals back to the Cochlear over the lateral and medial efferents. The medial efferents stimulate the motors in the outer hair cells and they in turn generate movement at the inner hair cells which start the process again ... over and over again ... the end result is a mecho-neural standing wave ... or 'tinnitus'. This type of tinnitus masks low level sound heard through the ear ... however if the external sound gets loud enough, then it masks the tinnitus !

What do you think ?


On 09/10/2012 08:22 AM, Matt Winn wrote:

Mark and everyone,

Although I am not a tinnitus researcher, I have had lots of experience with patients with tinnitus in the audiology clinic. Generally, we try to avoid the confusion of tinnitus with testing tones by using pulsed and/or warbled tones. As you point out, this doesn’t always work out perfectly.

It has been my experience that dips in the audiogram are indeed frequently accompanied by tinnitus. having measuring hearing at the VA, this connection might be limited to hearing loss that is noise-induced. The two most common explanations I have heard for this are 1) damage to the auditory system at the site of the hearing loss underlies both the threshold elevation and improper firing by damaged nerves, and 2) tinnitus that exists in the region of the dip is not masked out by external stimulation because the external sounds are less audible; thus rendering tinnitus more noticeable. This latter explanation accounts for the relief from tinnitus experienced by many people who use hearing aids. Specifically, tinnitus isn’t “cured,” but it is masked out by the amplified input, and then the tinnitus returns after the hearing aid is removed.

Returning to the point of tinnitus without apparent hearing loss, I have found that salt intake and stress level are two (among many) contributing factors to and my own tinnitus, and I don’t have hearing loss. The dependence of OHCs on metabolic factors underscores this connection, which seems anecdotally to be exacerbated in patients with Ménière’s.