Hi Magpie, in "hyperacusis reserach" I have read: the results suggest a role for cochlear primary neuronal degeneration.
Gradual desensitisation or gradual nerve regeneration?
You have the text here:
Hyperacusis Research Lunch with Charlie Liberman, Ann Hickox, and Amanda Lauer at ARO 2014
The first hyperacusis discussions were with Charlie Liberman (Professor of Otology and Laryngology at Harvard Medical School), Ann Hickox (Postdocto...ral Research Associate at Purdue University), Amanda Lauer (Assistant Professor, Johns Hopkins University School of Medicine), and Hyperacusis Research supporters Ken Devore and Kimberlie Hamilton. Professor Liberman and Ann Hickox published a paper last year titled: "Is noise-induced cochlear neuropathy key to the generation of hyperacusis or tinnitus?" In the paper, they describe recent work in animals which has shown that a "neuropathic" noise exposure can cause immediate, permanent degeneration of the cochlear nerve despite complete threshold recovery and lack of hair cell damage. They show that mice with cochlear neuropathy displayed hyper-responsivity to sound, evidenced by enhanced ASR (Acoustic Startle Reflex) and PPI, while exposed mice without neuronal loss showed control-like responses. Gap PPI tests, often used to assess tinnitus, revealed limited gap detection deficits in mice with cochlear neuropathy only for certain gap-startle latencies, inconsistent with the presence of tinnitus "filling in the gap". Despite significantly reduced wave 1 of the auditory brainstem response, representing cochlear nerve activity, later peaks were unchanged or enhanced, suggesting compensatory neural hyperactivity in the auditory brainstem. Considering the rapid post-exposure onset of both cochlear neuropathy and exaggerated startle-based behavior, the results suggest a role for cochlear primary neuronal degeneration, per se, in the central neural excitability that could underlie the generation of hyperacusis. Charlie Liberman also presented on this topic at ARO with a talk on: "Primary Degeneration of the Cochlear Nerve in Noise and Aging: Putting the "Neural" Back in Sensorineural Hearing Loss." These works show that the synaptic ribbon fibers that connect the hair cells to the auditory pathway can be damaged and the hair cells survive and more importantly, this type of damage is typically not detectable with normal auditory tests.
To summarize, it is probable that some hyperacusis patients have this type of neural damage in the cochlear hair cells and this damage contributes to hyper-responsivity to sound. All of the researchers were very interested in learning more about patients who suffer significant pain from hyperacusis. Charlie, Ann, and Amanda felt that there should be at least 2 categories of hyperacusis – one with and one without pain. Charlie thinks the pain may come from type II fibers which may transmit pain signals to various parts of the brain from the cochlea.
One possible diagnostic test that may help differentiate levels of hyperacusis better than the subjective LDL testing is reaction time. Amanda Lauer published a paper in 2007 titled: "Evidence of Hyperacusis in Canaries with Permanent Hereditary High-Frequency Hearing Loss." The abstract states the following: "The mechanisms that underlie hyperacusis are poorly understood, due in part to the lack of a behavioral animal model. Traditional self-report methods used to measure loudness and loudness discomfort are not suitable for use with animals because the animals cannot provide subjective responses about the magnitude of an internal psychological perception. Instead, reaction time (RT) measures have been used in animals to estimate loudness perception. In the present study, the authors demonstrate that RTs are shorter at moderate and high sound levels in canaries of a strain with a hereditary high-frequency hearing loss than in normal canaries, indicating increased loudness. As far as we know, this is the first report of hyperacusis in a nonhuman animal and demonstrates that RT is a potentially useful measure in animal models of hyperacusis." Hyperacusis Research would like to see additional testing for reaction time with hyperacusis patients to move to a more objective measure which could possibly better differentiate levels of hyperacusis.
Pictured: Ken Devore, Bryan Pollard, Charlie Liberman, Amanda Lauer, Ann Hickox
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