Also search the paper's keywords for central gain, noxacusis, synaptopathy, neuropathy, neuralgia, allodynia, demyelination.
Researchers often use these terms to describe issues associated with hyperacusis with pain and hidden hearing loss when they speak formal.
They do talk about central gain theory.
This is the only mention of synaptopathy in the main body of text. Everything else is just citations from other papers talking about it.
"Repeated or long-term exposures increase the risk that the swelling will not diminish and will result in PTS and functional problems for listeners. The process by which synapses are damaged even as hair cell integrity is maintained is termed synaptopathy.Sound levels associated with synaptopathy are lower than those required to produce hair cell damage. After reporting 40 dB TTS following 105 dB SPL broadband noise expo-sure, Kujawa and Liberman (2015) deter-mined that hearing returned to normal, and synapses regenerated if the experimental ani-mals survived for 4 weeks following exposure. Also investigated by this group were the effects of longer-term moderate exposure levels on mice, and they employed a week-long 84 dB SPL noise focused in the 8 to 16 kHz region, which is in the middle of the mouse's audible range. This level was chosen in an attempt to mimic the exposure levels encountered by humans in industrial settings. Although the reported TTS was less severe (on average <12 dB) as many as 22% of the synapses were affected (Maison, Usubuchi, & Liberman, 2013). The cumulative effects of several simi-lar and repeated exposures would most likely exacerbate the damage."
It seems as if the discussion of neuropathy is limited because they cannot find a clear measure to correlate neuropathy to tinnitus.
"Electrocochleography has the potential to detect cochlear neuropathy but is a more invasive technique. Moving up the auditory pathway, measurement of temporal processing in the auditory midbrain by assessing neural phase locking at different depths of AM has been proposed as a possible correlate of cochlear neuropathy (Bharadwaj, Masud, Mehraei, Verhulst, & Shinn-Cunningham, 2015). This technique applied to tinnitus may improve our understanding of the role of cochlear factors in tinnitus and the relation between tinnitus and other problems of hearing (e.g., difficulty in hearing in noise) in which impaired tempo-ral processing is likely present"
Looks like they quote Liberman's work.
"Similarly, Hickox and Liberman reported that mice exposed to acoustic levels that produced clear evidence of cochlear neuropathy, as well as first-order afferent degeneration, also showed exaggerated acoustic startle and PPI (Hickox & Liberman, 2014). Interestingly, they reported that this level of neuropathy did not yield convincing evidence of tinnitus using GPIAS."
They do in fact discuss trigeminal neuralgia:
"An understanding of TTTS may facilitate the clinician's explanations regarding the observation that patients with severe hyper-acusis report frequent or constant pain that is triggered by intolerable sound exposure. Trigeminal nerve irritability potentially leads to chronic trigeminal neuralgia, TMD, or myo-fascial pain syndrome (Ramirez et al., 2008; Schames, Schames, Boyd, King, & Ulansey, 2002)."
However, they do talk about central pain:
"Central pain sensitization can develop from this chronic pain, as indicated by the development of muscle trigger points in the neck, shoulder, and arm in many patients with severe TTTS, hyperacusis, or ASD."
References
Baguley, D., & Fagelson, M. (2013). Tinnitus : Clinical and Research Perspectives. San Diego: Plural Publishing, Inc.
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