Hidden Hearing Loss, Tinnitus and Trouble Hearing Conversations in Noise

Weak middle-Ear-Muscle Reflex in Humans with Noise-Induced Tinnitus and Normal Hearing May Reflect Cochlear Synaptopathy

Abstract
Chronic tinnitus is a prevalent hearing disorder and yet no successful treatments or objective diagnostic tests are currently available. The aim of this study was to investigate the relationship between the presence of tinnitus and the strength of the middle-ear-muscle reflex in humans with normal and near-normal hearing. Clicks were used as test stimuli to obtain a wideband measure of the effect of reflex activation on ear-canal sound pressure. The reflex was elicited using a contralateral broadband noise. The results show that the reflex strength is significantly reduced in individuals with noise-induced continuous tinnitus and normal or near-normal audiometric thresholds compared with no-tinnitus controls. Due to a shallower growth of the reflex strength in the tinnitus group, the difference between the two groups increased with increasing elicitor level. No significant difference in the effect of tinnitus on the strength of the middle-ear muscle reflex was found between males and females. The weaker reflex could not be accounted for by differences in audiometric hearing thresholds between the tinnitus and control groups. Similarity between our findings in humans and the findings of a reduced middle-ear muscle reflex in noise-exposed animals suggests that noise-induced tinnitus in individuals with clinically normal hearing may be a consequence of cochlear synaptopathy – a loss of synaptic connections between inner-hair cells in the cochlea and auditory-nerve fibers that has been termed hidden hearing loss.

Significance Statement Chronic tinnitus is a prevalent condition that in some cases can lead to debilitating consequences. It may also indicate some damage to the inner ear, termed cochlear synaptopathy, even in cases of clinically normal hearing. However, there are currently no objective diagnostic tests for either tinnitus or cochlear synaptopathy in humans. This study compares the strength of the middle-ear muscle reflex in people with clinically normal or near-normal hearing but suffering from noise-induced tinnitus to that in an age-matched control group without tinnitus. The results show that the tinnitus group had greatly reduced reflex strength. The outcomes are consistent with recent results obtained in mice and suggest that it may be possible to diagnose tinnitus and cochlear synaptopathy in humans.

http://www.eneuro.org/content/early/2017/11/16/ENEURO.0363-17.2017

 

@lapidus are there any theories expanding on the scientific/anatomical cause behind the reflex strength reduction after tinnitus?

 

Not that I'm aware of.

 

This is explained on page 5 of the paper:

"There are several reasons why the wideband MEMR measure is expected to be affected by cochlear synaptopathy. First, the MEMR is absent or significantly reduced in individuals with auditory neuropathy (Berlin et al., 2005), a more severe AN disorder. Second, the neural circuit of the MEMR involves afferent neurons with relatively high thresholds and low spontaneous firing rates (Liberman and Kiang, 1984, Kobler et al., 1992), which appear to be preferentially affected by cochlear synaptopathy (Furman et al., 2013). Finally, mice with noise induced synaptopathy (Valero et al., 2016) have a significantly reduced MEMR strength. To our knowledge, the relationship between tinnitus and a wideband measure of MEMR strength has not been previously investigated in humans."

Liberman and a co-author had a poster at the 2017 ARO Midwinter Meeting looking at the MEMR in mice. The first paragraph explains why a weakened MEMR may be a problem in and of itself.

PS 144

Effects of Cochlear Synaptopathy on the Middle-Ear Muscle Reflex in Unanesthetized Mice

Michelle D. Valero; M. Charles Liberman

Massachusetts Eye and Ear Infirmary, Harvard Medical School

Cochlear synaptopathy is an important problem in aging, noise damage, ototoxicity, and possibly other types of acquired sensorineural hearing loss. Because behavioral thresholds are insensitive to the pathology until ~90% of the cochlear nerve fibers are lost, new approaches are needed to diagnose this condition in humans. The subset of cochlear nerve fibers with high thresholds and low spontaneous rates (SRs) are the most vulnerable to many types of damage, and they may be particularly important drivers of the middle-ear muscle reflex (MEMR). Because one role of the MEMR is to protect the inner ear from noise damage, loss of low-SR fibers could lead to a vicious cycle wherein the ear becomes progressively more damaged by subsequent trauma. Because therapeutic interventions may be possible, an early diagnostic tool would be of great value.

To cleanly separate the MEMR from the medial olivocochlear reflex (MOCR), we used a mutant mouse strain that is functionally de-efferented due to the absence of the alpha-9 nicotinic acetylcholine receptor expressed on outer hair cells. We first titrated the exposure level required to induce temporary threshold shifts, as measured by auditory brainstem responses (ABRs) and distortion-product otoacoustic emissions (DPOAEs), and permanent cochlear synaptopathy. The optimal exposure level was 4-dB lower than that required for CBA/CaJ mice (93.5 vs. 97.5 dB SPL), but there was no difference between knockout (KO) and wild-type (WT) mice of the same strain.

We compared contralaterally evoked MEMRs in unanesthetized, head-fixed a9-KO vs. a9-WT mice, with synaptopathy ranging from 0 50% in the basal half of the cochlea, as confirmed by cochlear histopathology. Reflex
threshold was strongly correlated with the percentage of synapses lost. When the reflex elicitor spanned the synaptopathic region (22.6-45.2 kHz passband), the threshold was elevated by up to ~16 dB in synaptopathic mice,
but there was no difference in reflex threshold when the elicitor spanned the non-synaptopathic region (5.6-11.3 kHz passband). This internal control indicated that reflex threshold elevation was caused by a reduced input from
the afferent limb of the circuit, rather than a central deficit or reduced motor output to the stapedius muscle. The
data confirm our prior report on anesthetized mice and further highlight the potential utility of the MEMR in the
early detection of cochlear synaptopathy.

 

Here's a very interesting video of a lecture given by Charles Liberman on hidden hearing loss:

Hidden Hearing Loss: M. Charles Liberman PhD

Lots of discussion of his experiments with Kujawa, aging as a cause in addition to noise, etc. No inside information on Decibel or treatment beyond what we already know about NT-3.

 

Hidden hearing loss?
https://liu.se/en/news-item/upptack...on-kan-forbattra-diagnostik-for-horselskadade

 

Missed hearing loss in tinnitus patients with normal audiograms.
Xiong B, et al. Hear Res. 2019.
Show full citation
Abstract
The prevalence of tinnitus is positively correlated with hearing loss, although, tinnitus can also present alongside clinically normal pure-tone thresholds. As standard pure tone audiograms (PTA) only sample at octave or inter-octaves, they potentially can miss lesions between the tested frequencies. Here we investigate if tinnitus patients with normal audiograms have hearing loss missed by standard PTA testing, referred as "missed hearing loss" in the paper. Hearing thresholds in 106 tinnitus patients who have a normal PTA were tested using fine frequency resolution (1/24 octave step) audiometry, referred as precision PTA (P-PTA), at ±1/3 octave band centered at their tinnitus frequencies. Tinnitus pitch, loudness and residual inhibition were evaluated based on the result of P-PTA. DPOAEs were also tested to evaluate the function of outer hair cells (OHC). Using the P-PTA test, we found that 49% (52 out of 106) of tinnitus patients with normal audiograms showed sharply notched hearing loss and most of the notches were at their tinnitus frequencies. Using a fine frequency step (1/24 octave) to assess tinnitus pitch, the successful matching rate increased to 84%, significantly higher than the rate measured in traditional method (51%, Fisher's test, P < 0.0001, n = 106). The number of patients whose tinnitus loudness was less than 5 dB SL increased from 26% to 55% after the loudness reassessment based on the tinnitus pitch match (n = 106, Chi-Square test, P < 0.01). The percentage of patients who showed positive residual inhibition of tinnitus also increased from 31% to 54% (Chi-Square test, P < 0.05). DPOAEs revealed significantly reduced OAE amplitude in the tinnitus patients, suggesting that OHC dysfunction may contribute to their notched hearing loss. However, in 13 out of 31 patients with notched hearing loss, their DPOAE did not show any reduction which suggests that their notched hearing loss may be induced by the dysfunction of the inner hair cells or afferent synapses (synaptopathy). Our study confirmed hidden cochlear impairments in tinnitus patients with seemingly normal audiograms. We conclude that P-PTA can help identify a mild hearing impairment that may otherwise be missed by conventional PTA and that P-PTA can also improve tinnitus evaluation accuracy.

Published by Elsevier B.V.

https://www.ncbi.nlm.nih.gov/pubmed/31683074/