noisy environments, hearing speech
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PhD students Courtney Coburn Glavin, Kailyn A. McFarlane, and Assistant Professor Jason Tait Sanchez discuss the mechanisms, barriers, and future progress for hearing speech in noisy environments

When you find yourself struggling to hear in a noisy restaurant, chances are you aren’t alone. Difficulty understanding speech-in-noise (SIN) is one of the most common hearing-related complaints1. This problem is not unique to individuals with clinically defined hearing loss; estimates suggest that as many as 26 million people complain of hearing difficulties in noisy situations despite having clinically “normal” hearing2. Even with renewed attention to this problem in the fields of audiology and hearing science, its etiology, and thus, diagnosis and treatment in humans remains elusive.

In this research profile we: 1) explore potential mechanisms underlying this phenomenon, 2) consider barriers to validating and identifying this problem, and 3) discuss our lab’s novel approach to this problem.

Potential mechanisms

Cochlear synaptopathy – a term used to describe synapse damage and loss between inner hair cells of the cochlea and auditory nerve fibers – has been demonstrated to occur after noise exposure in animal models3,4,5. This form of hearing impairment is termed “hidden” hearing loss because traditional tests of hearing integrity are not sensitive enough to detect this synaptic disruption. Some theorize that synaptopathy could explain SIN deficits in humans, given that it occurs after auditory insult and is a deficit “hidden” from traditional hearing tests.

However, the presence of synaptopathy following noise insult is not ubiquitous, even in animal models6. Results in humans are further complicated by the fact that synaptic damage cannot be directly verified because of the invasive nature of doing so. Many studies, using proxy measures of synaptopathy, have failed to find systematic evidence of this pathology in humans7,8. This could be due to the inability to directly measure the phenomenon, the lack of experimental control in exposing humans to environmental insults, or the true absence of synaptopathy in humans. Based on existing evidence, synaptopathy is likely not the sole explanation for SIN deficits in humans.

Hearing loss in frequency regions not typically evaluated with traditional hearing tests has also been suggested as a reason for SIN difficulty. Though the range of human hearing extends up to 20,000 Hz, traditional hearing tests evaluate frequency sensitivity only to 8,000 Hz. Testing higher frequencies is time-consuming and there are equipment limitations in presenting high-frequency stimuli. Both of these factors have resulted in a significant portion of the human hearing range left unevaluated.

This dilemma is important because the cochlea of the inner ear is frequency-tuned (i.e., tonotopic); specific regions are most sensitive to high-frequency sounds, while other regions are most sensitive to low-frequency sounds. The region sensitive to higher frequencies is also believed to be most susceptible to environmental insult, making the relationship between high-frequency hearing loss above 8,000 Hz and SIN difficulties conceivable. More research in this area is needed to better understand this potential relationship.

Limitations to validation and identification

A major barrier to identifying SIN difficulties in humans is the shortage of diagnostic tests that are sensitive enough to evaluate the integrity of specific anatomical locations within the complex auditory pathway. This prevents us from obtaining a clear picture of functional and structural changes that occur with age or environmental insult. The traditional test of hearing is the behavioural audiogram. Though it is the current gold standard for assessing auditory function, it is a gross measure of hearing.

While the health of some anatomical sites of the auditory pathway can be reliably assessed through existing diagnostic tools (e.g., integrity of outer hair cells is thought to be captured by measures of otoacoustic emissions), others, such as inner hair cells, cochlear synapses, and more central structures cannot be assessed and interpreted in a straightforward manner in humans.

For example, Wave I of the auditory brainstem response (ABR) is thought to reflect the integrity of the synaptic connection between inner hair cells and auditory nerve fibers. However, studies investigating the use of Wave I as a biomarker for functional SIN deficits have yielded mixed results in humans9,10,11.

The clinical use of diagnostic measures beyond the audiogram is another problem in characterising SIN deficits in humans. Fewer than 15% of audiologists report routinely assessing SIN performance in their patients2. Even when used clinically, existing SIN tests are highly variable and may not assess the same constructs.

For example, some SIN tests use speech babble as background noise, whereas others use steady-state noise; some use an adaptive procedure that changes based on performance, whereas others use a fixed procedure. Thus, some SIN procedures may not accurately reflect real-world listening situations, and their variability limits cross-study comparisons of patient performance. This limits reliable identification of SIN problems and their relationship to other measures of hearing.

Future progress

Ultimately, the largest barrier to identifying the etiology of SIN deficits lies in the complexity of the human experience. Over the course of a lifetime, a person is exposed to an amalgamation of environmental insults, each of which interact with the person’s genetic makeup. Mechanisms underlying problems with SIN are multifaceted in nature and are likely more complex in humans than other animals.

“Sound conditioning” and “toughening”, for example, are ideas that previous noise exposure leads to reduced susceptibility of the auditory system to noise12,13. Individuals who have a history of noise exposure may then be less vulnerable to future auditory insults. Sound conditioning has been proposed as one explanation for the mixed evidence of SIN etiology and difficulties in humans.

The research conducted in the Sanchez Laboratory at Northwestern University takes a unique approach to examining SIN deficits in humans. Specifically, we compare individuals with self-reported SIN deficits to those with no reported SIN issues on an extensive battery of auditory diagnostic tests. In this way, we do not rely solely on objective measures of SIN ability, which are highly variable and may not reflect real-world experiences.

From our extensive test battery and large pool of participants, we hope to identify clinically viable measures that validate patient complaints and are sensitive to the underlying mechanisms behind SIN deficits. Given the number of individuals who experience SIN-related problems, there is a tremendous need to improve their communication abilities. Treatment options, however, cannot fully be explored until we understand the etiology of this issue and can reliably validate and identify it in humans.



1 Abrams, H.B, & Kihm, J. (2015). An introduction to MarkeTrak IX: A new baseline for the hearing aid market. Hearing Review, 22(6), 16.

2 Beck, D.L., Danhauer, J.L., Abrams, H.B., Atcherson, S.R., Brown, D.K., Chasin, M., Clark, J.G., De Placido, C., Edwards, B., Fabry, D.A., Flexer, C., Fligor, B., Frazer, G., Galster, J.A., Gifford, L., Johnson, C.E., Madell, J., Moore, D.R., Roeser, R.J., Saunders, G.H., Searchfield, G.D., Spankovich, C., Valente, M., & Wolfe, J. (2018). Audiologic considerations for people with normal hearing sensitivity yet hearing difficulty and/or speech-in-noise problems. Hearing Review, 25(10), 28-38.

3 Kujawa, S. G., & Liberman, M. C. (2009). Adding Insult to Injury: Cochlear Nerve Degeneration after “Temporary” Noise-Induced Hearing Loss. The Journal of Neuroscience, 29(45), 14077–14085.

4 Lobarinas, E., Spankovich, C., & Le Prell, C.G. (2017). Evidence of “hidden hearing loss” following noise exposures that produce robust TTS and ABR wave-I amplitude reductions. Hearing Research, 349, 155-163.

5 Hickox, A. E., Larsen, E., Heinz, M. G., Shinobu, L., & Whitton, J. P. (2017). Translational issues in cochlear synaptopathy. Hearing Research, 349, 164–171.

6 Fernandez, K.A., Jeffers, P.W., Lall, K., Liberman, M.C., & Kujawa, S.G. (2015). Aging after noise exposure: acceleration of cochlear synaptopathy in “recovered” ears. J. Neuroscience, 35(19), 7509-7520.

7 Prendergast, G., Guest, H., Munro, K.J., Kluk, K., Léger, A., Hall, D.A., Heinz, M.G., & Plack, C.J. (2016). Effects of noise exposure on young adults with normal audiograms I: Electrophysiology. Hearing Research, 344, 68-81.

8 Guest, H., Munro, K. J., Prendergast, G., Millman, R. E., & Plack, C. J. (2018). Impaired speech perception in noise with a normal audiogram: No evidence for cochlear synaptopathy and no relation to lifetime noise exposure. Hearing Research, 364, 142–151.

9 Grose, J.H., Buss, E., & Hall, J.W. (2017). Loud music exposure and cochlear synaptopathy in young adults: Isolated auditory brainstem response effects but no perceptual consequences. Trends Hear. 21, 1-18.

10 Grinn, S.K., Wiseman, K.B., Baker, J.A., & Le Prell, C.G. (2017). Hidden Hearing Loss? No effect of common recreational noise exposure on cochlear nerve response amplitude in humans. Front. Neurosci. 11(465).

11 Valderrama, J.T., Beach, E.F., Yeend, I., Sharma, M., Van Dun., B., & Dillon, H. (2018). Effects of lifetime noise exposure on the middle-age human auditory brainstem response, tinnitus and speech-in-noise intelligibility. Hearing Research, 365, 36-48.

12 Canlon B, Borg E, Flock A (1988) Protection against noise trauma by pre-exposure to a low level acoustic stimulus. Hearing Research, 34(2), 197–200.

13 Mannström, P., Kirkegaard, M., & Ulfendahl, M. (2015). Repeated Moderate Noise Exposure in the Rat—an Early Adulthood Noise Exposure Model. Journal of the Association for Research in Otolaryngology, 16(6), 763–772.



The Roxelyn and Richard Pepper Department of Communication Sciences and Disorders.

The Department of Neurobiology.

The Hugh Knowles Hearing Research Center. Northwestern University. Evanston, Illinois, 60208, USA.



Courtney Coburn Glavin, Au.D., FAAA

Ph.D. Student

Northwestern University

Tel: +1 847 467 0123


Kailyn A. McFarlane

Au.D./Ph.D. Student

Northwestern University

Tel: +1 972 832 8744


Jason Tait Sanchez, Ph.D., CCC-A, FAAA

Assistant Professor

Northwestern University

Tel: +1 847 491 4648

Central Auditory Physiology Laboratory


Please note: This is a commercial profile


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