Le Prell, Colleen G.

Permanent URI for this collectionhttps://hdl.handle.net/10735.1/5917

Colleen Le Prell holds the Emile and Phil Schepps Professorship in Hearing Science. She also serves as the Program Head for the Audiology AuD program at the Callier Center for Communication Disorders. Dr. Le Prell is "one of the leading researchers in the area of hearing loss prevention." He research interests include:

  • The identification of cell death pathways activated by noise,
  • The assessment of therapeutic agents that prevent cell death and hearing loss,
  • Prevention of age-related hearing loss.
  • Noise-induced hearing loss,
  • Prevention of temporary music-player induced changes in hearing.

ORCID page


Recent Submissions

Now showing 1 - 4 of 4
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    Effects of Noise Exposure on Auditory Brainstem Response and Speech-in-Noise Tasks: A Review of the Literature
    (Taylor & Francis Ltd, 2018-12-18) Le Prell, Colleen G.; 0000-0002-6161-3033 (Le Prell CG); Le Prell, Colleen G.
    Objective: Short-term noise exposure that induces transient changes in thresholds has induced permanent cochlear synaptopathy in multiple species. Here, the literature was reviewed to gain translational insight into the relationships between noise exposure, ABR metrics, speech-in-noise performance and TTS in humans.Design: PubMed-based literature search, retrieval and review of full-text articles. Study Sample: Peer-reviewed literature identified using PubMed search.Results: Permanent occupational noise-induced hearing loss (NIHL) is frequently accompanied by abnormal ABR amplitude and latency. In the absence of NIHL, there are mixed results for relationships between noise exposure and ABR metrics. Interpretation of speech-in-noise deficits is difficult as both cochlear synaptopathy and outer hair cell (OHC) loss can drive deficits. Reductions in Wave I amplitude during TTS may reflect temporary OHC pathology rather than cochlear synaptopathy. Use of diverse protocols across studies reduces the ability to compare outcomes across studies.Conclusions: Longitudinal ABR and speech-in-noise data collected using consistent protocols are needed. Although speech-in-noise testing may not reflect cochlear synaptopathy, speech-in-noise testing should be completed as part of a comprehensive test battery to provide the objective measurement of patient difficulty.
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    Otoprotectants: From Research to Clinical Application
    (Thieme Medical Publishers, Inc., 2019) Le Prell, Colleen G.; 0000-0002-6161-3033 (Le Prell, CG); Le Prell, Colleen G.
    There is an urgent need for otoprotective drug agents. Prevention of noise-induced hearing loss continues to be a major challenge for military personnel and workers in a variety of industries despite the requirements that at-risk individuals use hearing protection devices such as ear plugs or ear muffs. Drug-induced hearing loss is also a major quality-of-life issue with many patients experiencing clinically significant hearing loss as a side effect of treatment with life-saving drug agents such as cisplatin and aminoglycoside antibiotics. There are no pharmaceutical agents approved by the United States Food and Drug Administration for the purpose of protecting the inner ear against damage, and preventing associated hearing loss (otoprotection). However, a variety of preclinical studies have suggested promise, with some supporting data from clinical trials now being available as well. Additional research within this promising area is urgently needed. © Georg Thieme Verlag KG, Stuttgart. New York.
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    The Search for Noise-Induced Cochlear Synaptopathy in Humans: Mission Impossible?
    (Elsevier B.V.) Bramhall, N.; Beach, E. F.; Epp, B.; Le Prell, Colleen G.; Lopez-Poveda, E. A.; Plack, C. J.; Schaette, R.; Verhulst, S.; Canlon, B.; 0000-0002-6161-3033 (LePrell, CG); Le Prell, Colleen G.
    Animal studies demonstrate that noise exposure can permanently damage the synapses between inner hair cells and auditory nerve fibers, even when outer hair cells are intact and there is no clinically relevant permanent threshold shift. Synaptopathy disrupts the afferent connection between the cochlea and the central auditory system and is predicted to impair speech understanding in noisy environments and potentially result in tinnitus and/or hyperacusis. While cochlear synaptopathy has been demonstrated in numerous experimental animal models, synaptopathy can only be confirmed through post-mortem temporal bone analysis, making it difficult to study in living humans. A variety of non-invasive measures have been used to determine whether noise-induced synaptopathy occurs in humans, but the results are conflicting. The overall objective of this article is to synthesize the existing data on the functional impact of noise-induced synaptopathy in the human auditory system. The first section of the article summarizes the studies that provide evidence for and against noise-induced synaptopathy in humans. The second section offers potential explanations for the differing results between studies. The final section outlines suggested methodologies for diagnosing synaptopathy in humans with the aim of improving consistency across studies. ©2019 Elsevier B.V.
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    Hidden Hearing Loss? No Effect of Common Recreational Noise Exposure on Cochlear Nerve Response Amplitude in Humans
    Grinn, Sarah K.; Wiseman, Kathryn B.; Baker, Jason A.; Le Prell, Colleen G.; Grinn, Sarah K.; Wiseman, Kathryn B.; Baker, Jason A.; Le Prell, Colleen G.
    This study tested hypothesized relationships between noise exposure and auditory deficits. Both retrospective assessment of potential associations between noise exposure history and performance on an audiologic test battery and prospective assessment of potential changes in performance after new recreational noise exposure were completed. Methods: 32 participants (13M, 19F) with normal hearing (25-dB HL or better, 0.25-8 kHz) were asked to participate in 3 pre- and post-exposure sessions including: otoscopy, tympanometry, distortion product otoacoustic emissions (DPOAEs) (f2 frequencies 1-8 kHz), pure-tone audiometry (0.25-8 kHz), Words-in-Noise (WIN) test, and electrocochleography (eCochG) measurements at 70, 80, and 90-dB nHL (click and 2-4 kHz tone-bursts). The first session was used to collect baseline data, the second session was collected the day after a loud recreational event, and the third session was collected 1-week later. Of the 32 participants, 26 completed all 3 sessions. Results: The retrospective analysis did not reveal statistically significant relationships between noise exposure history and any auditory deficits. The day after new exposure, there was a statistically significant correlation between noise "dose" and WIN performance overall, and within the 4-dB signal-to-babble ratio. In contrast, there were no statistically significant correlations between noise dose and changes in threshold, DPOAE amplitude, or AP amplitude the day after new noise exposure. Additional analyses revealed a statistically significant relationship between TTS and DPOAE amplitude at 6 kHz, with temporarily decreased DPOAE amplitude observed with increasing TTS. Conclusions: There was no evidence of auditory deficits as a function of previous noise exposure history, and no permanent changes in audiometric, electrophysiologic, or functional measures after new recreational noise exposure. There were very few participants with TTS the day after exposure - a test time selected to be consistent with previous animal studies. The largest observed TTS was approximately 20-dB. The observed pattern of small TTS suggests little risk of synaptopathy from common recreational noise exposure, and that we should not expect to observe changes in evoked potentials for this reason. No such changes were observed in this study. These data do not support suggestions that common, recreational noise exposure is likely to result in "hidden hearing loss".

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