Investigating the Interaction of Auditory and Pain Pathways
By Senthilvelan Manohar, Ph.D.
As the intensity of a sound increases, typical-hearing listeners experience an increase in loudness, but for levels above 120 decibels (dB), listeners not only perceive the sound as extremely loud, but also painful—the aural threshold of pain. Some individuals with hearing loss and other neurological disorders perceive even moderate-intensity sounds as both painful and loud, a condition known as pain hyperacusis.
At the same time, in many individuals moderate-intensity sounds have been shown to reduce sensitivity to pain, a phenomenon termed audio-analgesia. This has led to the use of white noise and music in some medical settings. And it has long been known that very intense sounds around 130 dB can evoke aural pain, termed audio-hyperalgesia, but it is not clear whether pain sensitivity is also exacerbated.
To investigate the multisensory interactions between auditory and pain pathways, we performed a series of experiments using a rat model, with results published in Hearing Research in August 2020. After confirming that sounds up to 90 dB reduced pain sensitivity (specifically thermal, or pain from heat), a major new finding was that high intensity sounds exacerbated the experience of thermal pain. Our results show for the first time that audio-analgesia in rats is limited to intensities below 100 dB, that thermal pain sensitivity begins to increase above 110 dB, and that audio-hyperalgesia emerges for intensities near the aural thresholds of pain.
We also modified the opioid pain pathway by treating rats with a high dose of the opioid fentanyl, known to induce increased pain sensitivity after its effects diminish. In ambient noise, pain sensitivity remained typical 10 days after the fentanyl dose. But at 90 to 110 dB, pain sensitivity increased, indicating that the pre-treatment with fentanyl had converted audio-analgesia to audio-hyperalgesia.
Finally, we tested the hypothesis that hearing loss could alter pain sensitivity by exposing rats to an intense noise leading to hearing loss. Three and four weeks after the noise exposure, pain sensitivity significantly increased. To our knowledge, these results show for the first time that noise-induced hearing loss can lead to increased thermal pain sensitivity.
Taken together, our results suggest that auditory and pain pathways interact in ways that depend on intensity, hearing loss, and opioid pain signaling, data that may be relevant to better understanding pain hyperacusis.
A 2017 ERG scientist generously funded by Hyperacusis Research Ltd., Senthilvelan Manohar is a research assistant professor at the University at Buffalo, the State University of New York. Coauthors on this paper include ERG alumni Kelly Radziwon, Ph.D. (also funded by Hyperacusis Research Ltd.), and Richard Salvi, Ph.D.