In October our partner Hyperacusis Research hosted a webinar that highlighted both the human impact of hyperacusis—pain triggered by everyday sounds—and the scientific progress being made to understand and treat it.
HHF’s Timothy Higdon (second from left) with (from left) Hyperacusis Research’s Steven Barad, M.D., Mike Maholchic, and Ana Raab, at the ARO MidWinter Meeting in February 2025.
The field was revolutionized in 2011 when Hyperacusis Research was founded by Bryan Pollard, who unfortunately passed away in 2022. Hyperacusis Research continues his legacy, and to date has awarded nearly $400,000 in research grants.
Moderated by Steven Barad, M.D., the incoming president of Hyperacusis Research, scientists shared major advances in identifying the biological mechanisms behind sound-induced pain, from the discovery of specialized auditory neurons that transmit pain signals to the development of promising new drugs targeting hyperactive brain circuits.
Several Types of Ear Pain
James Henry, Ph.D., a retired research audiologist, provides an overview of the potential mechanisms causing hyperacusis, including central auditory gain, middle ear muscle dysfunction, and specific nerve pathways. He also clarifies distinctions between different types of sound sensitivity disorders, which can be confusing. For instance “otalgia,” a word often used in the field, describes ear pain that is unrelated to sound—unlike hyperacusis, where ear pain is a result of exposure to sound.
He explains how to differentiate hyperacusis from other conditions with which it is often confused, highlighting each condition’s key characteristics.
Otalgia: Ear pain unrelated to sound exposure.
Loudness hyperacusis: Uncomfortable to unbearable physical sensations (exclusive of piercing or stabbing pain) when exposed to sounds that are comfortable for most people.
Pain hyperacusis: Burning, stabbing, or jabbing pain in the ears or head when exposed to sounds that are comfortable for most people.
Misophonia: A negative and distressing emotional reaction to specific sounds, sometimes soft mouth-related sounds like chewing or sniffling. This is not ear pain.
Noise sensitivity: A general emotional reactivity where sound, in general, is bothersome.
Phonophobia: An excessive fear that sound will be uncomfortable or painful.
Henry says loudness hyperacusis could be due to increased central auditory gain or to dysfunction in the middle ear muscles. Pain hyperacusis could be caused by dysfunction of the type II auditory neurons, which connect to outer hair cells in the cochlea. Another possible source is inflammation of the trigeminal nerve, which innervates the face, head and ear. (Henry has previously written about the five distinct sound sensitivity disorders.)
Modeling Auditory Pain
Megan Beers Wood, Ph.D., of Vanderbilt University, details her work on modeling auditory pain in animals. She presents evidence that unmyelinated type II afferent neurons—which share characteristics with pain-sensing nerve fibers after tissue damage—may be a key component of pain hyperacusis.
Type II afferent neurons share characteristics with C-fibers, the primary pain-sensing neurons in the skin. These unmyelinated neurons express genes for pain-related neuropeptides like CGRP and Substance P, and respond to ATP, a chemical released by damaged cells. Noise exposure can cause physical and functional changes to these neurons, with an increase in the number of ribbon synapses connecting them to outer hair cells.
Her lab demonstrates that these nerves become activated after noise exposure and confirms that a functional cochlea is necessary to generate these auditory pain signals. In mice, auditory pain can be measured using changes in facial grimace and body position. Deaf mice cannot detect sound, demonstrating that the initial detection of sound by a functional cochlea is necessary for the generation of auditory pain.
Wood says her lab also used AI to help analyze thousands of video frames for a mouse grimace study and expects that AI will be critical in accelerating research by analyzing large and complex data sets.
A Potential Pharmacological Treatment
Thanos Tzounopoulos, Ph.D., of the University of Pittsburgh, explains the “central gain” (neural hyperactivity) mechanism: After noise-induced damage reduces the signal from the ear, the brain turns up an internal gain to compensate, and neurons become hyperactive. This hyperactivity is caused by the dysfunction of potassium channels called KCNQ, which fail to open properly after noise injury.
An epilepsy drug, Retigabine, was previously shown to force these channels open but produced unacceptable side effects. Building on this knowledge, Tzounopoulos and his team have developed a new, more specific molecule called RL81 that also opens KCNQ channels, quieting hyperactive neurons.
RL81 is still in preclinical development. While drug delivery remains a challenge, this compound represents a promising new approach to correcting the neural hyperactivity underlying tinnitus. Once it enters testing, RL81 will likely be evaluated first for tinnitus.
Lives Destroyed
Steven Barad, M.D., a retired orthopedic surgeon, will take over as president of Hyperacusis Research on January 1, 2026, succeeding Michael Maholchic. Both have adult sons suffering from severe pain hyperacusis.
Barad spoke about his son’s situation. He was once a popular high school student who now lives an isolated life at home. “He is imprisoned by his house,” Barad says. His son played loud music in a garage band and attended dozens of concerts.
Barad says that, like almost everyone back then, his son knew nothing about protecting his ears. As his son’s symptoms worsened, his friends slipped away. Barad notes an enormous lack of empathy from people who are lucky enough not to know about hyperacusis.
The webinar also highlighted a recent BBC News feature on Karen Cook, a former flight attendant in the U.K. whose life was forever changed when she developed severe pain hyperacusis, along with tinnitus. Her pain feels like “burning lava” inside her ears, along with severe pressure in her face and head.
In the interview, Cook says that sound keeps her captive. The impact has been devastating, Cook says: “It completely erased me.” The voices of her two young sons are torture. “Everything we knew as a family has changed,” says her husband.
Next Steps
Hyperacusis Research has announced a $50,000 matching gift challenge for its 2025 Fall 2025 fundraiser, as scientists continue to search for a cure.
The webinar underscored the immense personal toll of hyperacusis and the promising scientific progress already underway. With sustained research investment and public awareness, relief for those living with sound-induced pain moves closer to reality.
Hyperacusis Research is a nonprofit organization focused on advocating for individuals whose lives are impacted by hyperacusis. The organization is staffed entirely by volunteers and directs its revenue toward funding scientific research through Hearing Health Foundation’s Emerging Research Grants program. HHF is grateful for our long partnership with Hyperacusis Research, founded by the late Bryan Pollard. Megan Beers Wood, Ph.D., is a 2022–2023 ERG scientist funded by Hyperacusis Research, where she is now a member of their scientific advisory board.
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Our partner Hyperacusis Research recently hosted a webinar that highlighted both the human impact of hyperacusis—pain triggered by everyday sounds—and the scientific progress being made to understand and treat it.