By James A. Henry, PhD, and Kelly N. Jahn, AuD, PhD
Originally published in the Spring 2025 issue of "Tinnitus Today" magazine.

As many as 17 percent of people have difficulty tolerating everyday sounds that do not bother others. These people are hypersensitive to sound compared to the typical person. In general, a sound hypersensitivity disorder is characterized by interference with or prevention of participation in normal life activities because everyday sounds cause physical discomfort, pain, negative emotional reactions, fear, or some combination of these symptoms.

The term hyperacusis is often used to describe a sound hypersensitivity disorder, but at least five different sound hypersensitivity disorders have been distinguished in the scientific literature:

• Loudness hyperacusis: Sounds are perceived as unbearably loud when they seem normal to most other people.
• Pain hyperacusis (noxacusis): Sound causes physical pain in or around the ears.
• Misophonia: Certain sounds cause negative emotional reactions, especially sounds from the mouth and nose of others.
• Noise sensitivity: Sound in general causes irritation or annoyance.
• Phonophobia: Excessive fear that sound will be too loud, distressing, or painful.

The Hyperacusis and Misophonia Book: When Everyday Sounds Are Too Loud, Distressing, or Painful was written to explain these disorders, how they differ, and how they can be diagnosed and treated. This article focuses on explaining how loudness hyperacusis differs from pain hyperacusis.

Definition
Loudness hyperacusis is the experience of uncomfortable-to-unbearable physical sensations (exclusive of piercing, burning, or stabbing pain) in the ears and/or head when exposed to any sound at intensity levels that would not be uncomfortable for the typical person.

Symptoms
This definition is the basis for diagnosing loudness hyperacusis. The physical symptoms might involve an uncomfortable sense of fullness in one or both ears (like a balloon being blown up inside the ear), dull earache, or headache. The sensations are often difficult to describe, but they are not typically characterized using adjectives such as "piercing," "burning," or "stabbing" that would indicate severe physical pain.

Although loudness hyperacusis can occur in isolation, it is commonly associated with a range of audiovestibular, neurological, psychological, and neurodevelopmental conditions, including tinnitus, hearing loss, migraine, autism spectrum disorder, brain injury, William's syndrome, and post-traumatic stress disorder, to name a few.

Theorized Mechanisms
Loudness hyperacusis is widely believed to be caused by heightened central auditory gain (i.e., the "volume control" in the brain is turned up too high). "A consensus is emerging in the auditory neuroscience literature that hyperacusis may be associated with a sustained and persistent increase in central auditory gain."

What is central auditory gain? Briefly, all neurons in the central auditory system fire spontaneously even in the absence of sound, which is normal for everyone. The spontaneous activity has a "set point," which is recalibrated depending on the level of sound entering the ears. During an extended period of quiet or when there is hearing loss, the set point may be raised such that the central auditory system amplifies sound more than usual, which could result in loudness hyperacusis.

Another source of physical discomfort can be caused by tightening of the tensor tympani muscle—one of the two middle-ear muscles that contracts to stiffen the middle-ear bones (ossicles)—which reduces the amount of sound energy entering the cochlea. Physical discomfort associated with loudness hyperacusis could be due to everyday sounds causing contraction of the tensor tympani muscle, which would cause fullness in the ear and other uncomfortable sensations, often described as "pain" but not meeting the definition for pain hyperacusis as explained below. Some people have tensor tympani syndrome, which could explain why the tensor tympani contracts so easily with sound exposure.

Treatment
Treatment often involves some type of systematic sound exposure to desensitize (or recalibrate) central auditory gain. These interventions typically focus on alleviating the physical discomfort caused by sound. If a patient also has negative emotional reactions to this physical discomfort, then resolving the sound-related discomfort may also positively impact emotional well-being. Sometimes, however, intense emotional reactions to sound may need to be treated separately from the physical discomfort. In such cases, patients should be referred to behavioral health specialists to address the emotional impact of sound exposure.

The most effective approaches to managing loudness hyperacusis typically involve a combination of graded sound exposure and counseling. A common intervention for loudness hyperacusis is Tinnitus Retraining Therapy, which uses a specific form of sound therapy along with a structured counseling protocol. Other approaches that use different forms of sound therapy and counseling include Hyperacusis Activities Treatment and Progressive Tinnitus Management. Transitional Intervention is a unique and relatively new approach that uses output-limiting sound-protection devices combined with counseling to recalibrate the hyper-gain response associated with loudness hyperacusis.

It is important to note that sound therapy may not be effective for all patients and that other types of treatment or referrals to other healthcare professionals might be necessary. In all cases, educational counseling is essential so that patients understand the purpose of treatment, the plan of care, and how to address emotional well-being. Cognitive behavioral therapy (CBT) can be used to treat the negative emotional reactions to sound. Specifically, CBT has been used to treat sound-avoidance behaviors associated with loudness hyperacusis. Reducing sound avoidance results in more sound entering the ears, which could augment sound therapy approaches.

In some cases, surgery may be used as a last resort to treat loudness hyperacusis. A surgical technique has been developed to impede the transmission of sound waves to the cochlea—effectively reducing the loudness of sound. In essence, the surgery stiffens the membranes (round and oval windows) in the bony cochlea that are necessary to transmit sound to the inner ear. The majority of patients undergoing this surgery showed long-term improvement in hyperacusis symptoms.

Definition
Pain hyperacusis (noxacusis) is the experience of burning, stabbing, or jabbing pain in the ears or head when exposed to and/or following any sound at an intensity level that would be comfortable for the typical person.

Symptoms
Both loudness hyperacusis and pain hyperacusis are defined by physical reactions to sound at intensity levels that are comfortable for most people. The main difference between the two conditions is how these sensations manifest. Whereas loudness hyperacusis is described as discomfort, intolerance, or hypersensitivity, pain hyperacusis is described as piercing pain, including burning, stabbing, or jabbing sensations. Pain hyperacusis can also result in delayed or prolonged pain, and patients often experience "setbacks" where the pain is exacerbated for a period of time following sound exposure. Many patients experience some degree of both loudness and pain hyperacusis. Those who experience pain hyperacusis tend to exhibit more severe, debilitating, and life-altering symptoms.

Pain hyperacusis is not recognized by most healthcare professionals. "The old way of thinking is that there is one kind of hyperacusis, where everything sounds louder. Fortunately, science has progressed, and it's now known that there is a more severe form, pain hyperacusis, where loudness passes some threshold and turns into actual pain. And that pain lingers and worsens. It's impossible to describe how much suffering this condition entails."

Theorized Mechanisms
Whereas loudness hyperacusis is thought to be caused by an increase in central auditory gain, "there is little-to-no empirical evidence to support central gain as the underlying cause of pain hyperacusis per se." This does not mean that people with pain hyperacusis do not have elevated central auditory gain—there is simply not enough evidence one way or another to make that determination at this time.

So, which theories might explain the origin of sound-induced pain? Briefly, the inner ear (cochlea) is connected to the brainstem by the auditory nerve. This nerve is a bundle of nerve fibers, some of which have characteristics that could make them function like pain receptors. These fibers may be the source of the pain, but there are other possible sources, including structures in the middle ear and central auditory pathway.

In the middle ear, damage, overload, or myoclonus (uncontrollable twitching) of the tensor tympani muscle can irritate the trigeminal nerve and result in pain in or near the ear. Regarding the central auditory pathway, damage to the middle or inner ear can lead to an increase in neural activity or elevated central gain. It should be noted that patients with pain hyperacusis often have many other symptoms such as fullness, pressure, or fluttering in the ear that are consistent with a middle ear origin. However, more research is needed to pinpoint the underlying mechanisms of pain hyperacusis.

Treatment
Many people with loudness hyperacusis can benefit from graded sound exposure, but sound therapy may be ineffective for some people with pain hyperacusis and can even worsen the condition. One individual reported that sound therapy was "counterproductive and lowered my sound tolerance dramatically. I never recovered from that worsening." There are, however, some people with pain hyperacusis who do benefit from sound therapy, so it is important to explore all possible treatment avenues when working with these patients.

However, a patient should never be advised to "tough it out" by enduring painful sound under the pretense that sound exposure will eventually result in the ability to tolerate sound comfortably. Even if sound cannot be tolerated at all, it is important to leave the door open for possible sound therapy in the future. After all, the ultimate goal of therapy for pain hyperacusis is that the person is comfortable with reasonable levels of sound.

Counseling is essential for anyone with pain hyperacusis. Educational counseling should be used to explain what is known about pain hyperacusis and possible treatments. Counseling to reduce stress and anxiety should be done as needed, which may also have the benefit of relaxing the tensor tympani muscle. CBT has not yet been empirically studied in patients with pain hyperacusis, but its efficacy in treating other forms of pain suggests that CBT might be helpful, and certainly would not cause harm.

Perhaps the best source of data on different treatments used for pain hyperacusis is a study in which 32 adults described their use of pharmaceutical and non-pharmaceutical treatments for pain relief. In that study, "most participants reported low efficacy of interventions that are designed to counteract maladaptive gain in the central nervous system (e.g., sound therapy, Tinnitus Retraining Therapy) and six participants reported that those therapies made their noxacusis worse." In general, non-pharmaceutical treatments were reported to be largely ineffective for alleviating pain hyperacusis.

On the other hand, the patients in this study reported modest-to-excellent effects from pharmaceutical treatment with benzodiazepines, nerve blockers, anticonvulsants, Tylenol, oxycodone, and Botox. Two of the participants in the study reported an "excellent effect (>90% pain relief)" using nerve blockers such as lidocaine and ambroxol. Extensive evidence supports ambroxol for treating neuropathic pain in various conditions. One participant reported an excellent effect from Botox injections in the tensor veli palatini muscle. "The tensor veli palatini is innervated by the trigeminal motor root and may form a functional unit with the tensor tympani muscle to control middle ear pressure." The authors point out that their results are generally consistent with middle ear and trigeminal nerve theories of pain hyperacusis mechanisms, and they suggest that this hypothesis could be clinically tested using locally administered analgesics such as over-the-counter 4 percent lidocaine ear drops.

Another study showed promising results with benzodiazepines, opioids, and gabapentinoids—with a strong warning to use benzodiazepines "judiciously." Another study noted some minor improvement with clonazepam. Finally, an audiologist from the University of Iowa recommended lifestyle modifications to improve quality of life for individuals with pain hyperacusis.

Distinguishing between loudness hyperacusis and pain hyperacusis is a fairly recent development. The distinction has always existed for people who experience these different forms of hyperacusis, but clinicians and researchers have only recently become aware of the differences. It can be helpful to think of loudness hyperacusis as a disorder related to increased auditory gain, and pain hyperacusis as caused by pain receptors in or near the ear. Pain hyperacusis also tends to be a more severe condition than loudness hyperacusis.

Loudness hyperacusis can often be treated successfully using some combination of sound therapy and counseling, but pain hyperacusis presents more of a challenge. The study reviewed above that evaluated 32 adults with pain hyperacusis is an important resource that suggests specific treatment approaches that might be viable in addition to future directions for randomized controlled trials. Research is urgently needed to evaluate these different approaches.