The Best Tinnitus and Hyperacusis Treatment

Understanding the link between tinnitus and hyperacusis is crucial. The #1 problem with tinnitus and hyperacusis is that they often intensify each other, causing a vicious cycle of increased severity.

The good news is that treatment is possible! Here I cover important topics concerning tinnitus and hyperacusis and will describe the best hyperacusis treatment modern medicine has to offer.

• What is hyperacusis?
• How are tinnitus and hyperacusis related?
• What causes hyperacusis?
• Hyperacusis Treatment Options
• What is the best hyperacusis treatment?

What is hyperacusis?

Hyperacusis is an auditory condition characterized by heightened sensitivity to sounds. It’s typically accompanied by a range of psychological, emotional, and physiological responses to this increased sound sensitivity.

When hyperacusis becomes severe, it can profoundly affect one’s quality of life and daily functioning. Here are some of the prominent clinical features of hyperacusis:

• Stress / Anxiety: Individuals with hyperacusis often experience significant stress and anxiety, which goes beyond the fear of loud noises. It extends to a general apprehension about being in situations where they might encounter sounds that can trigger discomfort or pain. This can lead to heightened psychological stress in everyday environments, even those that are generally considered quiet or safe.

• Avoidance Behaviors: Due to the painful or uncomfortable sensations associated with normal environmental noises, people with hyperacusis develop avoidance behaviors. This includes avoiding social interactions, public spaces, and even common household environments that might unpredictably generate noise, such as kitchens during meal preparation. Such avoidance can lead to social isolation and can impact personal and professional relationships.

• Increasing Severity of Tinnitus: In cases where hyperacusis coexists with tinnitus, the symptoms of tinnitus can quickly escalate. Hyperacusis amplifies the perception of tinnitus, making the ringing or buzzing sounds more intrusive and harder to ignore. This combination can exacerbate the distress and difficulty in managing day-to-day activities.

• Decreased Quality of Life: The combined effects of anxiety, avoidance behavior, and worsening tinnitus contribute to a significant decrease in quality of life. Individuals may find themselves unable to participate in activities they once enjoyed, leading to a sense of loss and depression. The disruption to normal life can be profound, affecting both mental and physical health.

• Physical Pain: In some severe cases, hyperacusis can cause actual physical pain in the ears when exposed to certain sounds. This rare but troubling aspect means that even everyday sounds can lead to sharp pain, further encouraging avoidance behaviors. This is a particularly burdensome form of hyperacusis.

• Fatigue: The constant tension and stress of anticipating painful or uncomfortable sound exposure can lead to chronic fatigue. This is not only due to emotional stress but also from the exhaustion of constantly being on alert to manage or escape from potential sound exposure. Fatigue from hyperacusis significantly contributes to its burden in one’s life.

• Concentration Difficulties: The overwhelming nature of hyperacusis can make it challenging for sufferers to concentrate or focus on tasks. This may also be related to inattentive type ADHD, a condition that overlaps with tinnitus because of its involvement with the attention center of the brain. This is especially problematic in work or educational settings where background noise, where it becomes a significant obstacle to productivity and engagement.

How do you define hyperacusis subtypes?

Hyperacusis can manifest in several overlapping subtypes, which include the fear, annoyance, pain, and loudness subtypes. This a descriptive framework that researchers have developed to categorize what people experience.

• Fear Hyperacusis: Individuals with this subtype experience intense, often irrational fear of certain anticipated sounds, leading to avoidance behaviors that significantly disrupt daily life. The fear stems not just from a dislike of noise but from an anticipatory anxiety about the sound as a perceived threat.

• Annoyance Hyperacusis: Marked by a strong emotional reaction to sounds perceived as annoying or distressing, this form causes significant discomfort and agitation. Sounds that are normal or unnoticed by others can provoke negative reactions, leading to anger or frustration.

• Pain Hyperacusis: In this subtype, normal sound levels can induce physical pain in the ears or head, a response triggered by volumes harmless to those with normal hearing. The pain experienced is real and sharp, making the condition particularly debilitating.

• Loudness Hyperacusis: Individuals with this condition perceive moderately intense sounds as excessively loud, likening everyday noises to overwhelmingly loud disturbances, such as a jet engine. This skewed perception can render normal environments unbearably noisy and significantly impair quality of life.

Hearing Conditions Related to Hyperacusis

There are several related and often overlapping conditions that concern tinnitus and hyperacusis.

• Phonophobia: This is a specific type of anxiety disorder where there is an irrational fear of loud sounds. It’s more about fear than physical discomfort or pain. Someone with phonophobia may experience extreme anxiety or fear in anticipation of loud noises or in environments where unexpected noises may occur.

• Reactive Tinnitus: This is when one’s tinnitus disproportionately increases in loudness in response to external noises. The loudness of the tinnitus increases much more than the increase in the external sound level. This can make everyday environments seem intolerably loud or disturbing.

• Misophonia: This is a strong emotional and physiological reaction to specific sounds, which might not be loud or unpleasant to others. Common triggers include sounds like chewing, tapping, or clicking. Misophonia is characterized by feelings of anger, irritation, or even rage rather than fear or hypersensitivity to the loudness of sounds.

• Noxacusis: This condition involves experiencing pain as a direct response to sound that is not necessarily loud or normally painful. Noxacusis basically describes the “pain hyperacusis” subtype, specifically emphasizing the pain aspect rather than just discomfort or a general increase in sound sensitivity.

What is vestibular hyperacusis?

“Vestibular hyperacusis” is where certain sounds not only seem excessively loud but also trigger vestibular symptoms such as dizziness, nausea, and imbalance. It can be associated with inner ear disorders, migraine, or noise exposure. We are finding that people with this condition have excellent results using the same protocol we use at NeuroMed. The exception to this is a condition called “superior canal dehiscence” or “3^rd window syndrome”, a condition that can be surgically corrected.

Are hyperacusis and hearing loss related?

Hearing loss and hyperacusis often coexist, but one does not necessarily imply the presence of the other. You can have hyperacusis with normal hearing.

Importantly, experiencing hyperacusis does not mean you are losing hearing. The misconception goes like this:

• Hyperacusis makes my tinnitus worse, and
• Tinnitus is associated with hearing loss, so
• When I feel hyperacusis, it means I’m losing hearing.

However, this is incorrect. Hyperacusis reflects a reset in how your brain perceives sound, causing it to report sounds as louder than they are. Unlike hearing loss, hyperacusis is a treatable and reversible condition.

***This is important because the misconception that “hyperacusis means hearing loss” can exacerbate the condition by increasing anxiety.***

How are tinnitus and hyperacusis related?

Hyperacusis can occur independently of tinnitus, but most often, these conditions are connected. In fact, hyperacusis is present in approximately 80% of severe tinnitus cases [1].

Hyperacusis and tinnitus distress levels are closely linked:

• 8 Times More Likely: Individuals with moderate hyperacusis are about 8 times more likely to experience high levels of distress from tinnitus compared to those without hyperacusis.

• 77 Times More Likely: For those with severe hyperacusis, the likelihood of experiencing significant tinnitus distress increases dramatically to about 77 times greater than those without hyperacusis.

This relationship underscores a critical point: As hyperacusis becomes more severe, the probability of experiencing tinnitus distress also significantly rises.

Is there a hyperacusis test?

A patient’s report of hyperacusis symptoms is generally sufficient to establish the diagnosis.  However, for research purposes, there are both objective and subjective tests for hyperacusis:

• Objective: The Loudness Discomfort Level (LDL) test is commonly used to determine the threshold at which sounds become uncomfortably loud. In individuals with hyperacusis, this threshold is typically 16-18 decibels lower than the average threshold of 100 decibels, highlighting their heightened sensitivity to sound. LDLs of lower than 85 is considered in the hyperacusis range.

• Subjective: The most common subjective test is the Hyperacusis Questionnaire (HQ), a validated 14-item self-report tool used to understand how hyperacusis affects daily life. It provides insights into various aspects of sound sensitivity and its implications, offering a comprehensive view of the patient's experience that complements objective tests.

For a free copy of the Hyperacusis Questionnaire for personal or clinical use, please email us at [email protected].

What causes hyperacusis?

There are three related theories regarding the hyperacusis causes.  These include the central gain model, the chronic pain model, and the migraine hypothesis.

Central Gain Model

Central gain is a neuroscience concept that describes how the central auditory system adjusts its sensitivity to sound. The term “gain” refers to the amplification of a signal in this context. When there is a change in sound input, the central auditory system can actively increase (gain) or decrease (attenuate) its response to alter the perceived loudness of the signal.

The central gain model proposes the following sequence of events:

• Reduction in Auditory Input: This could be due to hearing loss, ear damage, or any condition that reduces the amount of sound information reaching the auditory cortex.

• Compensatory Increase in Gain: In response to reduced auditory input, the central auditory system compensates by increasing the gain. Essentially, the brain turns up the volume to make up for the diminished input. This increase in gain is the brain’s attempt to normalize auditory perception.

• Over-Amplification of Sound: This compensatory mechanism can become maladaptive, leading to an over-amplification of incoming sounds. The brain, having adjusted to a higher gain, now perceives even normal-level sounds as too loud or even painful.

• Development of Hyperacusis: As a result of this over-amplification, individuals develop hyperacusis, where ordinary sounds are perceived as uncomfortably or painfully loud. Over time, this leads to the psychological impact seen with moderate to severe hyperacusis.

Experimental studies supporting this model have shown that changes in the auditory pathway related to gain can occur due to various factors, including noise exposure, age-related changes, or brain wiring changes following auditory trauma.

The problem with the central gain model is that the focus is only on the auditory system. This is the #1 misconception about tinnitus and hyperacusis. The underlying causes are much broader than just the hearing centers.

Our research at the University of California, Irvine (UCI) indicates that central gain is related to an atypical migraine process. In these cases, patients may not experience headaches but exhibit many of the clinical characteristics of migraine. In fact, hyperacusis may be the sole manifestation of this atypical migraine (“migraine without a headache”).

Chronic Pain Model

An compelling alternative explanation for hyperacusis is using chronic pain as a model. This approach is based on an understanding of “central sensitization”, the process by which acute pain becomes chronic pain in the brain [2]. Central sensitization entails amplification of neural signaling within the central nervous system, caused by maladaptive brain wiring changes (i.e. “neuroplasticity”).

The key initiating event in central sensitization is acute pain. This causes the release of inflammatory mediators in the nervous system. If these mediators persist for more than a few days, they can trigger brain wiring changes that lead to chronic pain.

• What is CGRP? The primary inflammatory molecule implicated in central sensitization is called calcitonin gene-related peptide (CGRP) [3]. Discovery of how this molecule works in the brain has revolutionized neurology in the past decade. Bookmark CGRP in your mind, as it becomes important below.

Similarities Between Hyperacusis and Chronic Pain

Here are some important similarities between tinnitus, hyperacusis, and chronic pain:

• Hypersensitivity to Sensory Stimuli: Hyperacusis patients experience sound-induced discomfort at lower intensities compared to healthy controls, indicating a heightened sensitivity to auditory stimuli. This is precisely what is seen in chronic pain, but here the sensory gain is tactile (our sense of touch) as opposed to sound-based.

• Central Nervous System Involvement: Neuroimaging studies indicate that the functional and structural brain alterations seen in both hyperacusis and tinnitus are similar to those observed in chronic pain conditions, reinforcing the idea that central nervous system changes (i.e. central sensitization) are a common factor.

• Psychological Factors: Anxiety, fear, depression, stress, and catastrophizing are prevalent in both hyperacusis and chronic pain patients, indicating shared psychological burdens with chronic pain. This suggests a central mediating role between emotional and sensory processing in all three conditions.

• Lifestyle Factors: Sleep disturbances, stress, and environmental triggers in tinnitus, hyperacusis, and chronic pain. Again, these similarities point to central sensitization as the fundamental underlying mechanism.

A Better Theory

Central sensitization offers a compelling alternative hypothesis to the central gain theory for several reasons:

• Clinical Overlap: The clinical profiles of hyperacusis and tinnitus patients often include symptoms of chronic pain, such as temporomandibular joint pain, headaches, and neck pain, all of which are characterized by heightened sensory hypersensitivity (i.e. central sensitization).

• Neuroplastic Changes: Both tinnitus and chronic pain involve brain wiring changes (i.e. neuroplastic changes) in the central nervous system, the defining feature of central sensitization. Understanding this feature is critical for planning effective treatment strategies.

• Psychological and Lifestyle Correlations: The deterioration in psychological and lifestyle factors in patients with hyperacusis, tinnitus, and chronic pain suggests a common underlying process, which central sensitization could explain.

In addition, while both models explain how sensory information can be amplified centrally, they differ in terms of how they understand what initiates the process.

• Non-specific Origin: The central gain theory posits that any decrease in auditory input, regardless of the surrounding circumstances, leads to neuroplastic changes, resulting in central amplification of sound.

• Neuroinflammatory Origin: The central sensitization model of hyperacusis asserts that the initiating event must be inflammatory in nature. Specifically, this process involves CGRP expression in the acute phase, which in turn stimulates the brain rewiring changes responsible for the central amplification of sound.

In summary, the chronic pain model and phenomenon of central sensitization appears to present a more clinically coherent description of hyperacusis and tinnitus than the central gain theory.  

The Migraine Hypothesis of Hyperacusis

We believe that an atypical migraine reaction in the brain drives hyperacusis. Drawing from the central sensitization model, we have found that hyperacusis is initiated by an inflammatory condition in the brain (i.e., migraine). In other words, migraine is the dynamic cause of hyperacusis, while central gain simply describes the resulting effect.

Again, it’s important to emphasize that you can experience the effects of a migraine without having a headache (i.e. atypical migraine). For many people, loud tinnitus and hyperacusis can be the only manifestation of migraine that they experience.

How is migraine an inflammatory condition of the brain? 

Migraine is an inflammatory condition from a biochemical point of view. We now know that CGRP is the key molecule that triggers and sustains migraine processes in the brain. CGRP is not only a pro-inflammatory molecule, but also a key player in stimulating the brain wiring changes seen in central sensitization. Importantly, new research shows that CGRP acts directly on auditory system nerves, causing increased excitation [4].

How are hyperacusis and migraine related?

When we examine the migraine literature, we find several important clinical features that concern hyperacusis.

• Prevalence: Up to 81% of migraine patients report hyperacusis, compared to only 12.1% of non-migrainous headache sufferers, highlighting a significant prevalence of sound sensitivity among those with migraine [5].

• Hearing Discomfort: Migraineurs show lower sound discomfort thresholds both during and between migraine attacks, compared to healthy controls. This suggests heightened central auditory sensitivity (i.e. central gain).

• Migraine Triggers: Sounds can act as triggers for migraine attacks, indicating that hyperacusis may be an early manifestation of migraine symptoms rather than a separate condition.

• Cochlear Function: Otoacoustic emission tests reveal that migraine patients have less suppression of sound-induced signals, indicating abnormal auditory pathway function.

• Cortical Processing: In migraine patients, brain processing of hearing signals shows increase rather than the normal habituation response, suggesting an abnormal increase of sensory signals.

• Brainstem Auditory-Evoked Potentials: Migraine patients exhibit significant impairments in brainstem auditory processing during attacks, with altered latency and amplitude responses compared to controls.

Note: In many studies, hyperacusis is mislabeled as phonophobia, which inaccurately suggests a psychological fear of sound. In reality, it’s hyperacusis—a physical hypersensitivity—that migraine patients experience.

What does this mean for hyperacusis treatment?

Considering that:

• The migraine reaction initiates and drives the dynamic changes in hyperacusis and tinnitus, and
• The migraine reaction stimulates the brain wiring changes described in the central gain model;

We must conclude that without managing the underlying migraine process, sound-based treatment for hyperacusis alone is likely to fail.

Does hyperacusis go away?

The natural history of hyperacusis (its progression over time without treatment) can vary widely among individuals, but generally it will not get better on its own. Here's an overview of the typical case:

• Onset: Hyperacusis often begins suddenly, sometimes triggered by a specific event such as exposure to loud noise, head injury, ear infection, or an episode of severe stress or anxiety. We now believe that it is related to an atypical migraine process.

• Initial Symptoms: Individuals typically experience increased sensitivity to everyday sounds, which can be uncomfortable or even painful. This heightened sensitivity can lead to avoidance behaviors and anxiety about sound exposure.

• Progression: Without treatment, the severity of hyperacusis can fluctuate. Some individuals may experience worsening symptoms over time, while in others, the condition can remain stable for extended periods. Again, we now believe that the fluctuations are due to an atypical migraine process.

• Associated Conditions: Hyperacusis is often associated with other conditions such as tinnitus, migraine, anxiety disorders, and hearing loss. These associations can influence the natural course of hyperacusis. Hyperacusis and tinnitus are a particularly difficult combination as patients with hyperacusis protect their hearing (e.g., with ear muffs or ear plugs), and therefore, hear their tinnitus at a louder level.

• Long-Term Outlook: For some, hyperacusis may persist or progress to a severe state if left untreated. Others may experience a reduction in symptoms over time, usually after they adopt one of the common treatment strategies outlined below.

Overall, the natural history of hyperacusis is highly individualized. However, when we see hyperacusis combined with tinnitus, it is often a red flag that both conditions will escalate.

The good news is that treatment is possible, and people are recovering from hyperacusis and tinnitus under my care every day.

Hyperacusis Treatment Options

Effective treatment for hyperacusis often involves a combination of therapies tailored to individual needs. When you read through these, remember that while these interventions help, if they do not address the migraine issue, they are likely to be insufficient.

Mainstream hyperacusis treatments include:

• Sound Therapy: Gradual exposure to low-level noise helps desensitize the auditory system. Studies have shown that consistent use of sound therapy can reduce sensitivity over time and improve tolerance to everyday sounds.

• Cognitive-Behavioral Therapy (CBT): CBT addresses the emotional and psychological aspects of hyperacusis, helping patients manage anxiety and stress related to sound sensitivity. It is effective in reducing the overall impact of hyperacusis on daily life.

• Hearing Aids and Sound Generators: These devices can provide white noise to mask hyperacusis triggers, offering relief and improving sound tolerance in some patients.

• Tinnitus Retraining Therapy (TRT): TRT combines sound therapy with counseling to retrain the brain's response to sound, which can be particularly beneficial for those with both hyperacusis and tinnitus.

• Mental Health Treatments: When any of the common co-morbid mental health conditions are present, addressing these independently and parallel to treatment can help with hyperacusis outcomes.

• Lifestyle Adjustments: Avoiding loud environments, using ear protection, and practicing relaxation and stress management techniques can help manage symptoms. Educating patients about sound levels and safe listening practices is also crucial.

The efficacy of these treatments varies, with many patients experiencing the best results when combination therapies are used. Individual results depend on the severity of the condition and adherence to the treatment plan.

The problem is that none of these mainstream treatments address the underlying migraine (brain sensitivity) issue. As you’ll see below, addressing this aspect is crucial for achieving the best results.

Hyperacusis Ear Plugs – Good or Bad?

The use of ear plugs in hyperacusis can be complex. While prolonged use of ear plugs may delay recovery by hindering the auditory system's adjustment, they can be beneficial in a staged desensitization process.

Staged desensitization involves gradually exposing individuals to sounds to build tolerance. In such cases, ear plugs that offer partial protection (reducing sound intensity without completely blocking it) are preferable. For instance, you can find ear plugs that progressively step down in the level of protection from 25 dB, to 20 dB, to 15 dB, and so on. This approach helps balance ear protection with necessary sound exposure, aiding recovery.

What is the best hyperacusis treatment?

Based on all the information above, it should be clear that any treatment that does not address the migraine aspect of hyperacusis is suboptimal.

How do I know this? Because we conducted a clinical study for hyperacusis using a migraine protocol at my university that showed excellent results [6]. In this study, patients with hyperacusis were treated with migraine prevention medications along with lifestyle and dietary changes.

• We found that 88% of people who received the protocol reported a significant improvement in their symptoms. Objective tests showed that tolerance to sound increased (measured by LDL). In addition, patients reported a significant decrease in their discomfort levels and a notable improvement in their overall condition on a standardized questionnaire.

The protocol we use at NeuroMed to treat severe tinnitus and hyperacusis are based on these studies. In fact, hyperacusis treatment at NeuroMed is often more effective because we incorporate sound therapy, cognitive-behavioral therapy (CBT), and increased provider support – which helps with motivation, self-efficacy, and empowerment.

Conclusion: Hyperacusis Treatment Is Possible!

Understanding the link between tinnitus and hyperacusis is essential because these conditions often exacerbate each other. When someone with tinnitus develops hyperacusis, their symptoms typically become more severe and challenging to manage. Hyperacusis can significantly impact daily life and well-being. It often leads to anxiety, avoidance behaviors, increased tinnitus severity, physical pain, fatigue, and concentration difficulties, thus profoundly affecting one's quality of life.

To effectively treat hyperacusis, it is crucial to address the underlying migraine component. Our clinical trial success (88% success rate) demonstrates that a treatment regimen targeting migraine prevention significantly improves symptoms. Combining this migraine protocol with sound therapy, CBT, and consistent support (like we do at NeuroMed) can yield even better results, emphasizing the importance of a comprehensive treatment strategy for these interconnected conditions.

Tinnitus and Hyperacusis References

[1]           C. R. Cederroth et al., “Association between Hyperacusis and Tinnitus,” J. Clin. Med., vol. 9, no. 8, p. 2412, Jul. 2020, doi: 10.3390/jcm9082412.

[2]           K. De Meulemeester, M. Meeus, R. De Pauw, B. Cagnie, H. Keppler, and D. Lenoir, “Suffering from chronic tinnitus, chronic neck pain, or both: Does it impact the presence of signs and symptoms of central sensitization?,” PloS One, vol. 18, no. 8, p. e0290116, 2023, doi: 10.1371/journal.pone.0290116.

[3]           S. Iyengar, K. W. Johnson, M. H. Ossipov, and S. K. Aurora, “CGRP and the Trigeminal System in Migraine,” Headache, vol. 59, no. 5, pp. 659–681, May 2019, doi: 10.1111/head.13529.

[4]           C. G. Le Prell, L. F. Hughes, D. F. Dolan, and S. C. Bledsoe, “Effects of Calcitonin-Gene-Related-Peptide on Auditory Nerve Activity,” Front. Cell Dev. Biol., vol. 9, p. 752963, Nov. 2021, doi: 10.3389/fcell.2021.752963.

[5]           M. D. Villar-Martinez and P. J. Goadsby, “Pathophysiology and Therapy of Associated Features of Migraine,” Cells, vol. 11, no. 17, p. 2767, Sep. 2022, doi: 10.3390/cells11172767.

[6]           M. Abouzari, …, H. Djalilian, “Efficacy of Multi-Modal Migraine Prophylaxis Therapy on Hyperacusis Patients,” Ann. Otol. Rhinol. Laryngol., vol. 129, no. 5, pp. 421–427, May 2020, doi: 10.1177/0003489419892997.