Tinnitus and Hyperacusis Treatment: New Science, Real Recovery

Tinnitus and hyperacusis often occur together, creating a vicious cycle where each condition amplifies the other. This can lead to worsening symptoms, increased sound sensitivity, and a greater impact on daily life. However, both share a common underlying mechanism, meaning effective treatment is possible.

Quick spoiler: The real breakthrough in hyperacusis treatment about targeting the brain mechanisms that amplify sensitivity. If you read nothing else, make sure to check out the section on the best hyperacusis treatment.

Here I cover the following topics regarding tinnitus and hyperacusis:

• What Is Hyperacusis and Why Does It Happen?
• How are tinnitus and hyperacusis related?
• What causes hyperacusis?
• Hyperacusis Treatment Options
• What is the best hyperacusis treatment?

What Is Hyperacusis and Why Does It Happen?

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. In fact, when sound intolerance becomes severe, it can profoundly affect one’s quality of life and daily functioning.

Hyperacusis Pronunciation

Here is how to pronounce hyperacusis: Hy-per-ah-KOO-sis. Hyper- means “excessive” or “heightened,” while -acusis relates to “hearing” or “sound perception.” Together, hyperacusis refers to an abnormal sensitivity to everyday sounds, often causing discomfort or pain at normal volume levels.

What Are the Main Symptoms of Hyperacusis?

• Stress / Anxiety: People with auditory hypersensitivity often experience significant stress and anxiety, which goes beyond the fear of loud noises. It extends to a general fear of being in situations where they might encounter sounds that can trigger discomfort or pain. This can lead increased psychological stress in everyday environments, even when it's quiet or safe.

• Avoidance Behaviors: People with disabling sound sensitivity often develop avoidance behaviors. This includes avoiding social interactions, public spaces, and even home environments where unpredictable noises might occur. This avoidance leads to social isolation and its consequences.

• Increased Tinnitus Severity: When tinnitus and hyperacusis occur together, the symptoms of both can quickly escalate. Hyperacusis amplifies the perception of tinnitus, making the sounds more intrusive and harder to ignore.

• Decreased Quality of Life: The combined effects of anxiety, avoidance behavior, and worsening tinnitus contribute to a significant decrease in quality of life. People then find that they can't 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 cases, hyperacusis is associated with actual physical pain, a subtype called pain hyperacusis or noxacusis. This can lead to an acceleration of avoidance behaviors and in severe cases, leave affected people in a home-bound state.

• Fatigue: The constant tension and stress of anticipating sound exposure can lead to chronic fatigue. This is not only due to emotional stress but also from the hypervigilance that is caused by an increased sympathetic (fight-or-flight) drive.

• 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.

Hyperacusis symptoms are sometimes sorted by referring to general subtypes. In reality, these features often overlap, but they do help to roughly categorize the various hyperacusis symptoms people experience.

• Fear Hyperacusis: Refers to the 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: Refers to the when sounds are not just loud, but annoying or distressing, provoking emotional reactions, such as to anger or frustration. This is similar to the condition known as misophonia.

• Pain Hyperacusis (noxacusis): Refers to when 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: Refers to when moderately intense sounds feel excessively loud. This can render normal environments unbearably noisy and significantly impair quality of life.

What Other Conditions Are Linked to Hyperacusis and Tinnitus?

For clarity, there are several related and often overlapping conditions that concern tinnitus and hyperacusis that should be defined here:

• 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.

Is hyperacusis a disability?

Hyperacusis can be profoundly disabling, limiting daily activities, work, and social interactions. A recent 2025 study found that Hyperacusis Questionnaire scores were strong predictors of reduced work capacity, with nearly 65% of participants reporting that tinnitus and hyperacusis significantly impacted their ability to work.

At NeuroMed, we frequently complete disability paperwork for individuals with severe hyperacusis. Claims require comprehensive medical documentation of functional impairment, psychological impact, and daily limitations. While not always explicitly recognized, proper advocacy can help secure accommodations.

What Is Vestibular Hyperacusis and How Is It Treated?

“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 a normal hearing exam. Importantly, audiograms do not always pick up damage, such as with ‘hidden hearing loss' (also called cochlear synaptopathy).

Importantly, experiencing hyperacusis does not mean you are losing hearing. The misconception people suffering from this condition 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.

What’s the Relationship Between Tinnitus and Hyperacusis?

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 severity 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 info@neuromedcare.com.

What causes hyperacusis?

Much like with tinnitus, there are multiple pathways that can initiate hyperacusis. There is no single cause—rather, different factors can converge to trigger the same condition.

• Noise-Induced Hearing Damage – Prolonged or sudden exposure to loud sounds can damage the auditory system. This is one of the most common proximal cause of hyperacusis.
• Tonic Tensor Tympani Syndrome – This is a cluster of symptoms that occur after an acoustic shock and can include a fluttering in ear sensation, ear fullness or pain, hyperacusis, tinnitus, and a host of other symptoms.
• Medications – Certain drugs (e.g., some antibiotics, chemotherapy agents) can damage the auditory system. Some anti-depressants have been known to be the initiating factor
• Neurological Conditions – Conditions like multiple sclerosis, Bell’s palsy, or auditory processing disorders may be involved.
• Autism Spectrum Disorder (ASD) – Heightened sound sensitivity is common in individuals with ASD.
• Stress & Anxiety Disorders – Chronic stress can dysregulate the nervous system, leading to heightened sound sensitivity.
• Facial or Ear Nerve Damage – Injury to the facial nerve or auditory nerve can alter how the brain processes sound.
• Autoimmune Disorders – Conditions affecting the nervous system may contribute to hyperacusis.
• Post-Viral Syndromes – Viral infections (e.g., COVID-19, Epstein-Barr virus) have been linked to hyperacusis in some cases.
• Ear Surgeries or Procedures – Cochlear implants, ear infections, or surgeries can sometimes result in auditory hypersensitivity.

However in all of these cases, the initiation event does not explain the mechanistic cause of hyperacusis. For this, there are three related theories, including the central gain model, the chronic pain model, and the migraine hypothesis.

How the Central Gain Model Explains Hyperacusis

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 behavioral changes 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 hyperacusis and tinnitus. The underlying causes of increased sound sensitivity are much broader than just the gain in the hearing center.

Can Chronic Pain Help To Explain Hyperacusis?

An compelling alternative explanation for hyperacusis is using chronic pain as a model. This approach is based “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.

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 chronic pain, tinnitus and hyperacusis:

• 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 tinnitus and hyperacusis 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. This correlates with the fact that many of the inciting factors of hyperacusis are inflammatory in nature.

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.  

Is Hyperacusis a Form of Atypical Migraine?

Both tinnitus and hyperacusis are migraine-related sound disorders that manifest as sensory over-responsivity. We believe that an atypical migraine reaction in the brain drives auditory hypersensitivity. 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.

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 or 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 inflammatory, migraine-like 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.

Should You Use Ear Plugs for Hyperacusis?

The use of ear plugs or ear muffs in hyperacusis is a complex issue. To begin with, for people with severe, untreated hyperacusis, ear protection is a necessary survival strategy. Often times, ear protection in severe hyperacusis is a necessary starting point for therapy.

Furthermore, the initiation of sound therapy too early can cause significant setbacks. Without treating the underlying reactivity in the brain from the atypical migraine process, using sound can actually trigger a worsening as sound itself can be a migraine trigger. We often do not start any sound desensitization protocols until we first treat the brain medically.

However, we also know that the prolonged use of ear plugs can delay recovery by hindering the auditory system's adjustment. This is similar to photophobia (light sensitivity), where the use of dark glasses actually prolongs the duration of symptoms. We also see it with vertigo, where challenging the body to feel unsteady is an integral part of the path to recovery. The brain needs to re-learn normal.

Hyperacusis ear plugs can also be beneficial in a staged desensitization process, after we begin treatment for brain reactivity. Staged desensitization involves gradually exposing individuals to sounds to build tolerance.

For instance, there are some hyperacusis ear plugs that offer partial protection (reducing sound intensity without completely blocking it). We can used these to progressively step down the level of protection from 25 dB, to 20 dB, to 15 dB, and so on. This approach helps balance ear protection with the sound exposure necessary for recovery.

What is the best hyperacusis treatment?

At NeuroMed, we provide one of the most effective, evidence-based hyperacusis treatment protocols available today. This is because we recognize both tinnitus and hyperacusis as neurological sound disorders that require a medical approach to treatment, not just sound therapy.

Our approach is built on cutting-edge research, including a clinical study I conducted at my university, which demonstrated significant improvements in hyperacusis symptoms. By addressing the neurological and inflammatory drivers of sound sensitivity, we achieve better results than traditional treatments.

Why Hyperacusis Treatment Must Address Atypical Migraine

As the evidence shows, any treatment that ignores the migraine component of hyperacusis is incomplete. In our clinical study, patients were treated with migraine-prevention medications, lifestyle modifications, and dietary changes.

The Results Were Striking:

✔ 88% of patients reported that their hyperacusis symptoms significantly improved or completely resolved after treatment.
✔ Sound tolerance increased, meaning patients could handle louder sounds more comfortably.
✔ Discomfort levels dropped by more than half, a huge reduction in sound sensitivity and distress.
✔ Overall symptoms improved, with patients reporting feeling much less bothered by everyday sounds.

At NeuroMed, our hyperacusis treatment protocols are designed for your success, incorporating enhanced provider support and giving you the motivation, self-efficacy, and resilience needed for long-term success.

Final Thoughts: Is Hyperacusis Treatable?

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 leads to anxiety, avoidance behaviors, increased tinnitus severity, physical pain, fatigue, and concentration difficulties, thus profoundly affecting one's quality of life. The good news is that hyperacusis treatment is possible!

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.

Living with tinnitus or hyperacusis can be overwhelming, but you don’t have to navigate it alone. At NeuroMed, we offer comprehensive, science-backed treatments to help you manage symptoms, reduce sensitivity, and reclaim your quality of life.

Schedule a consultation today to explore personalized solutions and start your journey toward relief.

Hyperacusis and Tinnitus: FAQs

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.