Migraine and Hearing Disorders: Auditory Link

A systemic disorder of multisensory sensitization, migraine is now recognized as a major driver of auditory problems including hearing loss, tinnitus, and hyperacusis. A new review in the *Journal of Neurology* synthesizes the evidence, revealing that 15% to 49% of migraine patients experience comorbid auditory symptoms, with nearly two-thirds showing measurable abnormalities on auditory electrophysiological tests. The work by Xu, Zhai, Chen, and colleagues moves beyond simply noting this high comorbidity to propose a unified, three-axis pathophysiological model that explains how migraine can damage hearing health from the inner ear to the brain. This framework offers a new lens for clinicians to assess and treat patients whose hearing issues may be fundamentally linked to migraine pathology.

A High Prevalence of Overlooked Auditory Symptoms

The epidemiological data compiled by the research team is striking. Their analysis indicates that auditory dysfunction is not a rare complication of migraine but a common feature. The wide range of 15% to 49% reflects variability in study methods and patient populations, but the central finding is clear: auditory problems are a significant part of the migraine phenotype for many. Perhaps more compelling is the objective data showing that approximately 65% of migraine patients exhibit abnormalities on tests like auditory brainstem responses (ABRs) or otoacoustic emissions (OAEs), even in the absence of overt symptoms. This suggests the underlying pathology is active and measurable. For patients, this means symptoms like a persistent ringing (tinnitus) or an extreme sensitivity to everyday sounds (hyperacusis) should be actively discussed with healthcare providers if migraine is also present.

The Three-Axis Pathophysiological Model

The review’s primary contribution is its structured model explaining how migraine, typically considered a brain disorder, directly impairs auditory function. The authors describe a “peripheral-to-central continuum” across three interacting axes.

The first axis involves anatomical and hydrodynamic vulnerabilities. The delicate blood supply and fluid systems of the inner ear are susceptible to the microvascular changes and ischemia that occur during migraine. This can directly injure hair cells and neurons, potentially leading to sensorineural hearing loss.

The second axis centers on localized neurochemical imbalances in the cochlea and auditory nerve. Migraine-associated processes like glutamate excitotoxicity, the release of neuropeptides such as CGRP, and innate immune activation can create a toxic microenvironment for auditory structures, disrupting homeostasis.

The third and perhaps most far-reaching axis is central sensitization. Migraine primes the central nervous system to be hyper-responsive. In the auditory system, this manifests as impaired efferent inhibition (the brain’s ability to “turn down” irrelevant sound signals) and thalamocortical dysrhythmia—a disorganized pattern of brainwave activity linked to the perception of phantom sounds like tinnitus. This central component helps explain conditions like hyperacusis and misophonia, where the brain’s interpretation of sound is distorted. This mechanism shares features with other conditions of neural sensitization, such as the shared biology seen in PTSD and tinnitus.

From Mechanisms to Targeted Treatment Strategies

By defining these specific pathways, Xu and colleagues move the field toward rational, targeted therapies. They categorize emerging strategies by their clinical objective.

Blocking upstream migraine pathways is the most direct approach. If auditory dysfunction is a symptom of the migraine process itself, then effective migraine prophylaxis with CGRP monoclonal antibodies, beta-blockers, or neuromodulation should also benefit auditory symptoms. This treats the root cause.

Protecting the cochlear microenvironment involves interventions aimed at the inner ear. This could include antioxidants to combat oxidative stress, anti-excitotoxic agents, or drugs that stabilize inner ear fluid balance. Research into otoactive compounds is highly relevant to this therapeutic goal.

Correcting central hypersensitivity targets the maladaptive plasticity in the brain. Strategies here include sound therapy, cognitive behavioral therapy, and neuromodulation techniques like transcranial magnetic stimulation or vagus nerve stimulation to recalibrate neural networks. The success of such brain-directed therapies may depend on individual factors, much as baseline depression can predict long-term outcomes in CBT for insomnia.

Practical Implications for Patient Care

The review makes a strong case for integrated, cross-disciplinary care. For neurologists and headache specialists, it underscores the need to routinely ask migraine patients about hearing changes, tinnitus, or sound sensitivity. For audiologists and otolaryngologists, a patient presenting with idiopathic sensorineural hearing loss or sudden-onset hyperacusis should be screened for a history of migraine. Standardized audiological assessment protocols for migraine patients are needed.

This model also provides patients with a coherent explanation for symptoms that may seem unrelated. Understanding that their tinnitus and migraine may stem from the same underlying neural hypersensitivity can be validating and direct them toward more comprehensive treatment. It argues against treating auditory and neurological symptoms in isolation and promotes a holistic management plan that addresses the systemic nature of the disorder, aligning with broader trends in integrated auditory health.

The full review, “Migraine and auditory dysfunction: beyond comorbidity,” by Wandi Xu, Ni Zhai, Jingyu Chen et al., is available in the Journal of Neurology (doi: 10.1007/s00415-026-13957-0; PMID: 42371148).