Auditory Dysfunction in Migraine Sufferers

Migraine operates as a systemic disorder of multisensory sensitization, directly impacting auditory health. A 2026 review in *Journal of Neurology* synthesizes evidence showing that 15% to 49% of migraine patients experience comorbid auditory symptoms like tinnitus and hyperacusis, with nearly two-thirds showing electrophysiological abnormalities in their auditory systems. The review, authored by Wandi Xu, Ni Zhai, Jingyu Chen, and colleagues, moves beyond simple comorbidity to propose a unified pathological model connecting migraine to hearing dysfunction.

## A Shared Pathology: Three Interacting Axes

The researchers propose that migraine-related auditory dysfunction stems not from coincidence but from a shared “peripheral-to-central continuum.” This involves three distinct yet connected pathological axes.

First, anatomical and hydrodynamic vulnerabilities can drive localized microvascular ischemia and abnormal fluid exchange between the brain and inner ear. This creates a fragile environment for delicate cochlear structures. Second, localized neurochemical imbalances disrupt inner ear homeostasis. The review highlights glutamate excitotoxicity, abnormal neuropeptide signaling (like calcitonin gene-related peptide, or CGRP), and innate immune activation as key players. Third, and perhaps most significant for conditions like hyperacusis and tinnitus, is central sensitization. This process facilitates neural network plasticity, leading to impaired efferent gating (the brain’s ability to filter sound) and thalamocortical dysrhythmia, where brain rhythms become disordered.

This model explains why auditory symptoms are not merely a side effect but a core phenotype of the migraine disease process. It connects the dots from vascular events in the ear to maladaptive plasticity in the brain’s auditory cortex.

## From Mechanism to Management: A New Therapeutic Framework

The conventional approach of treating the migraine headache and the auditory symptom as separate issues is insufficient. The review by Xu et al. categorizes therapeutic strategies by their specific clinical objectives, based on the underlying pathways.

The first objective is **blocking upstream migraine pathways**. This includes established and emerging medications like CGRP monoclonal antibodies or gepants, which may prevent the neurochemical cascade that ultimately affects the auditory system. The second is **protecting the cochlear microenvironment**. Strategies here could involve antioxidants or agents that combat glutamate excitotoxicity to shield hair cells and neurons from damage during migraine attacks. The third objective is **correcting central hypersensitivity**. This aligns with neuromodulation approaches, such as sound therapy or cognitive behavioral therapy, designed to retrain hyperactive auditory neural networks.

This framework encourages clinicians to ask *which* pathological axis is most dominant in a given patient, allowing for more precise intervention. For instance, a patient with severe hyperacusis may benefit most from therapies targeting central sensitization, while one with fluctuating hearing loss might need a focus on cochlear protection.

## Practical Implications for Patients and Clinicians

The epidemiological finding that up to half of migraine patients have auditory symptoms is a call for routine audiological screening in this population. Patients experiencing tinnitus, sound sensitivity, or unexplained hearing fluctuations should be asked about migraine history. Conversely, neurologists and headache specialists should include basic questions about auditory health in their patient assessments.

This integrated view supports cross-disciplinary management. Effective care likely requires collaboration between neurologists, otolaryngologists, and audiologists. A patient’s treatment plan might combine a neurologist’s prescription for a CGRP inhibitor to prevent attacks, an audiologist’s guidance on sound-based management strategies, and therapeutic support for the distress caused by chronic symptoms.

For patients, this research validates their often-dismissed experiences. It provides a scientific explanation for why their hearing problems are linked to their migraines, moving them from anecdote to acknowledged phenotype. Understanding the mechanism—that it’s a systemic sensory sensitization disorder—can itself be therapeutic.

The review, “Migraine and auditory dysfunction: beyond comorbidity” (PMID: 42371148), concludes that future research must work to validate these mechanistic links. The goal is to promote early identification, precise clinical phenotyping, and treatments that address the root causes shared by migraine and auditory dysfunction. This work reinforces the concept of integrated auditory health, where disorders of the ear and brain are understood as interconnected. For a deeper look at the migraine-auditory link, our article on Migraine’s Link to Tinnitus and Hyperacusis explores this connection further.